Hypertension is not only a disorder but a significant riskfactor to many diseases and complications. Inparticular, hypertension contributes to cardiovascularmorbidity and mortality due to heart failure, rupture ofaortic aneurysms and aortic dissection. In presence ofother diseases like diabetes and other cardiovascularconditions like ischemic heart disease, hypertensionaggravates the condition. Regardless of whetherhypertension contributes directly to the etiology orincreases risk of cardiovascular mortality, systemicarterial hypertension has to be controlled.
REGULATION OF ARTERIAL BLOODPRESSURE ARTERIAL BLOOD PRESSURE- is the pressureexerted by blood against the wall of the arteries. 2 FACTORS DETERMINE ABP1. CARDIAC OUTPUT – the amount of blood thatthe heart ejects each minute.2. TOTAL PERIPHERAL RESISTANCE – theresistance that the blood encounters as it isbeing pumped through the peripheralcirculation. This reflects the tone of theresistance vessels and the viscosity of the blood.
REGULATION OF ARTERIAL BLOODPRESSUREBP = CO x TPR
The body maintains blood pressureby adjusting CO when TPR isincreased; and adjust TPR tocompensate changes in CO.
Normally, blood pressure is regulatedthrough the interplay of four factors:1. CARDIOVASCULAR COMPONENT AUTOREGULATION or the innate ability of thecardiovascular system to adjust flow of blood inrelation to pressure changes by vasoconstriction orvasodilatation. Heart adapts to changing volumes of venousreturn by altering stroke volume Changes in blood volume through fluid shifts fromcapillary to tissues
2. NEURAL REFLEXES mediated bybaroreceptors and chemoreceptors;responsible for short term regulation Baroreceptors are stretched receptors located inthe carotid sinus and aortic arch. Chemoreceptors located in carotid and aorticbodies; sensitive to chemical stimuli such aschanges in oxygen, carbon dioxide, andhydrogen ion content in the blood; wheneverarterial pressure drops below a critical level,chemoreceptors are stimulated because of theaccompanying hypoxia or hypercapnea.
3. HORMONAL MECHANISMS Renin-angiotensin mechanism Aldosterone secretion – promotes renal tubularabsorption of sodium directly, and waterindirectly, resulting in increase in plasma andextracellular blood volume leading to increasecardiac output and arterial blood pressure.
Renal Component by regulating sodiumand water secretion in the kidney tubulesand through the renin- angiotensin-aldosterone (RAA) mechanism
Hypertension - refers to systemic arterial hypertension.It means high blood pressure. Becauseblood pressure varies with age, genderand other factors, definition ofhypertension becomes an important issue.Thus, hypertension is defined assustained elevation in mean arterialpressure.
DEFINITIONS OF HYPERTENSION “ … SYSTOLIC BLOOD PRESSURE (SBP) of 140mmHg or greater, diastolic blood pressure (DBP)of 90 mmHg or greater, or takingantihypertensive medication.”-JOINT NATIONAL COMMITTEE ON PREVENTION,DETECTION, EVALUATION AND TREATMENT OFHIGH BLOOD PRESSURE (JNC VI), 1997 “… sustained SBP of 140 mmHg or greater andsustained DBP of 90 mmHg or more based onmeasurements done during at least 2 visits takenat least 1 week apart.”-Philippine Clinical Practice Guidelines on theDetection and Management of Hypertension
CLASSIFICATION OFHYPERTENSION According to Severity * Optimal blood pressurewith respect to cardiovascularrisk is below 120/80 mmHg.However, unusually lowreadings should be evaluatedfor clinical significance. # Based on the average oftwo or more readings takeneach of two or more visitsafter an initial Screening.CATEGORY SYSTOLIC(mmHg)DIASTOLIC(mmHg)Optimal * < 120 And <80Normal <130 And <85High-Normal 130-139 And 85-89Hypertension #Stage 1 140-159 Or 90-99Stage 2 160-179 Or 100-109Stage 3 ≥ 180 Or ≥110
According to etiology1. ESSENTIAL HYPERTENSION– refers to hypertension with no known medical disorder responsiblefor their high blood pressure. Also known as primary hypertensionand idiopathic hypertension.– There are several working hypotheses for essentialhypertension.a. Autoregulatory Hypothesis- High cardiac output states are associated with hypertension.High CO causes vessels to constrict through autoregulationresulting in diminished blood flow to tissues and increased TPR.In other words, HPN occurs as a compensatory response for highoutput states like hyperthyroidism and hypermetabolic states.
b. Renal Salt retention model- pressure natriuresis which means asblood pressure increases, kidneyssecrete more sodium and water toreduce blood volume and hence bloodpressure. This model proposes that thiscapability of kidney to regulate bloodpressure through pressure natriuresis isdefective in hypertensive individuals.
c. Sodium Transport Hypothesis- this hypotheis proposes thathypertensive individuals have a geneticdefect that prevents normal renal sodiumexcretion.
2. SECONDARY HYPERTENSION - refers to hypertension withidentifiable cause. In other words, HPNis literally secondary to other medicaldisorders. The most common causesinclude kidney diseases, endocrinedisorders, pheochromocytoma, coarctationof the aorta and acute brain lesions. Fluidoverload, drugs and foods, organdysfunction, tumors and pregnancy canalso include hypertension.
CARDIOVASCULAR COMPLICATIONS- include left ventricular hypertrophy,ischemic heart disease and acuteheart failure.
CORONARY ARTERY DISEASE CORONARY ATHEROSCLEROSIS- Abnormal accumulation of lipid or fattysubstance and fibrous tissue in vessel wall.These substances create blockage or narrow thevessel in a way that reduces blood flow tomyocardium.- Involves repetitious inflammatory response toarterial wall injury and an alteration in thebiophysical and biochemical properties of thearterial walls.
PATHOPHYSIOLOGY Deposition of small amounts of lipid material“fatty streaks” in the intima. Accumulation of lipid, especially cholesterol-rich beta lipoprotein in intima and inner media Fibrous encapsulation of the lesions creatingfibrous plaques Development of atheromas or complexatherosclerotic plaques consisting of lipid,fibrous tissue, collagen, calcium, cellulardebris, and capillaries. Degenerative changes in arterial wall.
ASSOCIATED RISK FACTORS: Modifiable:- use of tobacco- Hypertension- Elevated lipid levels- Lifestyle- DM
Non-modifiable:- family history of premature CVD (1stdegree relative with CVD at age 55 oryounger in women and age 65 or youngerin women- Age (More than 45 y/o in male and morethan 55 y/o in female)- Sex- Race
SIGNS AND SYMPTOMS Chest pain (angina pectoris) broughtabout by myocardial ischemia usuallymild to severe retrosternal pain Nausea and vomiting Dizziness and syncope Diaphoresis & cool and clammy skin Apprehension or a sense of impendingdoom
MANAGEMENT EDUCATION GUIDELINES TODECREASE RISK FOR CORONARY ARTERYDISEASE Daily management of hypertension. Takemedication at regular basis. Stop smoking immediately. Smoking reducesavailable O2 to the heart and can precipitateangina. Smoking increases HR and BP. Avoid passive smoke. Two hours of passivesmoke decreases O2 to heart, increases HRand BP. Plan a regular exercise under medicalsupervision.
If overweight, lose weight. Seek helpfrom professional. Follow a healthy heart diet. Reducecholesterol and increase fiber diet. Reduce stress. Allow adequate time for rest andrelaxation.
ANGINA PECTORIS A symptomatic paroxysmal pain orpressure sensation associated withtransient myocardial ischemia lasting nomore than 5-15 minutes
CARDIAC STRESSORSCAUSING ANGINA– Reduced blood flow to cardiac cells resultingfrom coronary blood vessel obstruction– Reduced O2 carrying capacity of blood– Increased O2 need of the heart in high COconditions
FACTORS ASSOCIATED WITHANGINA PECTORIS Physical exertion– Which can precipitate an attack by increasing myocardial O2demand. Exposure to cold– Which can cause vasoconstriction & an elevated BP whichincreases O2 demand. Eating heavy meal– Which can increase the blood flow to the mesenteric area fordigestion, thereby reducing the blood supply available to theheart Emotional stress– Causing release of adrenaline and increase BP which mayaccelerate the HR and increase myocardial workload.
SIGNS AND SYMPTOMS Chest pain– Duration: 5-15 minutes– Location: Substernal or retrosternal whichradiates to the neck, jaw, shoulder and inneraspects of the upper arm usually left arm– Description of pain: tightness, heaviness,choking, strangling sensation, crushing– Related factors: 5 E’s– Relief: rest; nitroglycerin, O2
pallor Diaphoresis Dyspnea Faintness Palpitation Dizziness Digestive disturbance due to vagal stimulation- Not all chest pain is angina. There are other conditionsthat can be mistaken for angina such as peptic ulcer,epigastric reflux, musculoskeletal disorders, extremeemotion, and hyperventilation.
TYPES OF ANGINA Classic/ Effort/ Exertional/ Stable– Associated with atherosclerotic disease ofthe coronary artery. Occurs when metabolicneeds of myocardium exceed the ability ofthe occluded coronary artery to deliveradequate blood flow.– Pain is usually precipitated by increasedemand of heart such as exertion, emotionalstress, and exposure to cold.– Relieved by rest, nitroglycerin.
Variant/ Rest/ Prinzmetal- Caused by spasm of coronary artery resultingto “vasospastic angina”- Occurs during rest or with minimal exercise- Frequently nocturnal associated with REMsleep- Dysrhythmia is often present when pain issevere- With reversible ST segment elevation
Unstable/ Pre infarction/ Crescendo/Intermittent coronary syndrome- An accelerated form of angina where pain ischaracterized by a changing pattern.- Begins and appear more frequently, last longerand occur at rest, pain last more than 15minutes but less than 30 minutes.
Silent ischemia- Occurs without complain of anginal pain.Caused by impaired blood flow due to effect ofcoronary atherosclerosis or vasospasm.- Affects 3 population:– People who are asymptomatic without otherevidence of coronary heart disease.– People with angina who also have episodes of silentischemia– Even people who had MI and continue to haveepisodes of silent ischemia.
DIAGNOSIS1. ECG2. CRP (C-reactive protein)Is a marker for inflammation of vascularendothelium. Increased level of CRP isassociated with increased coronary arterycalcification and risk of an acutecardiovascular event in healthy individuals.3. Increased level of homocysteine.
MEDICAL MANAGEMENT PTCA ( Percutaneous Transluminal CoronaryAngioplasty)– Mechanical dilatation of coronary vessel wall by compressingthe atheromatous plaque– It is recommended for client with single vessel coronarydisease– A specially designed balloon-tipped catheter is inserted underfluoroscopy and advanced to the site of coronary obstruction.– Inflation of the balloon and the catheter tip compresses andsplints the atherosclerotic plaque on the intimal layer of thevessel. Stretching and partial disruption of the medial andadventitial layers of the arterial wall also occurs which resultsto increase vessel diameter.
Intravascular stenting- Biologic stenting is produced throughcoagulation of collagen, elastin, and othertissues in the vessel wall by laser,photocoagulation or radiofrequency inducedheat.- Prosthetic intravascular cylindric stentsmaintain good luminal geometry after balloondeflation and withdrawal.- Intravenous stenting is done to preventrestenosis after PTCA.
SURGICAL MANAGEMENT CORONARY ARTERY BYPASS GRAFT (CABG)- Reduces angina and improves activity tolerane.- It is recommended for one or more branches of coronaryarteries exist.- Main purpose is myocardial revascularization.- Commonly used grafts are the saphenous vein from theleg and left internal mammary artery (LIMA) from thechest.- With saphenous vein bypass graft, one end of the veinsegment is anastomosed to the ascending aorta and theother end is attached beyond the site of vesselobstruction. Thus a vascular conduit is created to shuntblood around the lesion to the myocardium at risk.
NURSING MANAGEMENT INCABG1. Promote comfort Relieve pain Nitroglycerin is the drug of choice to relieve painfrom ischemic attack2. Promote tissue perfusion– Instruct the client to avoid over fatigue– Stop activity immediately in the presence of chest pain,dyspnea, light headedness or faintness which indicates lowtissue perfusion
3. Promote activity and rest Encourage slower activity or shorter periods of activitywith more rest periods. Avoid over exertion. Plan for regular activity programs Take nitroglycerin before exercise Increase extent of exercise gradually
4. Facilitate learning Promote a positive attitude and active participation ofthe client and family to encourage compliance.5. Promote relief of anxiety and feeling ofwell being Facilitate reduction in the client’s level of anxety Advise the client to minimize emotional outbursts,worry and tension Encourage to maintain an optimistic outlook to helprelieve the work of the heart.
MEDICAL MANAGEMENT1. NITROGLYCERIN Effects: Direct relaxing effect on vascular smooth muscle, resultingin generalized vasodilation. Decrease peripheral resistance, decrease systolic pressure,produce venous pooling, decrease preload. Coronary vasodilation, redistributes myocardial blood flowmore efficiently Routes: Sublingual (under the tongue or cheek[buccal pouch]), spray, topical agent, IVadministration.
Nursing Interventions: Assume sitting or supine position when taking the drug.To prevent orthostatic hypotension. Take maximum of 3 doses at five minutes interval. Gradual change of position to prevent orthostatichypotension. If taken sublingual, the medication causes burning orstinging sensation under the tongue. Sublingual routes produces onset of action within 1-2minutes, duration of action is 30 minutes. Offer sips of water before giving sublingual nitrates;dryness of the mouth may inhibit drug absorption.
Instruct patient to avoid drinking alcohol, to avoidhypotension, weakness and faintness. Advise client to always bring 3 tabs in his pocket. Store nitroglycerin in cool, dry place, use dark/amber-colored, air tight container; may be destroyed by heat,light or moisture. Change stock of nitroglycerin every 6 months. Observe for side effects: headache, flushed face,dizziness, faintness, tachycardia; these are common onthe first doses of medication. Do not discontinue thedrug. Transderm – nitropatch is applied once a day, usually inthe morning. Rotation of skin sites is necessary, usuallyon the chest wall. Evaluate effectiveness: relief of pain.
2. BETA-ADRENERGIC BLOCKINGAGENTS (Propanolol, Metoprolol,Atenolol) Effects:- Reduce myocardial O2 consumption byblocking the β-adrenergic sympatheticstimulation to the heart. The result isdecrease HR, hypotension, reducedmyocardial contractility.
Nursing Interventions Side effects and possible contraindications:hypotension, bradycardia, advanced AV block,decompensated heart failure. If given IV, ECG, BP & HR are monitored closelyafter the administration of the medication. Assess PR before administration of the drug;withhold if bradycardia is present. Administer with food to prevent GI upset.
Do not administer propanolol to clients withasthma. It causes bronchoconstriction. Do not stop taking them abruptly, angina mayworsen and MI may develop. Do not administer propanolol to clients with DM.It causes hypoglycemia. Give with extreme caution in clients with heartfailure. Observe for side effects: nausea and vomiting,mental depression, mild diarrhea, fatigue andimpotence, worsening of hyperlipidemia.
3. CALCIUM CHANNEL BLOCKERS(verapamil, Amlodipine, Diltiazem,Felodipine) Effects:- Inhibit Calcium ion transportation intomyocardial cells to depress inotropic andchronotropic activity, decrease myocardialworkload.- Reduces coronary vasospasm- It has vasodilating effect.
Side effects:- AV block- Bradycardia- Constipation- Gastric distress
NURSING INTERVENTIONS Assess HR and BP Monitor hepatic and renal function Administer 1 hour before or 2 hours aftermeals. Food delays absorption anddecrease plasma level of the drug.
4. ANTI-PLATELET &ANTICOAGULANT (ASA,Dipyridamole, Ticlopidine,Clopidogrel) Effects:- ASA- prevents platelet activation anddecrease incidence of MI and death inpatient with CAD.
Side effects:- GI upset and bleeding:- Intervention- Use H2 blocker to allow continuedaspirin therapy. Do not give ASA with coumadin,ASA should be given with food, observe for ASAtoxicity: tinnitus- Plavix and Ticlid are give to patients who areallergic to aspirin or given in addition to ASA inpatients at high risk for MI.
5. HEPARIN Effects:- Inactivates thrombin and other clottingfactors, inhibiting conversion offibrinogen to fibrin, fibrin clottingformation is prevented.
Nursing Interventions: The patient receiving heparin is placed on bleedingprecaution which include:– Applying pressure to the site of any needle puncture for a longertime than usual.– Avoiding intramuscular injection.– Avoiding tissue injury and bruising from trauma or use ofconstrictive devices. Assess for signs and symptoms of bleeding Keep protamine sulfate always available If administered Sc, do not aspirate, do not massage, toprevent hematoma formation. Use for a maximum of 2 weeks.
6. COUMADIN Effects:- Inhibits hepatic synthesis of vitamin K Nursing interventions:- Assess for signs and symptoms of bleeding- Keep Vitamin K always available- Monitor PT- Minimize green leafy vegetables in the diet.These contain Vit K.
DIET: Low sodium, lowcholesterol, high fiber diet. Avoidsaturated fats. White meat and fish arelow in cholesterol. ACTIVITY: No restrictions are placed onactivity, within the patient’s limitations. OXYGEN ADMINISTRATION: Toincrease the amount of O2 delivered tothe myocardium & to decrease pain.
MYOCARDIAL INFARCTION MYOCARDIAL INFARCTION- Other name: Heart attack, coronary occlusion.- If ischemia is prolonged over 30-45 minutes, thiscauses irreversible cellular damage and necrosisof affected myocardium.- MYOCARDIAL ISCHEMIA- causes imbalancebetween myocardial blood supply and demand.- MYOCARDIAL INFARCTION- is caused by totalobstruction in blood supply to a portion of theheart muscle.
OTHER CHANGES ASSOCIATEDWITH MYOCARDIAL INFARCTION Injured and ischemic cells revert to anaerobicmetabolism causing lactic acid production and severeangina. Necrotic cells release their intracellular contents likepotassium causing alterations in contractility andpossible left ventricular dysfunction. Alterations in conduction of impulse resulting in typicalECG changes. Cell death causes inflammation and release ofintracellular proteins and enzymes causing fever,leukocytosis, increased ESR and elevated serumenzymes like CPK and LDH.
MANIFESTATIONS: General Category of Clinical Manifestations:1. Chest pain– Duration- more than 15 minutes– Location- substernal or over precordium– Characteristic – crushing, severe and prolonged– Radiation- spreads widely throughout the chest, withpainful disability of the shoulders and hands.– Relief- Morphine SO4
Anxiety and Apprehension- Feeling of doom and restlessness, lightheadedness which may indicate increasesympathetic stimulation or a decrease incontractility and cerebral oxygenation.- Patient may also deny that anything is wrong. Murmur, (+) heart sounds S3 and S4,increased jugular vein distention seen ifpatient with AMI has HF.
Increased BP due to SNS response to decreased BPdue to reduced contractility and impending cardiogenicshock producing cold, clammy skin, diaphoresis, pallor,edema. Respiratory s/sx: SOB, dyspnea, tachypnea andcrackles if AMI has congestion. GI s/sx: vomiting, gas pain around the heart(indigestion) GUT: Oliguria (urine output less than 30 cc/hour)indicates renal hypoxia due to inadequate renalperfusion. Fever results from destruction of myocardial tissue andensuring inflammatory process.
DIAGNOSTIC PROCEDURE: Definitive diagnosis of AMI requires atleast 2 of the following:1. history of characteristic chest paindiscomfort2. evolutionary changes in ECG3. Elevated cardiac enzymes (elevated CPK-MB is the most definitive finding in MIespecially in the presence of elevatedlevels of LDH.)
COMPLICATIONS OF ACUTEMYOCARDIAL INFARCTION Dysrhythmia (75-90%) Heart failure (60%) cardiogenic shock (10%) – occurs when the heartis unable to contract with adequate force to deliver aCO sufficient to meet normal metabolic needs. Itcauses a shock-like state with inadequate perfusion totissues. In cardiogenic shock, this is due to failure ofthe heart as a pump. Rupture of free wall, septum or papillary muscle(1-5%) Other complication- pericarditis which mayoccur 2-4 weeks after infarction
PHARMACOLOGICMANAGEMENT THROMBOLYTIC THERAPY– Used to dissolve blood and platelet clots allowingblood to flow through coronary artery again.– STREPTOKINASE, UROKINASE, & TISSUEPLASMINOGEN ACTIVATOR (TPA) are examples.– Administration is most crucial between 3-12 hoursafter initial infarction has occurred (when tissue canstill be salvaged and infarction can be prevented)– Detect for occult bleeding during and afterthrombolytic therapy.– Assess neurologic status changes which mayindicate GI bleeding or cardiac tamponade.
NARCOTIC ANALGESIC MORPHINE SULFATE & MEPERIDINE HCL(DEMEROL)- To promote coronary blood supply- Morphine SO4 is most ideal because it not onlyaddresses pain but also relieves anxiety andinduces sleep, reducing myocardial workload.- Demerol is indicated because it does not causerespiratory depression- NALOXENE HCL 0.1-0.2 mg is the antidote ofmorphine.
ANGIOTENSIN CONVERTING ENZYMEINHIBITORS- Prevents conversion of angiotensin 1 toangiotensin II, reduces BP, and kidneyexcretes Na and fluid causing reduced O2demand of the heart IV LIDOCAINE- Maybe given within 24 hours to preventdysrhthmia. OTHER MEDS SAME AS IN ANGINA
SURGICAL MANAGEMENT: PTCA– Must be done within few hours of onset ofMI. CABG- To improve directly circulation to myocardium& therefore limit infarct size- To be successful, CABG should be done 4-5hours after the onset of AMI.- Not beneficial because most patient developAMI outside of hospital.
OTHER MANAGEMENT OXYGEN THERAPY:- At 3-5 lpm via nasal cannula for 24-48 hours to correctmild hypoxemia and relieve pain. BED REST:- To reduce O2 demand of the heart DIET:- Liquid diet for the 1st 24 hours, progressing to soft dietto avoid constipation, avoid large meals and avoidcaffeine contained in coffee, tea, &cola.- Low cholesterol, low salt diet.
HEART FAILURE HEART FAILURE - the heart as a pump isunable to deliver blood to meet the metabolicrequirements of the tissues. The effectiveness of the heart is determined bythe cardiac output, which is the amount ofblood ejected by the heart in a minute. Cardiacdeterminants include preload, afterload,myocardial contractility, heart rate. An indicator for the failure of the heart as apump is an alteration or decrease in cardiacoutput.
CAUSES OF HEART FAILURE Problems in the heart itself Non-cardiac disorders that place unduedemands on the heart
DIAGNOSIS OF HEARTFAILURE This will depend on the presence of twoconditions:- History of an underlying condition that can leadto heart failure- Signs and symptoms of heart failure based onhistory, physical assessment and routinelaboratory tests. Diagnosis of heart failure rarely requires use ofnon-invasive or invasive tests. The nursetherefore plays an important role in recognizingsigns and symptoms that may indicate heartfailure.
SIGNS AND SYMPTOMS Signs of compensatory mechanisms– Tachycardia– Elevation of blood pressure– Edema– Cardiac dilatation and hypertrophy based on PE (displacedapical pulse), EKG, chest X-ray and echocardiographic studies. Shortness of breath, dyspnea, orthopnea, and fatigueresulting from pulmonary congestion, and increased cardiacworkload. Physical examination may also reveal ventricular gallop orS3, which generally accompanies left ventricular failure. Fluid retention and edema Elevated central venous pressure based on examination ofthe neck for elevated jugular venous pressure, or moreaccurately obtained by using a catheter inserted.
MANAGEMENT OF HEARTFAILURE Improve ventricular pump performance- Increasing stroke volume and CO Reduce myocardial workload by:- Decreasing preload- Decreasing afterload- Regulating HR and correcting arrhythmias- Correcting other factors such as infection Increase myocardial perfusion and oxygenation
PHARMACOLOGIC TREATMENTOF HEART FAILURE DIGITALIS– A cardiac glycoside, is the mainstay oftreatment of heart failure.– The most common we use locally is digoxin(Lanoxin)– Digitalis increases force and velocity ofventricular contraction (positive inotropiceffect)
CAUTION! DIGITALIS may be dangerous. There is very narrowdifference between the therapeutic dose and the toxic dose.In other words, digitalis toxicity can easily develop. Watchout for DIGITALIS TOXICITY! Identify at risk patients. (elderly pts, those with advancedheart disease, severe arrhythmias, or acute MI.) Monitor for signs and symptoms of digitalis toxicity- take afull minute heart rate to determine abnormal slowing of theheart (possible heart block), GI symptoms etc. Teach patients and caregivers to recognize digitalis toxicity.
DIURETICS- Enhance renal excretion of sodium and water, whichreduces circulating blood volume, diminishespreload, and lessens systemic and pulmonarycongestion. Nursing Implications:- Monitor urine output to evaluate effectiveness oftreatment and to monitor for possible hypovolemia.- Diuretics should be given in the morning to preventdisturbing sleep at night.- Monitor serum electrolytes, particularly potassium levelespecially in patients taking digitalis.- Educate patient and caregivers.
VASODILATORS- Direct dilation of veins- Dilation of arterioles- Combined action on veins and arterioles- Inhibition of angiotensin convertingenzyme
ANGIOTENSIN CONVERTING ENZYME(ACE) Inhibitors- Suppress RAA system thereby blockingproduction of the potent vasoconstrictorangiotensin II.- This results in increase renal blood flow,and decrease renal vascular resistance,which enhances diuresis.
MORPHINE- The most useful drug for the treatment of pulmonaryedema.- Primary effect is peripheral vasodilation causingpooling of blood thereby reducing both venous returnand cardiac workload.- Allays anxiety associated with severe dyspnea.- It reduces afterload by decreasing arterial bloodpressure and resistance. BETA-ADRENERGIC BLOCKERS- Recent studies shown that administration of thismedication may result in improved symptomatic andfunctional status by slowing the heart rate.
OTHER MEDICAL ANDNURSING INTERVENTIONS POSITIONING- High fowler’s position to reduce pulmonary congestion and easedyspnea.- Legs are maintained in dependent position because if legs areraised, this will increase venous return and further aggaravatepulmonary congestion. BED REST- The overall pumping demand of the heart is decreased and slowsdown heart rate. FLUID AND SODIUM RESTRICTION- To prevent, control or eliminate edema. OXYGEN ADMINISTRATION- May be ordered if the patient is hypoxemic and dyspneic.Hypoxemia in HF is the result of pulmonary congestion, specificallyVQ mismatch.
References– Edition: Cardiovascular Care Made Incredibly easy Second– Style: Softbound ISBN 10:– 0-7817-8824-2– ISBN 13: 978-0-7817-8824-3– Publication Date: May, 2008N261 Cardiovascular Nursing Module– University of the Philippines Open University