| ID | 80 |
|---|---|
| Name | LEFT-SIDED HEART FAILURE |
| Cause | Causes: 1. Hypertension (commonest cause.) 2. Coronary thrombosis. 3. Myocardial infarction. 4. Aortic stenosis & incompetence. 5. Mitral incompetence. 6. Cardiomyopathy. 7. Severe anemia. 8. Coarctation of aorta. 9. Beriberi. |
| Signs Symptoms | |
| Diagnosis | |
| Investigations | Investigations: 1. Blood: Hb%, T.C, D.C, E.S.R; T.C. of R.B.C.- polycythaemia may present. 2. Biochemical studies: Blood urea, creatinine- may show renal insufficiency. Electrolytes- hyperkalaemia may develop due to drug effects (ACE inhibitors and spironolactone); hyponatraemia is a feature of severe heart failure, may be due to diuretic therapy and/or inappropriate water retention due to high ADH secretion. Liver function tests- to see any impaired liver function caused by hepatic venous congestion. 3. X-ray chest P/A view: a. Enlarged cardiac shadow (cardiomegaly). b. Prominence of pulmonary vascular markings, c. Butterfly wing shadows may be present, d. Hilar haziness due to pulmonary oedema. 4. E.C.G: show left ventricular hypertrophy. 5. Echocardiogram: This is the most useful test, which reveals the size and function of heart chambers, pericardia! effusion, valvular abnormalities, intracardiac shunts and other cardiac abnormalities. 6. Cardiac catheterization: In some patients left heart catheterization is necessary when valvular diseases are to be excluded and when the presence and extent of coronary artery disease is to be determined. |
| Management | Management: A. Management of acute pulmonary oedema: 1. Strict bed rest in propped up position (patient in sitting position with legs dangling over the side of the bed- this facilitates respiration and reduces venous return). 2. O2 inhalation by mask or nasal catheter at a rate of 6-8 litres/minute (to obtain an arterial PO2 greater than 60 mm Hg. 3. Inj. Morphine initial dosage 2-8mg i.v slowly or by i.m or s.c injection and an antiemetic such as cyclizine 50mg by i.v injection. Morphine may be repeated after 2-4 hours. Morphine increases venous capacitance, lowering left atrial pressure and relieves anxiety. Intravenous morphine should be given very cautiously only when the patients are in extreme condition. It reduces sympathetically mediated peripheral vasoconstriction but may cause respiratory depression and exacerbation of hypox aemia and hypercapnia. It should bvoided in opioid induced pulmonary oedema. 4. Inj. glyceryl trinitrate 10-200mcg/min. or oral glyceryl trinitrate 2-5mg under the tongue titrated upwards every 10 min. until clinical improvement occurs (systolic BP comes to <110 mmHg). 5. Diuresis: Diuretics are the most effective means of providing symptomatic relief to patients with moderate to severe congestive heart failure. In most symptomatic patients a combination of a diuretic and an ACE inhibitor should be the initial treatment. Heart failure patients with mild fluid retention, a thiazide or a related diuretic e.g hydrochlorothiazide 25-100mg, or metolazone 2.5-10mg, or chlorthalidone 25-100mg may be sufficient. Patients with more severe heart failure should be treated with one of the loop diuretics, e.g- Inj. Frusemide 40-80mg. i.v. stat, repeat if necessary with mist, potassium chloride-1 oz. 3 times daily. 6. Continuous monitoring of cardiac rhythm, BP, pulse and respiratory rate. B. Management of chronic heart failure: General management: 1. Educating the patients and/or their attendants about the causes and treatment plan of heart failure. 2. Weighing the patient for adjustment of therapy (specially diuretics). Drug therapy: 1. ACE (angiotensin-converting enzyme) inhibitor: Currently, the ACE inhibitors have become standard therapy for heart failure. Their beneficial effects include both vasodilation and inhibition of increased neurohormonal activity. Major benefit of it is a reduction in afterload, and also a reduction in preload. There is modest increase in the plasma potassium concentration. So, in the treatment of heart failure a combination of an ACE inhibitor and a potassium-losing diuretic has many potential advantages. As the ACE inhibitors may produce significant hypotension, particularly after the initial doses- so, before the therapy is started, other vasodilators should be discontinued and the dosages of diuretics should be reduced or withheld for 24 hours. Captopril- a short acting agent, is preferred for beginning ACE inhibior therapy- initial dose is 6.25mg 3 times daily then increase gradually up to 25mg 3 times daily. Patient may be sent home on a maintenance dose of 12.5mg three times daily. Enalapril- a long-acting agent, only active after conversion (to the active metabolite enalaprilat) in the liver; average dose is 20mg daily. Lisinopril- another ACE inhibitor with long half life, average dose is 10mg daily. 2. For long-term control potassium-sparing drugs like spironolactone, triamterene, or amiloride are often useful in combination with the loop diuretics and thiazides. 3. Angiotensin-II receptor antagonists (e.g losartan, valsartan): These drugs are now regarded as the first-line therapy option for treating high blood pressure; but they are also effective in congestive heart failure. They act by blocking the action of angiotensin II on the heart, peripheral vasculature and kidney and in heart failure, & the effects are almost similar to the effects of ACE inhibiors. The difference is that, they have no effect on the breakdown of bradykinin within the lungs and do not therefore cause cough, so it may be an effective alternative for patients who have to discontinue an ACE inhibitor because of persistent dry cough. The average dose of losartan, 50mg once daily. 4. Vasodilator drugs: In heart failure the use of vasodilator is limited due to its pharmacological tolerance and hypotension; and therapy with ACE inhibitors is usually preferable, because this combination prolongs life in patients with moderate to severe heart failure. Nitrates- e.g isosorbide dinitrate 20-80mg orally three times daily or glyceryl trinitrate 12.5-50mg every 8 hours may be used. 5. Digitalisation: Digitalis (digoxin) should be used as first-line therapy in patients of heart failure with atrial fibrillation; the role of digoxin in the treatment of heart failure with sinus rhythm is less certain. However, though it has a narrow therapeutic index, some physicians even use digoxin to treat patients with heart failure and sinus rhythm if treatment with a diuretic and an ACE inhibitor fails. Rapid digitalisation: Digoxin (0.25mg/tablet) 4 tablets stat & 2 tablets after 6 hour, then 1 tablet 6 hourly for 2 days, then 1 tablet daily as maintenance dose until the pulse rate becomes 60/minute. In very very emergency cases- Digoxin Img i.v stat then orally 2 tablets after 6 hour and 1 tablet once or twice daily as a maintenance dose. 6. Correction of reversible causes: The major reversible causes of heart failure include- ischaemic left ventricular dysfunction, thyrotoxicosis, myxoedema, valvular lesions, intra-cardiac shunts, arrhythmias, alcohol- or drug-induced myocardial depression and left ventricular hypertrophy due to hypertension. Once it is established that there is no reversible component, the measures outlined above are appopriate. 7. Antibiotic- if there is any sign of infection- appropriate antibiotic coverage should be given. 8. Proper nursing care & salt restricted diet, & avoid salt and fluid retaining drugs e.g NSAIDs, alcohols etc. 9. Advice for regular stamina-building exercise in patients with chronic heart failure. N.B: 1. p-blockers: The use of p-blockers in heart failure is not appreciated, because when given in standard doses, it may precipitate ‘acute on chronic heart failure’. 2. Calcium channel blockers and antiarrhythmic agents are important causes of worsening heart failure. |
| Introduction | It may be acute or chronic, and may be defined as the failure of the left ventricle acutely or chronically to propel blood forwards resulting in accumulation of blood in pulmonary circulation, characterized by- i. paroxysmal nocturnal dyspnoea, ii. gallop rhythm, iii. pulsus altemans & iv. basal crepitation. |
| History | |
| Etiology | |
| Clinical Features | Clinical features: Symptoms: 1. Dyspnoea of variable degree of severity. 2. Orthopnoea. 3. Paroxysmal nocturnal dyspnoea. 4. Cough with expectoration which may be frothy. 5. Haemoptysis & Nocturia. 6. Symptoms of acute pulmonary oedema, e.g patient is pale, sweating, cyanotic. Signs: 1. Cyanosis may or may not be present. 2. Pulsus altemans, gallop rhythm. 3. Apex beat thrusting in character, displaced laterally. 4. Wide spread fine & coarse crepitation & rhonchi at lung bases. 5. Accentuated pulmonary component of the 2nd heart sound. 6. Evidence of underlying cardiac pathology, e.g M.I, Aortic incompetence, Hypertension. |
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