Heart failure

Heart Failure

Diagnosis of heart failure
It requires evidence of cardiac dysfunction with appropriate investigation using objective measures of left ventricular function (usually echocardiography). The underlying cause of heart failure should be established in all patients. What are the aggravating factors of heart failure. Looking for complications of heart failure.

INVESTIGATIONS

Blood tests – full blood count, liver biochemistry, urea and electrolytescardiac enzymes in acute heart failure to diagnose myocardial infarction, thyroid function tests .

Echocardiography.

(Two-dimensional &Doppler echocardiography) establish the presence of systolic and/or diastolic impairment of the left or right ventricle. reveal the aetiology (valve disease, regional wall motion abnormalities in ischaemic heart disease, cardiomyopathy, amyloid), it may detect intracardiac thrombus. An ejection fraction of < %55 is generally accepted as evidence for systolic dysfunction.

2D echo

Doppler echo

Cardiomyopathy

Cardiac MRI.
recommended in selected patients with heart failure where other investigations do not provide satisfactory diagnosis. accurately measure cardiac volumes, wall thicknesses and left ventricular mass. detects thickened pericardium.

Cardiac catheterization . Cardiac biopsy for infiltrative disease, e.g. amyloid.

Complications of heart failure
Renal failure is caused by poor renal perfusion due to low cardiac output and may be exacerbated by diuretic therapy or by drugs Electrolytes disturbance.hypo kalemia,hyperkalemia and hypnatremia. Impaired liver function is caused by hepatic venous congestion and poor arterial perfusion. Thromboembolism. (Venous or arterial) Venous Deep vein thrombosis and pulmonary embolism may occur due to the effects of a low cardiac output and enforced immobility. systemic embolisation.in a patient with AF extensive MI ,V .aneurysem.

TREATMENT OF HEART FAILURE

Treatment is aimed at: relieving symptoms and improving quality of life. prevention and control of disease leading to cardiac dysfunction and heart failure. retarding disease progression .

Measures to prevent heart failure:

cessation of smoking & alcohol . effective treatment of hypertension, diabetes and hypercholesterolaemia. pharmacological therapy following myocardial infarction. any factor aggravating the failure should be identified and treated. the cause of heart failure must be identified and where possible corrected.

GENERAL MEASURES FOR THE MANAGEMENT OF HEART FAILURE Education : Explanation of nature of disease and treatment emphasizing weight monitoring and dose adjustment of diuretics may prevent hospitalization Diet : Good general nutrition and weight reduction for the obese Avoidance of high-salt foods and added salt, especially for patients with severe congestive heart failure Large meals should be avoided Fluid restriction is necessary. Alcohol : Alcohol-induced cardiomyopathy requires abstinence Smoking: Stopping Exercise :Regular moderate aerobic exercise within limits of symptoms Vaccination :Influenza and pneumococcal vaccination should be considered

Drug management

Diuretics Act by promoting the renal excretion of salt and water by blocking tubular reabsorption of sodium and chloride. The resulting loss of fluid reduces ventricular filling pressures (preload), produces consistent haemodynamic and symptomatic benefits in patients with heart failure, and rapidly improves dyspnoea and peripheral oedema. The intravenous administration of loop diuretics such as furosemide relieves pulmonary oedema rapidly by means of arteriolar vasodilatation reducing afterload, an action that is independent of its diuretic effect.

Loop diuretic

furosemide and bumetanide have a rapid onset of action (i.v. - 5 min; oral - 1-2 h) and generally short-lived (4-6 h) diuresis as the concentrating power of the kidney is reduced. They produce marked potassium loss and promote hyperuricaemia, and renal function should be monitored.

Thiazide diuretics

bendroflumethiazide have a mild diuretic effect. They enhanced Potassium excretion but they are less effective in patients with reduced glomerular filtration rates. Thiazide diuretics in combination with loop diuretics have a synergistic action and greater diuretic effect.

Potassium-sparing diuretics

Spironolactone is a specific competitive antagonist to aldosterone, producing a weak diuresis but with a potassium-sparing action. 30% reduction in all-cause mortality when spironolactone was added to conventional treatment in patients with moderate to severe heart failure. another aldosterone antagonist - eplerenone - that has less hormonal side-effects. Risk factors for developing hyperkalaemia include spironolactone dose > 50 mg/day, high-dose angiotensin-converting enzyme inhibitor (ACEI) and renal impairment. Potassium should be measured 5 days after the initiation of spironolactone until levels are stable and then every 1-3 months.

Angiotensin-converting enzyme inhibitors ACEI

Captopril, enalapril, lisinopril,ramipril. considerable symptomatic improvement in patients with symptomatic heart failure, prognosis is markedly improved and development of heart failure is slowed. Probably exert an indirect antiarrhythmic effect by reducing high circulating levels of norepinephrine (noradrenaline) and improving cardiac function.

ACEI

lower systemic vascular resistance and venous pressure. reduce levels of circulating catecholamines, thus improving myocardial performance.

ACEI

risk of first-dose hypotension in patients who are receiving large doses of diuretics and who have hyponatraemia. Start with testing dose and the preceding diuretic doses omitted.

Angiotensin receptor blockers(ARBS)

losartan, ibersartan, candesartan and valsartan. have similar haemodynamic effects to ACEI, but as they do not affect bradykinin metabolism, they do not produce a cough. Avoid the combination of ACEI and AII receptor antagonists.

Venodilators

Short- and long-acting nitrates (e.g. glyceryl trinitrate and isosorbide mononitrate) act by reducing preload and lowering venous pressure, with resulting reduction in pulmonary oedema. combination therapy of nitrate with hydralazine has been shown to improve mortality and exercise performance, and may be useful when ACEI are contraindicated.


β-Adrenoceptor blocking agents There is considerable evidence to support the use of beta-blockers in patients with chronic stable heart failure. metoprolol and bisoprolol have shown improved symptomatic class, exercise tolerance, left ventricular function and mortality in patients with heart failure of any cause. carvedilol, a non-selective vasodilator beta-blocker with additional vasodilator and antioxidant properties, has also demonstrated a significant improvement in mortality.


When initiated in standard doses they may precipitate acute-on-chronic heart failure, but when given in small incremental doses under carefully monitored conditions, they can increase ejection fraction, improve symptoms, reduce the frequency of hospitalisation and reduce mortality in patients with chronic heart failure,

Digitalis glycosides:

This should be used as first-line therapy in patients with heart failure and atrial fibrillation, when it usually provides adequate control of the ventricular rate together with a small positive inotropic effect. The role of digoxin in the treatment of patients with heart failure and sinus rhythm is less certain treatment with digoxin had no effect on overall survival but did reduce the need for hospitalisationused in patients with heart failure and atrial fibrillation.

The most common features of digoxin toxicity are: anorexia, nausea, altered vision arrhythmia (e.g. ventricular premature beats especially bigeminy, ventricular tachycardia and AV block.



Ivabradine
Act on the SA node resulting in reduction of heart rate. It reduces hospital admission and mortality rates in patients with heart failure due to moderate or severe left ventricular systolic impairment. its effects were most marked in patients with a relatively high heart rate ,so ivabradine is best suited to patients who cannot take β-blockers or in whom the heart rate remains high despite β-blockade. It is ineffective in patients in atrial fibrillation.

Coronary revascularisation

Coronary artery bypass surgery or percutaneous coronary intervention may improve function in areas of the myocardium that have inadequate blood supply, and can be used to treat carefully selected patients with heart failure and coronary artery disease. If necessary, such patients can be identified by stress echocardiography and specialised nuclear techniques

implantable cardioverter-defibrillator (ICD).

Patients with sustained episodes of ventricular tachycardia should receive treatment with an implantable cardioverter-defibrillator (ICD).


CRT
Cardiac resynchronization therapy. In advance heart failure with wide QRS complex.

Management of acute pulmonary oedema

acute medical emergency: Sit the patient up to reduce pulmonary congestion.• Give oxygen (high-flow, high-concentration).Non-invasive positive pressure ventilation(continuous positive airways pressure (CPAP) of 5–10 mmHg) by a tight-fitting facemask results in a more rapid clinical improvement. Administer nitrates, such as IV glyceryl trinitrate(10–200 μg/min, titrated , until clinical improvement occurs or systolic BP falls to less than 110 mmHg.• Administer a loop diuretic, such as furosemide ( IV).

The patient should initially be kept rested, with continuous monitoring of cardiac rhythm, BP and pulse oximetry. Intravenous opiates must be used cautiously in distressed patients, as they may cause respiratory depression and exacerbation of hypoxaemia and hypercapnia.



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