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SCENARIO Mrs. Florence Black is 60 year old, married with grown-up children.

She presents to the emegergency room after being brought in by the ambulace with an acute episode of shortness of breath, a noticeable swelling of the ankles and reports a decrease in appetite for the past week. Mrs. Black was admitted to the Coronary Care unit with a diagnosis of Congestive Heart Failure.

QUESTIONS: 1. Discuss the pathophysiology of CHF. 2. What diagnositc work- ups should be considered in caring for Mrs. Black?. Discuss its implications. 3. Formulate a nursing care plan (including drugs) integrating the nursing process and the 11 key areas of responsibility

Heart Failure, also called as congestive heart failure, is a clinical syndrome that results from the hearts inability to pump the amount of oxygenated blood necessary to meet the metabolic requirements of the body. The common pathophysiologic state that perpetuates the progression of heart failure is extremely complex, regardless of the precipitating event. Compensatory mechanisms exist on every level of organization, from subcellular all the way through organ-to-organ interactions. Only when this network of adaptations becomes overwhelmed does heart failure ensue. Cardiac compensatory mechanisms (increases in heart rate, vasoconstriction, heart enlargement) occur to assist the failing heart.

These mechanisms are able to compensate for the hearts inability to pump ineffectively and maintain sufficient blood flow to organs ad tissue at rest

Physiologis stressors that incraese the workload of the heart (exercise, infection) may cause these mechanisms to fail and precipitate the clinical syndrome associated with the failing heart (elevated ventricular/ atrial pressures, sodium and water retention, decrased cardiac output, ciculatory and pulmonary cogestion). The compensatory mechanisms may hasten the onset of failure because they increase afterload and cardiac work.

Left Sided Heart Failure (Forward Failure) Congestion occurs mainly in the lungs from backing up of blood into pulmonary veins and capillaries Fatigability from low cardiac output, nocturia, insomnia, dyspnea, catabolic effect of heart failure Insomnia, restlessness Tachycardia S3 ventricular gallop

Right Sided Heart Failure (Backward Failure


signs and symptms of elevated pressures and congestion in systemic veins and capillaries) Edema of the ankles; unexplained weight gain (pitting edema is obvious only after retention of atleast 4.5 kg of fluid) Liver congestion may produce upper abdominal pain Distended neck veins Abnormal fluid in body cavities (pleural space, abdominal cavity) Anorexia and nausea hepatic and visceral engorgement Nocturia diuresis occurs at night with rest and improved cardiac output Weakness

Cardiovascular finding in BOTH types Cardiomegaly - detected by physical examination and chest x ray Ventricular gallop evident on auscultation ; ECG Rapid heart rate Development of pulsus alternans (alternation in strength of beat

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ECG may show ventricular hypertrophy and strain Echocardiography may show ventricular hypertrophy, dilation of chambers, and abnormal wall motion Chest X Ray may show cardio megaly, pleural effusion, and vascular congestion ABG studies may show hypoxemia due to pulmonary vascular congestion Liver function studies may be altered because of heparic congestion

Treatment is directed at eliminating excessive accumulation of body water. Increasing the force and efficiency of myocardial contraction, and reducing the workload of the heart. These goals are achieved through promoting rest and administering pharmacologic agents which are the following:

DIURETICS 1. Eliminate excess body water and decrease ventricular pressures 2. A low soidum diet and restriction complement this therapy 3. Some diuretics may have slight venodilator properties

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INOTROPIC AGENTS Increase hearts ability to pump more effectively by improving the contractile force of the muscle. Digoxin (Lanoxin) may only be effective in severe cases of failure. Dopamine (Intropin) also improves renal blood flow in low dose range. Dobutamine (Dobutrex) Milrinone (Primacor) and Amrinone (Inocor) are potent vasodilators

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VASODILATOR THERAPY Decreases workload of the heart by dilating peripheral vessels. Reduces ventricular filling pressures (preload) and volumes by relaxing capacitance vessels (veins and venules) Reduce impedance to left ventricular ejection and improve stroke volume by relaxing resistance vessels (arterioles) Vasodilators used in CHF :
Nitrates such as niroglycerin (tridil), isosorbid dinitrate (Isordil), NTG ointment (Notrobid) predominantly dilate systemic veins. Hydralazine (Apresoline) affects arterioles; reduces arteriolar tone. Prazosin (Minipress) balance effects on both arterial and venous circulation Sodium nitroprusside (Nipride) affects arteriloes Morphine sulfate (Duramorph) decreases venous return, decreases pain and anxiety and thus cardiac work.

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ANGIOTENSIN

- CONVERTING ENZYME

INHIBITORS 1. Inhibit the adverse effects of angiotensin II (potent vasoconstrictor) 2. Decreases left ventricular afterload with subsequent decrease imn heart rate associated with heart failure, thereby reducing the workload of the heart and increasing cardiac output. 3. Captopril (Capoten) and enalapril (Vasotec) are commonly used.

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ADRENERGIC BLOCKING AGENTS Decrease myocardial workload and protect against fatal dysrhytmias by blocking norephinephrine effects of the sympathetic nervous system. Metoprolol (Lopressor) or metoprolol CR or XL (Toprol XL) are commonly used. Carvedilol is a nonselective beta and alpha blocking agent. Patiets may actually experience increase in general malaise for a 2 to 3 week period while they adjust to the medication.

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Place patient at physical and emotional rest to reduce work of heart Evaluate frequently for progression of left ventricular failure. Take frequent BP readings. Auscultate heart sounds frequently. Note presence os S3 and S4 gallop and monitor for premature ventricylar beats. Observe signs and symptoms of reduced peripheral tissue perfusion: cool temperature of skin, facial pallor, poor capillary refill of nailbeds. Administer pharmacotherapy as directed. Monitor clinical response of patient with respect to relief of symptoms (lessening dyspnea and orthopnea, decrease in crackles, relief of peripheral edema)

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Raise head of bed 20 to 30 cm (8-10 inches) reduces venous return to heart and lungs; alleviates pulmonary congestion Auscultate lung fields every 4 hours for crackles and wheezes in dependent lung fields (fluid accumulates in areas affected by gravity Obrserve for increased RR (could be indicative of falling arterial pH) Observe for Cheyne Stokes respirations Position client every 2 hours to prevent pneunomina and atelectasis Encourage deep breathing exercises every 1 -2 hours to avoid atelectasis Offer small amount frequent feedings to avoid excessive gastric filling and abdominal distention

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Administer prescribed diuretics as ordered. Keep input and output Weigh patient to determine pitting edema. Assess for weakness, malaise and muscle cramps Give oral potassium as prescribed. Observe for symptoms of electrolytes depletion lassitude, apathy, mental confusion, anorexia, decreasing urinary output, azotemia Limit IV fluid administratio through use of heparin lock Monitor pitting edema of lower extremeties and scaral area. Obrserve complications of bed rest. Monitor patients diet must be low salt.

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Increase patients activity gradually. Assist with self care activities early in the day (fatigue sets in as day progresses) Observe pulse, symptoms, and behavioral response to activity.. Relieve nighttime anxiety and provide rest and sleep patients with CHF tends to be restless at night because pf cerebral hypoxia with superimposed nitrigen retention. Give appropriate sedation to relieve insomnia and restlessness.