Medical Surgical Cardiovascular System: Congestive Heart Failure (CHF)

Hello Everyone, here is a Cardiovascular lecture on Congestive Heart Failure made easy to understand to help aide in your study sessions. I have gathered all of the important information from my Med- Surg Book (Brunners and Suddarth 12th edition) and NCLEX review (Saunders 6th edition) that will prepare you for your nursing test whether it is for school or NCLEX.

Part 2 of this lecture will be located under the Pharmacology section as it continues with cardiac meds that will further explains MOA, side effects, etc.

Here are some Extra information that may help and guide you...

Two major types of HF are identified by assessment of left ventricular functioning, usually by echocardiogram. The more common type is an alteration in ventricular contraction called systolic heart failure, which is characterized by a weakened heart muscle. The less common type is diastolic heart failure, which is characterized by a stiff and noncompliant heart muscle, making it difficult for the ventricle to fill. An assessment of the ejection fraction (EF) is performed to assist in determining the type of HF. EF is calculated by subtracting the amount of blood present in the left ventricle at the end of systole from the amount present at the end of diastole and calculating the percentage of blood that is ejected. A normal EF is 55% to 65% of the ventricular volume; the ventricle does not completely empty between contractions. The EF is normal in diastolic HF but severely reduced in systolic HF. Although a low EF is a hallmark of systolic HF, which is the most common type of HF, the severity of HF is frequently classified according to the patient’s symptoms.

Pathophysiology:

Systolic HF results in decreased blood volume being ejected from the ventricle. The decreased ventricular stretch is sensed by baroreceptors in the aortic and carotid bodies. The sympathetic nervous system is then stimulated to release epinephrine and norepinephrine. The purpose of this initial response is to increase heart rate and contractility and support the failing myocardium, but the continued response has multiple negative effects. Sympathetic stimulation causes vasoconstriction in the skin, gastrointestinal tract, and kidneys. A decrease in renal perfusion due to low CO and vasoconstriction then causes the release of renin by the kidneys. Renin promotes the formation of angiotensin I, a benign, inactive substance. Angiotensin- converting enzyme (ACE) in the lumen of pulmonary blood vessels converts angiotensin I to angiotensin II, a potent vasoconstrictor, which then increases the blood pressure and afterload. Angiotensin II also stimulates the release of aldosterone from the adrenal cortex, resulting in sodium and fluid retention by the renal tubules and stimulation of antidiuretic hormone. These mechanisms lead to the fluid volume overload commonly seen in HF. Angiotensin, aldosterone, and other neurohormones (eg, endothelin, prostacyclin) lead to an increase in preload and afterload, which increases stress on the ventricular wall, causing an increase in the workload of the heart. A counterregulatory mechanism is attempted through the release of natriuretic peptides. Atrial natriuretic peptide (ANP) and B-type (ie, brain type) natriuretic peptide (BNP) are released from the overdistended cardiac chambers. These substances promote vasodilation and diuresis. However, their effect is usually not strong enough to overcome the negative effects of the other mechanisms. As the heart’s workload increases, contractility of the myocardial muscle fibers decreases. Decreased contractility results in an increase in end-diastolic blood volume in the ventricle, stretching the myocardial muscle fibers and increasing the size of the ventricle (ventricular dilation). The increased size of the ventricle further increases the stress on the ventricular wall, adding to the workload of the heart. One way the heart compensates for the increased workload is to increase the thickness of the heart muscle (ventricular hypertrophy). However, hypertrophy results in an abnormal proliferation of myocardial cells, a process known as ventricular remodeling. Under the influence of neurohormones (eg, angiotensin II), large myocardial cells are produced that are dysfunctional and die early, leaving the other normal myocardial cells to struggle to maintain CO. The compensatory mechanisms of HF have been called the “vicious cycle of HF” because the heart does not pump sufficient blood to the body, which causes the body to stimulate the heart to work harder; thus, the heart cannot respond and failure becomes worse. Diastolic HF develops because of continued increased workload on the heart, which responds by increasing the number and size of myocardial cells (ie, ventricular hypertrophy and altered cellular functioning). These responses cause resistance to ventricular filling, which increases ventricular filling pressures despite a normal or reduced blood volume.

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