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UT Arlington NURS 5315 - MODULE 5

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1 N5315 Advanced Pathophysiology Heart Failure and Cardiac Contraction Heart Failure Is a syndrome which results from myocardial injury. It is the end result of myocardial damage from ischemic heart disease, cardiomyopathies, valvular heart disease, myocarditis, and results in a constellation of clinical manifestations which are consistent with volume overload, poor perfusion secondary to pump failure. Risk factors include age, ischemic heart disease, obesity, diabetes, HTN, excessive ETOH use, congenital heart disease, valvular heart disease, myocarditis, cardiomyopathies, and renal failure. Heart failure can be classified by its location (right-sided versus left-sided) or the effect on contractility (systolic versus diastolic dysfunction). Congestive heart failure is an old term which should not be used any longer. • Heart failure with Reduced Ejection Fraction (HFrEF): Systolic Heart Failure o Most commonly refers to the left side of the heart but right ventricular systolic dysfunction can happen too. o Is an impairment in left ventricular contraction (systole). Myocardial infarction is the most common cause of decreased systolic dysfunction. Other causes include myocarditis and cardiomyopathies. o A decrease in contractility in the left ventricle will lead to a decrease in stroke volume, decrease in cardiac output, an increase in left ventricular end diastolic volume (preload). This is the first step of ventricular remodeling, which over time, as preload increases causes a dilation of the ventricle and further compromises contraction and cardiac output. o Ventricular remodeling leads to the further pathological deterioration of the myocytes. The process is initially trigged by some pathologic insult to the myocardium which causes damage that leads to the dysfunction described above. The myocardial systolic dysfunction, low cardiac output, results in two different processes being triggered: ▪ Baroreceptor activation • Baroreceptors in the left ventricle, aortic arch and carotid sinus detect the low cardiac output (low blood pressure) and notify the medulla which in turns stimulates the sympathetic nervous system. The SNS stimulates the release of the catecholamines epinephrine and norepinephrine, which causes vasoconstriction and leads to increased afterload, increased blood pressure and increased heart rate. This increases the work load of the heart and causes hypertrophy and dilation of the left ventricle and further impairs contractility. ▪ Renin Angiotensin Aldosterone System activation by decreased renal blood flow. We have reviewed this process already. The end result of the RAAS system is the release of angiotensin II and aldosterone. study resource wasshared via CourseHero.com2 • AG II causes vasoconstriction which increases afterload, blood pressure and contributes to the worsening of left ventricular hypertrophy, dilation and worsening contraction. • Aldosterone enhances renal sodium retention and thereby water. This increases afterload again contributing to the worsening of the left ventricular hypertrophy, dilation and worsening contraction. ▪ Beta blockers are given to patients with HFrEF to block the effects of catecholamines on the heart. ACE Inhibitors and ARBS are given to block the effects of RAAS. These medications will prevent the progression of the heart failure, remodeling and may improve the systolic function. They decrease mortality too. ▪ Ultimately a person with HFrEF will experience pulmonary edema secondary to the back up of blood and high pressures into the pulmonary circulation. Additionally, they may experience edema from the sodium and water retention. • Heart Failure with Preserved Ejection Fraction (HFpEF) o This is characterized by the presence of pulmonary congestion in the setting of normal left systolic EF, stroke volume and cardiac output. It is more common in women and is most commonly caused by hypertension-induced hypertrophy or myocardial ischemia which result in remodeling. o Pathologically this disease results from the inability of the myocytes to actively pump calcium from the cytosol which impairs ventricular relaxation. This can happen in the left or right side of the heart. For our purposes we will refer to the left side of the heart. Since the left ventricle is unable to completely relax it does not fill with as much blood as it should. The contraction of the heart is completely normal and what blood the ventricle has, it is able to pump forward effectively. Because of the defect in relaxation the filling of the ventricle results in increased LVEDP. This pressure backs up into the left atrium and the pulmonary circulation and results in pulmonary edema. Over time pulmonary HTN and right-sided failure may develop. • HFrEF combined with HFpEF o This is a combination of systolic and diastolic heart failure. • Left-Sided Heart Failure o This is synonymous with HFrEF. • Right-Sided Heart Failure o Is characterized by a failing right ventricle which results in its inability to pump blood forward to the pulmonary circulation. The most common cause of right-sided heart failure is left-sided heart failure. When the pressures are too high in the left ventricle, the back flow of blood into the pulmonary circulation causes higher pressures in the pulmonary circulation against which the right ventricle must pump. The right ventricle is unable to effectively pump against the increase in pressure and ultimately dilates and fails. As a result, the pressure and volume backs up causing right atrial hypertrophy, jugular venous distention, hepatosplenomegaly, peripheral edema. study resource wasshared via CourseHero.com3 o Right-sided heart failure can occur without left-sided failure. When this happens it is usually related to a primary lung disorder such as COPD, cystic fibrosis, ARDS, pulmonary fibrosis, pulmonary hypertension. o Right-sided heart failure may also occur from right ventricular MI, cardiomyopathies, or pulmonic valvular disease. Cardiac Contraction The degree of tension (which is produced by the LVEDV aka preload) of the left ventricle and the amount of intracellular calcium are responsible for contraction. The greater the tension the

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