Congestive Heart Failure (CHF) is characterized by a decrease in cardiac output (CO) and the consequent decrease in blood flow throughout the body leads to many widespread effects. For example, when CO is too low, the body starts to prioritize and will decrease blood flow to certain organs, such as the digestive viscera, in order to maintain needed blood flow in organs such as the brain. As a result, a person with CHF will have issues with cachexia and malnutrition because the body is not digesting properly (Conelius, 2014). Patients will also experience fluid retention and edema because the pressure in the capillaries is greatly increased in both the peripheral and pulmonary circulations. The increase in capillary pressure reflects increased
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The first mechanism is the sympathetic nervous system (SNS). The SNS is meant to augment the blood pressure and CO and is the most immediate compensatory mechanism. It will sense the decrease in CO and release more norepinephrine and epinephrine to bind to beta-adrenergic receptors of the heart to increase the heart rate, which will increase contractility and CO consequently (Conelius, 2014). The second mechanism is the renin-angiotensin-aldosterone mechanism. If the kidneys sense that they are not receiving enough blood, they will release renin which is converted to angiotensin I by angiotensinogen and then angiotensin II an enzyme. Angiotensin II is a potent vasoconstrictor that will allow for an increase in preload, which will then increase contractility and an eventual increase in stroke volume and CO consequently; it will also lead to an increase in aldosterone that will help to increase sodium and water tubular reabsorption as well as an increase in ADH to prevent the loss of fluids which will all increase stroke volume (Conelius, 2014). The last compensatory mechanism is ventricular remodeling. The heart will begin to hypertrophy in the ventricles to improve its work performance in response to an increase in workload. Ventricular remodeling will occur in response to two stimuli including pressure overload, which leads to an increase in wall thickness and improves ventricular filling, or ventricular volume overload, which will decrease wall thickness and increase the diastolic volume and wall tension which will generate greater pumping capabilities. (Conelius,
The first mechanism is the sympathetic nervous system (SNS). The SNS is meant to augment the blood pressure and CO and is the most immediate compensatory mechanism. It will sense the decrease in CO and release more norepinephrine and epinephrine to bind to beta-adrenergic receptors of the heart to increase the heart rate, which will increase contractility and CO consequently (Conelius, 2014). The second mechanism is the renin-angiotensin-aldosterone mechanism. If the kidneys sense that they are not receiving enough blood, they will release renin which is converted to angiotensin I by angiotensinogen and then angiotensin II an enzyme. Angiotensin II is a potent vasoconstrictor that will allow for an increase in preload, which will then increase contractility and an eventual increase in stroke volume and CO consequently; it will also lead to an increase in aldosterone that will help to increase sodium and water tubular reabsorption as well as an increase in ADH to prevent the loss of fluids which will all increase stroke volume (Conelius, 2014). The last compensatory mechanism is ventricular remodeling. The heart will begin to hypertrophy in the ventricles to improve its work performance in response to an increase in workload. Ventricular remodeling will occur in response to two stimuli including pressure overload, which leads to an increase in wall thickness and improves ventricular filling, or ventricular volume overload, which will decrease wall thickness and increase the diastolic volume and wall tension which will generate greater pumping capabilities. (Conelius,