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CARDIOVASCULAR DISORDERS (CVD).pptx

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The document provides an overview of a course on cardiovascular diseases (CVD). The 16-hour course will cover the etiology, pathophysiology, manifestations, risk factors, and management of various CVDs. It will also address diagnostic tests, medications, treatments, and rehabilitation services for CVD patients. The main objective is for students to acquire knowledge and skills to promote health, prevent illness, diagnose, manage and coordinate rehabilitation of CVD patients. Specific topics to be covered include anatomy and physiology of the heart and vessels, assessment of the cardiovascular system, and common CVDs and their management.

Health & Medicine
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CARDIOVACULAR PROBLEMS BY MR ONSONGO DAVID
Course Outline For CVD Introduction • The cardiovascular diseases (CVD) conditions course will be covered within 16 hours. By the end of the course you will be able to compare and contrast the etiology, pathophysiology and manifestations of various cardiovascular conditions/diseases, explain risk factors and preventive measures, describe interdisciplinary and nursing care of CVS problems, relate the outcomes of diagnostic tests and procedures to pathophysiologies, discuss the effects and nursing implications for medications and treatments used, and describe rehabilitation services.
Main Objective • The student will be able to acquire knowledge, attitude, and skills to be able to promote health, prevent illness, diagnose, manage and coordinate rehabilitation of patients suffering from cardiovascular conditions/diseases. Specific Objectives • Review anatomy and physiology of the heart and blood vessels • Describe the assessment of cardiovascular system • Describe common cardiovascular diseases and conditions and their specific management
CONTENT • Review of anatomy and physiology of the heart and vessels • Assessment of cardiovascular system • Congestive cardiac failure • Rheumatic heart disease • Valvular heart disease • Coronary heart disease • Arteriosclerosis • Gangrene • Varicose vein • Thrombophlebitis (superficial and deep venous thrombosis) • Arterial Thrombosis • Arterial Embolism • Hypertension (essential/malignant)
Mode of teaching • Lectures/discussions • Assignments • Group discussions Teaching/learning materials • Handouts • LCD/PowerPoint slides • Flipcharts • Blackboard • White board • Overhead projector/transparencies • Textbooks
Mode of assessment for the course • Completion of assignment 10% • Quizzes 10% • Mid-Semister test 20% • End-block examination 60%
REFERENCE MATERIALS • Aghababian, R. et al (2006). Essentials of Emergency Medicine. Jones and Bartlett Publishers, London • Bilotta, K. et al (Eds) (2009). Nurse’s Quick Check Diseases. Wolters Kluwer, New York. • LeMone et al (2011). Medical-Surgical Nursing. Pearson Publishers, London. • Lewis et al (2011). Medical Surgical Nursing. Elsevier Publishers, London. • Smeltzer S et al (2014). Brunner and Suddarth’s Medical – Surgical Nursing. Lipppincot Company, Philadelphia. Facilitator: David Onsongo
NORMAL PHYSIOLOGY OF CIRCULATORY SYSTEM By David Onsongo
Aim: By the end of the study the students will be able to understand the concepts of how the heart functions
Anatomy and physiology of CVS Cardiovascular system(CVS) consists of: • Heart - muscular blood pump organ • Arteries– Carry blood away from the heart • Veins- Return venous blood to the heart • Capillaries- smallest blood vessels involved in actual exchange of materials between tissue cells and blood NB. Review more about the major blood vessels
Heart: • Hollow muscular organ • Occupies mediastinum space • Weighs about 300 g (about size of owner’s fist) • Pumps blood to supply oxygen and nutrients to all tissues Heart layers: • Inner layer (endocardium) • Middle layer (myocardium) • Outer layer (pericardium)  visceral pericardium  peripheral pericardium  pericardial space: contains 30 ml lubrication fluid
Heart chambers: • Right atrium –Receives venous (deoxygenated) blood • Left atrium – receives oxygenated blood from the lungs • Right ventricle – Sends deoxygenated blood to the lungs • Left ventricle – Distributes oxygenated blood to body tissues Cardiac wall thickness: • Atrial walls are thinner than ventricle walls • Left ventricle wall is two and half times thicker than right ventricle • Left ventricle has higher pressure than right ventricle and atria
Position: • Heart lies in rotated position in thoracic space • Right ventricle lies anteriorly just below the sternum • Left ventricle is located posteriorly • Apical beat obtained from left ventricle at left midclavicular line in the 5th intercostal space Valves: • Tricuspid valve- between R. atrium and R. ventricle • Bicuspid valve- between L. atrium and L. ventricle • Pulmonic valve- between R. ventricle and pulmonary artery • Aortic valve- between L. ventricle and Aorta
Heart Sounds: • Mitral and tricuspid valve closure produces first heart sound (S1) • Aortic and pulmonic valves closure produces second sound (S2) Abnormal Heart Sounds: • Gallop sounds – occurs during ventricular filling when there is impediment  gallop sounds comes in triplets with acoustic effect of a galloping horse (sound produced by a rapid moving horse)
Two kinds of gallop are S3 and S4  S3 results from rapid ventricular filling phase, may be normal in children and young adults. S3 is associated with:  myocardial diseases  inability of ventricles to eject all blood during contraction  S3 can be heard best when patient is lying on the left and sounds like, ‘Lub-dub-DUB’  S4, which sounds “LUB lub-dub” occurs during atrial contraction in:  enlarged ventricles which resist filling associated with hypertrophy common in hypertension, CHD, and aortic stenosis
Cont. of abnormal sounds • Snaps and Clicks:  Results from mitral stenosis (narrowing)  Characterised by high pitched sound heard very early in diastole  They are caused by high pressure in left atrium when it abruptly displaces a rigid mitral valve  It commonly causes murmurs specific to mitral stenosis
• Murmurs: caused by turbulent flow of blood due to  Serious narrowed valve  Malfunction valve that allows backflow of blood  congenital defect of ventricular wall  Defect between aorta and pulmonary artery  Increased blood flow thru normal structure in conditions with pyrexia, pregnancy, increased thyroid activity
Cont. of abnormal sounds •Friction rub:  Pericarditis causes a harsh, grating sound heard in both systole and diastole termed as friction rub  Pericardial rub is best heard when using diaphragm of stethoscope while patient is in upright position
Cardiac conducting system: • Organized atrial and ventricular contraction to ensure coordinated and controlled filling and empting • Cardiac cells contract and relax due to stimulation • Two major cardiac cells are: Unspecialized myocardial cells for contraction
Automatic cells specialized for impulse formation • Main bulk of atrial and ventricular muscles are unspecialized myocardial cells • Adjacent myocardial cells are held together by complex system of projections – intercalated discs – with relatively low electrical resistance
Cardiac conducting system cont. • Easy movement of electrically charged ions from one myocardial to others to propagate action potentials • Main ions are Na+, K+ and Ca++ • Myocardial cells are polarised in normal resting state • Stimulation of myocardial cells changes cell membrane permeability allowing ions movement, thereby changing electrical polarity (depolarisation)
• Depolarised myocardial cells have positive intracellular ions and negative extracellular ions • After depolarisation, repolarisation – returning to resting state – involves active pumping of ions against concentration gradient • Automatic cells regulate myocardial cells contraction by providing initial electrical stimulation
Cont of cardiac conducting syst. • Automatic cells consists of 3 properties:  Automaticity – ability to generate action potential, spontaneous and regularly  Excitability – ability to respond to electrical stimulation by stimulating action potential  Conductivity – ability to propagate action potential  Refractoriness – inability to respond to new stimuli while in contraction (depolarised) state
• Electrical charge on surface of automatic cell leaks away until certain threshold is reached • Then , spontaneous complete depolarisation occurs over the whole cell surface and spreads to adjacent cells (to both automatic and unspecialized cells) • Automatic cell with most rapid leak of charge becomes the pacemaker (normally located within SA node) • Automatic cell in cardiac conducting system are: SA node (Sinus node), AV node, Bundle of His, left and right bundle branches
Sequence of excitation: • Depolarisation begins at SA node and spreads through both atria • Activating impulse travel 1 m/s and reaches most distant atria in about 0.08 seconds (P wave in ECG) • Atria and ventricles remain electrically separate except via AV junction, which allows potential action be conducted from atrial to ventricular conducting system
• When impulse reaches AV node, there is a delay of about 0.04s to allow blood flow from atria to ventricles • After emerging from AV node, impulse reaches the rapidly conducting tissue of bundle of His and left and right bundle branches • Impulse spreads rapidly throughout ventricles via purkije fibres, thereby depolarising the ventricles causing efficient ventricular contraction to pump blood out of the heart
Electrocardiography (ECG): • Graphic recording from body surface of potential differences resulting from current generated in the heart • ECG is recorded on special graphic paper or on oscilloscope (monitor) and it is recorded against time • ECG detects and interprets Cardiac arrhythmias, diagnosis of CHD, ventrical enlargement or hypertrophy
• Electrical sequential events produced at each heart beat is labeled PQRS and T • P wave results from atrial activation (depolarisation), P width represent the time necessary for atrial activation process (0.08s) • Approximately 0.1 s after P wave begins, the atria contracts • PR interval is measured from starting of P wave to beginning of QRS complex that reflects time taken for action potential to spread from SA node, AV node, bundle of His into ventricular mass
Cont of ECG • QSR waves reflect ventricular activation. Q is downward deflection after P wave. R wave is the first upward deflection. Then, downward deflection after R is S wave. • P-R interval, represents time impulse takes to spread from atria to ventricles (takes 0.12-0.20 s, average 0.16 s) • QRS complex shows length of time action potential takes through the ventricles (ventricular depolarization time, 0.08 s)
• ST segment is a flat line between S wave and T wave, representing the early phase of ventricular muscle repolarisation (recovery) • Q-T interval represents electrical systole (varies in age, sex and heart rate)- takes up to 0.38-o.43s, normally inversely related to HR • T wave represents the actual recovery of the ventricle muscle (repolarisation)- takes about 0.16 seconds
Excitation – contraction coupling: • Excitation-contraction coupling describes the link between electrical events and myocardial muscle contraction • When action potential passes over cardiac cell membrane it passes into the interior of each muscle cell down a series of fine branching tubules until it reaches the cells contractile elements to stimulate release of Ca++ ions • Ca++ ions act as catalysts for chemical reaction to activate the sliding of thin muscle filaments (myofilaments) over each other to produce contraction • Myocardial contraction strength partly depends on intracellular concentration of free Ca++
Cardiac cycle: • Cardiac cycle – cyclical contraction (systole) and relaxation (diastole) of atria and ventricles • Initiation of each cycle is by spontaneous generation of action potential in SA node • Each chamber fills with blood during diastole • Diastole lasts 0.4 s during which blood enters atria and flows passively into ventricles
• Mitral and tricuspid valves open and aortic and pulmonic valves close during ventricular diastole • Blood is expelled from ventricles during systole • Atria contract fractionally before the ventricles and complete ventricular filling • Then ventricles begin to contract (systole), increasing pressure closes mitral and tricuspid valves and opens semilunar valves
Cont. of cardiac cycle • Ventricular contraction pushes blood into pulmonary artery and aorta • During diastole pressure within ventricles falls bellow the pressure in major arteries, thus pulmonic and aortic valves close. Then the cycle begins again. • Normal HR for a resting adult is approximately 60- 80 bpm • 65-75% of blood is ejected from the ventricles in each systole • SV is about 70-80 ml at rest • CO is the product of SV x HR • More informatively, CO can be measured using cardiac index, in which CO/min/m2 of BSA is about 3.2 L/m2
Primary factors determining CO: • Preload – the amount of tension on the ventricular muscle fibres before they contract, determined primarily by EDV • Afterload – the resistance against which the heart must pump, and its major components are:  Blood pressure in aorta  Resistance in the peripheral vessels  The size of aortic valve opening  Left ventricular size • Contractility of the heart • Heart rate  According to Frank-Starling law of the heart, cardiac out put matches venous return i.e. the heart adapts the changing loads of inflowing blood from systemic and pulmonary circulations
Continuation  Within certain limits, the more cardiac muscle contracts forcibly, the more they get stretched at the beginning of contraction  Once venous return increases beyond certain limit, the myocardium begin to fail  Regulation of the heart in response to the amount of blood to be pumped is termed as intrinsic regulation ANS regulation of cardiac function: • ANS alters rate of impulse generated by SA node, the speed of impulse conduction and the strength of cardiac contraction • Stimulation of sympathetic nervous system (fibres) increase HR, conduction speed through AV node and force of contraction
Ct of regulation cardiac function • Parasympathetic stimulation via vagus nerve decreases HR, conduction rate through AV node, and atrial conduction force • ANS control of the heart occurs by reflexes coordinated in medulla oblongata • Cardiac centre is the group of brain neurons controlling heart activity and blood vessels • Cardiac centre receives information from various sensory receptors e.g.  Baroreceptors – located in atria, aortic arch and carotid sinus- generate impulse in response to changes in blood pressure  Chemoreceptors – located in carotid artery respond to changes in the chemical composition of the blood
Blood supply: • Heart receives 5% of cardiac output to maintain cellular activity • Blood supply is through right and left coronary arteries • Branches of left coronary artery: left anterior interventri- cular (descending) artery (LAD) and circumflex artery (CX) • Right coronary branches: posterior interventricular artery (PIA) and marginal artery (MA) • LAD innervates interventricular septum and anterior walls of both ventricles. CX supplies lateral and posterior L. atrium and L. ventricle. • PIA innervates posterior ventricular walls. MA serves right ventricle • Normally, right coronary artery supplies blood to SA and AV nodes
Arterial blood pressure (ABP): • ABP is measurement of pressure exerted by blood as it flows through the arterial walls – systolic and diastolic pressure • Arterial blood pressure is the product of cardiac output times peripheral resistance (CO x PR) Determinants of blood pressure include:  the pumping action of the heart  the peripheral vascular resistance  blood volume  blood viscosity • Normal determinants of pressure are:  Autonomic nervous system  Renin-angiotensin-aldosterone system
Factors affecting BP values: • Age (increases with advancing age- arteriosclerosis) • Exercise (increases) • Emotional reaction (stress) • Race (common in the blacks) • Gender (common in males) • Medications (e.g. vasoconstrictors, Glucocorticoids) • Obesity • Diurnal variation (lowest in AM and highest in PM) • Position • Disease process (Renal diseases) • Sleep • Digestion
Assessment of cardiovascular system The CVS assessment comprises of  Health history  Physical exam  Diagnostic evaluation
Health history Common symptoms • Chest pain or discomfort (angina pectolaris, dysrrhythmia, valvular heart disease) • Shortness of breath or dyspnoea • Peripheral oedema, weight gain, abdominal distension due to enlarged spleen and liver or ascites • Palpitations (tachycardia from variety of causes) • Unusual fatigue, sometimes referred to as vital exhaustion • Dizziness, syncope or changes in level of consciousness (cardiogenic shock, cerebrovascular diseases, dysrrhythmia, hypotension, postural hypotension, vasovagal episode)
Health history Past health, family and social history • Any health changes within 5 years • Any cardiovascular problems • Any treatment of CVD • medications • Nutrition
Health history • elimination • activity and exercise • sleep and rest • self-perception and self-concept • roles and relationships • sexuality and reproduction • coping and stress tolerance
Physical exam Physical Assessment • general appearance • assessment of skin and extremities • blood pressure • pulse pressure • postural blood pressure changes • arterial pulses • pulse rate • pulse rhythm
Physical exam • pulse amplitude • pulse contour • palpation of arterial pulses • jugular venous pulsation • heart inspection and palpation • heart auscultation • normal heart sounds S1 and S2 • abnormal heart sounds S3 and S4 • Assessment of other systems • lungs
Physical exam • cough • hemoptysis • crackles • wheezes • abdomen • abdominal distension • hepatojugular reflux • bladder distension • gerontologic considerations
Diagnostic evaluation Diagnostic evaluation include: • Laboratory tests • Cardiac biomarker analysis • Creatinase secreted by necrotic cardiac muscles is part of diagnostic evaluation of CAD and proteins myoglobin, troponin T, and troponin I.
Diagnostic evaluation • Blood chemistry, hematology and coagulation studies • Lipid profile • Cholesterol levels normal is less than 200mg/dL • Triglycerides normal between 100-200mg/dL • LDLs normal levels less than 160mg/dL • HDLs normal levels in men is between 35-70 mg/dL and women 35-85mg/dL
Diagnostic evaluation • Brain (B-Type) natriuretic peptide – neurohormone that regulates BP and fluid volume • C-Reactive protein: protein from the liver in response to inflammation that plays a role in atherosclerosis • Homocysteine: an amino acid linked to development of atherosclerosis because it damages endothelial lining of arteries and promotes thrombus formation
Diagnostic evaluation • Chest X-Ray and Fluoroscopy • Determines size, contour and position of heart • Electrocardiography • Continuous electrocardiographic Monitoring • Hard wire cardiac monitoring • Telemetry • Ambulatory electrocardiography • Transtelephonic monitoring • Wireless mobile cardiac monitoring
Diagnostic evaluation • Cardiac stress testing • Exercise stress testing • Pharmacologic stress monitoring • Done in patients not able to perform exercise stress testing • Iv vasodilating drugs to mimic exercise effects by maximally dilating coronary arteries are given e.g. dipyridamole and adenosine
Diagnostic evaluation • Echocardiography • Transthoracic echocardiography • Transesophageal echocardiography • Radionuclide imaging • Myocardial perfusion imaging • Test of ventricular function and wall motion • Computed tomography • Positron emission tomography • Magnetic resonance angiography
Diagnostic evaluation • Cardiac catheterization • Right heart catheterization • Left heart catheterization • Electrophysiologic testing • Hemodynamic monitoring • Central venous pressure monitoring • Pulmonary artery pressure monitoring • Intra-arterial blood pressure monitoring • Minimally invasive cardiac output monitoring devices
CARDIOVACULAR PROBLEMS BY MR ONSONGO DAVID
Hypertension Introduction  Intermittent or sustained elevation of diastolic equal/above 90 mmHg or systolic blood pressure equal/above 140 mmHg on three separate readings recorded weeks apart  Associated with: premature death, vascular disease of the brain, heart and kidneys  Usually begins as benign disease, slowly progressing to accelerated or Malignant state  Two major types: Essential (primary or idiopathic) hypertension and secondary hypertension, which result from renal disease or another identifiable cause  Malignant hypertension, a medical emergency: a
Pathophysiology • There several theories about pathophysiology of hypertension Changes in arteriolar bed cause increased peripheral vascular resistance Abnormally increased tone in the sympathetic nervous system originating in the vasomotor system centres causes increased peripheral vascular resistance
pathophysiology Increase in arteriolar thickening caused by genetic factors leads to increased peripheral resistance Increased activity of renin-angiotensin- aldosterone system, resulting in expansion of extracellular fluid volume and increased vascular resistance due to constriction of arterioles by the effects of angiotensin II.
• Resistance to insulin action, which may be a common factor linking hypertension, type two diabetes, hypertriglyridemia, obesity, and glucose intolerance • Adaptation of the innate and adaptive components of the immune response that may contribute to renal inflammation and dysfunction
• Increased renal reabsorption of sodium, chloride, and water related to a genetic variation in the pathways by which the kidneys handle sodium
causes • Causes for primary hypertension are unknown in most cases, but with various predisposing factors • 5% - 10% (secondary hypertension): due to underlying conditions to include:  Kidney disease e.g renal failure  Coarctation (narrowing) of the aorta, causing hypertension  Endocrine disorders e.g. Cushings Syndrome, pheochromocytoma (tumour in adrenal gland that releases catecholamines; causes 2% of all hypertensions)  Neurologic disorders e.g. increased intracranial pressure  Certain medications, or illicit drugs  Pregnancy
Factors implicated as causes of HPN Many factors have been implicated as causes of hypertension: • Increased sympathetic nervous system activity related to dysfunction of the autonomic nervous system • Increased renal reabsorption of sodium, chloride, and water related to a genetic variation in the pathways by which the kidneys handle sodium
Factors implicated as causes of HPN • Increased activity of the renin–angiotensin– aldosterone system, resulting in expansion of extracellular fluid volume and increased systemic vascular resistance • Decreased vasodilation of the arterioles related to dysfunction of the vascular endothelium • Resistance to insulin action, which may be a common factor linking hypertension, type 2 diabetes mellitus, hypertriglyceridemia, obesity, and glucose intolerance
Risk Factors • Family history of cardiovascular disease • Genetic factors • Race: Africans (the blacks) • Stress • Obesity • High sodium intake • Low potassium, calcium , and magnesium intake • High-saturated fat diet • Impaired renal function (GFR < 60 ml/min and/or microalbuminuria)
• Use of hormonal contraceptives • Excess alcohol intake • Use of tobacco • Sedentary lifestyle • Low socio-economic status • Insulin resistance/ diabetes mellitus type 2 • Aging, above 55 years for men, above 65 years for women
Incidence • Primarily affects middle aged and older adults • Primary hypertension: 90% - 95% of cases • More than 50% of people aged 60 -74 years are hypertensive • 75% of those aged 75 and older are hypertensive • Incidence of hypertension is her in the blacks than the whites
Common characteristics/classifications of blood pressure for adults • Serial blood measurements in mmHg: CATEGORY SYSTOLIC DIASTOLIC Normal < 120 and < 80 Pre-hypertension 120 – 139 or 80 – 89 Hypertension: stage I 140 – 159 or 90 – 99 stage II Equal or above or Equal or above 160 100
Complications/Target organ damage • Cardiac disease: Left ventricular hypertrophy Coronary artery disease Myocardial infarction  Congestive heart failure • Stroke or transient • Peripheral vascular/arterial disease • Renal failure • Retinopathy/Blindness
Diagnostic assessments • History: Many cases have no symptoms and the disorder is revealed incidentally during an evaluation of another disorder or during a routine blood pressure screening program Symptoms that reflect the effect of hypertension on the organ system Awakening with occipital headache, subsides spontaneously after a few hours
History of: • Fatigue, dizziness and confusion • Palpitation, chest pain and dyspnoea • Epistaxis • Haematuria • Blurred vision
Physical exam findings include: • Bounding pulse • S4 • Peripheral oedema in the late stages • Hemorrhages, exudates, and papilledema of the eye in late stage if hypertensive retinopathy present • Elevated blood pressure on at least two consecutive occasions after initial screening • Bruits over the abdominal aorta and femoral arteries or the carotids • Palpating abdominal mass, suggesting an abdominal aneurysm.
Lab Test Results • Urinalysis: protein, RBCs, or WBCs, suggesting renal disease, or glucose suggesting DM • Serum potassium levels <5.5 mEq/L may indicate adrenal dysfunction (primary hypertension) • Blood urea nitrogen normal or elevated above 20 mg/dl suggesting renal disease • Serum creatinine levels normal or elevated above 1.5 mg/dl suggesting renal disease
Imaging Tests • Excretory urography reveals renal atrophy, indicating chronic renal disease, one kidney more than 1.6 cm shorter than the other suggests unilateral renal disease • Chest x-ray may demonstrate cardiomegaly • Renal arteriography may show renal artery stenosis
Diagnostic procedures • Electrocardiography may show left ventricular or ischemia • An oral captopril challenge may be done to test for renovascular hypertension • Ophthalmoscopy reveals arteriovenous nicking and, in hypertensive encephalopathy, oedema
Management General Management: • Lifestyle modification including Weight control Limiting alcohol intake Regular exercise Smoking cessation Decrease of stress
General management • For a patient with secondary hypertension, correction of the underlying cause and control of hypertensive effects • Low saturated fat and low sodium diet • Adequate calcium, potassium, and magnesium in diet
Medications • Diuretics to reduce blood volume, such as furosemide, hydrochlorothiazide and indapamide • Beta-adrenergic blockers such as atenolol and meteprolol • Calcium channel blockers to block Ca+ access to cardiac muscle to reduce contractility and conductivity, reduce oxygen demand, relaxes arterioles (lowers periveral vascular resistance): such as, verapamil, nifedipine, felodipine, and nisoldipine • Angiotensin converting enzyme inhibitors: such as benazepril, captopril, and enalapril. Mainstay of vasodilator therapy. More effective when used with diuretics. • Alpha-blockers, such as doxazosine, and prazosin • Angiotensin-receptor blockers such as olmesartan, candesartan, and irbesartan
Medications • Vasodilators such as hydralazine, minoxidil • Aldosterone antagonists such as eplerenone and spironolactone • Combination alpha-and beta-blockers such as carvedilol and labetalol • Alpha-receptor antagonist such as clonidine • Direct Renin inhibiters e.g. alskiren (Tektuma), indicated in mild to moderate hypertension to block the conversion of angiotensinogen to angiotensin I by inhibiting the activity of enzyme renin. C/I in pregnancy.
Nursing management Nursing diagnoses: • Ineffective self-health management related to lack of knowledge of the condition, complications, management, unpleasant side-effects of drugs, failure to achieve goal BP while on medication, return of BP to normal while on medications, high cost of some medications, inconvenient of taking drugs, lack of trusting relationship with health care provider • Anxiety related to complexity of management regimen, possible complications and lifestyle changes associated with hypertension • Sexual dysfunction related to side-effects of antihypertensive medications
Nursing diagnoses • Disturbed body image related to diagnosis of hypertension • Imbalanced nutrition: more than body requirement related to obesity, and alcohol intake • Excess fluid volume related to sodium retention, disruption of renin-angiotensin- aldosterone system • Risk for decreased cardiac tissue perfusion • Risk for ineffective cerebral tissue perfusion • Risk for ineffective renal perfusion
Collaborative problems • Potential complication: adverse effects from antihypertensive therapy • Potential complication: hypertensive crisis • Potential complication: stroke • Potential complication: myocardial infarction
Key nursing outcomes • The patient will: Maintain adequate cardiac output Maintain hemodynamic stability Develop no arrhythmias Express feelings of increased energy Comply with the therapy regimen Develop no renal failure and stroke
Nursing interventions • Administer prescribed drugs • Encourage dietary changes as appropriate • Help patient identify risk factors and modify his/her lifestyle
Monitoring: o Vital signs, especially blood pressure o Signs and symptoms of target end-organ damage o Complications o Response to treatment o Risk factor modification o Adverse effects of antihypertensive agents
Patient teaching:  Be sure to cover: The disorder, diagnosis and treatment How to use a self-monitoring blood pressure cuff and to record the reading in a journal for review by the physician The importance of compliance with antihypertensive therapy and establishing a daily routine for taking prescribed drugs
The need to report adverse effect of drugs The need to avoid high-sodium antacids and over- the-counter cold and sinus medications containing harmful vasoconstrictors Examining and modifying life-style including diet The need for routine exercise program, particularly aerobic walking Dietary restrictions: adopt DASH eating plan (consuming diet rich in fruits, vegetables and low fat) Cessation of alcohol consumption The importance of follow-up care
Dietary Approach to Stop Hypertension (DASH) • Grains: seven to eight servings per day • Vegetables: four to five servings per day • Fruits: four to five servings per day • Nonfat/low-fat dairy products: two to three servings per day • Meats, poultry, and fish: two or less 3 oz servings per day • Nuts, seeds and dry beans: four to five servings per a week • Fats and oils: two to three servings per day • Sweets: five servings per a week (should be low in fat)
Discharge Planning:  Refer the patient to stress-reduction therapies or support groups as needed
Hypertensive Crisis • Significant, rapid elevations in systolic and/or diastolic pressure. Two types: Hypertensive emergency and hypertensive urgency. • In hypertensive emergency or malignant hypertension, the systolic pressure is above 180 mmHg or the diastolic pressure is above 120 mmHg, associated with impending or progressive organ dysfunction • Immediate treatment, just within one hour, is vital to prevent cardiac, brain, renal and vascular damage, and reduce morbidity and mortality. • Intensive cerebral artery spasm occurs to protect brain from high pressure, but in turn, it complicates to cerebral oedema
Hypertensive Emergency • Associated with following organ dysfunction: o hypertensive encephalopathy o Hypertensive left ventricular infarction o Hypertension with myocardial infarction o Hypertension with unstable angina o Hypertension with dissection of the aorta o Hypertension with subarachnoid haemmorrhage or CVA o Severe pre-eclampsia or eclampsia o Crisis associated with phaechromocytoma o Hypertension perioperatively o Use of creational drugs e.g. Amphetamines, LSD, Cocaine
Signs and symptoms of hypertensive crises • Rapid onset elevation of BP • Blurred vision, papilledema • Systolic pressure greater than 180 mmHg • Diastolic pressure greater than 120 mmHg • Severe headache • Confusion/anxiety • Nasal bleeding • Motor and sensory deficits
Hypertensive Urgencies • Isolated large blood pressure elevations without evidence of acute Organ Dysfunction • Elevated blood pressures with severe headaches, nose- bleedings, or anxiety are classified as urgencies • It is associated with treatment discontinuation or reduction as well as anxiety • It should not be treated as emergency but treated by reinstitution or intensification of drug therapy and treatment of anxiety • Oral agents e.g. Labetalol (Beta blocker) and captopril (CCB)or clonidine (Catapres) are given to reduce blood pressure to normal in 24 to 48 hours. • Monitor blood pressure in every 30 minutes till stable
Management of hypertensive emergency • Acute life-threatening blood pressure elevations requiring prompt treatment in an intensive care setting because of serious target organ damage that may occur • This Pressure must be reduced by 20 to 25% in one hour of treatment, and a further reduction to a goal pressure of about 160/100 mmHg over a period of 6 hours • Vasodilators e.g. sodium nitropruside, nitroglycerin, diazoxide, hydralazine • Calcium-channel blockers e.g. nicardipine • ACE inhibitor e.g. enalaprilat • Adrenergic blockers: labetalol, esmolol, phentolamine • Monitor vital signs esp. BP in every 5 min, then 15 to 30 min interval when stable
HEART FAILURE Introduction: • Definition: It is a clinical syndrome resulting from structural or functional cardiac disorders that impair the ability of ventricles to fill or eject blood (to meet the metabolic needs of the body) [Hinkle & Cheever, 2014] • Fluid buildup in the heart from myocardium that can’t provide sufficient cardiac output • Usually occurs in a damaged left ventricle but may occur in right ventricle, either primarily or secondary to left-sided heart failure
• Heart failure (HF) was referred to congestive heart/Cardiac failure (CHF or CCF) due to many patients present with pulmonary or peripheral congestion with oedema • Currently, HF is recognized as clinical syndrome characterized by signs and symptoms of fluid overload or inadequate tissue perfusion • Fluid overload and decreased tissue perfusion occurs when heart cannot generate sufficient cardiac (CO) to meet body’s demand for oxygen and nutrients • In heart failure, impaired contraction of the heart (systolic dysfunction) or filling of the heart (diastolic dysfunction) may cause pulmonary or systemic congestion
Pathophysiology Given according to the cause:  Left-sided verses right-sided failure  Systolic or diastolic failure  Low-output or high output failure  Acute or chronic failure  Forward or backward failure
Pathophysiology • Left-sided Heart Failure:  Pumping ability of the left ventricle fails and cardiac output falls  Blood backs up in the left atrium and lungs, causing pulmonary congestion and decreased cardiac output.  Causes include: hypertension, myocardial infarction of left ventricle, or valvular heart disease • Right-sided Heart Failure: (Cor pulmonale)  Ineffective contractile function of the right ventricle leads to blood backing up into the right atrium, in the vena cava and the peripheral circulation (venous system), which results in peripheral edema and engorgement of the kidneys and other organs.  Causes include: severe pulmonary disease and myocardial infarction
Systolic or diastolic failure Systolic heart failure:  Due to ventricle failure to contract adequately to eject enough blood through aorta into arterial system. Causes decreased ventricular blood ejection  Caused by loss of myocardial cells in ischemia, myocardial infarction (contractile dysfunction), cardiomyopathy or inflammations, increased afterload (hypertension), mechanical abnormalities (e.g. valvular disease)  manifested in effects of low CO e.g. weakness, fatigue, exercise intolerance Over time, it causes left ventricle dilatation and hypertrophy
Diastolic heart failure:  Occurs when heart is unable to completely relax (stiffness and non-compliant heart muscle) in diastole, thus disrupts normal filling  Passive diastole filling decreases thereby decreasing stroke volume and cardiac output, but increases atrial contraction to preload  Diastolic function occurs from chronic hypertension ( most common), decreased ventricular compliance due to hypertrophy, and impaired heart muscle contraction  Manifested by dyspnoea, tachypnoea, respiratory crackles in if left ventricle affected and pulmonary hypertension. Neck vein distension, liver enlargement, anorexia, nausea, if right ventricle is affected
Low-output VS high-out failure:  Low-output failure • Develops when there is a decrease in the biventricular output resulting from: coronary heart disease, hypertension, cardiomyopathy, and other primary cardiac disorders.  High-output failure (increased/normal cardiac output) • Hypermetabolic states increases CO to maintain blood flow and O2 to tissues • This activates compensatory mechanisms to increase CO thus further increasing O2 demand • Though high CO, the heart is unable to meet increased demands of the tissues and thus fails • Causes include: septicemia, anaemia, hyperthyroidism or AV shunting
Acute VS chronic failure: Acute failure: it’s life-threatening and occurs abruptly resulting from myocardial injury e.g. massive myocardial infarction manifested by sudden decrease in cardiac function and signs of decreased CO. Manifests as pulmonary oedema and congestion  Chronic failure: progressive (gradual) decline or deterioration of heart muscle, which allows compensatory mechanisms to come into play. It causes decreased cardiac output. Causes include: cardiomyopathies, valvular disease, or coronary heart disease (CHD)
Pathophysiology of Compensatory mechanism leading to heart failure • There are three primary compensatory mechanisms are: 1. The Frank-Starling mechanism: that is, the greater the stretch of the cardiac muscle, the greater the force of contraction. This increases contractile force thereby increasing CO. Complications include: increased myocardial demand; limited by overstretching.
pathophysiology 2. Neuroendocrine response including activation of SNS and RAAS • Decreased CO induces SNS and catecholamine release, thereby increasing HR, BP, contractility, vascular resistance and venous return. • Complications include: tachycardia, decreased filling time, low CO, increased vascular resistance, increased myocardial work and O2 demand
pathophysiology • Decreased CO and renal perfusion induce renin- angiotensin system. This causes vasoconstriction and increased BP. Complications include: increased myocardial work, renal vasoconstriction, and decreased renal perfusion • ACE converts angiotensin I to angiotensin II, which stimulates aldosterone release from renal cortex resulting in salt and water retention by kidneys, and increased vascular volume overload and vasoconstriction, increasing BP and afterload. Complications include: increased preload and afterload; pulmonary congestion; increased stress on ventricular wall (increased cardiac work-load).
pathophysiology • ADH is released from neurohypophysis, which inhibits water excretion; while atrial natriuretic factor that is released from the heart increases Na excretion and diuresis. Complications include; fluid retention and increased preload and afterload • Blood flow is redistributed to vital organs (heart and brain) thereby decreasing perfusion of other organ systems, skin and muscles. Complications include: renal failure, anaerobic metabolism, and lactic acidosis.
pathophysiology 3. Ventricular hypertrophy: • Increased cardiac workload causes myocardial muscle to hypertrophy and ventricles to dilate. • This in turn leads to increased contractile force to maintain CO. • This effect complicates into: increased myocardial O2 demand and cellular enlargement • The enlarged myocardial cells become dysfunctional and die early (apoptosis), thus leading to low CO.
causes • Mitral stenosis secondary to rheumatic heart disease, constrictive pericarditis, or atrial fibrillation • Mitral and aortic insufficiency • Arrhythmias • Hypertension • Atherosclerosis with myocardial infarction (MI) • Myocarditis • Ventricular and atrial septal defects
causes • Endocarditis • Pregnancy • Thyrotoxicosis • Pulmonary embolism • Infections • Anaemia • Emotional • Increased sodium or water intake • Renal failure
Incidence • Affects less than 5% in ages between 55 – 64 years • Affects about 10% of people older than 65 years common characteristics • Reduced cardiac output • Shortness of breath • Peripheral oedema • Dyspnoea on exertion
Classification heart disease by New York Heart Association Class I: No limitation of physical activity Ordinary activity does not cause fatigue, dyspnoea, palpitation or anginal pain Class II: Slight limitation of physical activity No symptoms at rest Ordinary physical activity causes fatigue, dyspnoea, palpitations or anginal pain
Classification cont. Class III: Marked limitation of physical activity but usually comfortable at rest Ordinary physical activity causes fatigue, dyspnoea, palpitations, or anginal pain Class IV: Inability to carry on any physical activity without any discomfort Cardiac insufficiency symptoms or angina may be present Increased discomfort for any activity undertaken
complications • Pulmonary oedema • Organ failure, especially the brain and kidneys • Myocardial infarction • Pleural effusion • Left ventricular thrombus
Complications cont. o Hepatomegaly (right ventricular failure) o Splenomegaly (in right ventricular failure) o Ascites (in right ventricular failure) o Dysarrhythmias- due to enlargement of chambers of the heart o Cardiomyogenic shock
Diagnostic assessments History of: • A disorder or condition that can precipitate heart failure • Dyspnoea or paroxysmal nocturnal dyspnoea • Peripheral oedema • Fatigue • Weakness • Insomnia
History of: • Anorexia • Nausea • Sense of abdominal fullness, due to right- sided heart failure • Substance abuse e.g. alcohol, drugs, tobacco.
Physical exam findings • Cough that produces pink, frothy sputum • Cyanosis of the lips and nail beds • Orthopnoea • Pale, cool, clammy skin • Diaphoresis • Jugular vein distension • Ascites resulting poor venous return from abdomen and liver congestion • Tachycardia • Pulsus alternans- weak pulse alternating with strong one
Physical findings cont. • Hepatomegaly and, possibly, splenomegaly • Decreased pulse pressure • S3 and S4 heart sounds • Moist, bibasilar crackles, rhonchi, and expiratory wheezing • Decreased pulse oximetry • Peripheral oedema • Decreased urinary output
Lab test results: • B-type natriuretic peptide immunoassay is elevated • Liver function tests e.g. ALT, AST, LDH, serum bilirubin, and total protein and albumin levels are evaluated to show effect of heart failure on the liver • Thyroid function tests e.g. TSH, TH levels done because both hypothyroidism and hyperthyroidism can be primary or contributory factor for heart failure • In acute heart failure, ABGs done to evaluate gas exchange in lung tissues
Imaging results • Chest x-ray shows increased pulmonary markings, interstitial oedema, or pleural effusion and cardiomegaly • Radionuclide imaging to evaluate ventricular function and size • Serum electrolytes measured to evaluate fluid and electrolyte status • Urinalysis, BUN and serum creatinine done to evaluate renal function
Diagnostic procedures • ECG reflects heart strain or enlargement or ischemia; atrial enlargement, tachycardia, extrasystole, or atrial fibrillations • Pulmonary artery pressure monitoring typically shows elevated pulmonary artery wedge pressures, left ventricular end-diastolic pressure in left-sided heart failure, and elevated right atrial or central venous pressure in right-sided heart failure
Management General management: • Antiembolism stockings to promote venous return • Elevation of lower extremities to relieve oedema • Sodium restricted diet to prevent fluid retention • Fluid restriction to prevent fluid overload • Calorie restriction if indicated to prevent obessity • Low-fat fat diet to prevent atherosclerosis • Walking programs to reduce weight to optimum level • Activity as tolerated to keep fit and prevent dependance
Medications • Oxygen therapy as necessary • Diuretics, such as frusemide, bumetanide, torsemide, metolazone and hydrochlorothiazide • Inotropic drugs such as digoxin (digitalis), dobutamine, and dopamine to reduce heart rate and improve cardiac output • Vasodilators such as nitrates (nitroglycerin), sodium nitroprusside, isosorbide, and nesiritide- causes dilatation of arteries and veins • Angiotensin-converting enzyme inhibitors, such as captopril, enalapril, and lisinopril
• Angiotensin-receptor blockers, such as losartan, valsartan, and irbesartan to prevent action of angiotensin II and produce vasoconstriction and increased salt and water excretion. Full effect experienced after 3-6 weeks. • Calcium channel blockers, such as amiodipine, felodipine, nefedipine, verapamil to block movement of extracellular Ca++ into cells, causing vasodilation and decreased HR, conractility and systemic vascular resistance
• Potassium –sparing diuretics e.g. amiloride and spilonolactone (Aldactone) for exchange of K+ and Na+ in distal renal tubules and reduce excretion of K+, H+, Ca++ and Mg++ • Beta-adrenergic blockers, such as atenolol, metoprolol, propranolol (inderal) and carvedilol • Anticoagulants, such as warfarin • Morphine- decreases preload and afterload in acute decompesated heart failure and pulmonary oedema, dilates pulmonary and systemic blood vessels.
Surgical intervention • For valvular dysfunction with recurrent acute heart failure, surgical replacement • Heart transplant – transfer of a heart from one person (especially for one who has suffered massive brain dead) to another • Ventricular assist device • Stent placement
Nursing management Nursing Diagnoses • Decreased cardiac output related to altered contractility, altered preload and altered stroke volume as evidenced by jugular vein distension, orthopnoea, S3, S4 • Impaired gas exchange related to increased preload and alveolar capillary membrane changes AEB dyspnoea, tachypnoea, restlessness, verbalisation , “am short of breath”
• Excess fluid volume related to increased venous pressure and decreased renal perfusion secondary to HF AEB edema, rapid weight gain, oliguria. • Activity intolerance related to fatigue secondary to cardiac insufficiency and pulmonary congestion • Deficient knowledge: low sodium diet related to lack of information about disease process
Expected client outcomes • The client will: Maintain haemodynamic stability Maintain cardiac output Carry out activities of daily living without excess fatigue or decreased energy Maintain adequate ventilation Maintain adequate fluid balance
Nursing interventions • Place patient in Fowler’s position • Give supplemental oxygen • Provide continuous cardiac monitoring during acute and advanced stages • Assist the patient with range-of-motion exercises • Apply antiembolism stockings • Check for calf pain and tenderness • Administer prescribed drugs • Provide emotional support
Monitor closely for the following: • Daily weight for peripheral oedema and other signs and symptoms of fluid overload • Cardiac rhythm • Intake and output • Response to treatment • Vital signs: TPR and BP and report to physician any deviation • Mental status • Peripheral oedema
monitoring • Auscultate for abnormal heart beat and breath sounds, report any changes immediately • Blood urea and nitrogen and serum creatinine, potassium, sodium, and magnesium levels • Prothrombin time
Patient Teachings • You must the following patient teachings: Heart failure disorder, diagnosis and treatment Signs and symptoms of worsening heart failure When to notify the physician The importance of follow up-care The need to avoid high-sodium foods The need to avoid fatigue Instructions about fluid restrictions
Patient teaching The need to take weight every morning, at the same time, before eating, and after urinating, keeping record of this weight, and reporting weight gain of 1.5 to 2.5 kg in a week The importance of smoking cessation, if appropriate Diet education to include low sodium and low cholesterol diet intake Weight reduction as needed for optimal wt management Medication administration, dosage, possible adverse effects, and monitoring needs
Discharge planning • Encourage client to attend for follow-ups • Refer the client to a smoking-cessation program, if appropriate
Rheumatic Heart Disease Definition: Rheumatic heart disease (RHD) is a slowly progressive valvular deformity that may follow acute or repeated attacks of rheumatic fever
Risk factors • Streptococcal infection of pharynx • Crowded environmental conditions • Low socioeconomic factors • Malnutrition • Immunodeficiency • Poor access to health care • Unknown genetic factor in susceptibility to rheumatic fever
Incidence • Occurs worldwide • More common in developing countries • More common before age 15, though it can affect any age
Pathophysiology • Rheumatic heart disease occurs as a result of autoimmune response to group A streptococcal throat infection, causing inflammation of tissue containing M proteins. • Carditis occurs in about 50% of rheumatic fever: endocarditis, myocarditis and pericarditis • Aschoff bodies, localized areas of necrotic tissue surrounded by immune cells, develop in cardiac tissues • Endocardial inflammation causes swelling and erythema of valve structures and small vegetative lesions on valve leaflets, making them rigid and deformed • As a result, stenosis and regurgitation occurs , most commonly on the mitral valve, and heart failure ensues
Diagnostic Test Characteristics of RHD • Elevated WBC • Reduced RBC • Elevated erythrocyte sedimentation rate • C-reactive protein is positive • Elevated antistreptolysin titer • Throat culture usually positive of group beta-hemolytic streptococci • Elevated cardiac enzymes in severe carditis • ECG changes: prolonged PR interval • Chest X-ray may show cardiac enlargement • Echocardiogram may show valvular damage, enlarged chambers, decreased ventricular function, pericardial efffusion
Clinical features • Chest pain • Tachycardia • Pericardial friction rub • Evidence of heart failure (manifestations of heart failure) • Heart murmur: S3 and S4 sounds on auscultation • Cardiomegally • Pericardial effusion • Manifestation of rheumatic fever, including polyarthritis
Medical Management  antibiotics to eliminate streptococcal infection, penicillin for at least 10 days  Erythromycin or clindamycin for a patient allergic to penicillin  Prophylactic antibiotic therapy continued for 5 to 10 years, penicillin G 1.2 mu IM every 3-4 weeks  Analgesics for pain relief e.g. aspirin or ibuprofen  Corticosteroids e.g. Prednisone to relieve inflammation (carditis)
Nursing intervention • Find out whether patient reacts with penicillins • Administer prescribed antibiotics • Administer analgesics as prescribed • Administer prescribed corticosteroids • Stress the importance of bed rest • Position patient in high Fowler’s position • Provide oxygen therapy as necessary • Monitor vital signs
Nursing interventions • Monitor heart rhythm • Monitor heart and respiratory sounds • Provide warm moist compresses for local pain relief • Allow patient express feelings and concerns • Provide psychological and spiritual support • Give balanced diet, low in sodium and fats
Patient teaching • Inform the patient on the disorder, diagnosis and treatment • Importance of resuming activities of daily living slowly and scheduling frequent rest periods • Inform patient what to do if reacts with penicillin • Importance of reporting signs of heart failure e.g. severe dyspnoea • Prevention of respiratory infections • Good oral care to prevent gingival infections • Continue with prescribed prophylactic antibiotics • Medication administration, dosages and possible adverse effects • Clinic follow-up for check-ups
VALVULAR HEART DISEASE Tricuspid insufficiency (regurgitation, incompetence)
TRCUSPID INSUFFICIENCY Introduction • Heart condition in which the tricuspid valve doesn’t function properly • Also called tricuspid regurgidation Causes Rheumatic heart disease Papillary muscle dysfunction Carcinod heart disease Connective tissue disease Trauma  Endocarditis Valvular prolapse  Epstein anomaly
Incidence: o Affects both sexes equally o Usually occurs in childhood Common characteristics: • Dyspnoea on exertion • Peripheral oedema • Tachycardia • Fatigue
Pathophysiology • The tricuspid valve is incompetent • Blood flows back into the atrium • Fluid overload occurs in the atrium • Congestive failure occurs, and impendance to the pulmonary vasculature may result in hypoxaemia and polycythemia
Complications • Heart failure • Pulmonary oedema • Thrombolism • Endocarditis • Arrhythmias
Assessment History of: Occurrence of one listed causes Orthopnoea Dyspnoea Fatigue Angina Palpitations
Physical findings • Tachycardia • Crackles in the lungs • Hepatomegaly in right-sided failure • Jugular vein distension • S3 heart sound • Diminished peripheral pulses • Ascites • Atrial fibrillations • Peripheral oedema • Pansystolic murmur- murmur throughout systolic perriod
Test results  Imaging: o Chest X-ray show right atrial and ventricular enlargement o Echocardiography shows right ventricular dilation and prolapse or flailing of the tricuspid triplets
Test results  Diagnostic procedures Electrocardiography shows right atrial hypertrophy, right or left ventricular hypertrophy, and atrial fibrillation, and incomplete right bundle-branch block Right-sided heart catheterization shows high atrial pressure, tricuspid insufficiency, and decreased and normal output
Treatment and medication • General treatment include o Underlying cause o Low-sodium diet o Fluid restriction o Activity as tolerated
Medications • Diuretics • Cardiac glycoside • Anticoagulants • Angiotensin-converting enzyme inhibitors • Oxygen • Prophylactic antibiotics in some patients before and after surgery or dental care to prevent endocarditis
Surgery o Annuloplasty or valvuloplasty to reconstruct or repair the valve o valve replacement with a prosthetic valve
NURSING CONSIDERATION Key Outcomes The patient will: o Carry out activities of daily living without weakness or fatigue o Maintain haemodynamic stability o Maintain adequate ventilation
NURSING INTERVETIONS • Administer oxygen • Watch for signs of heart failure or pulmonary edema • Alternate periods of activity and rest • Keep patient’s legs elevated to improve venous return to the heart
Monitoring • Vital signs and oximetry • Cardiac rhythm • Pulmonary artery catheter readings • Intake and output • Adverse effects of drug therapy
Patient teachings • Be sure to cover The disorder, diagnosis and treatment  dietary restrictions and medications Signs and symptoms that should be reported The importance of consistent follow-up care The need to elevated his/her legs when sitting to relieve oedema
Tricuspid valve stenosis • Is a valvular disease which results in the narrowing of the orifice of the tricuspid valve of the heart. • Obstructs blood flow from the right atrium to right ventricle • Fibrosed, retracted tricuspid valve cusps and fused leaflets narrow the valve orifice and prevent closure
Causes • Rheumatic fever • Carcinoid heart disease • Infective endorcarditis • Tricuspid atresia • Mitral and aortic valve disorders • Endomyocardial fibrosis • Systemic lupus erythematosus
Pathophysiology • Alterations in the structure of the tricuspid valve cause incompetence of valve • Restriction of blood flow into the right ventricle and, subsequently, to the pulmonary vasculature occurs • Obstructed venous return results in hepatic enlargement, decreased pulmonary blood flow, peripheral oedema, and right atrial enlargement
Incidence • Affects females slightly more common than males Common characteristic • Dyspnoea on exertion • Peripheral oedema • Fatigue • Ascites
Complications • Heart failure • Pulmonary oedema • Thromboembolism • Endocarditis • Arrhythmias
Diagnostic findings • Assessment History of:  orthopnea  dyspnea  fatigue  angina  palpitations
• Physical findings: A low rumbling crescendo-decrescendo murmur in the tricuspid area heard in 4th intercostal space at left sternal boarder or over xiphoid process Split S1 Hepatomegaly Ascites Jugular venous distension Peripheral oedema
Test result • Imaging Chest x-ray-reveals cardiomegaly Echocardiography- used to examine the size shape and motion of the cardiac structure Electrocardiography-this is a graphic recording of the electrical activity of the heart
Medication • Diuretics eg furosemide • Digoxin • oxygen therapy • Angiotensin converting enzyme inhibitor eg captropil
• Surgical management Balloon valvuloplasty Valvotomy-incision to a stenosed cardiac valve tot relieve obstruction
Complication • Heart failure • Pulmonary edema • Thromboembolism • Endocarditis
Aortic stenosis • Narrowing of the aortic valve that affect blood flow in the heart • It is classified as either acquired or rheumatic
Incidence • Possibly asymptomatic till age 50 and 70 • About 80% are males
Causes • Idiopathic calcification • Congenital aortic bicuspid valve • Rheumatic fever • Artherosclerosis
Pathophysiology of aortic stenosis • Stenosis of the aortic valve results in impendance to foward blood flow • The left ventricle requires greater pressure to open the aortic valve • Added work load increases myocardial oxygen demands • Diminished cardiac output reduces coronary artery blood flow • Left ventricular hypertrophy and failure result
Common characteristics • Note; many are asymptomatic • Exertional dyspnea • Orthopnea • Pulmonary edema • Dizziness • Syncope • Angina
Assessment and diagnostic findings • History taking • Physical examination: a loud rough systolic murmur is heard over the aortic area. Which may radiate to carotid arteries Other distinguishing finding: • Diminished carotid pulse • Distinct lag between carotid artery pulse and apical pulse
• Diagnostic procedures include: Echocardiography- shows decreased valve area and hypertrophied left ventricle. Chest x-ray-shows cardiomegaly Catheterization-shows increased pressure across the aortic valve and in the left ventricle Electrocardiography-shows left ventricular hypertrophy and artrial fibrillation
Medications • Cardiac glycosides eg digoxin • Antibiotic for infective endorcaditis prophylaxis • Anticoagulant eg warfarin Surgical management include: Balloon valvuloplasty Commissurotomy
Complications • Left-sided heart failure • Right-sided heart failure • Infective endorcarditis • Left ventricular hypertrophy
Aortic insufficiency • Is the back-flow of blood into the ventricles causing fluid excess. Incidence • Occurs most commonly in males • When associated with mitral valve disease, it more common in females
Causes • Rheumatic fever • Hypertension • Infective endocarditis • Aortic dissection- tearing or rupturing of the aorta • Aortic aneurysm- weakening, thinning and distension of the walls of the aorta
pathophysiology • Blood flows back into the left ventricle during diastole causing increased left ventricular diastolic pressure • This results in volume overload, dilation and eventually hypertrophy of the left ventricle • Excess fluid volume also eventually results in increased left arterial pressure and increased pulmonary vascular pressure.
Clinical manifestation • Most develop without symptoms • Palpitations • Marked and visible carotid pulses • Fatigue • Orthopnea • Angina • Paroxysmal nocturnal dyspnea
Physical findings • Corrigans pulse-carotid (also called water- hammer pulse) pulse that increases rapidly then collapses • Pulses bisferiens (having two beats)-striking twice • Pulsating nail bed and Quincke's’ sign- visible pulsation of red coloration on the nail bed (seen in aortic regurgitation)
• Wide pulse pressure (systolic pressure minus diastolic pressure ) • A high pitched blowing decrescendo murmur that radiates from the aortic valve area to the left sternal border.
Imaging studies includes Chest x-ray-shows cardiomegaly and pulmonary vein congestion Echocardiography- shows cardiomegaly and thickening of the valve cusps Other tests include • Electrocardiography – shows sinus tachycardia and hypertrophy • Cardiac catheterization-shows degree of aortic insufficiency
Medical management • Cardiac glycoside eg digoxin • Diuretics eg furosemide • Vasodilators eg, nitrates • Antihypertensive eg adalat • Antiarrhythmic eg amiodarone • Anticoagulants eg heparin
Repair of aortic valve incompetence Surgical management Valvuloplasty- this is the repair of the cardiac valve.
complications • Left sided heart failure • Pulmonary edema • Myocardial ischemia
Nursing consideration Key outcomes The patient will • Perform activities of daily living without excess fatigue or exhaustion • Avoid complications • Maintain cardiac output
Nursing consideration • Demonstrate hemodynamic instability • Maintain balanced fluid status • Maintain joint mobility and range of motion • Develop an demonstrate adequate coping skills
Nursing interventions • Give prescribed drugs • Maintain a low sodium diet • Stress the importance of bed rest • Alternate periods of activity with rest • Allow the pateint to voice concerns about the effect of activity restrictions
Nursing interventions • Keep the patients legs elevated while he sits on a chair • Place the patient in an upright position and administer oxygen as needed • Allow patient express fears and concerns
Monitoring • Vital signs • Intake and output • Signs and symptoms of heart failure • Signs and symptoms of progressive aortic stenosis • Daily weight • Arrythmias • Respiratory status
monitoring If patient had surgery, monitor • Signs and symptoms of thrombus formation • Hemodynamic stability • Arterial blood gases levels • Blood chemistry results • Chest x-ray result
Patient teaching • Teach on diagnosis, progressive nature of the valvular heart disease and the treatment plan • Patient is taught to report new symptoms to the health care provider • Emphasize the need for prophylactic antibiotic therapy before any invasive procedure • Patient is advised to rest and sleep sitting in chair/ bed with head elevated when experiencing symptoms of pulmonary congestion
Mitral stenosis • Is a valvular heart disease characterized by the narrowing of the orifice of the mitral valve of the heart, thereby obstructing blood flow from the left atrium into left ventricle during diastole • The disorder is chronic and progressive • Normally the orifice is 3-6cm • Mild mitral stenosis: orifice is 2cm • Severe mitral stenosis: orifice of 1cm
Causes • Rheumatic fever • Congenital anomalies • Atrial myxoma- a benign mucous tumor of the connective tissues. • Endocarditis • Rheumatoid arthritis
Incidence • Two-third of the patients are female • It also occurs in 40% of patients with rheumatic heart disease
Pathophysiology • The opening narrows to the width of a pencil • The left atrium has difficulty moving blood into the ventricle because of the increased resistance • The left atrium stretches and hypertrophies because of the increased blood volume.
pathophysiology • The pulmonary circulation becomes congested, leading to pulmonary hypertension • As a result the right atrium must contract against the high pressure of the pulmonary hypertension causing right- sided heart failure
Clinical manifestation • Shortness of breath • Dyspnea on exertion • Chest pain • Palpitations • Hemoptysis • Peripheral and facial cyanosis
Diagnostic findings • History taking: for specific symptoms • Physical examination: a loud S1, a split S2, mitral opening snap may be heard Identify the murmur: a low rumbling crescendo- decresendo murmur in the mitral valve area, accompanied by palpable thrill (vibration) • Diagnostic procedures Cardiac catheterization-shows increased pressure in the left atrium Electrocardiography reveals left artrial enlargement
Medical management • Digitalis e.g. Digoxin • Diuretics e.g. frusemide • Oxygen therapy • Anticoagulant e.g. warfarin • Nitrates e.g. nitroglycerin • Calcium channel blockers e.g. nifedipine • Beta-adrenergic blockers e.g. atenolol
Surgical intervention Surgical management includes Balloon valvuloplasty
Balloon inflated in mitral stenotic valve
Mitral valve insufficiency • This is a valvular disease of the mitral valve that allows the backflow of blood from the left ventricle to the left atrium. • It may be: Acute. Chronic compensated. Chronic decompensated.
Causes • Rheumatic fever • Cardiomyopathy- chronic disorder of the heart muscles • Infective endocarditis • Mitral valve prolapse • Myocardial infarction- death or necrosis of myocardial cells • Congenital anomalies
Pathophysiology • Blood from the left ventricle flows back into the right atrium during systole causing the atrium to enlarge to accommodate the backflow • Left ventricles dilate to accommodate the increased volume from the atrium and to compensate for diminishing cardiac output
Pathophysiology • Ventricular hypertrophy and increased end-diastolic results in increased pulmonary artery pressure, eventually leading to left sided and right sided heart failure
Common characteristics • Dyspnea • Orthopnea • Tachycardia • Angina • palpitations
Diagnostic findings • History taking: orthopnea, dyspnea, fatigue, angina, palpitations • Physical examination: tachycardia, crackles. • A high pitched rumbling pansystolic murmur that radiates from the mitral area to the left axillary line
Test result • Imaging Chest x-ray-reveals left atrial and ventricular enlargement Echocardiography- shows abnormal valves structure
management Medications such as • Diuretics e.g. furosemide • Inotropic agents such as digoxin • Angiotensin converting enzyme inhibitors eg captopril • Oxygen • Anticoagulant e.g. warfarin • Prophylactic antibiotic • Vasodilators such as nitroprusside
Surgery • Annuloplasty-the repair of the valve annulus • Valve replacement with prosthetic valve
Complications • Heart failure • Pulmonary edema • Thromboembolism • Endorcarditis • Shock
Summary • Valvular diseases mainly affect the valves. They can be congenital or acquired. • There are various types of valve disorders classified broadly as stenotic disorders or regurgitation disorders. • Symptoms present as those of heart failure. • Management involves medical, surgical and nursing management. • Common complication is heart failure.
Conclusion on valvular diseases • If valvular diseases progress they lead to heart failure. • Proper management and follow-up should therefore be emphasized: Surgical treatment Treament include medications and surgical interventions: Valvuloplasty- repair of valves Commissurotomy- separating fused leaflets
Surgical treatment of valvular disorders Annuloplasty-repair of junction of valve and muscular heart wall Leaflet repair- to remove extra tissue leaflets Chordoplasty- repair of chordae tendineae Valve replacement- when above measures have failed, valve replacement is perfomed, two types: mechanical valves (bileaflet, tilting-disk, ball-and- cage design) and tissue valves: 3 types (bioprostheses, homografts, autoggrafts)
Coronary Artery Disease Introduction • Type of blood vessel disorder including atherosclerosis, that is, deposits of fat (atheromas) that hardens with age • Atherosclerosis occludes the coronary artery by fibrous, fatty plaque, manifested by angina pectoris, acute coronary syndrome and /or myocardial infarction • Primary effect include: loss of oxygen and nutrients to myocardial tissue because of diminished coronary blood flow
Pathophysiology • Increased blood levels of low-density lipoprotein (LDL) irritate or damage the inner layer of coronary vessels • LDL enters the vessel after damaging the protective barrier, accumulates, and forms a fatty streak • Smooth muscle cells move to the inner layer to engulf the fatty substance, produce fibrous tissue, and stimulate calcium deposition • Cycle continues, resulting in transformation of fatty streak into fibrous plaque, and eventually, a coronary artery disease (CAD) evolves
Pathophysiology • Oxygen deprivation forces the myocardium to shift from aerobic to anaerobic metabolism, leading to accumulation of lactic acid and reduction of cellular pH cause angina pectoris • The combination of hypoxia and reduced energy availability, and acidosis rapidly impairs left ventricular function
Pathophysiology • The strength of contractions in the affected myocardial region is reduced as the fibres shorten inadequately, result in less force and velocity • Wall motion is abnormal in ischemic area, resulting in less blood being ejected from the heart with each contraction
causes • Atherosclerosis • Dissecting aneurysm • Infectious vasculitis • Syphylis • Congenital defects • Coronary artery spasm
Risk factors • Family history • High serum cholesterol levels above 200 mg/dL • Smoking • Diabetes • Hormonal contraceptives • Obesity: BMI above 30 kg/m2 or waist over 40 inches • Sedentary lifestyle • Stress/psychological states e.g. depression, increased stimulation of SNS
Risk factors • Increased homocysteine levels : broken products of aminoacid methionine, which lead to atherosclerosis • Hypertension • Substance abuse e.g. cocaine, methamphetamine cause coronary spasms resulting in myocardial ischemia • Metabolic syndrome: cluster risk factors e.g. insulin resistance, obesity, hypertension, high serum lipids levels
Incidence • Occurs after age 40 • Males eight times more susceptible than premenopausal females • Risk increased by family history • White males more susceptible than nonwhite males; nonwhite females more susceptible than white females • In America alone, more than 11 million people affected by CAD Common characteristic  Angina
Complications • Arrhythmias- heart beat irregularities • Myocardial infarction- death of cardiac myocytes • Heart failure- insufficient cardiac out to meet body’s metabolic activities • Cardiac shock due to inadequate oxygen and nutrient supply • Ventricular aneurysm • Pericarditis due to cardiac compression • Dressler syndrome: pericarditis with effusion and fever • Papillary muscle dysfunction: if infarcted area includes/adjacent papillary muscle attached to mitral valve
Diagnostic assessment History of: • Angina that may radiate to the left arm, neck, jaw, of shoulder blade • Commonly occurring after physical exertion but possibly following emotional excitement, exposure to cold, or ingestion of a large meal • May develop during sleep; symptoms wake the patient • Nausea • Vomiting • Fainting • Sweating • Stable angina: predictable and relieved by rest or nitrates
History of: • Unstable angina: increases in frequency and duration and is more easily induced and generally indicates extensive or worsening disease, and, untreated, may progress to myocardial infarction • Crescendo angina: an effort pain-induced occurring with increasing frequency and decreasing provocation • Prinzmental’s or variant angina pectoris: severe non-effort produced pain occurs at rest without provocation to spasm
Physical findings • Cool extremities- due to poor blood supply • Xanthoma- soft, yellow skin plaques or nodules containing lipoprotein deposits inside histiocytes related to hyperlipidemia • Arteriovenous nicking of the eye • Obesity- • Hypertension • Positive Levine’s sign (holding fist to chest) • Decreased or absent peripheral pulses
Imaging test results • Myocardial perfusion imaging with radionucleotide during treadmill exercise shows ischemic areas of myocardium, visualized as “cold spots”. • Pharmacologic myocardial perfusion imaging in arteries with stenosis shows decrease in blood flow proportional to the percentage of occlusion • Stress echocardiography may show abnormal wall motion
Imaging test results • Coronary angiography reveals the location and the degree of coronary artery stenosis or obstruction, collateral circulation, and the condition of the artery beyond the narrowing • Multiple-gated acquisition scanning demonstrates cardiac wall motion and reflects injury to cardiac tissue
Diagnostic procedures findings • ECG may be normal between anginal episodes • During angina, ECG may show ischemic changes • Exercise stress testing may be done to detect ST- segment changes during exercise, indicating ischemia, and to determine a safe exercise prescription
Treatment/Management General management: • Stress reduction techniques essential especially if known stressors precipitate pain • Lifestyle modifications, such as smoking cessation and maintaining ideal body weight • Low-fat, low-sodium diet • Activity restrictions possible • Regular exercise as tolerated
Medications • Antianginals, such as ranolazine and nitroglycerin • Beta adrenergic blocker such as metoprolol • Calcium channel blocker such as diltiazem • Antiplatelets, such as ticlopidine and aspirin • Antilipemic such as simvastatin, atorvastatin, pravastatin • Antihypertensive such as lisinopril
Surgery • Coronary artery bypass graft • “Keyhole” or minimally invasive surgery • Angioplasty • Endovascular stent placement • Laser angioplasty • Atherectomy
Nursing Management Nursing diagnoses: • Acute pain related to imbalance between myocardial oxygen supply and demand • Decreased cardiac output related to myocardial injury • Anxiety related to actual thread of death, pain, possible lifestyle changes • Activity intolerance related to fatigue • Imbalanced nutrition: more than body requirement related to obesity • Ineffective self-health management related to lack of knowledge of disease process
Expected patient outcomes The client will: Maintain hemodynamic stability Plan menus appropriate to prescribed diet Demonstrate understanding of the disease process Express concern about self-concept, self-esteem, and body image Express feeling of increased comfort and decreased pain
Nursing interventions • Ask the patient to grade the severity of his/pain on scale of 0 to 10 • Keep nitroglycerin available for immediate use • Instruct patient to call immediately whenever he or she feels pain and before taking nitroglycerin • Observe for signs and symptoms that may signify worsening of condition
Nursing interventions • Prepare patient for surgical intervention if indicated • Maintain bed rest immediately postoperatively with the head of the bed elevated at least 30 degrees • Encourage coughing, deep breathing and incentive spirometer use postoperatively • Encourage early ambulation after surgery
Monitoring • Vital signs to identify any abnormality • Hemodynamic status • Fluid intake and output • Effectiveness of pain medication during anginal episodes • Abnormal bleeding and distal pulses following intervention procedures • Respiratory status • Chest tube drainage, after surgery • Cardiac rate and rhythm • Cardiovascular status
Patient teaching On patient teaching, ensure to cover the following: Risk factors for CAD Avoidance of activities that precipitate pain The need to follow the prescribed drug regimen Effective coping mechanism to deal with stress Low-sodium and low-calorie diet The importance of regular, moderate exercise
Discharge planning • Refer the patient to a weight-loss program, if needed • Refer the patient to a smoking-cessation program, if needed • Refer the patient to cardiac rehabilitation program, if indicated
THROMBOPHLEBITIS
OBJECTIVES 1. To describe Thrombophlebitis. 2. To state the cause of Thrombophlebitis. 3. To list the risk factors of Thrombophlebitis. 4. To state the incidence of Thrombophlebitis. 5. To describe the pathophysiology of Thrombophlebitis. 6. To list the signs and symptoms of Thrombophlebitis. 7. To explain the diagnosis of Thrombophlebitis. 8. To discuss the management of Thrombophlebitis. 9. To describe the complications of Thrombophlebitis. 10 . To highlight patient teaching on the condition Thrombophlebitis.
Introduction • It is an acute condition that’s characterized by inflammation of the vein accompanied by thrombus formation. • Typically occurs in the cusps because the venous stasis encourages accumulation of and adherence of fibrin and platelets.
Cause of Thrombophlebitis • Inflammation due to a blood clot in the vein. Risk Factors • Prolonged bed rest • Trauma • Surgery • pregnancy and childbirth • Hormonal contraceptives or estrogen replacement therapy.
Risk factors • Fracture of the spine, femur, pelvis • Smoking • Obesity • Venous stasis • Family Hx of clotting disorder Incidence • Increase use of subclavian vein catheters • Risk for DVT increases after age 20.
Pathophysiology • Alteration in epithelial cell lining causes platelet aggregation and fibrin entrapment of RBCs, WBCs and platelets. • The thrombus initiates a chemical inflammatory process in the vessel epithelium that leads to fibrosis which may occlude the vessel lumen or embolize.
Signs and symptoms • Inflammation (swelling) in the part of the body affected • Pain in the part of the body affected • Skin redness (not always present) • Warmth and tenderness over the vein
Diagnosis and Assessment i. History  Asymptomatic in up to 50% of patients with DVT  Possible tenderness, aching, severe pain in affected leg or arm, fever, chills, malaise in the past. ii. Physical findings • Possible tenderness, aching, severe pain in affected leg or arm, fever, chills, malaise • Positive Homan’s sign. • Lymphadenitis in case of extensive vein involvement.
• iii. Test results Diagnostic procedures: Doppler ultrasonography indicates reduced blood flow to a specific area and any obstruction to venous blood flow. Phlebography confirms the diagnosis and shows filling defects and diverted blood flow.
Management General: • Application of warm moist compresses to the affected area. • Antiembolism stockings • Bed rest with elevation of the affected extremity. Medications • Anticoagulants i.e. heparin and warfarin • Thrombolytics (e.g., alteplase) is given within the first 3 days after acute thrombosis • Analgesics i.e. NSAIDs
Management Surgery  Simple ligation or clipping of the vein  Embolectomy- is the emergency surgical removal of emboli which are blocking blood circulation.  Caval interruption with a transvenous placement of a vena cava filter. Nursing Management Key outcomes: The patient will:
Nursing consideration • Maintain collateral circulation • Express feelings of increased comfort and decreased pain • Maintain tissue perfusion and tissue oxygenation • Develop no signs of infection Nursing Interventions • Enforce bed rest and elevate affected leg • Apply warm compresses • Administer prescribed antibiotics • Regulary measure circumference of the affected leg and compare with the other • Administer prescribed anticoagulants
Nursing interventions • Encourage or perform ROM exercises • Apply antiembolic stockings • Encourage early ambulation. Monitoring • Signs and Symptoms of bleeding • Vital signs • Clinical features of heparin induced thrombocytopenia • Manifestations of pulmonary embolism • Response to treatment
Patient Teaching • Stress on the importance of follow up studies to monitor anticoagulant therapy • Avoid prolonged sitting or standing • Proper application of antiembolism stockings • Importance of adequate hydration
Thrombophlebitis (venous thrombosis) Introduction: • Inflammation of the vessel wall with information of a clot (thrombus); may affect superficial or deep veins (deep venous thrombosis) • Most frequent veins affected are the saphenous, femoral and popliteal • Can result in damage to the surrounding tissues, ischemia, and necrosis • Risk factors include: obesity, HF, prolonged immobility, MI, pregnancy, oral contraceptives, trauma, sepsis, cigarette smoking, dehydration, severe anaemia, venous cannulation, complication of surgery
Pathophysiology • The three major pathologic factors (Virchow’s triad) predisposing to thrombus formation are: Blood stasis Injury to venous endothelial lining, and Hypercoagulability of blood • A venous thrombosis usually being in a valve cusp where platelets adhere to the endothelium and then to each other. As the process continues, a fibrin mesh covers the platelets (white thrombus).
Pathophysiology cont. • As the thrombus grows, it causes obstruction to blood flow. This allows red blood cells, platelets and fibrin to stagnate and form a red thrombus • If thrombus occludes blood flow, venous congestion will develop unless collateral circulation is established • Within a few days of thrombus formation, the body can dissolve the clot or may convert it to fibrous tissue that could incorporate and destroy the valve • Complications of venous thrombus are pulmonary emboli, and venous insufficiency
Assessment findings • Pain in the affected area/extremity • Superficial vein: tenderness, redness, induration along course of the vein, palpable cord, distension of superficial veins, prominent venous collaterals • Deep vein: swelling, extreme oedema formation, venous distension of limb, tenderness over involved vein, positive Homan’s sign, cyanosis • Elevated WBC, and ESR
Causes (Hinkle, 2014) • Endothelial damage: Trauma Surgery Pacing wires Central venous catheters Dialysis access catheters Local vein damage Repetitive motion injury
Causes • Venous stasis: bed rest or immobilisation Obesity History of vasicosities Spinal cord injury Age > 65 years
causes • Altered Coagulation: Cancer  pregnancy Oral contraceptive use Protein S deficiency Antiphospholipid antibody syndrome Factor V Leiden defect Prothrombin G20210A defect Hyperhomocysteinemia Elevated factors II, VIII, IX, XI Polycythemia Septicemia
Diagnostic evaluation • Venography (phlebography): increased uptake of radio • Plethysmography: non-invasive test measuring venous flow • Duplex ultrasonography: non-invasive visualization of vein and measurement of velocity of venous blood flow • I-125 fibrinogen scanning • Magnetic resonance imaging: non-invasive detection of deep vein thrombosis • Ascending contrast venography: uses injected contrast medium to locate site of thrombus and size
Prevention • Leg exercises • Elastic compression • Low dose heparin • External pneumatic compression • Dextran • Warfarin
Treatment • Bed rest • Elevate extremities • Local heat • Elastic hose • Analgesics/antiinflammatories e.g. indomethacin or naproxen • Anticoagulation initially with low-moleculat weight heparin • Anticoagulate with warfarin (comoudin) • May use thrombolytic drugs e.g. streptokinase or tissue plasminogen activator to acccelerate clot lysis • Iliofemoral venous thrombectomy
Nursing diagnoses • Pain related to inflammation secondary to thrombosis in the involved vein • Ineffective peripheral tissue perfusion related to occlusion of vein, obstruction of blood flow • Ineffective protection related to use of anticoagulants causing bleeding/hemorrhage • Impaired physical mobility related to severe pain, oedema • Risk for ineffective tissue perfusion: cardiopulmonary related to pulmonary embolism
Nursing interventions • Promote resolution of thrombus and prevent further thrombus formation by: promoting bed rest Administering anticoagulants as ordered Applying elastic or pneumatic hose as ordered Elevating affected extremity Frequent position changes Deep breathing and fluid intake Providing good skin care
Promote resolution and thrombus formation Teaching patient to cease smoking Not massaging the affected extremity Not to stand or sit in any position for long periods of time To avoid use of constricting garments like …… To perform calf and quadriceps contractions several times per hour
• Monitor status of extremity by: Assessing quality of pulses Assessing colour Assessing temperature Assessing rapidity of capillary refill Assessing for presence of oedema and pain Monitoring of circumference of the leg daily Monitoring for skin breakdown or ulcers
• Promote pain relief by: Providing analgesics as ordered Elastic or pneumatic stockings as ordered Applying warm compresses as ordered Encouraging frequent position changes Elevation of affected extremity and rest periods
On-going monitoring and assessments • Monitor complications of pulmonary embolus and bleeding by: Monitoring for tachycardia Monitoring for dyspnoea Monitoring for chest pain Monitoring for hemoptysis Monitoring for changes in breath sounds Monitoring for changes in vital signs
On-going monitoring and assessment Monitoring for changes in arterial blood gases Assessing results of serial hemoglobin and hematocrits Assessing PT’s, PTT’s, or APTT’s every day Observing for blood in urine Observing for bleeding from gums and epistaxis • Assessing for and instituting measures to alleviate anxiety
Client’s teaching • Teach patient about: Treatment measures including, laboratory tests, and their purposes, Medications and side effects Basic pathophysiology of thrombus formation Measures to prevent future episodes of the condition Prescribed exercises Monitoring for signs of bleeding Recurrent thrombus and pulmonary emboli Need to stop smoking Correct use of elastic hose/pneumatic stockings
Client teachings Not using constricting clothing Appropriate methods of heat applications Need for frequent change of position while standing or sitting Wearing of a medic alert bracelet if anticoagulated Importance of follow-up visits and laboratory tests as scheduled
Complications • Chronic venous oclusion • Pulmonary emboli • Valvular destruction: Chronic venous insufficiency Increased venous pressure Varicosities Venous ulcers • Venous destruction Increased distal pressure Fluid stasis Edema Venous gangrene
VARICOSITY (VARICOSE VEINS) • Dilated tortuous veins, engorged with blood resulting from improper venous valve function • Primary varicose veins originating in superficial veins, especially saphenous and branches • Secondary varicose veins occurring in deep and perforating
Pathophysiology • A weakened valve allows backflow of blood to the previous valve • If the valve can’t hold the pooling blood, it becomes incompetent, allowing even more blood to flow backward • As volume of venous blood builds, pressure in the vein increases and the vein becomes distended. • As the vein stretches, it loses elasticity, enlarges, and becomes tortuous • Hydrostatic pressure increases, plasma is forced out into surrounding tissue, and oedema results
causes • Congenital weakness of valves or venous wall • Pregnancy • Tight clothing • Occupations that require long standing • Deep venous thrombosis • Trauma
Risk factors • Prolonged standing or time on feet • Obesity • Heavy lifting • Pregnancy Incidence  Common in middle adult  Primary varicose veins: family tendency, affect both legs, twice as common in females as males  Secondary varicose veins: usually in only one leg
Common characteristics • Dilated, purple, rope-like veins • Oedema of calves and ankles • Venous stasis ulcers Complications  Venous insufficiency  Venous stasis ulcers
Assessment History include:  May be asymptomatic  Feeling of heaviness in the legs, worsening in evenings and during warm whether  Leg cramp at night  Diffuse, dull, aching leg pain after prolonged standing or sitting  Aching legs during menses in women  Exercise relieves pain due to venous return improvement
Physical findings • Dilated, purplish, ropelike veins in the calf • Orthostatic oedema and stasis of the calves • Nodules along affected veins and valve incompetence • In chronic condition, venous stasis ulcers, which should be differentiated from arterial and diabetic ulcers
Test results • Imaging Ascending and descending venography reveals venous occlusion and collateral circulation • Diagnostic procedures Photoplethysmography, a noninvasive test, characterizes venous blood flow by showing changes in the skin’s circulation Dopler ultrasonography quickly and acurately shows presence or absence of venous backflow in deep or superficial veins Venous outflow and reflux plethysmography may be used to identify deep venous occlusion
Treatment General: • Put on elastic bandage • Avoid tight clothing • Wear antiembolism stockings for moderate varicosity • Severe varicosities are treated with custorm fitted, surgical weight stockings with graduated pressure • Avoid prolonged standing • Routine exercise • Elevation of the legs
Medication/surgery • Medication: Sclerotherapy- the injection of irritating chemicals into a vein to destroy it • Surgical interventions include: Stripping (removing all contents from affected vein) and ligation (the application of a ligature) Laser surgery- use of intense beam of light to vaporize the blockage Catheter-assisted procedure Phlebectomy: surgical removal of a vein or part of a vein Endoscopic vein surgery
Nursing considerations Key outcomes The patient will: • Express understanding of disorder and treatment • Maintain adequate distal and collateral circulation • Express feelings of increased comfort and decreased pain • Carry out activities of daily living without excess fatigue or discomfort
Nursing considerations • After stripping and ligation or after injection of a sclerosing agent, administer agent analgesics as ordered to relieve pain • Frequently check circulation in toes and observe elastic bandages for bleeding • When ordered, rewrap bandages at least once per a shift, wrapping from toe to thigh, with the leg elevated
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CARDIOVASCULAR DISORDERS (CVD).pptx

  • 2. Course Outline For CVD Introduction • The cardiovascular diseases (CVD) conditions course will be covered within 16 hours. By the end of the course you will be able to compare and contrast the etiology, pathophysiology and manifestations of various cardiovascular conditions/diseases, explain risk factors and preventive measures, describe interdisciplinary and nursing care of CVS problems, relate the outcomes of diagnostic tests and procedures to pathophysiologies, discuss the effects and nursing implications for medications and treatments used, and describe rehabilitation services.
  • 3. Main Objective • The student will be able to acquire knowledge, attitude, and skills to be able to promote health, prevent illness, diagnose, manage and coordinate rehabilitation of patients suffering from cardiovascular conditions/diseases. Specific Objectives • Review anatomy and physiology of the heart and blood vessels • Describe the assessment of cardiovascular system • Describe common cardiovascular diseases and conditions and their specific management
  • 4. CONTENT • Review of anatomy and physiology of the heart and vessels • Assessment of cardiovascular system • Congestive cardiac failure • Rheumatic heart disease • Valvular heart disease • Coronary heart disease • Arteriosclerosis • Gangrene • Varicose vein • Thrombophlebitis (superficial and deep venous thrombosis) • Arterial Thrombosis • Arterial Embolism • Hypertension (essential/malignant)
  • 5. Mode of teaching • Lectures/discussions • Assignments • Group discussions Teaching/learning materials • Handouts • LCD/PowerPoint slides • Flipcharts • Blackboard • White board • Overhead projector/transparencies • Textbooks
  • 6. Mode of assessment for the course • Completion of assignment 10% • Quizzes 10% • Mid-Semister test 20% • End-block examination 60%
  • 7. REFERENCE MATERIALS • Aghababian, R. et al (2006). Essentials of Emergency Medicine. Jones and Bartlett Publishers, London • Bilotta, K. et al (Eds) (2009). Nurse’s Quick Check Diseases. Wolters Kluwer, New York. • LeMone et al (2011). Medical-Surgical Nursing. Pearson Publishers, London. • Lewis et al (2011). Medical Surgical Nursing. Elsevier Publishers, London. • Smeltzer S et al (2014). Brunner and Suddarth’s Medical – Surgical Nursing. Lipppincot Company, Philadelphia. Facilitator: David Onsongo
  • 8. NORMAL PHYSIOLOGY OF CIRCULATORY SYSTEM By David Onsongo
  • 9. Aim: By the end of the study the students will be able to understand the concepts of how the heart functions
  • 10. Anatomy and physiology of CVS Cardiovascular system(CVS) consists of: • Heart - muscular blood pump organ • Arteries– Carry blood away from the heart • Veins- Return venous blood to the heart • Capillaries- smallest blood vessels involved in actual exchange of materials between tissue cells and blood NB. Review more about the major blood vessels
  • 11. Heart: • Hollow muscular organ • Occupies mediastinum space • Weighs about 300 g (about size of owner’s fist) • Pumps blood to supply oxygen and nutrients to all tissues Heart layers: • Inner layer (endocardium) • Middle layer (myocardium) • Outer layer (pericardium)  visceral pericardium  peripheral pericardium  pericardial space: contains 30 ml lubrication fluid
  • 12. Heart chambers: • Right atrium –Receives venous (deoxygenated) blood • Left atrium – receives oxygenated blood from the lungs • Right ventricle – Sends deoxygenated blood to the lungs • Left ventricle – Distributes oxygenated blood to body tissues Cardiac wall thickness: • Atrial walls are thinner than ventricle walls • Left ventricle wall is two and half times thicker than right ventricle • Left ventricle has higher pressure than right ventricle and atria
  • 13. Position: • Heart lies in rotated position in thoracic space • Right ventricle lies anteriorly just below the sternum • Left ventricle is located posteriorly • Apical beat obtained from left ventricle at left midclavicular line in the 5th intercostal space Valves: • Tricuspid valve- between R. atrium and R. ventricle • Bicuspid valve- between L. atrium and L. ventricle • Pulmonic valve- between R. ventricle and pulmonary artery • Aortic valve- between L. ventricle and Aorta
  • 14. Heart Sounds: • Mitral and tricuspid valve closure produces first heart sound (S1) • Aortic and pulmonic valves closure produces second sound (S2) Abnormal Heart Sounds: • Gallop sounds – occurs during ventricular filling when there is impediment  gallop sounds comes in triplets with acoustic effect of a galloping horse (sound produced by a rapid moving horse)
  • 15. Two kinds of gallop are S3 and S4  S3 results from rapid ventricular filling phase, may be normal in children and young adults. S3 is associated with:  myocardial diseases  inability of ventricles to eject all blood during contraction  S3 can be heard best when patient is lying on the left and sounds like, ‘Lub-dub-DUB’  S4, which sounds “LUB lub-dub” occurs during atrial contraction in:  enlarged ventricles which resist filling associated with hypertrophy common in hypertension, CHD, and aortic stenosis
  • 16. Cont. of abnormal sounds • Snaps and Clicks:  Results from mitral stenosis (narrowing)  Characterised by high pitched sound heard very early in diastole  They are caused by high pressure in left atrium when it abruptly displaces a rigid mitral valve  It commonly causes murmurs specific to mitral stenosis
  • 17. • Murmurs: caused by turbulent flow of blood due to  Serious narrowed valve  Malfunction valve that allows backflow of blood  congenital defect of ventricular wall  Defect between aorta and pulmonary artery  Increased blood flow thru normal structure in conditions with pyrexia, pregnancy, increased thyroid activity
  • 18. Cont. of abnormal sounds •Friction rub:  Pericarditis causes a harsh, grating sound heard in both systole and diastole termed as friction rub  Pericardial rub is best heard when using diaphragm of stethoscope while patient is in upright position
  • 19. Cardiac conducting system: • Organized atrial and ventricular contraction to ensure coordinated and controlled filling and empting • Cardiac cells contract and relax due to stimulation • Two major cardiac cells are: Unspecialized myocardial cells for contraction
  • 20. Automatic cells specialized for impulse formation • Main bulk of atrial and ventricular muscles are unspecialized myocardial cells • Adjacent myocardial cells are held together by complex system of projections – intercalated discs – with relatively low electrical resistance
  • 21. Cardiac conducting system cont. • Easy movement of electrically charged ions from one myocardial to others to propagate action potentials • Main ions are Na+, K+ and Ca++ • Myocardial cells are polarised in normal resting state • Stimulation of myocardial cells changes cell membrane permeability allowing ions movement, thereby changing electrical polarity (depolarisation)
  • 22. • Depolarised myocardial cells have positive intracellular ions and negative extracellular ions • After depolarisation, repolarisation – returning to resting state – involves active pumping of ions against concentration gradient • Automatic cells regulate myocardial cells contraction by providing initial electrical stimulation
  • 23. Cont of cardiac conducting syst. • Automatic cells consists of 3 properties:  Automaticity – ability to generate action potential, spontaneous and regularly  Excitability – ability to respond to electrical stimulation by stimulating action potential  Conductivity – ability to propagate action potential  Refractoriness – inability to respond to new stimuli while in contraction (depolarised) state
  • 24. • Electrical charge on surface of automatic cell leaks away until certain threshold is reached • Then , spontaneous complete depolarisation occurs over the whole cell surface and spreads to adjacent cells (to both automatic and unspecialized cells) • Automatic cell with most rapid leak of charge becomes the pacemaker (normally located within SA node) • Automatic cell in cardiac conducting system are: SA node (Sinus node), AV node, Bundle of His, left and right bundle branches
  • 25. Sequence of excitation: • Depolarisation begins at SA node and spreads through both atria • Activating impulse travel 1 m/s and reaches most distant atria in about 0.08 seconds (P wave in ECG) • Atria and ventricles remain electrically separate except via AV junction, which allows potential action be conducted from atrial to ventricular conducting system
  • 26. • When impulse reaches AV node, there is a delay of about 0.04s to allow blood flow from atria to ventricles • After emerging from AV node, impulse reaches the rapidly conducting tissue of bundle of His and left and right bundle branches • Impulse spreads rapidly throughout ventricles via purkije fibres, thereby depolarising the ventricles causing efficient ventricular contraction to pump blood out of the heart
  • 27. Electrocardiography (ECG): • Graphic recording from body surface of potential differences resulting from current generated in the heart • ECG is recorded on special graphic paper or on oscilloscope (monitor) and it is recorded against time • ECG detects and interprets Cardiac arrhythmias, diagnosis of CHD, ventrical enlargement or hypertrophy
  • 28. • Electrical sequential events produced at each heart beat is labeled PQRS and T • P wave results from atrial activation (depolarisation), P width represent the time necessary for atrial activation process (0.08s) • Approximately 0.1 s after P wave begins, the atria contracts • PR interval is measured from starting of P wave to beginning of QRS complex that reflects time taken for action potential to spread from SA node, AV node, bundle of His into ventricular mass
  • 29. Cont of ECG • QSR waves reflect ventricular activation. Q is downward deflection after P wave. R wave is the first upward deflection. Then, downward deflection after R is S wave. • P-R interval, represents time impulse takes to spread from atria to ventricles (takes 0.12-0.20 s, average 0.16 s) • QRS complex shows length of time action potential takes through the ventricles (ventricular depolarization time, 0.08 s)
  • 30. • ST segment is a flat line between S wave and T wave, representing the early phase of ventricular muscle repolarisation (recovery) • Q-T interval represents electrical systole (varies in age, sex and heart rate)- takes up to 0.38-o.43s, normally inversely related to HR • T wave represents the actual recovery of the ventricle muscle (repolarisation)- takes about 0.16 seconds
  • 31. Excitation – contraction coupling: • Excitation-contraction coupling describes the link between electrical events and myocardial muscle contraction • When action potential passes over cardiac cell membrane it passes into the interior of each muscle cell down a series of fine branching tubules until it reaches the cells contractile elements to stimulate release of Ca++ ions • Ca++ ions act as catalysts for chemical reaction to activate the sliding of thin muscle filaments (myofilaments) over each other to produce contraction • Myocardial contraction strength partly depends on intracellular concentration of free Ca++
  • 32. Cardiac cycle: • Cardiac cycle – cyclical contraction (systole) and relaxation (diastole) of atria and ventricles • Initiation of each cycle is by spontaneous generation of action potential in SA node • Each chamber fills with blood during diastole • Diastole lasts 0.4 s during which blood enters atria and flows passively into ventricles
  • 33. • Mitral and tricuspid valves open and aortic and pulmonic valves close during ventricular diastole • Blood is expelled from ventricles during systole • Atria contract fractionally before the ventricles and complete ventricular filling • Then ventricles begin to contract (systole), increasing pressure closes mitral and tricuspid valves and opens semilunar valves
  • 34. Cont. of cardiac cycle • Ventricular contraction pushes blood into pulmonary artery and aorta • During diastole pressure within ventricles falls bellow the pressure in major arteries, thus pulmonic and aortic valves close. Then the cycle begins again. • Normal HR for a resting adult is approximately 60- 80 bpm • 65-75% of blood is ejected from the ventricles in each systole • SV is about 70-80 ml at rest • CO is the product of SV x HR • More informatively, CO can be measured using cardiac index, in which CO/min/m2 of BSA is about 3.2 L/m2
  • 35. Primary factors determining CO: • Preload – the amount of tension on the ventricular muscle fibres before they contract, determined primarily by EDV • Afterload – the resistance against which the heart must pump, and its major components are:  Blood pressure in aorta  Resistance in the peripheral vessels  The size of aortic valve opening  Left ventricular size • Contractility of the heart • Heart rate  According to Frank-Starling law of the heart, cardiac out put matches venous return i.e. the heart adapts the changing loads of inflowing blood from systemic and pulmonary circulations
  • 36. Continuation  Within certain limits, the more cardiac muscle contracts forcibly, the more they get stretched at the beginning of contraction  Once venous return increases beyond certain limit, the myocardium begin to fail  Regulation of the heart in response to the amount of blood to be pumped is termed as intrinsic regulation ANS regulation of cardiac function: • ANS alters rate of impulse generated by SA node, the speed of impulse conduction and the strength of cardiac contraction • Stimulation of sympathetic nervous system (fibres) increase HR, conduction speed through AV node and force of contraction
  • 37. Ct of regulation cardiac function • Parasympathetic stimulation via vagus nerve decreases HR, conduction rate through AV node, and atrial conduction force • ANS control of the heart occurs by reflexes coordinated in medulla oblongata • Cardiac centre is the group of brain neurons controlling heart activity and blood vessels • Cardiac centre receives information from various sensory receptors e.g.  Baroreceptors – located in atria, aortic arch and carotid sinus- generate impulse in response to changes in blood pressure  Chemoreceptors – located in carotid artery respond to changes in the chemical composition of the blood
  • 38. Blood supply: • Heart receives 5% of cardiac output to maintain cellular activity • Blood supply is through right and left coronary arteries • Branches of left coronary artery: left anterior interventri- cular (descending) artery (LAD) and circumflex artery (CX) • Right coronary branches: posterior interventricular artery (PIA) and marginal artery (MA) • LAD innervates interventricular septum and anterior walls of both ventricles. CX supplies lateral and posterior L. atrium and L. ventricle. • PIA innervates posterior ventricular walls. MA serves right ventricle • Normally, right coronary artery supplies blood to SA and AV nodes
  • 39. Arterial blood pressure (ABP): • ABP is measurement of pressure exerted by blood as it flows through the arterial walls – systolic and diastolic pressure • Arterial blood pressure is the product of cardiac output times peripheral resistance (CO x PR) Determinants of blood pressure include:  the pumping action of the heart  the peripheral vascular resistance  blood volume  blood viscosity • Normal determinants of pressure are:  Autonomic nervous system  Renin-angiotensin-aldosterone system
  • 40. Factors affecting BP values: • Age (increases with advancing age- arteriosclerosis) • Exercise (increases) • Emotional reaction (stress) • Race (common in the blacks) • Gender (common in males) • Medications (e.g. vasoconstrictors, Glucocorticoids) • Obesity • Diurnal variation (lowest in AM and highest in PM) • Position • Disease process (Renal diseases) • Sleep • Digestion
  • 41. Assessment of cardiovascular system The CVS assessment comprises of  Health history  Physical exam  Diagnostic evaluation
  • 42. Health history Common symptoms • Chest pain or discomfort (angina pectolaris, dysrrhythmia, valvular heart disease) • Shortness of breath or dyspnoea • Peripheral oedema, weight gain, abdominal distension due to enlarged spleen and liver or ascites • Palpitations (tachycardia from variety of causes) • Unusual fatigue, sometimes referred to as vital exhaustion • Dizziness, syncope or changes in level of consciousness (cardiogenic shock, cerebrovascular diseases, dysrrhythmia, hypotension, postural hypotension, vasovagal episode)
  • 43. Health history Past health, family and social history • Any health changes within 5 years • Any cardiovascular problems • Any treatment of CVD • medications • Nutrition
  • 44. Health history • elimination • activity and exercise • sleep and rest • self-perception and self-concept • roles and relationships • sexuality and reproduction • coping and stress tolerance
  • 45. Physical exam Physical Assessment • general appearance • assessment of skin and extremities • blood pressure • pulse pressure • postural blood pressure changes • arterial pulses • pulse rate • pulse rhythm
  • 46. Physical exam • pulse amplitude • pulse contour • palpation of arterial pulses • jugular venous pulsation • heart inspection and palpation • heart auscultation • normal heart sounds S1 and S2 • abnormal heart sounds S3 and S4 • Assessment of other systems • lungs
  • 47. Physical exam • cough • hemoptysis • crackles • wheezes • abdomen • abdominal distension • hepatojugular reflux • bladder distension • gerontologic considerations
  • 48. Diagnostic evaluation Diagnostic evaluation include: • Laboratory tests • Cardiac biomarker analysis • Creatinase secreted by necrotic cardiac muscles is part of diagnostic evaluation of CAD and proteins myoglobin, troponin T, and troponin I.
  • 49. Diagnostic evaluation • Blood chemistry, hematology and coagulation studies • Lipid profile • Cholesterol levels normal is less than 200mg/dL • Triglycerides normal between 100-200mg/dL • LDLs normal levels less than 160mg/dL • HDLs normal levels in men is between 35-70 mg/dL and women 35-85mg/dL
  • 50. Diagnostic evaluation • Brain (B-Type) natriuretic peptide – neurohormone that regulates BP and fluid volume • C-Reactive protein: protein from the liver in response to inflammation that plays a role in atherosclerosis • Homocysteine: an amino acid linked to development of atherosclerosis because it damages endothelial lining of arteries and promotes thrombus formation
  • 51. Diagnostic evaluation • Chest X-Ray and Fluoroscopy • Determines size, contour and position of heart • Electrocardiography • Continuous electrocardiographic Monitoring • Hard wire cardiac monitoring • Telemetry • Ambulatory electrocardiography • Transtelephonic monitoring • Wireless mobile cardiac monitoring
  • 52. Diagnostic evaluation • Cardiac stress testing • Exercise stress testing • Pharmacologic stress monitoring • Done in patients not able to perform exercise stress testing • Iv vasodilating drugs to mimic exercise effects by maximally dilating coronary arteries are given e.g. dipyridamole and adenosine
  • 53. Diagnostic evaluation • Echocardiography • Transthoracic echocardiography • Transesophageal echocardiography • Radionuclide imaging • Myocardial perfusion imaging • Test of ventricular function and wall motion • Computed tomography • Positron emission tomography • Magnetic resonance angiography
  • 54. Diagnostic evaluation • Cardiac catheterization • Right heart catheterization • Left heart catheterization • Electrophysiologic testing • Hemodynamic monitoring • Central venous pressure monitoring • Pulmonary artery pressure monitoring • Intra-arterial blood pressure monitoring • Minimally invasive cardiac output monitoring devices
  • 56. Hypertension Introduction  Intermittent or sustained elevation of diastolic equal/above 90 mmHg or systolic blood pressure equal/above 140 mmHg on three separate readings recorded weeks apart  Associated with: premature death, vascular disease of the brain, heart and kidneys  Usually begins as benign disease, slowly progressing to accelerated or Malignant state  Two major types: Essential (primary or idiopathic) hypertension and secondary hypertension, which result from renal disease or another identifiable cause  Malignant hypertension, a medical emergency: a
  • 57. Pathophysiology • There several theories about pathophysiology of hypertension Changes in arteriolar bed cause increased peripheral vascular resistance Abnormally increased tone in the sympathetic nervous system originating in the vasomotor system centres causes increased peripheral vascular resistance
  • 58. pathophysiology Increase in arteriolar thickening caused by genetic factors leads to increased peripheral resistance Increased activity of renin-angiotensin- aldosterone system, resulting in expansion of extracellular fluid volume and increased vascular resistance due to constriction of arterioles by the effects of angiotensin II.
  • 59. • Resistance to insulin action, which may be a common factor linking hypertension, type two diabetes, hypertriglyridemia, obesity, and glucose intolerance • Adaptation of the innate and adaptive components of the immune response that may contribute to renal inflammation and dysfunction
  • 60. • Increased renal reabsorption of sodium, chloride, and water related to a genetic variation in the pathways by which the kidneys handle sodium
  • 61. causes • Causes for primary hypertension are unknown in most cases, but with various predisposing factors • 5% - 10% (secondary hypertension): due to underlying conditions to include:  Kidney disease e.g renal failure  Coarctation (narrowing) of the aorta, causing hypertension  Endocrine disorders e.g. Cushings Syndrome, pheochromocytoma (tumour in adrenal gland that releases catecholamines; causes 2% of all hypertensions)  Neurologic disorders e.g. increased intracranial pressure  Certain medications, or illicit drugs  Pregnancy
  • 62. Factors implicated as causes of HPN Many factors have been implicated as causes of hypertension: • Increased sympathetic nervous system activity related to dysfunction of the autonomic nervous system • Increased renal reabsorption of sodium, chloride, and water related to a genetic variation in the pathways by which the kidneys handle sodium
  • 63. Factors implicated as causes of HPN • Increased activity of the renin–angiotensin– aldosterone system, resulting in expansion of extracellular fluid volume and increased systemic vascular resistance • Decreased vasodilation of the arterioles related to dysfunction of the vascular endothelium • Resistance to insulin action, which may be a common factor linking hypertension, type 2 diabetes mellitus, hypertriglyceridemia, obesity, and glucose intolerance
  • 64. Risk Factors • Family history of cardiovascular disease • Genetic factors • Race: Africans (the blacks) • Stress • Obesity • High sodium intake • Low potassium, calcium , and magnesium intake • High-saturated fat diet • Impaired renal function (GFR < 60 ml/min and/or microalbuminuria)
  • 65. • Use of hormonal contraceptives • Excess alcohol intake • Use of tobacco • Sedentary lifestyle • Low socio-economic status • Insulin resistance/ diabetes mellitus type 2 • Aging, above 55 years for men, above 65 years for women
  • 66. Incidence • Primarily affects middle aged and older adults • Primary hypertension: 90% - 95% of cases • More than 50% of people aged 60 -74 years are hypertensive • 75% of those aged 75 and older are hypertensive • Incidence of hypertension is her in the blacks than the whites
  • 67. Common characteristics/classifications of blood pressure for adults • Serial blood measurements in mmHg: CATEGORY SYSTOLIC DIASTOLIC Normal < 120 and < 80 Pre-hypertension 120 – 139 or 80 – 89 Hypertension: stage I 140 – 159 or 90 – 99 stage II Equal or above or Equal or above 160 100
  • 68. Complications/Target organ damage • Cardiac disease: Left ventricular hypertrophy Coronary artery disease Myocardial infarction  Congestive heart failure • Stroke or transient • Peripheral vascular/arterial disease • Renal failure • Retinopathy/Blindness
  • 69. Diagnostic assessments • History: Many cases have no symptoms and the disorder is revealed incidentally during an evaluation of another disorder or during a routine blood pressure screening program Symptoms that reflect the effect of hypertension on the organ system Awakening with occipital headache, subsides spontaneously after a few hours
  • 70. History of: • Fatigue, dizziness and confusion • Palpitation, chest pain and dyspnoea • Epistaxis • Haematuria • Blurred vision
  • 71. Physical exam findings include: • Bounding pulse • S4 • Peripheral oedema in the late stages • Hemorrhages, exudates, and papilledema of the eye in late stage if hypertensive retinopathy present • Elevated blood pressure on at least two consecutive occasions after initial screening • Bruits over the abdominal aorta and femoral arteries or the carotids • Palpating abdominal mass, suggesting an abdominal aneurysm.
  • 72. Lab Test Results • Urinalysis: protein, RBCs, or WBCs, suggesting renal disease, or glucose suggesting DM • Serum potassium levels <5.5 mEq/L may indicate adrenal dysfunction (primary hypertension) • Blood urea nitrogen normal or elevated above 20 mg/dl suggesting renal disease • Serum creatinine levels normal or elevated above 1.5 mg/dl suggesting renal disease
  • 73. Imaging Tests • Excretory urography reveals renal atrophy, indicating chronic renal disease, one kidney more than 1.6 cm shorter than the other suggests unilateral renal disease • Chest x-ray may demonstrate cardiomegaly • Renal arteriography may show renal artery stenosis
  • 74. Diagnostic procedures • Electrocardiography may show left ventricular or ischemia • An oral captopril challenge may be done to test for renovascular hypertension • Ophthalmoscopy reveals arteriovenous nicking and, in hypertensive encephalopathy, oedema
  • 75. Management General Management: • Lifestyle modification including Weight control Limiting alcohol intake Regular exercise Smoking cessation Decrease of stress
  • 76. General management • For a patient with secondary hypertension, correction of the underlying cause and control of hypertensive effects • Low saturated fat and low sodium diet • Adequate calcium, potassium, and magnesium in diet
  • 77. Medications • Diuretics to reduce blood volume, such as furosemide, hydrochlorothiazide and indapamide • Beta-adrenergic blockers such as atenolol and meteprolol • Calcium channel blockers to block Ca+ access to cardiac muscle to reduce contractility and conductivity, reduce oxygen demand, relaxes arterioles (lowers periveral vascular resistance): such as, verapamil, nifedipine, felodipine, and nisoldipine • Angiotensin converting enzyme inhibitors: such as benazepril, captopril, and enalapril. Mainstay of vasodilator therapy. More effective when used with diuretics. • Alpha-blockers, such as doxazosine, and prazosin • Angiotensin-receptor blockers such as olmesartan, candesartan, and irbesartan
  • 78. Medications • Vasodilators such as hydralazine, minoxidil • Aldosterone antagonists such as eplerenone and spironolactone • Combination alpha-and beta-blockers such as carvedilol and labetalol • Alpha-receptor antagonist such as clonidine • Direct Renin inhibiters e.g. alskiren (Tektuma), indicated in mild to moderate hypertension to block the conversion of angiotensinogen to angiotensin I by inhibiting the activity of enzyme renin. C/I in pregnancy.
  • 79. Nursing management Nursing diagnoses: • Ineffective self-health management related to lack of knowledge of the condition, complications, management, unpleasant side-effects of drugs, failure to achieve goal BP while on medication, return of BP to normal while on medications, high cost of some medications, inconvenient of taking drugs, lack of trusting relationship with health care provider • Anxiety related to complexity of management regimen, possible complications and lifestyle changes associated with hypertension • Sexual dysfunction related to side-effects of antihypertensive medications
  • 80. Nursing diagnoses • Disturbed body image related to diagnosis of hypertension • Imbalanced nutrition: more than body requirement related to obesity, and alcohol intake • Excess fluid volume related to sodium retention, disruption of renin-angiotensin- aldosterone system • Risk for decreased cardiac tissue perfusion • Risk for ineffective cerebral tissue perfusion • Risk for ineffective renal perfusion
  • 81. Collaborative problems • Potential complication: adverse effects from antihypertensive therapy • Potential complication: hypertensive crisis • Potential complication: stroke • Potential complication: myocardial infarction
  • 82. Key nursing outcomes • The patient will: Maintain adequate cardiac output Maintain hemodynamic stability Develop no arrhythmias Express feelings of increased energy Comply with the therapy regimen Develop no renal failure and stroke
  • 83. Nursing interventions • Administer prescribed drugs • Encourage dietary changes as appropriate • Help patient identify risk factors and modify his/her lifestyle
  • 84. Monitoring: o Vital signs, especially blood pressure o Signs and symptoms of target end-organ damage o Complications o Response to treatment o Risk factor modification o Adverse effects of antihypertensive agents
  • 85. Patient teaching:  Be sure to cover: The disorder, diagnosis and treatment How to use a self-monitoring blood pressure cuff and to record the reading in a journal for review by the physician The importance of compliance with antihypertensive therapy and establishing a daily routine for taking prescribed drugs
  • 86. The need to report adverse effect of drugs The need to avoid high-sodium antacids and over- the-counter cold and sinus medications containing harmful vasoconstrictors Examining and modifying life-style including diet The need for routine exercise program, particularly aerobic walking Dietary restrictions: adopt DASH eating plan (consuming diet rich in fruits, vegetables and low fat) Cessation of alcohol consumption The importance of follow-up care
  • 87. Dietary Approach to Stop Hypertension (DASH) • Grains: seven to eight servings per day • Vegetables: four to five servings per day • Fruits: four to five servings per day • Nonfat/low-fat dairy products: two to three servings per day • Meats, poultry, and fish: two or less 3 oz servings per day • Nuts, seeds and dry beans: four to five servings per a week • Fats and oils: two to three servings per day • Sweets: five servings per a week (should be low in fat)
  • 88. Discharge Planning:  Refer the patient to stress-reduction therapies or support groups as needed
  • 89. Hypertensive Crisis • Significant, rapid elevations in systolic and/or diastolic pressure. Two types: Hypertensive emergency and hypertensive urgency. • In hypertensive emergency or malignant hypertension, the systolic pressure is above 180 mmHg or the diastolic pressure is above 120 mmHg, associated with impending or progressive organ dysfunction • Immediate treatment, just within one hour, is vital to prevent cardiac, brain, renal and vascular damage, and reduce morbidity and mortality. • Intensive cerebral artery spasm occurs to protect brain from high pressure, but in turn, it complicates to cerebral oedema
  • 90. Hypertensive Emergency • Associated with following organ dysfunction: o hypertensive encephalopathy o Hypertensive left ventricular infarction o Hypertension with myocardial infarction o Hypertension with unstable angina o Hypertension with dissection of the aorta o Hypertension with subarachnoid haemmorrhage or CVA o Severe pre-eclampsia or eclampsia o Crisis associated with phaechromocytoma o Hypertension perioperatively o Use of creational drugs e.g. Amphetamines, LSD, Cocaine
  • 91. Signs and symptoms of hypertensive crises • Rapid onset elevation of BP • Blurred vision, papilledema • Systolic pressure greater than 180 mmHg • Diastolic pressure greater than 120 mmHg • Severe headache • Confusion/anxiety • Nasal bleeding • Motor and sensory deficits
  • 92. Hypertensive Urgencies • Isolated large blood pressure elevations without evidence of acute Organ Dysfunction • Elevated blood pressures with severe headaches, nose- bleedings, or anxiety are classified as urgencies • It is associated with treatment discontinuation or reduction as well as anxiety • It should not be treated as emergency but treated by reinstitution or intensification of drug therapy and treatment of anxiety • Oral agents e.g. Labetalol (Beta blocker) and captopril (CCB)or clonidine (Catapres) are given to reduce blood pressure to normal in 24 to 48 hours. • Monitor blood pressure in every 30 minutes till stable
  • 93. Management of hypertensive emergency • Acute life-threatening blood pressure elevations requiring prompt treatment in an intensive care setting because of serious target organ damage that may occur • This Pressure must be reduced by 20 to 25% in one hour of treatment, and a further reduction to a goal pressure of about 160/100 mmHg over a period of 6 hours • Vasodilators e.g. sodium nitropruside, nitroglycerin, diazoxide, hydralazine • Calcium-channel blockers e.g. nicardipine • ACE inhibitor e.g. enalaprilat • Adrenergic blockers: labetalol, esmolol, phentolamine • Monitor vital signs esp. BP in every 5 min, then 15 to 30 min interval when stable
  • 94. HEART FAILURE Introduction: • Definition: It is a clinical syndrome resulting from structural or functional cardiac disorders that impair the ability of ventricles to fill or eject blood (to meet the metabolic needs of the body) [Hinkle & Cheever, 2014] • Fluid buildup in the heart from myocardium that can’t provide sufficient cardiac output • Usually occurs in a damaged left ventricle but may occur in right ventricle, either primarily or secondary to left-sided heart failure
  • 95. • Heart failure (HF) was referred to congestive heart/Cardiac failure (CHF or CCF) due to many patients present with pulmonary or peripheral congestion with oedema • Currently, HF is recognized as clinical syndrome characterized by signs and symptoms of fluid overload or inadequate tissue perfusion • Fluid overload and decreased tissue perfusion occurs when heart cannot generate sufficient cardiac (CO) to meet body’s demand for oxygen and nutrients • In heart failure, impaired contraction of the heart (systolic dysfunction) or filling of the heart (diastolic dysfunction) may cause pulmonary or systemic congestion
  • 96. Pathophysiology Given according to the cause:  Left-sided verses right-sided failure  Systolic or diastolic failure  Low-output or high output failure  Acute or chronic failure  Forward or backward failure
  • 97. Pathophysiology • Left-sided Heart Failure:  Pumping ability of the left ventricle fails and cardiac output falls  Blood backs up in the left atrium and lungs, causing pulmonary congestion and decreased cardiac output.  Causes include: hypertension, myocardial infarction of left ventricle, or valvular heart disease • Right-sided Heart Failure: (Cor pulmonale)  Ineffective contractile function of the right ventricle leads to blood backing up into the right atrium, in the vena cava and the peripheral circulation (venous system), which results in peripheral edema and engorgement of the kidneys and other organs.  Causes include: severe pulmonary disease and myocardial infarction
  • 98. Systolic or diastolic failure Systolic heart failure:  Due to ventricle failure to contract adequately to eject enough blood through aorta into arterial system. Causes decreased ventricular blood ejection  Caused by loss of myocardial cells in ischemia, myocardial infarction (contractile dysfunction), cardiomyopathy or inflammations, increased afterload (hypertension), mechanical abnormalities (e.g. valvular disease)  manifested in effects of low CO e.g. weakness, fatigue, exercise intolerance Over time, it causes left ventricle dilatation and hypertrophy
  • 99. Diastolic heart failure:  Occurs when heart is unable to completely relax (stiffness and non-compliant heart muscle) in diastole, thus disrupts normal filling  Passive diastole filling decreases thereby decreasing stroke volume and cardiac output, but increases atrial contraction to preload  Diastolic function occurs from chronic hypertension ( most common), decreased ventricular compliance due to hypertrophy, and impaired heart muscle contraction  Manifested by dyspnoea, tachypnoea, respiratory crackles in if left ventricle affected and pulmonary hypertension. Neck vein distension, liver enlargement, anorexia, nausea, if right ventricle is affected
  • 100. Low-output VS high-out failure:  Low-output failure • Develops when there is a decrease in the biventricular output resulting from: coronary heart disease, hypertension, cardiomyopathy, and other primary cardiac disorders.  High-output failure (increased/normal cardiac output) • Hypermetabolic states increases CO to maintain blood flow and O2 to tissues • This activates compensatory mechanisms to increase CO thus further increasing O2 demand • Though high CO, the heart is unable to meet increased demands of the tissues and thus fails • Causes include: septicemia, anaemia, hyperthyroidism or AV shunting
  • 101. Acute VS chronic failure: Acute failure: it’s life-threatening and occurs abruptly resulting from myocardial injury e.g. massive myocardial infarction manifested by sudden decrease in cardiac function and signs of decreased CO. Manifests as pulmonary oedema and congestion  Chronic failure: progressive (gradual) decline or deterioration of heart muscle, which allows compensatory mechanisms to come into play. It causes decreased cardiac output. Causes include: cardiomyopathies, valvular disease, or coronary heart disease (CHD)
  • 102. Pathophysiology of Compensatory mechanism leading to heart failure • There are three primary compensatory mechanisms are: 1. The Frank-Starling mechanism: that is, the greater the stretch of the cardiac muscle, the greater the force of contraction. This increases contractile force thereby increasing CO. Complications include: increased myocardial demand; limited by overstretching.
  • 103. pathophysiology 2. Neuroendocrine response including activation of SNS and RAAS • Decreased CO induces SNS and catecholamine release, thereby increasing HR, BP, contractility, vascular resistance and venous return. • Complications include: tachycardia, decreased filling time, low CO, increased vascular resistance, increased myocardial work and O2 demand
  • 104. pathophysiology • Decreased CO and renal perfusion induce renin- angiotensin system. This causes vasoconstriction and increased BP. Complications include: increased myocardial work, renal vasoconstriction, and decreased renal perfusion • ACE converts angiotensin I to angiotensin II, which stimulates aldosterone release from renal cortex resulting in salt and water retention by kidneys, and increased vascular volume overload and vasoconstriction, increasing BP and afterload. Complications include: increased preload and afterload; pulmonary congestion; increased stress on ventricular wall (increased cardiac work-load).
  • 105. pathophysiology • ADH is released from neurohypophysis, which inhibits water excretion; while atrial natriuretic factor that is released from the heart increases Na excretion and diuresis. Complications include; fluid retention and increased preload and afterload • Blood flow is redistributed to vital organs (heart and brain) thereby decreasing perfusion of other organ systems, skin and muscles. Complications include: renal failure, anaerobic metabolism, and lactic acidosis.
  • 106. pathophysiology 3. Ventricular hypertrophy: • Increased cardiac workload causes myocardial muscle to hypertrophy and ventricles to dilate. • This in turn leads to increased contractile force to maintain CO. • This effect complicates into: increased myocardial O2 demand and cellular enlargement • The enlarged myocardial cells become dysfunctional and die early (apoptosis), thus leading to low CO.
  • 107. causes • Mitral stenosis secondary to rheumatic heart disease, constrictive pericarditis, or atrial fibrillation • Mitral and aortic insufficiency • Arrhythmias • Hypertension • Atherosclerosis with myocardial infarction (MI) • Myocarditis • Ventricular and atrial septal defects
  • 108. causes • Endocarditis • Pregnancy • Thyrotoxicosis • Pulmonary embolism • Infections • Anaemia • Emotional • Increased sodium or water intake • Renal failure
  • 109. Incidence • Affects less than 5% in ages between 55 – 64 years • Affects about 10% of people older than 65 years common characteristics • Reduced cardiac output • Shortness of breath • Peripheral oedema • Dyspnoea on exertion
  • 110. Classification heart disease by New York Heart Association Class I: No limitation of physical activity Ordinary activity does not cause fatigue, dyspnoea, palpitation or anginal pain Class II: Slight limitation of physical activity No symptoms at rest Ordinary physical activity causes fatigue, dyspnoea, palpitations or anginal pain
  • 111. Classification cont. Class III: Marked limitation of physical activity but usually comfortable at rest Ordinary physical activity causes fatigue, dyspnoea, palpitations, or anginal pain Class IV: Inability to carry on any physical activity without any discomfort Cardiac insufficiency symptoms or angina may be present Increased discomfort for any activity undertaken
  • 112. complications • Pulmonary oedema • Organ failure, especially the brain and kidneys • Myocardial infarction • Pleural effusion • Left ventricular thrombus
  • 113. Complications cont. o Hepatomegaly (right ventricular failure) o Splenomegaly (in right ventricular failure) o Ascites (in right ventricular failure) o Dysarrhythmias- due to enlargement of chambers of the heart o Cardiomyogenic shock
  • 114. Diagnostic assessments History of: • A disorder or condition that can precipitate heart failure • Dyspnoea or paroxysmal nocturnal dyspnoea • Peripheral oedema • Fatigue • Weakness • Insomnia
  • 115. History of: • Anorexia • Nausea • Sense of abdominal fullness, due to right- sided heart failure • Substance abuse e.g. alcohol, drugs, tobacco.
  • 116. Physical exam findings • Cough that produces pink, frothy sputum • Cyanosis of the lips and nail beds • Orthopnoea • Pale, cool, clammy skin • Diaphoresis • Jugular vein distension • Ascites resulting poor venous return from abdomen and liver congestion • Tachycardia • Pulsus alternans- weak pulse alternating with strong one
  • 117. Physical findings cont. • Hepatomegaly and, possibly, splenomegaly • Decreased pulse pressure • S3 and S4 heart sounds • Moist, bibasilar crackles, rhonchi, and expiratory wheezing • Decreased pulse oximetry • Peripheral oedema • Decreased urinary output
  • 118. Lab test results: • B-type natriuretic peptide immunoassay is elevated • Liver function tests e.g. ALT, AST, LDH, serum bilirubin, and total protein and albumin levels are evaluated to show effect of heart failure on the liver • Thyroid function tests e.g. TSH, TH levels done because both hypothyroidism and hyperthyroidism can be primary or contributory factor for heart failure • In acute heart failure, ABGs done to evaluate gas exchange in lung tissues
  • 119. Imaging results • Chest x-ray shows increased pulmonary markings, interstitial oedema, or pleural effusion and cardiomegaly • Radionuclide imaging to evaluate ventricular function and size • Serum electrolytes measured to evaluate fluid and electrolyte status • Urinalysis, BUN and serum creatinine done to evaluate renal function
  • 120. Diagnostic procedures • ECG reflects heart strain or enlargement or ischemia; atrial enlargement, tachycardia, extrasystole, or atrial fibrillations • Pulmonary artery pressure monitoring typically shows elevated pulmonary artery wedge pressures, left ventricular end-diastolic pressure in left-sided heart failure, and elevated right atrial or central venous pressure in right-sided heart failure
  • 121. Management General management: • Antiembolism stockings to promote venous return • Elevation of lower extremities to relieve oedema • Sodium restricted diet to prevent fluid retention • Fluid restriction to prevent fluid overload • Calorie restriction if indicated to prevent obessity • Low-fat fat diet to prevent atherosclerosis • Walking programs to reduce weight to optimum level • Activity as tolerated to keep fit and prevent dependance
  • 122. Medications • Oxygen therapy as necessary • Diuretics, such as frusemide, bumetanide, torsemide, metolazone and hydrochlorothiazide • Inotropic drugs such as digoxin (digitalis), dobutamine, and dopamine to reduce heart rate and improve cardiac output • Vasodilators such as nitrates (nitroglycerin), sodium nitroprusside, isosorbide, and nesiritide- causes dilatation of arteries and veins • Angiotensin-converting enzyme inhibitors, such as captopril, enalapril, and lisinopril
  • 123. • Angiotensin-receptor blockers, such as losartan, valsartan, and irbesartan to prevent action of angiotensin II and produce vasoconstriction and increased salt and water excretion. Full effect experienced after 3-6 weeks. • Calcium channel blockers, such as amiodipine, felodipine, nefedipine, verapamil to block movement of extracellular Ca++ into cells, causing vasodilation and decreased HR, conractility and systemic vascular resistance
  • 124. • Potassium –sparing diuretics e.g. amiloride and spilonolactone (Aldactone) for exchange of K+ and Na+ in distal renal tubules and reduce excretion of K+, H+, Ca++ and Mg++ • Beta-adrenergic blockers, such as atenolol, metoprolol, propranolol (inderal) and carvedilol • Anticoagulants, such as warfarin • Morphine- decreases preload and afterload in acute decompesated heart failure and pulmonary oedema, dilates pulmonary and systemic blood vessels.
  • 125. Surgical intervention • For valvular dysfunction with recurrent acute heart failure, surgical replacement • Heart transplant – transfer of a heart from one person (especially for one who has suffered massive brain dead) to another • Ventricular assist device • Stent placement
  • 126. Nursing management Nursing Diagnoses • Decreased cardiac output related to altered contractility, altered preload and altered stroke volume as evidenced by jugular vein distension, orthopnoea, S3, S4 • Impaired gas exchange related to increased preload and alveolar capillary membrane changes AEB dyspnoea, tachypnoea, restlessness, verbalisation , “am short of breath”
  • 127. • Excess fluid volume related to increased venous pressure and decreased renal perfusion secondary to HF AEB edema, rapid weight gain, oliguria. • Activity intolerance related to fatigue secondary to cardiac insufficiency and pulmonary congestion • Deficient knowledge: low sodium diet related to lack of information about disease process
  • 128. Expected client outcomes • The client will: Maintain haemodynamic stability Maintain cardiac output Carry out activities of daily living without excess fatigue or decreased energy Maintain adequate ventilation Maintain adequate fluid balance
  • 129. Nursing interventions • Place patient in Fowler’s position • Give supplemental oxygen • Provide continuous cardiac monitoring during acute and advanced stages • Assist the patient with range-of-motion exercises • Apply antiembolism stockings • Check for calf pain and tenderness • Administer prescribed drugs • Provide emotional support
  • 130. Monitor closely for the following: • Daily weight for peripheral oedema and other signs and symptoms of fluid overload • Cardiac rhythm • Intake and output • Response to treatment • Vital signs: TPR and BP and report to physician any deviation • Mental status • Peripheral oedema
  • 131. monitoring • Auscultate for abnormal heart beat and breath sounds, report any changes immediately • Blood urea and nitrogen and serum creatinine, potassium, sodium, and magnesium levels • Prothrombin time
  • 132. Patient Teachings • You must the following patient teachings: Heart failure disorder, diagnosis and treatment Signs and symptoms of worsening heart failure When to notify the physician The importance of follow up-care The need to avoid high-sodium foods The need to avoid fatigue Instructions about fluid restrictions
  • 133. Patient teaching The need to take weight every morning, at the same time, before eating, and after urinating, keeping record of this weight, and reporting weight gain of 1.5 to 2.5 kg in a week The importance of smoking cessation, if appropriate Diet education to include low sodium and low cholesterol diet intake Weight reduction as needed for optimal wt management Medication administration, dosage, possible adverse effects, and monitoring needs
  • 134. Discharge planning • Encourage client to attend for follow-ups • Refer the client to a smoking-cessation program, if appropriate
  • 135. Rheumatic Heart Disease Definition: Rheumatic heart disease (RHD) is a slowly progressive valvular deformity that may follow acute or repeated attacks of rheumatic fever
  • 136. Risk factors • Streptococcal infection of pharynx • Crowded environmental conditions • Low socioeconomic factors • Malnutrition • Immunodeficiency • Poor access to health care • Unknown genetic factor in susceptibility to rheumatic fever
  • 137. Incidence • Occurs worldwide • More common in developing countries • More common before age 15, though it can affect any age
  • 138. Pathophysiology • Rheumatic heart disease occurs as a result of autoimmune response to group A streptococcal throat infection, causing inflammation of tissue containing M proteins. • Carditis occurs in about 50% of rheumatic fever: endocarditis, myocarditis and pericarditis • Aschoff bodies, localized areas of necrotic tissue surrounded by immune cells, develop in cardiac tissues • Endocardial inflammation causes swelling and erythema of valve structures and small vegetative lesions on valve leaflets, making them rigid and deformed • As a result, stenosis and regurgitation occurs , most commonly on the mitral valve, and heart failure ensues
  • 139. Diagnostic Test Characteristics of RHD • Elevated WBC • Reduced RBC • Elevated erythrocyte sedimentation rate • C-reactive protein is positive • Elevated antistreptolysin titer • Throat culture usually positive of group beta-hemolytic streptococci • Elevated cardiac enzymes in severe carditis • ECG changes: prolonged PR interval • Chest X-ray may show cardiac enlargement • Echocardiogram may show valvular damage, enlarged chambers, decreased ventricular function, pericardial efffusion
  • 140. Clinical features • Chest pain • Tachycardia • Pericardial friction rub • Evidence of heart failure (manifestations of heart failure) • Heart murmur: S3 and S4 sounds on auscultation • Cardiomegally • Pericardial effusion • Manifestation of rheumatic fever, including polyarthritis
  • 141. Medical Management  antibiotics to eliminate streptococcal infection, penicillin for at least 10 days  Erythromycin or clindamycin for a patient allergic to penicillin  Prophylactic antibiotic therapy continued for 5 to 10 years, penicillin G 1.2 mu IM every 3-4 weeks  Analgesics for pain relief e.g. aspirin or ibuprofen  Corticosteroids e.g. Prednisone to relieve inflammation (carditis)
  • 142. Nursing intervention • Find out whether patient reacts with penicillins • Administer prescribed antibiotics • Administer analgesics as prescribed • Administer prescribed corticosteroids • Stress the importance of bed rest • Position patient in high Fowler’s position • Provide oxygen therapy as necessary • Monitor vital signs
  • 143. Nursing interventions • Monitor heart rhythm • Monitor heart and respiratory sounds • Provide warm moist compresses for local pain relief • Allow patient express feelings and concerns • Provide psychological and spiritual support • Give balanced diet, low in sodium and fats
  • 144. Patient teaching • Inform the patient on the disorder, diagnosis and treatment • Importance of resuming activities of daily living slowly and scheduling frequent rest periods • Inform patient what to do if reacts with penicillin • Importance of reporting signs of heart failure e.g. severe dyspnoea • Prevention of respiratory infections • Good oral care to prevent gingival infections • Continue with prescribed prophylactic antibiotics • Medication administration, dosages and possible adverse effects • Clinic follow-up for check-ups
  • 145. VALVULAR HEART DISEASE Tricuspid insufficiency (regurgitation, incompetence)
  • 146. TRCUSPID INSUFFICIENCY Introduction • Heart condition in which the tricuspid valve doesn’t function properly • Also called tricuspid regurgidation Causes Rheumatic heart disease Papillary muscle dysfunction Carcinod heart disease Connective tissue disease Trauma  Endocarditis Valvular prolapse  Epstein anomaly
  • 147. Incidence: o Affects both sexes equally o Usually occurs in childhood Common characteristics: • Dyspnoea on exertion • Peripheral oedema • Tachycardia • Fatigue
  • 148. Pathophysiology • The tricuspid valve is incompetent • Blood flows back into the atrium • Fluid overload occurs in the atrium • Congestive failure occurs, and impendance to the pulmonary vasculature may result in hypoxaemia and polycythemia
  • 149. Complications • Heart failure • Pulmonary oedema • Thrombolism • Endocarditis • Arrhythmias
  • 150.
  • 151. Assessment History of: Occurrence of one listed causes Orthopnoea Dyspnoea Fatigue Angina Palpitations
  • 152. Physical findings • Tachycardia • Crackles in the lungs • Hepatomegaly in right-sided failure • Jugular vein distension • S3 heart sound • Diminished peripheral pulses • Ascites • Atrial fibrillations • Peripheral oedema • Pansystolic murmur- murmur throughout systolic perriod
  • 153. Test results  Imaging: o Chest X-ray show right atrial and ventricular enlargement o Echocardiography shows right ventricular dilation and prolapse or flailing of the tricuspid triplets
  • 154. Test results  Diagnostic procedures Electrocardiography shows right atrial hypertrophy, right or left ventricular hypertrophy, and atrial fibrillation, and incomplete right bundle-branch block Right-sided heart catheterization shows high atrial pressure, tricuspid insufficiency, and decreased and normal output
  • 155. Treatment and medication • General treatment include o Underlying cause o Low-sodium diet o Fluid restriction o Activity as tolerated
  • 156. Medications • Diuretics • Cardiac glycoside • Anticoagulants • Angiotensin-converting enzyme inhibitors • Oxygen • Prophylactic antibiotics in some patients before and after surgery or dental care to prevent endocarditis
  • 157. Surgery o Annuloplasty or valvuloplasty to reconstruct or repair the valve o valve replacement with a prosthetic valve
  • 158. NURSING CONSIDERATION Key Outcomes The patient will: o Carry out activities of daily living without weakness or fatigue o Maintain haemodynamic stability o Maintain adequate ventilation
  • 159. NURSING INTERVETIONS • Administer oxygen • Watch for signs of heart failure or pulmonary edema • Alternate periods of activity and rest • Keep patient’s legs elevated to improve venous return to the heart
  • 160. Monitoring • Vital signs and oximetry • Cardiac rhythm • Pulmonary artery catheter readings • Intake and output • Adverse effects of drug therapy
  • 161. Patient teachings • Be sure to cover The disorder, diagnosis and treatment  dietary restrictions and medications Signs and symptoms that should be reported The importance of consistent follow-up care The need to elevated his/her legs when sitting to relieve oedema
  • 162. Tricuspid valve stenosis • Is a valvular disease which results in the narrowing of the orifice of the tricuspid valve of the heart. • Obstructs blood flow from the right atrium to right ventricle • Fibrosed, retracted tricuspid valve cusps and fused leaflets narrow the valve orifice and prevent closure
  • 163.
  • 164. Causes • Rheumatic fever • Carcinoid heart disease • Infective endorcarditis • Tricuspid atresia • Mitral and aortic valve disorders • Endomyocardial fibrosis • Systemic lupus erythematosus
  • 165. Pathophysiology • Alterations in the structure of the tricuspid valve cause incompetence of valve • Restriction of blood flow into the right ventricle and, subsequently, to the pulmonary vasculature occurs • Obstructed venous return results in hepatic enlargement, decreased pulmonary blood flow, peripheral oedema, and right atrial enlargement
  • 166. Incidence • Affects females slightly more common than males Common characteristic • Dyspnoea on exertion • Peripheral oedema • Fatigue • Ascites
  • 167. Complications • Heart failure • Pulmonary oedema • Thromboembolism • Endocarditis • Arrhythmias
  • 168. Diagnostic findings • Assessment History of:  orthopnea  dyspnea  fatigue  angina  palpitations
  • 169. • Physical findings: A low rumbling crescendo-decrescendo murmur in the tricuspid area heard in 4th intercostal space at left sternal boarder or over xiphoid process Split S1 Hepatomegaly Ascites Jugular venous distension Peripheral oedema
  • 170. Test result • Imaging Chest x-ray-reveals cardiomegaly Echocardiography- used to examine the size shape and motion of the cardiac structure Electrocardiography-this is a graphic recording of the electrical activity of the heart
  • 171. Medication • Diuretics eg furosemide • Digoxin • oxygen therapy • Angiotensin converting enzyme inhibitor eg captropil
  • 172. • Surgical management Balloon valvuloplasty Valvotomy-incision to a stenosed cardiac valve tot relieve obstruction
  • 173. Complication • Heart failure • Pulmonary edema • Thromboembolism • Endocarditis
  • 174. Aortic stenosis • Narrowing of the aortic valve that affect blood flow in the heart • It is classified as either acquired or rheumatic
  • 175.
  • 176. Incidence • Possibly asymptomatic till age 50 and 70 • About 80% are males
  • 177. Causes • Idiopathic calcification • Congenital aortic bicuspid valve • Rheumatic fever • Artherosclerosis
  • 178. Pathophysiology of aortic stenosis • Stenosis of the aortic valve results in impendance to foward blood flow • The left ventricle requires greater pressure to open the aortic valve • Added work load increases myocardial oxygen demands • Diminished cardiac output reduces coronary artery blood flow • Left ventricular hypertrophy and failure result
  • 179. Common characteristics • Note; many are asymptomatic • Exertional dyspnea • Orthopnea • Pulmonary edema • Dizziness • Syncope • Angina
  • 180. Assessment and diagnostic findings • History taking • Physical examination: a loud rough systolic murmur is heard over the aortic area. Which may radiate to carotid arteries Other distinguishing finding: • Diminished carotid pulse • Distinct lag between carotid artery pulse and apical pulse
  • 181. • Diagnostic procedures include: Echocardiography- shows decreased valve area and hypertrophied left ventricle. Chest x-ray-shows cardiomegaly Catheterization-shows increased pressure across the aortic valve and in the left ventricle Electrocardiography-shows left ventricular hypertrophy and artrial fibrillation
  • 182. Medications • Cardiac glycosides eg digoxin • Antibiotic for infective endorcaditis prophylaxis • Anticoagulant eg warfarin Surgical management include: Balloon valvuloplasty Commissurotomy
  • 183. Complications • Left-sided heart failure • Right-sided heart failure • Infective endorcarditis • Left ventricular hypertrophy
  • 184. Aortic insufficiency • Is the back-flow of blood into the ventricles causing fluid excess. Incidence • Occurs most commonly in males • When associated with mitral valve disease, it more common in females
  • 185. Causes • Rheumatic fever • Hypertension • Infective endocarditis • Aortic dissection- tearing or rupturing of the aorta • Aortic aneurysm- weakening, thinning and distension of the walls of the aorta
  • 186. pathophysiology • Blood flows back into the left ventricle during diastole causing increased left ventricular diastolic pressure • This results in volume overload, dilation and eventually hypertrophy of the left ventricle • Excess fluid volume also eventually results in increased left arterial pressure and increased pulmonary vascular pressure.
  • 187. Clinical manifestation • Most develop without symptoms • Palpitations • Marked and visible carotid pulses • Fatigue • Orthopnea • Angina • Paroxysmal nocturnal dyspnea
  • 188. Physical findings • Corrigans pulse-carotid (also called water- hammer pulse) pulse that increases rapidly then collapses • Pulses bisferiens (having two beats)-striking twice • Pulsating nail bed and Quincke's’ sign- visible pulsation of red coloration on the nail bed (seen in aortic regurgitation)
  • 189. • Wide pulse pressure (systolic pressure minus diastolic pressure ) • A high pitched blowing decrescendo murmur that radiates from the aortic valve area to the left sternal border.
  • 190. Imaging studies includes Chest x-ray-shows cardiomegaly and pulmonary vein congestion Echocardiography- shows cardiomegaly and thickening of the valve cusps Other tests include • Electrocardiography – shows sinus tachycardia and hypertrophy • Cardiac catheterization-shows degree of aortic insufficiency
  • 191. Medical management • Cardiac glycoside eg digoxin • Diuretics eg furosemide • Vasodilators eg, nitrates • Antihypertensive eg adalat • Antiarrhythmic eg amiodarone • Anticoagulants eg heparin
  • 192. Repair of aortic valve incompetence Surgical management Valvuloplasty- this is the repair of the cardiac valve.
  • 193. complications • Left sided heart failure • Pulmonary edema • Myocardial ischemia
  • 194. Nursing consideration Key outcomes The patient will • Perform activities of daily living without excess fatigue or exhaustion • Avoid complications • Maintain cardiac output
  • 195. Nursing consideration • Demonstrate hemodynamic instability • Maintain balanced fluid status • Maintain joint mobility and range of motion • Develop an demonstrate adequate coping skills
  • 196. Nursing interventions • Give prescribed drugs • Maintain a low sodium diet • Stress the importance of bed rest • Alternate periods of activity with rest • Allow the pateint to voice concerns about the effect of activity restrictions
  • 197. Nursing interventions • Keep the patients legs elevated while he sits on a chair • Place the patient in an upright position and administer oxygen as needed • Allow patient express fears and concerns
  • 198. Monitoring • Vital signs • Intake and output • Signs and symptoms of heart failure • Signs and symptoms of progressive aortic stenosis • Daily weight • Arrythmias • Respiratory status
  • 199. monitoring If patient had surgery, monitor • Signs and symptoms of thrombus formation • Hemodynamic stability • Arterial blood gases levels • Blood chemistry results • Chest x-ray result
  • 200. Patient teaching • Teach on diagnosis, progressive nature of the valvular heart disease and the treatment plan • Patient is taught to report new symptoms to the health care provider • Emphasize the need for prophylactic antibiotic therapy before any invasive procedure • Patient is advised to rest and sleep sitting in chair/ bed with head elevated when experiencing symptoms of pulmonary congestion
  • 201. Mitral stenosis • Is a valvular heart disease characterized by the narrowing of the orifice of the mitral valve of the heart, thereby obstructing blood flow from the left atrium into left ventricle during diastole • The disorder is chronic and progressive • Normally the orifice is 3-6cm • Mild mitral stenosis: orifice is 2cm • Severe mitral stenosis: orifice of 1cm
  • 202. Causes • Rheumatic fever • Congenital anomalies • Atrial myxoma- a benign mucous tumor of the connective tissues. • Endocarditis • Rheumatoid arthritis
  • 203. Incidence • Two-third of the patients are female • It also occurs in 40% of patients with rheumatic heart disease
  • 204. Pathophysiology • The opening narrows to the width of a pencil • The left atrium has difficulty moving blood into the ventricle because of the increased resistance • The left atrium stretches and hypertrophies because of the increased blood volume.
  • 205. pathophysiology • The pulmonary circulation becomes congested, leading to pulmonary hypertension • As a result the right atrium must contract against the high pressure of the pulmonary hypertension causing right- sided heart failure
  • 206. Clinical manifestation • Shortness of breath • Dyspnea on exertion • Chest pain • Palpitations • Hemoptysis • Peripheral and facial cyanosis
  • 207. Diagnostic findings • History taking: for specific symptoms • Physical examination: a loud S1, a split S2, mitral opening snap may be heard Identify the murmur: a low rumbling crescendo- decresendo murmur in the mitral valve area, accompanied by palpable thrill (vibration) • Diagnostic procedures Cardiac catheterization-shows increased pressure in the left atrium Electrocardiography reveals left artrial enlargement
  • 208. Medical management • Digitalis e.g. Digoxin • Diuretics e.g. frusemide • Oxygen therapy • Anticoagulant e.g. warfarin • Nitrates e.g. nitroglycerin • Calcium channel blockers e.g. nifedipine • Beta-adrenergic blockers e.g. atenolol
  • 209. Surgical intervention Surgical management includes Balloon valvuloplasty
  • 210. Balloon inflated in mitral stenotic valve
  • 211. Mitral valve insufficiency • This is a valvular disease of the mitral valve that allows the backflow of blood from the left ventricle to the left atrium. • It may be: Acute. Chronic compensated. Chronic decompensated.
  • 212. Causes • Rheumatic fever • Cardiomyopathy- chronic disorder of the heart muscles • Infective endocarditis • Mitral valve prolapse • Myocardial infarction- death or necrosis of myocardial cells • Congenital anomalies
  • 213. Pathophysiology • Blood from the left ventricle flows back into the right atrium during systole causing the atrium to enlarge to accommodate the backflow • Left ventricles dilate to accommodate the increased volume from the atrium and to compensate for diminishing cardiac output
  • 214. Pathophysiology • Ventricular hypertrophy and increased end-diastolic results in increased pulmonary artery pressure, eventually leading to left sided and right sided heart failure
  • 215. Common characteristics • Dyspnea • Orthopnea • Tachycardia • Angina • palpitations
  • 216. Diagnostic findings • History taking: orthopnea, dyspnea, fatigue, angina, palpitations • Physical examination: tachycardia, crackles. • A high pitched rumbling pansystolic murmur that radiates from the mitral area to the left axillary line
  • 217. Test result • Imaging Chest x-ray-reveals left atrial and ventricular enlargement Echocardiography- shows abnormal valves structure
  • 218. management Medications such as • Diuretics e.g. furosemide • Inotropic agents such as digoxin • Angiotensin converting enzyme inhibitors eg captopril • Oxygen • Anticoagulant e.g. warfarin • Prophylactic antibiotic • Vasodilators such as nitroprusside
  • 219. Surgery • Annuloplasty-the repair of the valve annulus • Valve replacement with prosthetic valve
  • 220. Complications • Heart failure • Pulmonary edema • Thromboembolism • Endorcarditis • Shock
  • 221. Summary • Valvular diseases mainly affect the valves. They can be congenital or acquired. • There are various types of valve disorders classified broadly as stenotic disorders or regurgitation disorders. • Symptoms present as those of heart failure. • Management involves medical, surgical and nursing management. • Common complication is heart failure.
  • 222. Conclusion on valvular diseases • If valvular diseases progress they lead to heart failure. • Proper management and follow-up should therefore be emphasized: Surgical treatment Treament include medications and surgical interventions: Valvuloplasty- repair of valves Commissurotomy- separating fused leaflets
  • 223. Surgical treatment of valvular disorders Annuloplasty-repair of junction of valve and muscular heart wall Leaflet repair- to remove extra tissue leaflets Chordoplasty- repair of chordae tendineae Valve replacement- when above measures have failed, valve replacement is perfomed, two types: mechanical valves (bileaflet, tilting-disk, ball-and- cage design) and tissue valves: 3 types (bioprostheses, homografts, autoggrafts)
  • 224. Coronary Artery Disease Introduction • Type of blood vessel disorder including atherosclerosis, that is, deposits of fat (atheromas) that hardens with age • Atherosclerosis occludes the coronary artery by fibrous, fatty plaque, manifested by angina pectoris, acute coronary syndrome and /or myocardial infarction • Primary effect include: loss of oxygen and nutrients to myocardial tissue because of diminished coronary blood flow
  • 225. Pathophysiology • Increased blood levels of low-density lipoprotein (LDL) irritate or damage the inner layer of coronary vessels • LDL enters the vessel after damaging the protective barrier, accumulates, and forms a fatty streak • Smooth muscle cells move to the inner layer to engulf the fatty substance, produce fibrous tissue, and stimulate calcium deposition • Cycle continues, resulting in transformation of fatty streak into fibrous plaque, and eventually, a coronary artery disease (CAD) evolves
  • 226. Pathophysiology • Oxygen deprivation forces the myocardium to shift from aerobic to anaerobic metabolism, leading to accumulation of lactic acid and reduction of cellular pH cause angina pectoris • The combination of hypoxia and reduced energy availability, and acidosis rapidly impairs left ventricular function
  • 227. Pathophysiology • The strength of contractions in the affected myocardial region is reduced as the fibres shorten inadequately, result in less force and velocity • Wall motion is abnormal in ischemic area, resulting in less blood being ejected from the heart with each contraction
  • 228. causes • Atherosclerosis • Dissecting aneurysm • Infectious vasculitis • Syphylis • Congenital defects • Coronary artery spasm
  • 229. Risk factors • Family history • High serum cholesterol levels above 200 mg/dL • Smoking • Diabetes • Hormonal contraceptives • Obesity: BMI above 30 kg/m2 or waist over 40 inches • Sedentary lifestyle • Stress/psychological states e.g. depression, increased stimulation of SNS
  • 230. Risk factors • Increased homocysteine levels : broken products of aminoacid methionine, which lead to atherosclerosis • Hypertension • Substance abuse e.g. cocaine, methamphetamine cause coronary spasms resulting in myocardial ischemia • Metabolic syndrome: cluster risk factors e.g. insulin resistance, obesity, hypertension, high serum lipids levels
  • 231. Incidence • Occurs after age 40 • Males eight times more susceptible than premenopausal females • Risk increased by family history • White males more susceptible than nonwhite males; nonwhite females more susceptible than white females • In America alone, more than 11 million people affected by CAD Common characteristic  Angina
  • 232. Complications • Arrhythmias- heart beat irregularities • Myocardial infarction- death of cardiac myocytes • Heart failure- insufficient cardiac out to meet body’s metabolic activities • Cardiac shock due to inadequate oxygen and nutrient supply • Ventricular aneurysm • Pericarditis due to cardiac compression • Dressler syndrome: pericarditis with effusion and fever • Papillary muscle dysfunction: if infarcted area includes/adjacent papillary muscle attached to mitral valve
  • 233. Diagnostic assessment History of: • Angina that may radiate to the left arm, neck, jaw, of shoulder blade • Commonly occurring after physical exertion but possibly following emotional excitement, exposure to cold, or ingestion of a large meal • May develop during sleep; symptoms wake the patient • Nausea • Vomiting • Fainting • Sweating • Stable angina: predictable and relieved by rest or nitrates
  • 234. History of: • Unstable angina: increases in frequency and duration and is more easily induced and generally indicates extensive or worsening disease, and, untreated, may progress to myocardial infarction • Crescendo angina: an effort pain-induced occurring with increasing frequency and decreasing provocation • Prinzmental’s or variant angina pectoris: severe non-effort produced pain occurs at rest without provocation to spasm
  • 235. Physical findings • Cool extremities- due to poor blood supply • Xanthoma- soft, yellow skin plaques or nodules containing lipoprotein deposits inside histiocytes related to hyperlipidemia • Arteriovenous nicking of the eye • Obesity- • Hypertension • Positive Levine’s sign (holding fist to chest) • Decreased or absent peripheral pulses
  • 236. Imaging test results • Myocardial perfusion imaging with radionucleotide during treadmill exercise shows ischemic areas of myocardium, visualized as “cold spots”. • Pharmacologic myocardial perfusion imaging in arteries with stenosis shows decrease in blood flow proportional to the percentage of occlusion • Stress echocardiography may show abnormal wall motion
  • 237. Imaging test results • Coronary angiography reveals the location and the degree of coronary artery stenosis or obstruction, collateral circulation, and the condition of the artery beyond the narrowing • Multiple-gated acquisition scanning demonstrates cardiac wall motion and reflects injury to cardiac tissue
  • 238. Diagnostic procedures findings • ECG may be normal between anginal episodes • During angina, ECG may show ischemic changes • Exercise stress testing may be done to detect ST- segment changes during exercise, indicating ischemia, and to determine a safe exercise prescription
  • 239. Treatment/Management General management: • Stress reduction techniques essential especially if known stressors precipitate pain • Lifestyle modifications, such as smoking cessation and maintaining ideal body weight • Low-fat, low-sodium diet • Activity restrictions possible • Regular exercise as tolerated
  • 240. Medications • Antianginals, such as ranolazine and nitroglycerin • Beta adrenergic blocker such as metoprolol • Calcium channel blocker such as diltiazem • Antiplatelets, such as ticlopidine and aspirin • Antilipemic such as simvastatin, atorvastatin, pravastatin • Antihypertensive such as lisinopril
  • 241. Surgery • Coronary artery bypass graft • “Keyhole” or minimally invasive surgery • Angioplasty • Endovascular stent placement • Laser angioplasty • Atherectomy
  • 242. Nursing Management Nursing diagnoses: • Acute pain related to imbalance between myocardial oxygen supply and demand • Decreased cardiac output related to myocardial injury • Anxiety related to actual thread of death, pain, possible lifestyle changes • Activity intolerance related to fatigue • Imbalanced nutrition: more than body requirement related to obesity • Ineffective self-health management related to lack of knowledge of disease process
  • 243. Expected patient outcomes The client will: Maintain hemodynamic stability Plan menus appropriate to prescribed diet Demonstrate understanding of the disease process Express concern about self-concept, self-esteem, and body image Express feeling of increased comfort and decreased pain
  • 244. Nursing interventions • Ask the patient to grade the severity of his/pain on scale of 0 to 10 • Keep nitroglycerin available for immediate use • Instruct patient to call immediately whenever he or she feels pain and before taking nitroglycerin • Observe for signs and symptoms that may signify worsening of condition
  • 245. Nursing interventions • Prepare patient for surgical intervention if indicated • Maintain bed rest immediately postoperatively with the head of the bed elevated at least 30 degrees • Encourage coughing, deep breathing and incentive spirometer use postoperatively • Encourage early ambulation after surgery
  • 246. Monitoring • Vital signs to identify any abnormality • Hemodynamic status • Fluid intake and output • Effectiveness of pain medication during anginal episodes • Abnormal bleeding and distal pulses following intervention procedures • Respiratory status • Chest tube drainage, after surgery • Cardiac rate and rhythm • Cardiovascular status
  • 247. Patient teaching On patient teaching, ensure to cover the following: Risk factors for CAD Avoidance of activities that precipitate pain The need to follow the prescribed drug regimen Effective coping mechanism to deal with stress Low-sodium and low-calorie diet The importance of regular, moderate exercise
  • 248. Discharge planning • Refer the patient to a weight-loss program, if needed • Refer the patient to a smoking-cessation program, if needed • Refer the patient to cardiac rehabilitation program, if indicated
  • 250. OBJECTIVES 1. To describe Thrombophlebitis. 2. To state the cause of Thrombophlebitis. 3. To list the risk factors of Thrombophlebitis. 4. To state the incidence of Thrombophlebitis. 5. To describe the pathophysiology of Thrombophlebitis. 6. To list the signs and symptoms of Thrombophlebitis. 7. To explain the diagnosis of Thrombophlebitis. 8. To discuss the management of Thrombophlebitis. 9. To describe the complications of Thrombophlebitis. 10 . To highlight patient teaching on the condition Thrombophlebitis.
  • 251. Introduction • It is an acute condition that’s characterized by inflammation of the vein accompanied by thrombus formation. • Typically occurs in the cusps because the venous stasis encourages accumulation of and adherence of fibrin and platelets.
  • 252. Cause of Thrombophlebitis • Inflammation due to a blood clot in the vein. Risk Factors • Prolonged bed rest • Trauma • Surgery • pregnancy and childbirth • Hormonal contraceptives or estrogen replacement therapy.
  • 253. Risk factors • Fracture of the spine, femur, pelvis • Smoking • Obesity • Venous stasis • Family Hx of clotting disorder Incidence • Increase use of subclavian vein catheters • Risk for DVT increases after age 20.
  • 254. Pathophysiology • Alteration in epithelial cell lining causes platelet aggregation and fibrin entrapment of RBCs, WBCs and platelets. • The thrombus initiates a chemical inflammatory process in the vessel epithelium that leads to fibrosis which may occlude the vessel lumen or embolize.
  • 255. Signs and symptoms • Inflammation (swelling) in the part of the body affected • Pain in the part of the body affected • Skin redness (not always present) • Warmth and tenderness over the vein
  • 256. Diagnosis and Assessment i. History  Asymptomatic in up to 50% of patients with DVT  Possible tenderness, aching, severe pain in affected leg or arm, fever, chills, malaise in the past. ii. Physical findings • Possible tenderness, aching, severe pain in affected leg or arm, fever, chills, malaise • Positive Homan’s sign. • Lymphadenitis in case of extensive vein involvement.
  • 257. • iii. Test results Diagnostic procedures: Doppler ultrasonography indicates reduced blood flow to a specific area and any obstruction to venous blood flow. Phlebography confirms the diagnosis and shows filling defects and diverted blood flow.
  • 258. Management General: • Application of warm moist compresses to the affected area. • Antiembolism stockings • Bed rest with elevation of the affected extremity. Medications • Anticoagulants i.e. heparin and warfarin • Thrombolytics (e.g., alteplase) is given within the first 3 days after acute thrombosis • Analgesics i.e. NSAIDs
  • 259. Management Surgery  Simple ligation or clipping of the vein  Embolectomy- is the emergency surgical removal of emboli which are blocking blood circulation.  Caval interruption with a transvenous placement of a vena cava filter. Nursing Management Key outcomes: The patient will:
  • 260. Nursing consideration • Maintain collateral circulation • Express feelings of increased comfort and decreased pain • Maintain tissue perfusion and tissue oxygenation • Develop no signs of infection Nursing Interventions • Enforce bed rest and elevate affected leg • Apply warm compresses • Administer prescribed antibiotics • Regulary measure circumference of the affected leg and compare with the other • Administer prescribed anticoagulants
  • 261. Nursing interventions • Encourage or perform ROM exercises • Apply antiembolic stockings • Encourage early ambulation. Monitoring • Signs and Symptoms of bleeding • Vital signs • Clinical features of heparin induced thrombocytopenia • Manifestations of pulmonary embolism • Response to treatment
  • 262. Patient Teaching • Stress on the importance of follow up studies to monitor anticoagulant therapy • Avoid prolonged sitting or standing • Proper application of antiembolism stockings • Importance of adequate hydration
  • 263. Thrombophlebitis (venous thrombosis) Introduction: • Inflammation of the vessel wall with information of a clot (thrombus); may affect superficial or deep veins (deep venous thrombosis) • Most frequent veins affected are the saphenous, femoral and popliteal • Can result in damage to the surrounding tissues, ischemia, and necrosis • Risk factors include: obesity, HF, prolonged immobility, MI, pregnancy, oral contraceptives, trauma, sepsis, cigarette smoking, dehydration, severe anaemia, venous cannulation, complication of surgery
  • 264. Pathophysiology • The three major pathologic factors (Virchow’s triad) predisposing to thrombus formation are: Blood stasis Injury to venous endothelial lining, and Hypercoagulability of blood • A venous thrombosis usually being in a valve cusp where platelets adhere to the endothelium and then to each other. As the process continues, a fibrin mesh covers the platelets (white thrombus).
  • 265. Pathophysiology cont. • As the thrombus grows, it causes obstruction to blood flow. This allows red blood cells, platelets and fibrin to stagnate and form a red thrombus • If thrombus occludes blood flow, venous congestion will develop unless collateral circulation is established • Within a few days of thrombus formation, the body can dissolve the clot or may convert it to fibrous tissue that could incorporate and destroy the valve • Complications of venous thrombus are pulmonary emboli, and venous insufficiency
  • 266. Assessment findings • Pain in the affected area/extremity • Superficial vein: tenderness, redness, induration along course of the vein, palpable cord, distension of superficial veins, prominent venous collaterals • Deep vein: swelling, extreme oedema formation, venous distension of limb, tenderness over involved vein, positive Homan’s sign, cyanosis • Elevated WBC, and ESR
  • 267. Causes (Hinkle, 2014) • Endothelial damage: Trauma Surgery Pacing wires Central venous catheters Dialysis access catheters Local vein damage Repetitive motion injury
  • 268. Causes • Venous stasis: bed rest or immobilisation Obesity History of vasicosities Spinal cord injury Age > 65 years
  • 269. causes • Altered Coagulation: Cancer  pregnancy Oral contraceptive use Protein S deficiency Antiphospholipid antibody syndrome Factor V Leiden defect Prothrombin G20210A defect Hyperhomocysteinemia Elevated factors II, VIII, IX, XI Polycythemia Septicemia
  • 270. Diagnostic evaluation • Venography (phlebography): increased uptake of radio • Plethysmography: non-invasive test measuring venous flow • Duplex ultrasonography: non-invasive visualization of vein and measurement of velocity of venous blood flow • I-125 fibrinogen scanning • Magnetic resonance imaging: non-invasive detection of deep vein thrombosis • Ascending contrast venography: uses injected contrast medium to locate site of thrombus and size
  • 271. Prevention • Leg exercises • Elastic compression • Low dose heparin • External pneumatic compression • Dextran • Warfarin
  • 272. Treatment • Bed rest • Elevate extremities • Local heat • Elastic hose • Analgesics/antiinflammatories e.g. indomethacin or naproxen • Anticoagulation initially with low-moleculat weight heparin • Anticoagulate with warfarin (comoudin) • May use thrombolytic drugs e.g. streptokinase or tissue plasminogen activator to acccelerate clot lysis • Iliofemoral venous thrombectomy
  • 273. Nursing diagnoses • Pain related to inflammation secondary to thrombosis in the involved vein • Ineffective peripheral tissue perfusion related to occlusion of vein, obstruction of blood flow • Ineffective protection related to use of anticoagulants causing bleeding/hemorrhage • Impaired physical mobility related to severe pain, oedema • Risk for ineffective tissue perfusion: cardiopulmonary related to pulmonary embolism
  • 274. Nursing interventions • Promote resolution of thrombus and prevent further thrombus formation by: promoting bed rest Administering anticoagulants as ordered Applying elastic or pneumatic hose as ordered Elevating affected extremity Frequent position changes Deep breathing and fluid intake Providing good skin care
  • 275. Promote resolution and thrombus formation Teaching patient to cease smoking Not massaging the affected extremity Not to stand or sit in any position for long periods of time To avoid use of constricting garments like …… To perform calf and quadriceps contractions several times per hour
  • 276. • Monitor status of extremity by: Assessing quality of pulses Assessing colour Assessing temperature Assessing rapidity of capillary refill Assessing for presence of oedema and pain Monitoring of circumference of the leg daily Monitoring for skin breakdown or ulcers
  • 277. • Promote pain relief by: Providing analgesics as ordered Elastic or pneumatic stockings as ordered Applying warm compresses as ordered Encouraging frequent position changes Elevation of affected extremity and rest periods
  • 278. On-going monitoring and assessments • Monitor complications of pulmonary embolus and bleeding by: Monitoring for tachycardia Monitoring for dyspnoea Monitoring for chest pain Monitoring for hemoptysis Monitoring for changes in breath sounds Monitoring for changes in vital signs
  • 279. On-going monitoring and assessment Monitoring for changes in arterial blood gases Assessing results of serial hemoglobin and hematocrits Assessing PT’s, PTT’s, or APTT’s every day Observing for blood in urine Observing for bleeding from gums and epistaxis • Assessing for and instituting measures to alleviate anxiety
  • 280. Client’s teaching • Teach patient about: Treatment measures including, laboratory tests, and their purposes, Medications and side effects Basic pathophysiology of thrombus formation Measures to prevent future episodes of the condition Prescribed exercises Monitoring for signs of bleeding Recurrent thrombus and pulmonary emboli Need to stop smoking Correct use of elastic hose/pneumatic stockings
  • 281. Client teachings Not using constricting clothing Appropriate methods of heat applications Need for frequent change of position while standing or sitting Wearing of a medic alert bracelet if anticoagulated Importance of follow-up visits and laboratory tests as scheduled
  • 282. Complications • Chronic venous oclusion • Pulmonary emboli • Valvular destruction: Chronic venous insufficiency Increased venous pressure Varicosities Venous ulcers • Venous destruction Increased distal pressure Fluid stasis Edema Venous gangrene
  • 283. VARICOSITY (VARICOSE VEINS) • Dilated tortuous veins, engorged with blood resulting from improper venous valve function • Primary varicose veins originating in superficial veins, especially saphenous and branches • Secondary varicose veins occurring in deep and perforating
  • 284. Pathophysiology • A weakened valve allows backflow of blood to the previous valve • If the valve can’t hold the pooling blood, it becomes incompetent, allowing even more blood to flow backward • As volume of venous blood builds, pressure in the vein increases and the vein becomes distended. • As the vein stretches, it loses elasticity, enlarges, and becomes tortuous • Hydrostatic pressure increases, plasma is forced out into surrounding tissue, and oedema results
  • 285. causes • Congenital weakness of valves or venous wall • Pregnancy • Tight clothing • Occupations that require long standing • Deep venous thrombosis • Trauma
  • 286. Risk factors • Prolonged standing or time on feet • Obesity • Heavy lifting • Pregnancy Incidence  Common in middle adult  Primary varicose veins: family tendency, affect both legs, twice as common in females as males  Secondary varicose veins: usually in only one leg
  • 287. Common characteristics • Dilated, purple, rope-like veins • Oedema of calves and ankles • Venous stasis ulcers Complications  Venous insufficiency  Venous stasis ulcers
  • 288. Assessment History include:  May be asymptomatic  Feeling of heaviness in the legs, worsening in evenings and during warm whether  Leg cramp at night  Diffuse, dull, aching leg pain after prolonged standing or sitting  Aching legs during menses in women  Exercise relieves pain due to venous return improvement
  • 289. Physical findings • Dilated, purplish, ropelike veins in the calf • Orthostatic oedema and stasis of the calves • Nodules along affected veins and valve incompetence • In chronic condition, venous stasis ulcers, which should be differentiated from arterial and diabetic ulcers
  • 290. Test results • Imaging Ascending and descending venography reveals venous occlusion and collateral circulation • Diagnostic procedures Photoplethysmography, a noninvasive test, characterizes venous blood flow by showing changes in the skin’s circulation Dopler ultrasonography quickly and acurately shows presence or absence of venous backflow in deep or superficial veins Venous outflow and reflux plethysmography may be used to identify deep venous occlusion
  • 291. Treatment General: • Put on elastic bandage • Avoid tight clothing • Wear antiembolism stockings for moderate varicosity • Severe varicosities are treated with custorm fitted, surgical weight stockings with graduated pressure • Avoid prolonged standing • Routine exercise • Elevation of the legs
  • 292. Medication/surgery • Medication: Sclerotherapy- the injection of irritating chemicals into a vein to destroy it • Surgical interventions include: Stripping (removing all contents from affected vein) and ligation (the application of a ligature) Laser surgery- use of intense beam of light to vaporize the blockage Catheter-assisted procedure Phlebectomy: surgical removal of a vein or part of a vein Endoscopic vein surgery
  • 293. Nursing considerations Key outcomes The patient will: • Express understanding of disorder and treatment • Maintain adequate distal and collateral circulation • Express feelings of increased comfort and decreased pain • Carry out activities of daily living without excess fatigue or discomfort
  • 294. Nursing considerations • After stripping and ligation or after injection of a sclerosing agent, administer agent analgesics as ordered to relieve pain • Frequently check circulation in toes and observe elastic bandages for bleeding • When ordered, rewrap bandages at least once per a shift, wrapping from toe to thigh, with the leg elevated