In case of heart failure, the body has several adaptations, both in the heart and systemically. If both ventricular stroke volume is reduced, therefore the emphasis contractility or afterload was increased, the volume and end-diastolic pressure in the two chambers of the heart increased. This will increase the length of myocardial fibers end-diastolic, systolic rise time becomes shorter. If this condition persists, ventricular dilatation occurs. Cardiac output at rest can still be good, but the increase in diastolic pressure that lasts longer / chronicle will spread to both the atrium and the pulmonary circulation and the systemic circulation. Finally, capillary pressure will increase which will lead to transudation of fluid and edema arising systemic or pulmonary edema. Decrease in cardiac output, especially if associated with a reduction in arterial pressure or decreased renal perfusion, will activate several neural and humoral systems. Increased activity of the sympathetic nervous system will stimulate myocardial contraction, heart rate and veins; recent changes that will increase central blood volume, which in turn increase the preload. Although these adaptations are designed to increase cardiac output, adaptation itself can interfere with the body. Therefore, tachycardia and increased myocardial contractility can stimulate the occurrence of ischemia in patients with coronary artery disease earlier and increased preload may worsen pulmonary congestion.
Activation of the sympathetic nervous system will also increase peripheral resistance; adaptation designed to maintain perfusion to vital organs, but if activation is increased instead will decrease the flow to the kidneys and tissues. Peripheral vascular resistance may also be a major determinant of ventricular afterload, so that excessive sympathetic activity can improve the function of the heart itself. One important effect is a decrease in cardiac output decreased renal blood flow and filtration rate decreased glomerolus, which will cause sodium and fluid retention. Sitem renin - angiotensin - aldosterone system will also be activated, leading to increased peripheral vascular resistance and penigkatan selanjutnta left ventricular afterload as sodium and fluid retention. Heart failure is associated with increased levels of arginine vasopressin in the circulation increases, which also is vasokontriktor and inhibiting the excretion of fluids. In heart failure increased atrial natriuretic peptide due to increased atrial pressure, which indicates that here there is resistance to the effects of natriuretic and vasodilator.
