Heart failure

Heart failure is a clinical syndrome that is characterized by rapid onset of high-grade congestive heart failure in addition develop acute pulmonary edema, cardiac asthma, acute systemic venous stasis or rapid onset of strong decrease of cardiac output with tissue hypoperfusion and subsequent development of cardiogenic shock . Described clinical findings respond to the development of acute heart failure.
In regard to classification, acute heart failure is left ventricle, which is dominated by stagnation type, with dominant syndrome venous pulmonary hypertension and pulmonary edema and development of cardiac asthma. Left ventricular heart failure is mainly low output, which dominates syndrome decrease in cardiac output and development of severe tissue hypoperfusion. Subsequently began development of acute cardiogenic shock. There is also a mixed form of left ventricular heart failure, in which the combined clinical picture of congestive failure and hipodebitna leading to even more acute in clinical development, with a very poor prognosis in the absence of medical intervention.
The other type Acute heart failure is right ventricular type. It occurs primarily as congestive failure with acute venous stasis. Like the taxonomic description of left ventricular heart failure, here pathogenetic plan also meets the development of low output crisis, which develops clinic generalized cardiogenic shock.
There is another kind of impending acute heart failure, in which the effect develops in both chambers. This is a two-chamber or biventrikulna heart failure. The most common causes of acute heart failure have occurred acute myocardial infarction, myocarditis, severe hypertensive crisis occurring acute mitral insufficiency, rupture of the ventricular septum and others. In acute congestive left ventricular insufficiency is decreased contractility cameras due to loss of contractile mass. A similar type of damage occurs in the development of acute myocardial infarction. In response, the body responds with the reaction mechanism of Frank-Starling, which naturally increases the pumping function of the heart, though the effect is temporary. Accompanied by elevated pressure in the pulmonary venous system. Increases and pulmonary capillary pressure, and when the oncotic pressure is substantially increased over 30 mmHg, and occurs leakage of fluid and proteins in the interstitium of the lungs. Subsequently developing severe pulmonary edema and subsequent development of cardiac asthma.
The second major compensation mechanism is to increase the activity of Simpatico-adrenal system through increased release of norepinephrine from beta-adrenergic receptors in the myocardium and medulnata part of the kidney. This in turn leads to enhancement of myocardial contractility, development of sinus tachycardia and spasm, peripheral arterial and venous vessels. Subsequently developed generalized redirecting blood flow to zhiezneno important organs - brain, heart, kidney and lung.
The third mechanism for self-defense in conditions of acute heart failure occurred is the rise of the renin-angiotensin-aldosterone secretion. Begins direct retention time of fluid in the bloodstream for the purpose of protection of the plunging blood pressure and slow the development of cardiogenic shock.

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The main events occurring in acute heart failure is the development of cardiac asthma, pulmonary edema and subsequent development of cardiogenic shock. Cardiac asthma is manifested by shortness of breath, accompanied by shallow and rapid breathing. Most often, symptoms begin during the night, when a person is relaxed and calm. Patients wake up with a strong shortness of breath. The only way to master is borrowing ortopnoichno position - sit in bed or stand up and opened the window. Breathlessness not soothe - rather, begins to deepen. Develops dry and irritating cough, pallor, sweating, and cyanosis of the lips, tachycardia, restlessness and a sense of fear. During auscultation is perceptible noise finding for lung wet wheezing primarily in the foundations of the lung.