Pathophysiology of Congestive Heart Failure (CHF)
Congestive Heart Failure (CHF)
Congestive heart failure, or heart failure, is a condition in which the heart is unable to adequately pump blood throughout the body and/or unable to prevent blood from "backing up" into the lungs.
In most cases, heart failure is a process that occurs over time, when an underlying condition damages the heart or makes it work too hard, weakening the organ. Heart failure is characterized by shortness of breath (dyspnea) and abnormal fluid retention, which usually results in swelling (edema) in the feet and legs.
Pathophysiology of Congestive Heart Failure (CHF)
Heart failure occurs, the body undergoes some adaptation, both in heart and systemically. If the stroke volume of both ventricles is reduced, because of pressure contractility, or afterload are greatly increased, the volume and pressure at the end of diastolic heart in two space will increase. This will increase the end diastolic myocardial fiber length, causing systolic time becomes shorter. If this condition lasts long, there was dilatation of the ventricles. Cardiac output at rest can still be good, but the increase in diastolic pressure that persists / chronicle will spread to both the atrium and the pulmonary circulation and systemic circulation.
Finally, capillary pressure will increase which will cause fluid transudation and pulmonary edema or systemic edema. Decrease in cardiac output, especially if associated with a decrease 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 venous; changes that last time, will increase central blood volume which in turn increases the preload.
Although the adaptation was designed to increase cardiac output, the adaptation itself can interfere with the body. Therefore, tachycardia and increased myocardial contractility stimulated the occurrence of ischemia in patients with previous coronary artery disease and increased preload may worsen pulmonary congestion.
Activation of the sympathetic nervous system will also increase peripheral resistance, this adaptation designed to maintain perfusion to vital organs, but if the activation is greatly increased, will decrease the flow to the kidneys and tissues. Peripheral vascular resistance may also be the main determinant of ventricular afterload, so that excessive sympathetic activity can improve heart function. One important effect is the decrease in cardiac output decreased renal blood flow and decrease in filtration velocity glomerolus, which will cause sodium and fluid retention.
System renin - angiotensin - aldosterone also be activated, causing further increase in peripheral vascular resistance and increased 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 atrial natriuretic peptide increased due to increased atrial pressure, which indicates that there is resistance to the effects of natriuretic and vasodilator.
Congestive heart failure, or heart failure, is a condition in which the heart is unable to adequately pump blood throughout the body and/or unable to prevent blood from "backing up" into the lungs.
In most cases, heart failure is a process that occurs over time, when an underlying condition damages the heart or makes it work too hard, weakening the organ. Heart failure is characterized by shortness of breath (dyspnea) and abnormal fluid retention, which usually results in swelling (edema) in the feet and legs.
Pathophysiology of Congestive Heart Failure (CHF)
Heart failure occurs, the body undergoes some adaptation, both in heart and systemically. If the stroke volume of both ventricles is reduced, because of pressure contractility, or afterload are greatly increased, the volume and pressure at the end of diastolic heart in two space will increase. This will increase the end diastolic myocardial fiber length, causing systolic time becomes shorter. If this condition lasts long, there was dilatation of the ventricles. Cardiac output at rest can still be good, but the increase in diastolic pressure that persists / chronicle will spread to both the atrium and the pulmonary circulation and systemic circulation.
Finally, capillary pressure will increase which will cause fluid transudation and pulmonary edema or systemic edema. Decrease in cardiac output, especially if associated with a decrease 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 venous; changes that last time, will increase central blood volume which in turn increases the preload.
Although the adaptation was designed to increase cardiac output, the adaptation itself can interfere with the body. Therefore, tachycardia and increased myocardial contractility stimulated the occurrence of ischemia in patients with previous coronary artery disease and increased preload may worsen pulmonary congestion.
Activation of the sympathetic nervous system will also increase peripheral resistance, this adaptation designed to maintain perfusion to vital organs, but if the activation is greatly increased, will decrease the flow to the kidneys and tissues. Peripheral vascular resistance may also be the main determinant of ventricular afterload, so that excessive sympathetic activity can improve heart function. One important effect is the decrease in cardiac output decreased renal blood flow and decrease in filtration velocity glomerolus, which will cause sodium and fluid retention.
System renin - angiotensin - aldosterone also be activated, causing further increase in peripheral vascular resistance and increased 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 atrial natriuretic peptide increased due to increased atrial pressure, which indicates that there is resistance to the effects of natriuretic and vasodilator.
