Heart Failure Case Study: Part B of Trevor's Pathophysiology Report

This report presents Part B of a case study concerning Trevor, a patient suffering from congestive heart failure (CHF). The report details the pathophysiology of CHF, explaining how hypertension can lead to the heart's inability to pump sufficient blood, causing reduced cardiac output and fluid leakage. It explores compensatory mechanisms such as cardiac hypertrophy and tachycardia, and the role of the Starling law. The report further discusses pharmacological interventions, including ACE inhibitors, beta-blockers, and diuretics, and their mechanisms of action in managing CHF. References to relevant medical literature support the analysis, providing a comprehensive overview of the condition and its treatment.

Running head: PART B OF TREVOR CASE STUDY
PART B OF TREVOR CASE STUDY
Name of the student:
Name of the university:
Author note:

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).

4
PART B OF TREVOR CASE STUDY
References:
Bardy, G. (2016). U.S. Patent No. 9,232,900. Washington, DC: U.S. Patent and Trademark Office.
Brown, D., Edwards, H., Seaton, L., & Buckley, T. (2017). Lewis's Medical-Surgical Nursing:
Assessment and Management of Clinical Problems. Elsevier Health Sciences. Bullock,
Hales. Principles of Pathophysiology.
Marieb, E. (2011). Essentials of Human Anatomy and Physiology (10th) (Vol. 10). San
Francisco, CA: Benjamin Cummings/Pearson Education.
McMurray, J. J., Packer, M., Desai, A. S., Gong, J., Lefkowitz, M. P., Rizkala, A. R., ... & Zile,
M. R. (2014). Angiotensin–neprilysin inhibition versus enalapril in heart failure. New
England Journal of Medicine, 371(11), 993-1004.
Norhammar, A., Johansson, I., Thrainsdottir, I. S., & Rydén, L. (2017). Congestive heart
failure. Textbook of Diabetes, 659-672.
Okuyama, H., Langsjoen, P. H., Hamazaki, T., Ogushi, Y., Hama, R., Kobayashi, T., & Uchino, H.
(2015). Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms. Expert
review of clinical pharmacology, 8(2), 189-199.
Volpe, M., Carnovali, M., & Mastromarino, V. (2016). The natriuretic peptides system in the
pathophysiology of heart failure: from molecular basis to treatment. Clinical Science, 130(2), 57-
77.

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.