Contact us:
+1 (520) 226-8615
Email:
[email protected]
NURS 250 CHF SIM Preparation Questions
(McCulloch & Osborn, 2014, p. 1026, American Heart Association, 2016, National Heart, Lung and Blood Institute, 2016)
2. Explain the cause of the compensations for chronic heart failure.
The initial response to decreased cardiac output is activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Substances that are released with eventual detrimental cardiac effects include norepinephrine, angiotensin II, aldosterone, endothelin, vasopressin, and cytokines. Circulating levels play an important role in vasoconstriction, sodium retention, and toxic effects on the architecture of the heart.
In the early phases of heart failure, SNS and RAAS activation augments preload, ventricular contractility, and heart rate, thereby maintaining cardiac output. As cardiac function gets worse, these compensatory mechanisms can no longer maintain cardiac output, and ventricular function is further compromised. Increased SNS activity leads to increased norepinephrine and vasoconstriction in the pulmonary and systemic vasculature and enhances tone. This initially maintains bp and increased ventricular preload.
Norepinephrine also causes renal vasoconstriction that allows for the GFR to remain stable despite decreased perfusion of renal blood flow. Circulating norepinephrine also increases Na absorption, leading to fluid retention that initially increases intravascular volume with subsequent temporary improvements in cardiac output and blood pressure. Myocardial contractility and heart rate are stimulated and therefore increase cardiac output. Long term these effects are deleterious causing increased cardiac wall stress, hypertrophy, chamber dilation, increased myocardial oxygen consumption, worsening myocardial ischemia, and pulmonary and systemic congestion.
(McCullouch & Osborn, 2014, p. 1028-1029)
3. Describe the manifestations and effects of right-sided and left-sided heart failure.
Manifestations of right-sided heart failure are congestion of peripheral tissue, liver and gastrointestinal tract. Right sided heart failure impairs the ability to move blood from the systemic venous circulation into the pulmonary circulation which leads to the development of peripheral edema in lower extremities. The impaired ability to move blood causes congestion of the viscera (ascites) and as distention progresses, blood backs up in the hepatic veins that leads to vena cava and liver engorgement. Hepatomegaly can cause pain in the right upper quadrant, decrease liver function and engorgement of the spleen. Congestion of the GI tract can interfere with digestion and absorption of nutrients, causing anorexia and abdominal distress.
Manifestations of left-sided heart failure include activity intolerance, fatigue, shortness of breath, frothy sputum, orthopnea, paroxysmal nocturnal dyspnea, cyanosis, hypoxia and respiratory crackles. Left-sided heart failure is an abnormal cardiac condition that causes a pumping inability of the left side of the heart, which eventually backs the blood up into the pulmonary circulation
(Porth, 2015, p. 492-494).
…
KINDLY ORDER NOW FOR A MORE RESOURCEFUL AND COMPLETE SET OF REVIEW QUESTIONÂ