Heart failure (short for "heart failure") is a condition where heart does not provide enough blood flow to meet body's needs, or is unable to perform this "task" with great difficulty.

cause

Cardiac dysfunction can be systolic or diastolic.

Systolic dysfunctionSystole is act of contracting heart, defined by two properties of heart: (1) contractility (the ability of muscle to contract) and (2) afterload (the force on heart pressure).

Reduced contractility: myocardial infarction, valvular heart disease, arterial hypertension, cardiomyopathy.

Increased afterload, eg hypertension, aortic stenosis.

Diastolic dysfunction Diastole is period of relaxation after heart beats, defined by active and passive properties. When Ca2+ is pumped out of myocardium, diastolic phase occurs earlier. It is active because it uses energy and is disrupted by ischemia. Passive relaxation occurs when mitral and tricuspid valves open, allowing blood from atria to pool into ventricles. It is affected by increased ventricular stiffness, as seen in concentric hypertrophy and infiltrative disease.

Clinical suspicion

Clinical manifestations suggest heart failure. Symptoms include shortness of breath on exertion, palpitations, fainting, coughing, and leg swelling. The suspicion was supported by extensive radiological evidence of heart size and pulmonary vascular redistribution.

Diagnostics

The diagnosis must be confirmed by echocardiography, radionuclide ventriculography, or cardiac catheterization combined with left ventricular angiography.

treatment

The ideal treatment would be to eliminate cause, and if not, then try to eliminate cause of deposits, but in most cases this is not possible.

Treatment of systolic heart failure in patients with blood pressure >90/60 Vasodilators

They dilate blood vessels in body.

Angiotensin converting enzyme inhibitors (ACE inhibitors)

First line treatment for any congestive heart failure, both asymptomatic and severe, with exception of smuggling.

Rationale: Heart failure is accompanied by compensatory mechanisms of vasoconstriction. This increases venous return and arterial tone while maintaining blood pressure and perfusion. However, it also increases ventricular ejection resistance (afterload). This leads to a vicious cycle in which a decrease in stroke volume results in greater vasoconstriction, further reducing stroke volume. Thus, vasodilator therapy breaks cycle. Vasodilation therapy is only treatment for congestive heart failure that increases survival and improves quality of life.

Contraindications. Patients with heart failure due to aortic/mitral stenosis or patients with heart failure due to aortic stenosis are not treated. Patients with impaired functioncheck or bilateral stenosis of renal arteries, drug was not prescribed. Do not supplement potassium with ACE, control blood pressure with ACE, and carefully monitor blood pressure at start of concomitant use with diuretics.

ACE inhibition should be started 72 hours after any acute myocardial infarction with symptoms or echocardiographic evidence of systolic dysfunction.

ACE inhibition should not be started within 24 hours of an acute myocardial infarction.

Dose and type: Start with a small dose (1/4 to 1/2, one tablet) of ACE inhibitors and give them in a sitting position to avoid hypotension at first dose. The dose was gradually titrated and each other's program reached 3 tablets per day (maximum dose was 50 mg TDS).

Isosorbide dinitrate hydrochloride hydrochloride:

The combination of these two drugs may also improve survival. Patients with intolerance to ACE inhibitors are prescribed as a second line.

Diuretics

Diuretics are useful for congestion.

Digoxin

If above drugs do not control condition or are accompanied by supraventricular arrhythmia

Dosage: maintenance dose of 0.25 mg per day, controlled by serum levels. in

The elderly and people of short stature and with renal insufficiency.

Treatment of systolic heart failure in patients with hypotension

Mimics sympathetic amine and amrinone (see below).

refractory heart failure

Heart failure is considered refractory when there is insufficient response to conventional treatments. Before assuming that this condition simply reflects late, possibly terminal, myocardial depression, several possible scenarios need to be carefully considered: (1) underlying and overlooked causes of heart disease that may be specific to surgical or medical treatment, such as asymptomatic aortic or mitral stenosis, constrictive pericarditis, infective endocarditis, hypertension or thyrotoxicosis, (2) predisposing factors to heart failure such as pulmonary or urinary tract infection, recurrent pulmonary embolism, hypoxemia or thyrotoxicity; (2) one or a combination of causes of heart failure failure such as lung or urinary tract infection, recurrent pulmonary embolism, hypoxemia, anemia or cardiac arrhythmia, and (3) complications of over-heavy treatment such as digitalis poisoning, hypovolemia or electrolyte imbalance.

Intravenous vasodilators (eg, nitroprusside) in combination with potent sympathetic amines (eg, dopamine or dobutamine) often have an additive effect, increasing cardiac output and decreasing filling pressure. Intravenous amrinone, sometimes used with a converting enzyme inhibitor, may also be useful in patients with refractory heart failure.

sympathetic amines

Dopamine, immediate precursor of norepinephrine, has multiple actions, making it particularly useful in treatment of various hypotensive conditions and congestive heart failure. At very low doses, i.e. 1 to 2 (µg/kg)/min, it increases renal and mesenteric blood flow and sodium excretion by stimulating specific dopaminergic receptors that dilate renal and mesenteric blood vessels. In range of 2-10 (µg/kg)/min, dopamine stimulates myocardial β-receptors, but induced tachycardia is relatively small; high doses of dopamine can also stimulate α-adrenergic receptors and increase blood pressure.

Dobutamine Catecholamine is a synthetic catecholamine that acts on β1, β2 and α receptors. It has a strong inotropic effect, causes only a slight acceleration of heart rate and reduces peripheral vascular resistance, but has little effect on systemic arterial pressure, since it simultaneously increases cardiac output. Continuous infusion of dobutamine at a dose of 2.5–10 mcg/kg/min is useful in acute heart failure without hypotension. Like other similar sympathetic amines, it is useful in patients requiring relatively short-term inotropic support - up to 1 week - for reversible conditions such as cardiac depression after open heart surgery, or in preparation for surgery, may be of particular importance in patients with acute heart failure. Side effects include sinus tachycardia, tachyarrhythmia, and hypertension.

The main problem for all sympathoids is loss of sensation, apparently due to "down regulation" of adrenergic receptors, which becomes apparent within 8 hours of continuous use. This problem can be solved with intermittent treatment.

Heart transplant Survival increased from 50% at 1 year to 50% at 5 years.

Diastolic heart failure

Diuretics for congestion

Calcium channel blockers in some cases

Digoxin doesn't work.

When diastolic dysfunction is secondary to this condition, prompt resolution of acute myocardial ischemia is usually effective. The slowing of heart rate caused by β-blockers has a positive effect on diastolic function, including prolonging filling period and reducing ischemia. Calcium channel blockers, especially verapamil, have been shown to accelerate ventricular diastolic function in patients with hypertrophic cardiomyopathy and are reported to be useful in treatment of diastolic dysfunction in this condition. Other beneficial mechanisms include reduction in heart rate, control of hypertension, reduction in microvascular ischemia and oxygen consumption, improvement in intracellular calcium overload, and reduction in left ventricular hypertrophy.

Sodium restriction and use of diuretics and venodilators reduce ventricular filling pressure and secondary venous congestion. Even in absence of ischemia, nitrates, by reducing preload, are useful in treatment of diastolic dysfunction and in treatment and prevention of subsequent severe pulmonary congestion. In an emergency, nitroglycerin can be given intravenously or subcutaneously, and long-acting nitrates, such as isosorbide dinitrate, are often long-acting. However, excessive reduction in preload should be avoided in long term, as these patients often require higher than normal filling pressures to maintain adequate filling.

Maintaining heart rate and heart rate is critical. Tachycardia, regardless of underlying mechanism, must be controlled so that proportion of each cardiac cycle required to fill ventricles is increased. Sequential AV pacing that synchronously maintains sinus rhythm may be key to atrial expansion and ventricular filling. Digoxin and other inotropes do not have a fixed place in these patients, in whom ejection fraction is better preserved, and in principle may have an adverse effect on this group of patients. Exercise significantly improves exercise tolerance and left ventricular diastolic dysfunction in patients with dilated cardiomyopathy. Finally, study showed that endogenous nitric oxide released from coronary microcirculation selectively enhances left ventricular diastolic function in isolated guinea pig hearts. These results may lead to a new approach to treatment of diastolic heart failure that focuses on coronary microcirculation.

The American College of Cardiology/American Heart Association Task Force divides drug therapy into three categories for treatment of diastolic heart failure: Category I refers to commonly prescribed drugs such as diuretics and nitrates and, in presence of atrial fibrillation, drugs that depress atrioventricular conduction and anticoagulants. Category 2 drugs are "acceptable" but their efficacy is questionable. These drugs include calcium channel blockers, beta blockers, ACE inhibitors, and anticoagulants in patients with intracardiac thrombosis. Class III drugs are not listed and include drugs with a positive inotropic effect.