1 PART B OF TREVOR CASE STUDY Pathophysiology of Trevor’s condition: The patient named Trevor is suffering from congestive heart failure. It is the condition when the heart becomes unable to pump enough blood to the organs and tissue to supply oxygen and nutrients. This results in decrease of cardiac output, as the amount of the blood that is pumped by the heart is not adequate for circulation throughout the body and return from the body and the lungs to heart. This results in leaking of the fluid into the capillary blood vessels causing symptoms of shiftlessness of breath as well as weakness and swelling (Norhammer et al., 2017). Many of the disorders may result in occurrence of the symptoms like coronary heart diseases, hypertension, alcohol abuse, disorders of valves and many others. In case of Trevor, hypertension can be considered as the causal factor. It can lead to orthopnea that makes patients face difficult in breathing when they lay flat. In order to maintain cardiac output under normal condition, several compensatory mechanisms are seen to play important roles like that of the compensatory enlargement (Marieb, 2017). This may be in form of cardiac hypertrophy, cardiac dilation or can be both of them. Tachycardia is the situation when increase in the heart rate place due to functioning of the neurohumoral system. This includes realeasing of the nor epinephrine as atrial natrouretic peptide along with the activation of the rennin-angiotensin aldosterone mechanism. Researchers also point the Starling law that states that within limits, the force applied by ventricular contraction can be considered as the cardiac muscle that is in turn seen to be closely related to that of the ventricular end diastolic heart (Bardy, 2016). This is in turn achieved by the increase of the different lengths of the sarcomeres in the dilated heart and thereby increases the contractility of the myocardium. This helps to maintain the stroke volume. When heart failure takes place, there is depression of the ventricular curve function (Volpe et al., 2016). As a result, compensation in the form of myocardial fibres, results. Stretching takes place
2 PART B OF TREVOR CASE STUDY that leads to cardiac dilation when the left ventricle is seen to fail for ejecting end diastolic volume. When left ventricular and right ventricular failure takes place, there are compensatory mechanisms that take place. Due to this myocardial contractility as well as cardiac workload increase causing cell stretching and therefore, compensatory hypertrophy and dilation take place. However, under abnormal conditions, activated activation of the rennin-angiotensin-aldosterone mechanism results in sodium and water retention. This causes stress on myocardium and congestive heart failure. Plasma volume, preload and cardiac workload increases causing failure of heart. Peripheral vasoconstriction takes place, after load increases and cardiac output decreases causing failure. Again activation of the nor epinephrine as atrial natrouretic peptide causes tachycardia creating stress on myocardium resulting in congestive heart failure. Pharmacology: Ace inhibitors also called the angiotensinogen converting enzyme inhibitors as well as ARBs called the angiotension receptor blockers are some of the medications that helps in increasing the survival by decreasing the systematic resistance and causes favourable alteration of the hormonal milieu. These are seen to affect the cardiac performance. These are often seen to be utilised with other forms of the drugs. Beta-blockers is also another form of medication that can be also used for this purpose. It controls heart rate and increases cardiac output as well as ejection fraction (Yancy et al., 2016). This helps in providing the beneficial response to circulating epinephrine. On the other hand, dioxin is also extensively used to increase cardiac output and thereby control symptoms. In many other situation, role of diuretics are also found to be useful in heart failure. They are mainly seen to helpful in the cases of atrial fibrillation, atrial flutter as well as paroxysmal supraventricular tachycardia (Okuyama et al., 2015). They are mainly seen to force contraction and cardiac output, decreases heart rate, increases refractory
3 PART B OF TREVOR CASE STUDY period and conduction velocity. It also increases automaticity. High ceiling diuretics also called the loop diuretics are also found (Brown et al al.2017), . They are mainly seen to increase salt as well as water excretion. They are also seen to decrease the blood volume. They reduce the preload as well as venous pressure, also help in the improvement of cardiac performance, and thereby relieve oedema. Angiotensin receptor blockers in the heart are mainly seen to block AT1 receptor of the Heart, peripheral vasculature as well as kidney. They are used mainly in patients who cannot tolerate ACE inhibitors because of cough, neutropena and angioedema (McMurray et al., 2014).
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5 PART B OF TREVOR CASE STUDY Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Colvin, M. M., ... & Hollenberg, S. M. (2016). 2016 ACC/AHA/HFSA focused update on new pharmacological therapy for heart failure: an update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America.Journal of Cardiac Failure,22(9), 659-669.