Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN                                       ...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN               Upper Chamber (connecti...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN                AV Node( Atrioventricul...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MANGeneral Variables of Cardiac Output    ...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN                                       ...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN      Location: over pericardium. Upri...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MANB. Non-Invasive Procedure1. Cardiac Mon...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN3. Stress Test           A non-invasiv...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN                o     Perfusion imaging...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN               Prosthetic intravascula...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN                                       ...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN            9.     Sedentary lifestyle ...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN                     Make sex as an app...
Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN     C.    NURSING INTERVENTIONS       ...
Cardiovascular Nursing
Cardiovascular Nursing
Cardiovascular Nursing
Cardiovascular Nursing
Upcoming SlideShare
Loading in …5
×

Cardiovascular Nursing

21,982 views

Published on

  • Hi, I'm an RMTU Level IV student, and your reviewers would be a huge help when I study for the upcoming NLE. Can you please send me a copy through e-mail? Mine is t_johanross@yahoo.ca. I would much appreciate it. Thank you!
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • hello Mr Abejo, I can't seem to download your cardiac lecture..please email to nrobinso@sunyrockland.edu
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • Hi Sir,, I would like to ask a copy of your review notes. for my review.. it's a big help for me Sir Please.. Thank you.. this is my email krizzle.tulio@yahoo.com
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • Thank for the notes but would be able to send me the note in my email: aishaahmedmh@gmail.com
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • Your notes are absolutely amazing and very well thought out. Not to mention, the idea is very clear, which is extremely helpful! If you don't mind, could you please send me all of your presentations/notes regarding nursing? I am a nursing student and start clinical in the fall and your notes would be very well appreciated! I hope you take this into consideration. My email is: llancas@siue.edu.
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here

Cardiovascular Nursing

  1. 1. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN MEDICAL AND SURGICAL NURSING Cardiovascular System Lecturer: Mark Fredderick R. Abejo RN, MAN Anatomy and Physiology of the Heart Cardiovascular system consists of the heart, arteries,  Pericardium – invaginated sacveins & capillaries. The major function are circulation of blood,  Visceral – attached to the exterior ofdelivery of O2 & other nutrients to the tissues of the body & myocardiumremoval of CO2 & other cellular products metabolism  Parietal – attached to the great vessels and diaphragmHeart  Papillary Muscle Muscular pumping organ that propel blood into the arerial Arise from the endocardial & myocardial surface of the system & receive blood from the venous system of the body. ventricles & attach to the chordae tendinae Hollow muscular behind the sternum and between the lungs Located on the middle of mediastinum  Chordae Tendinae Resemble like a close fist Attach to the tricuspid & mitral valves & prevent eversion Weighs approximately 300 – 400 grams during systole Has heart wall has 3 layers  Endocardium – lines the inner chambers of the  Separated into 2 pumps: heart, valves, chordate tendinae and papillary  right heart – pumps blood through the lungs muscles.  left heart – pumps blood through the peripheral  Myocardium – muscular layer, middle layer, organs responsible for the major pumping action of the ventricles.  Chamber of the Heart  Epicardium – thin covering(mesothelium), Atria covers the outer surface of the heart  2 chambers, function as receiving chambers, lies above the ventricles Medical and Surgical Nursing 1 Abejo
  2. 2. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN  Upper Chamber (connecting or receiving)  Coronary Veins  Right Atrium: receives systemic venous blood Coronary sinus – main vein of the heart through the superior vena cava, inferior vena cava & Great Cardiac vein – main tributary of the coronary sinus coronary sinus Oblique vein – remnant of SVC, small unsignificant  Left Atrium: receives oxygenated blood returning to the heart from the lungs trough the pulmonary veins Heart Circulation Ventricles  2 thick-walled chambers; major responsibility for forcing blood out of the heart; lie below the atria  Lower Chamber (contracting or pumping)  Right Ventricle: contracts & propels deoxygenated blood into pulmonary circulation via the aorta during ventricular systole; Right atrium has decreased pressure which is 60 – 80 mmHg  Left Ventricle: propels blood into the systemic circulation via aortaduring ventricular systole; Left ventricle has increased pressure which is 120 – 180 mmHg in order to propel blood to the systemic circulation Heart Valves  Tricuspid  Pulmonic  Mitral  Aortic Cardiac Conduction System Properties of Heart Conduction System • Automaticity • Excitability  Coronary artery – 1st branch of aorta • Conductivity Right Coronary • Contractility  SA nodal Branch – supplies SA node  Right marginal Branch – supplies the right border of the heart Structure of Heart Conduction System  AV nodal branch – supplies the AV node  Posterior interventricular artery – supplies both ventricles Left Coronary  Circumflex branch – supplies SA node in 40 % of people  Left marginal – supplies the left ventricle  Anterior interventricular branch aka Left anterior descending(LAD)–supplies both ventricles and interventricular septum  Lateral branch – terminates in ant surface of the heart  Nodal tissues SA Node( Sino-atrial, Keith and Flack)  Primary Pacemaker  Between SVC and RA  Vagal and symphatetic innervation  Sinus RhythmsMedical and Surgical Nursing 2 Abejo
  3. 3. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN AV Node( Atrioventricular , Kent and Tawara) The Normal Cardiac Cycle  At the right atrium  3 zones General Concepts  AN Zone(atrionodal) Systole - period of chamber contraction  N Zone (nodal) Diastole - period of chamber relaxation  NH zone (nodal –HIS) Cardiac cycle - all events of systole and diastole during one heart flow cycle  Internodal and Interatrial Pathways Connects SA and AV Node Ant. Internodal(bachman) tract Middle Internodal(wenkebach) tract Events of Cardiac Cycle Posterior internodal(Thorel) tract 1. mid-to-late ventricular diastole: ventricles filled  Bundle of His/ Purkinje Fibers  the AV valves are open Provides for ventricular conduction system  pressure: LOW in chambers; HIGH in Fastest conduction among cardiac tissues aorta/pulmonary trunk Right bundle  aortic/pulmonary semilunar valves CLOSED Left Bundle  blood flows from vena cavas/pulmonary vein INTO atriaCardiac Action Potential  blood flows through AV valves INTO ventricles (70%)  Depolarization: electrical activation of a cell caused by the influx of sodium into the cell while potassium exits 2. ventricular systole: blood ejected from heart the cell  filled ventricles begin to contract, AV valves CLOSE  Repolarization: return of the cell to the resting state  contraction of closed ventricles increases pressure caused by re-entry of potassium into the cell while  ventricular ejection phase - blood forced out sodium exits  semilunar valves open, blood -> aorta & pulmonary trunk  Refractory periods: Effective refractory period: phase in which cells 3. isovolumetric relaxation: early ventricular diastole are incapable of depolarizing Relative refractory period: phase in which cells  ventricles relax, ventricular pressure becomes LOW require a stronger-than-normal stimulus to  semilunar valves close, aorta & pulmonary trunk depolarize backflow TOTAL CARDIAC CYCLE TIME = 0.8 secondAnatomical Sequence of Excitation of the Heart (normal 70 beats/minute)  (right atrium)  sinoatrial node (SA) atrial systole (contraction) = 0.1 second  (right AV valve) ventricular systole (contraction) = 0.3 second  atrioventricular node (AV) quiescent period (relaxation) = 0.4 second  atrioventricular bundle (bundle of His)  right & left bundle of His branches  Purkinje fibers of ventricular walls Cardiac Output - Blood Pumping of the Heart(from SA through complete heart contraction = 220 ms = 0.22 s) General Concepts • Stroke volume: the amount of blood ejected with eacha. Sinoatrial node (SA node) "the pacemaker" - has the heartbeat fastest autorhythmic rate (70-80 per minute), and sets the • Cardiac output: amount of blood pumped by the pace for the entire heart; this rhythm is called the sinus ventricle in liters per minute rhythm; located in right atrial wall, just inferior to the • Preload: degree of stretch of the cardiac muscle fibers at superior vena cava the end of diastole • Contractility: ability of the cardiac muscle to shorten inb. Atrioventricular node (AV node) - impulses pass from response to an electrical impulse SA via gap junctions in about 40 ms.; impulses are • Afterload: the resistance to ejection of blood from the delayed about 100 ms to allow completion of the ventricle contraction of both atria; located just above tricuspid • Ejection fraction: the percent of end-diastolic volume valve (between right atrium & ventricle) ejected with each heartbeatc. Atrioventricular bundle (bundle of His) - in the interATRIAL septum (connects L and R atria)d. L and R bundle of His branches - within the interVENTRICULAR septum (between L and R ventricles)e. Purkinje fibers - within the lateral walls of both the L and R ventricles; since left ventricle much larger, Purkinjes more elaborate here; Purkinje fibers innervate “papillary muscles” before ventricle walls so AV can valves prevent backflowMedical and Surgical Nursing 3 Abejo
  4. 4. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MANGeneral Variables of Cardiac Output hypernatremia - HIGH Na+ concentration; can block Na+ transport & muscle contraction1. Cardiac Output (CO) - blood amount pumped per minute  CO (ml/min) = HR (beats/min) X SV (ml/beat) 3. Other Factors Effecting Heart Rate (HR)  Normal CO = 75 beats/min X 70 ml/beat = 5.25 L/min normal heart rate - fetus 140 - 160 beats/minute female 72 - 80 beats/minute2. Heart Rate (HR) - cardiac cycles per minute male 64 - 72 beats/minute  Normal range is 60-100 beats per minute  Tachycardia is greater than 100 bpm 1. exercise - lowers resting heart rate (40-60)  Bradycardia is less than 60 bpm 2. heat - increases heart rate significantly  Sympathetic system INCREASES HR 3. cold - decreases heart rate significantly  Parasympathetic system (Vagus) DECREASES HR 4. tachycardia - HIGHER than normal resting heart rate (over 100); may lead to fibrillation3. Blood pressure - Cardiac output X peripheral resistance 5. bradycardia - LOWER than normal resting heart rate  Control is neural (central and peripheral) and (below 60); parasympathetic drug side effects; physical hormonal conditioning; sign of pathology in non-healthy patient  Baroreceptors in the carotid and aorta  Hormones- ADH, aldosterone, epinephrine can increase BP; ANF can decrease BP Vascular SystemRegulation of Stroke Volume (SV) Major function of the blood vessels isto supply the tissue  End diastolic volume (EDV) - total blood collected in with blood, remove wastes, & carry unoxygenated blood ventricle at end of diastole; determined by length of back to the heart diastole and venous pressure (~ 120 ml)  End systolic volume (ESV) - blood left over in ventricle at end of contraction (not pumped out); determined by Types of Blood Vessels force of ventricle contraction and arterial blood pressure (~50 ml) ArteriesSV (ml/beat) = EDV (ml/beat) - ESV (ml/beat)Normal SV = 120 ml/beat - 50 ml/beat = 70 ml/beat Elastic-walled vessels that can stretch during systole & recoil during diastole; they carry blood away from theFrank-Starling Law of the Heart - critical factor for stroke heart & distribute oxygenated blood throughout the bodyvolume is "degree of stretch of cardiac muscle cells"; Arteriolesmore stretch = more contraction force Small arteries that distribute blood to the capillaries & increased EDV = more contraction force function in controlling systemic vascular resistance & slow heart rate = more time to fill exercise = more venous blood return therefore arterial pressure CapilliariesRegulation of Heart Rate (Autonomic, Chemical, Other) The following exchanges occurs in the capilliaries O2 & CO21. Autonomic Regulation of Heart Rate (HR) Solutes between the blood & tissue  Sympathetic - NOREPINEPHRINE (NE) increases heart Fluid volume transfer between the plasma & rate (maintains stroke volume which leads to increased Cardiac Output) interstitial space Venules  Parasympathetic - ACETYLCHOLINE (ACh) decreases heart rate Small veins that receive blood from capillaries & function as collecting channels between the capillaries &  Vagal tone - parasympathetic inhibition of inherent rate of SA node, allowing normal HR veins Veins  Baroreceptors, pressoreceptors - monitor changes in blood pressure and allow reflex activity with the Low-pressure vessels with thin small & less muscles than autonomic nervous system arteries; most contains valves that prevent retrograde blood flow; they carry deoxygenated blood back to the2. Hormonal and Chemical Regulation of Heart Rate (HR) heart. When the skeletal surrounding veins contract, the  epinephrine - hormone released by adrenal medulla veins are compressed, promoting movement of blood during stress; increases heart rate back to the heart.  thyroxine - hormone released by thyroid; increases heart rate in large quantities; amplifies effect of epinephrine  Ca++, K+, and Na+ levels very important; hyperkalemia - increased K+ level; KCl used to stop heart on lethal injection hypokalemia - lower K+ levels; leads to abnormal heart rate rhythms hypocalcemia - depresses heart function hypercalcemia - increases contraction phaseMedical and Surgical Nursing 4 Abejo
  5. 5. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN Palpation: Assessment of the Client with Cardiovascular DisordersNursing HistoryRisk FactorsA. Non – Modifiable Risk Factor  Age  Gender  Race  Heredity Heart Sounds: Stethoscope ListeningB. Modifiable Risk Factor Overview of Heart Sounds (lub-du ; lub, dub )  Stress  Diet lub - closure of AV valves, onset of ventricular systole  Exercise dub - closure of semilunar valves, onset of diastole  Sedentary lifestyle  Cigarette smoking  Tricuspid valve (lub) - RT 5th intercostal, medial  Alcohol  Mitral valve (lub) - LT 5th intercostal, lateral  Hypertension  Aortic semilunar valve (dub) - RT 2nd intercostal  Hyperlipidemia  Pulmonary semilunar valve (dub) - LT 2nd intercostals  DM  Obesity S1 - due to closure of the AV(mitral/tricuspid) valves  Type A personality - timing: beginning of systole  Contraceptive Pills - loudest at the apexCommon Clinical Manifestations of Cardiovascular Disorders S2 - due to the closure of the semi-lunar (pulmonic/aortic) valves - timing: diastole a. Dyspnea - loudest at the base - Exertional - Orthopnea - Paroxysmal Noctural Dyspnea - Cheyne-stokes b. Chest Pain c. Edema - Ascites - Hydrothorax - Anasarca d. Palpitation S3 – Ventricular Diastolic Gallop e. Hemoptysis Mechanism: vibration resulting from resistance to rapid f. Fatigue ventricular filling secondary to poor compliance g. Syncope and Fainting Timing: early diastole h. Cyanosis Location: Apex (LV) or LLSB (RV) i. Abdominal Pain Pitch: faint and low pitched j. Clubbing of fingers k. Jaundice S4 - Atrial Diastolic Gallop Mechanism: vibration resulting from resistance to latePhysical Assessment ventricular filling during atrial systole Timing: late diastole ( before S1)Inspection: Location: Apex ( LV) or LLSB (RV) – Skin color Pitch: low ( use bell) – Neck vein distention Heart Murmurs Murmur - sounds other than the typical "lub-dub"; typically caused by disruptions in flow  Incompetent valve - swishing sound just AFTER the normal "lub" or "dub"; valve does not completely close, some regurgitation of blood  Stenotic valve - high pitched swishing sound when blood should be flowing through valve; narrowing of outlet in the open state – Respirations – Pulsations Pericardial Friction Rub – Clubbing – Capillary refill  It is an extra heart sound originating from the pericardial sac  Mechanism: Originates from the pericardial sac as it moves  Timing: with each heartbeatMedical and Surgical Nursing 5 Abejo
  6. 6. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN  Location: over pericardium. Upright position, leaning 2. Coagulation Screening Test forward  Pitch: high pitched and scratchy. Sounds like sandpaper a. Bleeding Time – measures the ability to stop bleeding after being rubbed together small puncture wound  Significance: inflammation, infection, infiltration b. Partial Thromboplastin Time (PTT) – used to identify deficiencies of coagulation factors, prothrombin and fibrinogen;Classification of Clients with Diseases of the monitors heparin therapy.Heart ( Functional Capacity ) c. Prothrombin Time (Pro-time) – determines activity and  Class I. Patients with cardiac disease but without interaction of the Prothrombin group: factors V (preacclerin), VII resulting limitations of physical activity. (proconvertin), X (Stuart-Power factor), prothrombin and  Class II. Patients with cardiac disease resulting to slight fibrinogen; used to determine dosages of oral anti-coagulant. limitation of physical activity  Class III. Patients with cardiac disease resulting in Normal Values marked limitation of physical activity. They are comfortable at rest. Bleeding Time: 2.75-8 min  Class IV. Patients with cardiac disease resulting in Partial Thromboplastin Time (PTT): 60 - 70 sec. inability to carry on any physical activity without Prothrombin Time (PT): 12-14 sec. discomfortDiagnostic Assessment 3. Erythrocyte sedimentation rate ( ESR) It is a measurement of the rate at which RBC’s settle outPurposes: of anticoagulated blood in an hour It is elevated in infectious heart disorder or myocardial1. To assist in diagnosing MI infarction2. To identify abnormalities3. To assess inflammation Normal Values4. To determine baseline value Male: 15-20 mm/hr5. To monitor serum level of medications Female: 20-30 mm/hr6. To assess the effects of medications 4. CARDIAC Proteins and enzymesA. Blood Studies a. CK- MB ( creatine kinase)1. Complete Blood Count  Most cardiac specific enzymes  Accurate indicator of myocardial dammagea. RBC count- # of RBCs/ mm3 of blood, to diagnose anemia and  Elevates in MI within 4 hours, peaks in 18 hours andploycythemia then declines till 3 days  Normal value is 0-7 U/L or males 50-325 mu/mlb. Hemoglobin- # of grams of hgb/ 100ml of blood; to measure the Female 50-250 mu/mloxygen-carrying capacity of the blood b. Lactic Dehydrogenase (LDH)c. Hematocrit – expressed in %; measures the volume of RBCs in  Most sensitive indicator of myocardial damageproportion to plasma; used also to diagnose anemia and  Elevates in MI in 24 hours, peaks in 48-72 hourspolycythemia and abnormal hydration states Return to normal in 10-14 days  Normally LDH1 is greater than LDH2d. RBC indices- measure RBC size and hemoglobin content  Lactic Dehydrogenase (LDH) a. MCV (mean corpuscular volume)  MI- LDH2 greater than LDH1 (flipped LDH pattern) b. MCH (mean corpuscular hemoglobin)  Normal value is 70-200 IU/L (100 – 225 mu/ml) c. MCHC (mean corpuscular hemoglobin concentrarion) c. Myoglobine. Platelet count- # of Platelet/ mm3; to diagnose  Rises within 1-3 hoursthrombocytopenia and subsequent bleeding tendencies  Peaks in 4-12 hours  Returns to normal in a dayf. WBC count- of WBCs/ mm3 of blood; to detect infection or  Not used aloneinflammation  Muscular and RENAL disease can have elevated myoglobing. WBC Differential count- determines proportion of each WBCin a sample of 100 WBCs; used to classify leukemias d. Troponin I and T  Troponin I is usually utilized for MINormal Values  Elevates within 3-4 hours, peaks in 4-24 hours and persists for 7 days to 3 weeks!RBC: Women – 4.2-5.4 million/mm3  Normal value for Troponin I is less than 0.6 ng/mL Men – 4.7-6.1 million/mm3  REMEMBER to AVOID IM injections beforeHgb: Women – 12-16 g/dl obtaining blood sample! Men – 13-18 g/dl  Early and late diagnosis can be made!Hct : Women – 36-42% Men – 42-48% e. SERUM LIPIDSWBC: 5000-10,000/mm3  Lipid profile measures the serum cholesterol,Granulocytes triglycerides and lipoprotein levels Neutrophils: 55-70%  Cholesterol= 200 mg/dL Eosinophils: 1-4%  Triglycerides- 40- 150 mg/dL Basophils: 0.5-1.0%  LDH- 130 mg/dLAgranulocytes  HDL- 30-70- mg/dL Lymphocytes: 20-40%  NPO post midnight (usually 12 hours) Monocytes: 2-8%Platelets: 150,000-450,000/mm3Medical and Surgical Nursing 6 Abejo
  7. 7. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MANB. Non-Invasive Procedure1. Cardiac Monitoring / Electrocardiography (ECG) A non-invasive procedure that evaluates the electricalactivity of the hearta. Limb Leadsb. Precordial Leads Deflection Waves of ECG 1. P wave - initial wave, demonstrates the depolarization from SA Node through both ATRIA; the ATRIA contract about 0.1 s after start of P Wave. 2. QRS complex - next series of deflections, demonstrates the depolarization of AV node through both ventricles; the ventricles contract throughout the period of the QRS complex, with a short delay after the end of atrial contraction; repolarization of atria also obscured The precordial leads VI –V6 are part of the 12 lead EKG. 3. T Wave - repolarization of the ventricles (0.16 s)They are not monitored with the standard limb leads 4. PR (PQ) Interval - time period from beginning of atrial contraction to beginning of ventricular contraction (0.16 s)c. 12 lead ECG 5. QT Interval - the time of ventricular contraction (about 0.36 s); from beginning of ventricular depolarization to end of repolarization. 2. Holter Monitoring  A non-invasive test in which the client wears a Holter monitor and an ECG tracing recorded continuously over a period of 24 hours  Instruct the client to resume normal activities and maintain a diary of activities and any symptoms that may develop ECG PaperMedical and Surgical Nursing 7 Abejo
  8. 8. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN3. Stress Test  A non-invasive test that studies the heart during C. Invasive Procedure activity and detects and evaluates CAD  Exercise test, pharmacologic test and emotional test 1. Cardiac Catheterization ( Coronary Angiography /  Treadmill testing is the most commonly used stress Arteriography ) test  Insertion of a catheter into the heart and surrounding  Used to determine CAD, Chest pain causes, drug vessels effects and dysrhythmias in exercise  Is an invasive procedure during which physician  Pre-test: consent may be required, adequate rest , eat injects dye into coronary arteries and immediately a light meal or fast for 4 hours and avoid smoking, takes a series of x-ray films to assess the structures alcohol and caffeine of the arteries  During the test: secure electrodes to appropriate  Determines the structure and performance of the location on chest, obtain baseline BP and ECG heart valves and surrounding vessels tracing, instruct client to exercise as instructed and  Used to diagnose CAD, assess coronary atery report any pain, weakness and SOB, monitor BP and patency and determine extent of atherosclerosis ECG continuously, record at frequent interval  Pretest: Ensure Consent, assess for allergy to  Post-test: instruct client to notify the physician if seafood and iodine, NPO, document weight and any chest pain, dizziness or shortness of breath . height, baseline VS, blood tests and document the Instruct client to avoid taking a hot shower for 10-12 peripheral pulses hours after the test  Pretest: Fasting for 8-12 hours, teachings, medications to allay anxiety  Intra-test: inform patient of a fluttery feeling as the4. Pharmacological stress test catheter passes through the heart; inform the patient  Use of dipyridamole that a feeling of warmth and metallic taste may  Maximally dilates coronary artery occur when dye is administered  Side-effect: flushing of face  Post-test: Monitor VS and cardiac rhythm  Pre-test: 4 hours fasting, avoid alcohol, caffeine  Monitor peripheral pulses, color and warmth and  Post test: report symptoms of chest pain sensation of the extremity distal to insertion site  Maintain sandbag to the insertion site if required to maintain pressure  Monitor for bleeding and hematoma formation5. ECHOCARDIOGRAM  Non-invasive test that studies the structural and functional changes of the heart with the use of ultrasound  Client Preparation: instruct client to remain still during the test, secure electrodes for simultaneous ECG tracing, 2. Nuclear Cardiology explain that there will be no pain or electrical shock,  Are safe methods of evaluating left ventricular muscle lubricant placed on the skin will be cool. function and coronary artery blood distribution.  Client Preparation: obtain written consent, explain procedure, instruct client that fasting may be required for6. Phonocardiography a short period before the exam, assess for iodine allergy.  Is a graphic recording of heart sound with simultaneous  Post Procedure: encourage client to drink fluids to ECG. facilitate the excretion of contrast material, assess venipuncture site for bleeding or hematoma.  Types of Nuclear Cardiology o Multigated acquisition (MUGA) or cardiac blood pool scan  Provides information on wall motion during systole and diastole, cardiac valves, and EF. o Single-photon emission computed tomography (SPECT)  Used to evaluate the myocardium at risk of infarction and to determine infarction size. o Positron emission tomography (PET) scanning  Uses two isotopes to distinguish viable and nonviable myocardial tissue.Medical and Surgical Nursing 8 Abejo
  9. 9. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN o Perfusion imaging with exercise testing  Determines whether the coronary  Client Preparation: obtain consent, insertion is under blood flow changes with increased strict sterile technique, usually at the bedside, explain to activity. client the sterile drapes may cover the face, assists to  Used to diagnose CAD, determine position client flat or slight T-postion as tolerated and the prognosis in already diagnosed instruct to remain still during the procedure CAD, assess the physiologic  Nursing Care During Insertion: Monitor and document significance of a known coronary HR,BP and ECG during the procedure lesion, and assess the effectiveness of various therapeutic modalities such as coronary artery bypass surgery, percutaneous coronary intervention, CARDIAC DISORDER or thrombolytic therapy.D. Hemodynamics Monitoring CORONARY ARTERIAL DISEASE ISCHEMIC HEART DISEASE1. CVP ( Central Venous Pressure )  Reflects the pressure of the blood in the right atrium.  Engorgement is estimated by the venous column that can Results from the focal narrowing of the large and be observed as it rises from an imagined angle at th point medium-sized coronary arteries due to deposition of atheromatous of manubrium ( angle of Louis). plaque in the vessel wall  With normal physiologic condition, the jugular venous column rises no higher than 2-3 cm above the clavicle Stages of Development of Coronary Artery Disease with the client in a sitting position at 45 degree angle. 1. Myocardial Injury: Atherosclerosis 2. Myocardial Ischemia: Angina Pectoris 3. Myocardial Necrosis: Myocardial Infarction  CVP is a measurement of: - cardiac efficiency I. ATHEROSCLEROSIS - blood volume - peripheral resistance ATHEROSCLEROSIS ARTERIOSCLEROSIS  Right ventricular pressure – a catheter is passed from a cutdown in the antecubital, subclavian jugular or basilica Narrowing of artery Hardening of artery vein to the right atrium and attached to a prescribed Lipid or fat deposits Calcium and protein manometer or tranducer. deposits Tunica intima  NORMAL CVP is 2 -8 cm h20 or 2-6 mm Hg Tunica media  Decrease indicates dec. circulating volume, increase indicates inc. blood volume or right heart beat failure. A. PRESDISPOSING FACTORS  To Measure: patient should be flat with zero point of 1. Sex: male manometer at the same level of the RA which 2. Race: black corresponds to the mid-axillary line of the patient or 3. Smoking approx. 5 cm below the sternum. 4. Obesity  Fluctuations follow patients respiratory function and will 5. Hyperlipidemia fall on inspiration and rise on expiration due to changes 6. Sedentary lifestyle in intrapulmonary pressure. Reading should be obtained 7. Diabetes Mellitus at the highest point of fluctuation. 8. Hypothyroidism 9. Diet: increased saturated fats 10. Type A personality2. Pulmonary Artery Pressure ( PAP) Monitoring  Appropriate for critically ill clients requiring more B. SIGNS AND SYMPTOMS accurate assessments of the left heart pressure 1. Chest pain  Swan-Ganz Catheter / Pulmonary Artery Catheter is use 2. Dyspnea 3. Tachycardia 4. Palpitations 5. Diaphoresis C. TREATMENT Percutaneous Transluminal Coronary Angioplasty and Intravascular Stenting  Mechanical dilation of the coronary vessel wall by compresing the atheromatous plaque.  It is recommended for clients with single-vessel coronary artery disease.Medical and Surgical Nursing 9 Abejo
  10. 10. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN  Prosthetic intravascular cylindric stent maintain Nursing Management: good luminal geometry after ballon deflation and withdrawal.  Nitroglycerine is the drug of choice for relief of pain  Intravascular stenting is done to prevent restenosis from acute ischemic attacks after PTCA  Instruct to avoid over fatigue  Plan regular activity program For Saphenous Vein Site:  Wear support stocking 4-6 week postop  Apply pressure dressing or sand bag on the site  Keep leg elevated when sitting 3 Complications of CABG 1. Pneumonia: encourage to perform deep breathing, coughing exercise and use of incentive spirometer 2. Shock 3. Thrombophlebitis II. ANGINA PECTORIS Transient paroxysmal chest pain produced by insufficient blood flow to the myocardium resulting to myocardial ischemia Clinical syndrome characterized by paroxysmal chest pain that is usually relieved by rest or nitroglycerine due to temporary myocardial ischemia Types of Angina Pectoris  Stable Angina: pain less than 15 minutes, recurrence is less frequent.  Unstable Angina : pain is more than 15 mins.,but not less than 30 minutes, recurrence is more frequent and theCoronary Arterial Bypass Graft Surgery intensity of pain increases.  Variant Angina ( Prinzmetal’s Angina ): Chest pain is on longer duration and may occur at rest. Result from coronary vasospasm.  Angina Decubitus: paroxysmal chest pain that occur when the client sits or stand. A. PRESDISPOSING FACTORS 1. Sex: male 2. Race: black 3. Smoking 4. Obesity 5. Hyperlipidemia 6. Sedentary lifestyleGreater and lesser saphenous veins are commonly used for 7. Diabetes Mellitusbypass graft procedures 8. Hypertension 9. CAD: Atherosclerosis 10. Thromboangiitis Obliterans 11. Severe Anemia 12. Aortic Insufficiency: heart valve that fails to open & close efficiently 13. Hypothyroidism 14. Diet: increased saturated fats 15. Type A personality B. PRESIPITATING FACTORS 4 E’s of Angina Pectoris 1. Excessive physical exertion: heavy exercises, sexual activity 2. Exposure to cold environment: vasoconstriction 3. Extreme emotional response: fear, anxiety, excitement, strong emotions 4. Excessive intake of foods or heavy meal C. SIGNS AND SYMPTOMS 1. Levine’s Sign: initial sign that shows the hand clutching the chest 2. Chest pain: characterized by sharp stabbing painObjectives of CABG located at sub sterna usually radiates from neck, 1. Revascularize myocardium back, arms, shoulder and jaw muscles usually 2. To prevent angina relieved by rest or taking nitroglycerine(NTG) 3. Increase survival rate 3. Dyspnea 4. Done to single occluded vessels 4. Tachycardia 5. If there is 2 or more occluded blood vessels CABG is 5. Palpitations done 6. DiaphoresisMedical and Surgical Nursing 10 Abejo
  11. 11. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN  Propanolol: not given to COPD cases: it causes D. DIAGNOSTIC PROCEDURE bronchospasm and DM cases: it cause 1. History taking and physical exam hypoglycemia 2. ECG: may reveals ST segment depression & T wave  Side Effects: Nausea and vomiting, mental inversion during chest pain depression and fatigue 3. Stress test / treadmill test: reveal abnormal ECG during exercise 4. Increase serum lipid levels C. Calcium – Channel Blockers: relaxes smooth 5. Serum cholesterol & uric acid is increased cardiac muscle, reduces coronary vasospasm Amlodipine ( norvasc ) E. MEDICAL MANAGEMENT Nifedipine ( calcibloc ) 1. Drug Therapy: if cholesterol is elevated Diltiazem ( cardizem ) Nitrates: Nitroglycerine (NTG)  Assess HR and BP Beta-adrenergic blocking agent: Propanolol  Adminester 1 hour before meal and 2 hours Calcium-blocking agent: nefedipine after meal ( foods delay absorption ) Ace Inhibitor: Enapril 2. Modification of diet & other risk factors 4. Administer oxygen inhalation 3. Surgery: Coronary artery bypass surgery 5. Place client on semi-to high fowlers position 4. Percutaneuos Transluminal Coronary Angioplasty 6. Monitor strictly V/S, I&O, status of (PTCA) cardiopulmonary fuction & ECG tracing 7. Provide decrease saturated fats sodium and caffeine F. NURSING INTERVENTIONS 8. Provide client health teachings and discharge 1. Enforce complete bed rest planning 2. Give prompt pain relievers with nitrates or narcotic  Avoidance of 4 E’s analgesic as ordered  Prevent complication (myocardial infarction) 3. Administer medications as ordered:  Instruct client to take medication before indulging into physical exertion to achieve the A. Nitroglycerine(NTG): when given in small maximum therapeutic effect of drug doses will act as venodilator, but in large doses  Reduce stress & anxiety: relaxation techniques will act as vasodilator & guided imagery  Give 1st dose of NTG: sublingual 3-5  Avoid overexertion & smoking minutes  Avoid extremes of temperature  Give 2nd dose of NTG: if pain persist after  Dress warmly in cold weather giving 1st dose with interval of 3-5  Participate in regular exercise program minutes  Space exercise periods & allow for rest periods  Give 3rd& last dose of NTG: if pain still  The importance of follow up care persist at 3-5 minutes interval 9. Instruct the client to notify the physician NTG Tablets(sublingual) immediately if pain occurs & persists despite rest &  Keep the drug in a dry place, avoid medication administration moisture and exposure to sunlight as it may inactivate the drug  Change stock every 6 months  Offer sips of water before giving III. MYOCARDIAL INFARCTION sublingual nitrates, dryness of mouth may inhibit drug absoprtion  Relax for 15 minutes after taking a tablet: Death of myocardial cells from inadequate oxygenation, to prevent dizziness often caused by sudden complete blockage of a coronary  Monitor side effects: orthostatic artery hypotension, flushed face. Transient Characterized by localized formation of necrosis (tissue headache & dizziness: frequent side effect destruction) with subsequent healing by scar formation &  Instruct the client to rise slowly from fibrosis sitting position Heart attack  Assist or supervise in ambulation Terminal stage of coronary artery disease characterized by malocclusion, necrosis & scarring. NTG Nitrol or Transdermal patch Types of M.I  Nitropatch is applied once a day, usually  Transmural Myocardial Infarction: most dangerous type in the morning. characterized by occlusion of both right and left coronary  Avoid placing near hairy areas as it may artery decrease drug absorption  Subendocardial Myocardial Infarction: characterized by  Avoid rotating transdermal patches as it occlusion of either right or left coronary artery may decrease drug absorption  Avoid placing near microwave ovens or The Most Critical Period Following Diagnosis of during defibrillation as it may lead to Myocardial Infarction burns (most important thing to remember) 6-8 hours because majority of death occurs due to arrhythmia leading to premature ventricular contractions B. Beta-blockers: decreases myocardial oxygen (PVC) demand by decreasing heart rate, cardiac output and BP A. PREDISPOSING FACTORS Propanolol 1. Sex: male Metropolol 2. Race: black Pindolol 3. Smoking Atenolol 4. Obesity  Assess PR, withhold if dec.PR 5. CAD: Atherosclerotic  Administer with food ( prevent GI upset ) 6. Thrombus Formation 7. Genetic Predisposition 8. HyperlipidemiaMedical and Surgical Nursing 11 Abejo
  12. 12. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN 9. Sedentary lifestyle 2. Administer oxygen low flow 2-3 L / min: to prevent 10. Diabetes Mellitus respiratory arrest or dyspnea & prevent arrhythmias 11. Hypothyroidism 3. Enforce CBR in semi-fowlers position without bathroom 12. Diet: increased saturated fats privileges(use bedside commode): to decrease cardiac 13. Type A personality workload 4. Instruct client to avoid forms of valsalva maneuver B. SIGNS AND SYMPTOMS 5. Place client on semi fowlers position 1. Chest pain 6. Monitor strictly V/S, I&O, ECG tracing & hemodynamic Excruciating visceral, viselike pain with sudden procedures onset located at substernal& rarely in 7. Perform complete lung / cardiovascular assessment precordial 8. Monitor urinary output & report output of less than 30 ml Usually radiates from neck, back, shoulder, / hr: indicates decrease cardiac output arms, jaw & abdominal muscles (abdominal 9. Provide a full liquid diet with gradual increase to soft diet: ischemia): severe crushing low in saturated fats, Na & caffeine Not usually relieved by rest or by 10. Maintain quiet environment nitroglycerine 11. Administer stool softeners as ordered:to facilitate bowel 2. N/V evacuation & prevent straining 3. Dyspnea 12. Relieve anxiety associated with coronary care 4. Increase in blood pressure & pulse, with gradual unit(CCU)environment drop in blood pressure (initial sign) 13. Administer medication as ordered: 5. Hyperthermia: elevated temp a. Vasodilators:Nitroglycirine (NTG), Isosorbide 6. Skin: cool, clammy, ashen Dinitrate, Isodil (ISD): sublingual 7. Mild restlessness & apprehension b. Anti Arrythmic Agents: Lidocaine (Xylocane), 8. Occasional findings: Brithylium Pericardial friction rub Side Effects: confusion and dizziness Split S1& S2 c. Beta-blockers: Propanolol (Inderal) Rales or Crackles upon auscultation d. ACE Inhibitors: Captopril (Enalapril) S4 or atrial gallop e. Calcium Antagonist: Nefedipine f. Thrombolytics / Fibrinolytic Agents: Streptokinase, C. DIAGNOSTIC PROCEDURED Urokinase, Tissue Plasminogen Activating Factor 1. Cardiac Enzymes (TIPAF) CPK-MB: elevated Side Effects:allergic reaction, urticaria, pruritus Creatinine phosphokinase(CPK):elevated Nursing Intervention: Monitor for bleeding time Heart only, 12 – 24 hours g. Anti Coagulant Lactic acid dehydrogenase(LDH): is increased Heparin Serum glutamic pyruvate transaminase(SGPT): Antidote: Protamine Sulfate is increased Nursing Intervention: Check for Partial Serum glutamic oxal-acetic transaminase(SGOT): is increased Thrombin Time (PTT) 2. Troponin Test: is increased Caumadin(Warfarin) 3. ECG tracing reveals Antidote:Vitamin K ST segment elevation Nursing Intervention: Check for T wave inversion Prothrombin Time (PT) Widening of QRS complexes: indicates that h. Anti Platelet: PASA (Aspirin): Anti thrombotic effect there is arrhythmia in MI Side Effects:Tinnitus, Heartburn, Indigestion / Dyspepsia Contraindication:Dengue, Peptic Ulcer Disease, Unknown cause of headache 14. Provide client health teaching & discharge planning concerning: a. Effects of MI healing process & treatment regimen b. Medication regimen including time name purpose, schedule, dosage, side effects c. Dietary restrictions: low Na, low cholesterol, avoidance of caffeine d. Encourage client to take 20 – 30 cc/week of wine, whisky and brandy:to induce vasodilation e. Avoidance of modifiable risk factors f. Prevent Complication 4. Serum Cholesterol & uric acid: are both increased 5. CBC: increased WBC Arrhythmia: caused by premature ventricular contraction D. NURSING INTERVENTIONS Cardiogenic shock: late sign is oliguria Left Congestive Heart Failure Goal: Decrease myocardial oxygen demand Thrombophlebitis: homan’s sign Stroke / CVA 1. Decrease myocardial workload (rest heart) Dressler’s Syndrome(Post MI Syndrome):client Establish a patent IV line is resistant to pharmacological agents: Administer narcotic analgesic as ordered: Morphine administer 150,000-450,000 units of Sulfate IV: provide pain relief(given IV because streptokinase as ordered after an infarction there is poor peripheral perfusion g. Importance of participation in a progressive activity & because serum enzyme would be affected by IM program injection as ordered) h. Resumption of ADL particularly sexual intercourse: Side Effects: Respiratory Depression is 4-6 weeks post cardiac rehab, post CABG & Antidote: Naloxone (Narcan) instruct to: Side Effects of Naloxone Toxicity: is tremorsMedical and Surgical Nursing 12 Abejo
  13. 13. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN Make sex as an appetizer rather than dessert Aminophylline to reduce Instruct client to assume a non weight bearing bronchospasm caused by severe position congestion. Client can resume sexual intercourse: if can Vasodilators to reduce venous return climb or use the staircase Diuretics to decrease circulating i. Need to report the ff s/sx: volume Increased persistent chest pain Dyspnea V. PERICARDITIS / DRESSLER’S SYNDROME Weakness Fatigue Is the inflammation of the pericardium which occurs Persistent palpitation approximately 1 – 6 weeks after AMI. Light headedness Results as an antigen – antibody response. The necrotic j. Enrollment of client in a cardiac rehabilitation tissues play the role of an antigen, which trigger antibody program formation. Inflammatory process follows. k. Strict compliance to mediation & importance of Constrictive Pericarditis is a condition in which a chronic follow up care inflammatory thickening of the pericardium compresses the heart so that it is unable to fill normally during diastole.IV. CARDIOGENIC SHOCK ( POWER/PUMP FAILURE ) A. SIGNS AND SYMPTOMS Is a shock state which result from profound left 1. Pain in the anterior chest, aggravated by coughing, ventricular failure usually from massive MI. yawning, swallowing, twisting and turning the torso, It result to low cardiac output, thereby systemic relieved by upright, leaning forward position. hypoperfusion. 2. Pericardial friction rub – scratchy, grating or cracking sound A. SIGNS AND SYMPTOMS 3. Dyspnea 1. Decrease systolic BP 4. Fever, sweating, chills 2. Oliguria 5. Joints pains 3. Cold, clammy skin 6. Arrhythmias 4. Weak pulse 5. Cyanosis B. NURSING INTERVENTIONS 6. Mental lethargy 7. Confusion 1. Elevate head of bed, place pillow on the overbed table so that the patient can lean on it. B. MEDICAL MANAGEMENT 2. Bed rest 1. Counterpulsation ( mechanical cardiac assistance / 3. Administer prescribed pharmacotherapy. diastolic augmentation ) a. ASA to suppress inflammatory process Involves introduction of the intra – aortic b. Corticosteriods for more severe symptoms balloon catheter via the femoral artery 4. Assist in pericardiocentesis if cardiac tamponade is Intra Aortic Balloon Pump augments present. 5. Pericardiocentesis is aspiration of blood or fluid diastole, resulting in increased perfusion from pericardial sac. of the coronary arteries and the myocardium and a decrease in left ventricular workload. VI. CARDIAC TAMPONADE The balloon is inflated during diastole, it is deflated during sytole. Also known as pericardial tamponade, is an emergency Indications: condition in which fluid accumulates in the pericardium  Cardiogenic shock (the sac in which the heart is enclosed).  AMI If the fluid significantly elevates the pressure on the heart  Unstable Angina it will prevent the hearts ventricles from filling properly.  Open heart surgery This in turn leads to a low stroke volume. C. NURSING INTERVENTIONS The end result is ineffective pumping of blood, shock, and often death. 1. Perform hemodynamic monitoring 2. Administer oxygen therapy A. PREDISPOSING FACTORS 3. Correct hypovolemia. Administer IV fluids as 1. Chest trauma ( blunt or penetrating ) ordered 2. Myocardial ruptured 4. Pharmacology: 3. Cancer a. Vasodilators: Nitroglycerine 4. Pericarditis b. Inotropic agents:Digitalis, Dopamine 5. Cardiac surgery ( first 24 – 48 hours ) c. Diuretics : Furosemide 6. Thrombolytic therapy d. Sodium Bicarbonate, Relieve lactic acidosis 5. Monitor hourly urine output, LOC and arrhythmias B. SIGNS AND SYMPTOMS 6. Provide psychosocial support 1. Beck’s Triad 7. Decrease pulmonary edema  Hypotension a. Auscultate lung fields for crackles and wheezes  Jugular venous distension b. Note for dyspnea, cough , hemoptysis and  Muffled heart sound orthopnea 2. Pulsus paradoxus ( drop of at least 10 mmHg in c. Monitor ABG for hypoxia and metabolic arterial BP on inspiration ) acidosis 3. Tachycardia d. Place in fowler’s position to reduce venous 4. Breathlessness return 5. Decrease in LOC e. Administer during therapy as ordered: Morphine sulfate to reduce venous return.Medical and Surgical Nursing 13 Abejo
  14. 14. Lecture Notes on Cardiovascular SystemPrepared By: Mark Fredderick R Abejo R.N, MAN C. NURSING INTERVENTIONS 3. Pulmonary embolism (char by chest pain and dyspnea) 1. Administer oxygen 4. Pulmonic stenosis 2. Elevate head of bed, place pillow on the overbed 5. Left sided heart failure table so that the patient can lean on it. 3. Bed rest B. SIGNS AND SYMPTOMS (Venous congestion) 4. Administer prescribed pharmacotherapy. 1. Jugular vein distention c. ASA to suppress inflammatory process 2. Pitting edema d. Corticosteriods for more severe symptoms 3. Ascites 5. Assist in pericardiocentesis and thoracotomy 4. Weight gain 6. Pericardiocentesis is aspiration of blood or fluid 5. Hepatosplenomegaly from pericardial sac. 6. Jaundice 7. Pruritus/ urticaria 8. Esophageal varices CONGESTIVE HEART FAILURE 9. Anorexia 10. Generalized body malaise Inability of the heart to pump blood towards systemic C. DIAGNOSTICScirculation 1. CXR – cardiomegaly 2. CVP – measures pressure in right atrium; N = 4-I. LEFT-SIDED HEART FAILURE 10cc H2O  During CVP: trendelenburg  to prevent A. PREDISPOSING FACTORS pulmo embolism and to promote ventricular 1. 90% - Mitral valve stenosis filling  RHD  Flat on bed post CVP, check CVP readings  Inflammation of mitral valve  Hypovolemia – fluid challenge  Anti-streptolysin O titer (ASO) – 300 todd  Hypervolemia – diuretics (loop) units 3. Echocardiography – reveals enlarged heart chamber  Penicillin, PASA, steroids  Muffled heart sounds  cardiomyopathy  Aging  Cyanotic heart diseases 2. MI  TOF  “tet” spells  cyanosis with 3. IHD hypoxemia 4. HPN  Tricuspid valve stenosis 5. Aortic valve stenosis  Transposition of aorta  Acyanotic B. SIGNS AND SYMPTOMS  PDA – machine-like murmur 1. Pulmonary edema/congestion  DOC: indomethacin SE: corneal  Dyspnea, PND (awakening at night d/t cloudiness difficulty in breathing), 2-3 pillow orthopnea 4. Liver enzymes  Productive cough (blood tinged)  SGPT up  Rales/crackles  SGOT up  Bronchial wheezing  Frothy salivation D. NURSING MANAGEMENT 2. Pulsus alternans (A unique pattern during which the amplitude of the pulse changes or alternates in size Goal: increase myocardial contraction  increase CO; with a stable heart rhythm.)This is common in Normal CO is 3-6L/min; N stroke volume is 60-70ml/h2o severe left ventricular dysfunction.) 3. Anorexia and general body malaise 1. Administer medications as ordered 4. PMI displaced laterally, cardiomegaly  Cardiac glycosides 5. S3 (ventricular gallop)  Digoxin (N=.5-1.5, tox=2)  Tox: Anorexia, N&V; A: Digibind C. DIAGNOSTICS  Digitoxin – given if (+) ARF; metabolized 1. CXR – cardiomegaly in liver and not in kidneys 2. PAP – pulmonary arterial pressure  Loop diuretics  Measures pressure in right ventricle  Lasix – IV push, mornings  Reveals cardiac status  Bronchodilators 3. PCWP – pulmonary capillary wedge pressure  Aminophylline (theophylline)  Measures end-systolic and end-diastolic  Tachycardia, palpitations pressure (elevated)  CNS hyperactivity, agitation  Done through cardiac catheterization (Swan-  Narcotic analgesics Ganz)  Morphine sulfate – induces vasodilation 4. Echocardiograph – reveals enlarged heart chamber  Vasodilators 5. ABG analysis reveals elevated PCO2 and decreased  NTG and ISDN PO2 (respiratory acidosis)  hypoxemia and  Anti-arrhythmic agents cyanosis  Lidocaine (SE: dizziness andTracheostomy  for severe respiratory distress and laryngospasm  confusion)performed at bedside within 10-15 minutes  Bretyllium  YOU DON’T GIVE BETA-BLOCKERS TOCVP  reveals fluid status; Normal = 4-10cm H2o; right atrium THESE PATIENTSPAP – cardiac status; left atrium 2. Administer O2 inhalation at 3-4 L/minute via NC asALLEN’S test – collateral circulation ordered  high flowCardiac Tamponade: pulsus paradoxus, muffled heart sounds, HPN 3. High fowler’s, 2-3 Pillows 4. Restrict Na and fluidsII. RIGHT SIDED HEART FAILURE 5. Monitor strictly VS and IO and Breath Sounds 6. Weigh pt daily and assess for pitting edema A. PREDISPOSING FACTORS 7. abdominal girth daily and notify MD 1. Tricuspid valve stenosis 8. provide meticulous skin care 2. COPDMedical and Surgical Nursing 14 Abejo

×