Case Study for a Heart Failure

This case study focuses on the pathophysiology, investigations, pharmacology, and management of heart failure. It discusses the signs and symptoms of cardiogenic shock and heart failure, the compensatory mechanisms of the body, and the importance of investigating the aetiology of heart failure before administering treatment. The paper also explains the use of ACE inhibitors and nitrates in treating heart failure and pulmonary oedema.

Running Head: CASE STUDY 1
Case Study for a Heart Failure
Student’s Name:
Name of the Institution:

CASE STUDY 2
Case Study for a Heart Failure
Pathophysiology
Cardiogenic Shock
Cardiogenic shock represents the heart’s inability to sufficiently supply enough blood to
the vital organs of the body. It is fatal if the steps are not taken to manage it. Signs and symptoms
of this condition include; rapid breathing, severe shortness of breath, tachycardia, pale skin, cold
hands and feet, low blood pressure (Voga, 2008). A Major cause of this kind of shock is
insufficient oxygen-rich blood circulating in the left ventricle of the heart. As for our case study,
Mrs. X displays enough of the above mentioned signs and symptoms to conclude she is
undergoing a cardiogenic shock. The CXR test requested by the medical officer shows an
enlarged heart, further proof of cardiogenic shock existence (Voga, 2008).
Mrs. X was subjected to various examination when she arrived at the hospital. Among the
trials, she was subjected to include: the AST, ALT, ALP, and Albumin tests. These tests
investigate the performance of the liver to deduce any liver damage. The average range values of
these tests are AST (9-32 U/L for females), ALT (7-55 U/L), and ALP (45-115 U/L). Results
displayed by Mrs. X were well off the normal range indicating proof of liver damage; this could
translate that the liver is not getting enough oxygen-rich blood. Conclusively, the patient could
be experiencing a cardiogenic shock (Voga, 2008).
Heart Failure
Heart failure can be diagnosed when the heart muscle fails to pump blood as efficiently
as it should. Among the signs and symptoms of this condition include, shortness of breath even
when lying down, fatigue and weakness, swelling especially ankles and feet, irregular heartbeat,

CASE STUDY 3
chest pains, and reduced appetite (Smiseth & Tendera, 2008). In our case study, Mrs. X shows
most of these symptoms and signs; this paper focuses on the shortness of breath and swelling of
ankles to illustrate the pathophysiology of heart failure.
There are numerous reasons for heart failure, the most common underlying problem in
the modern era being ventricular dysfunction. Myocardial infarction and hypertension contribute
markedly to this dysfunction. The myocardial infarction is responsible for systolic ventricular
dysfunction while hypertension leads to diastolic dysfunction (Smiseth & Tendera, 2008).
Critically, hypertension- a condition that Mrs. X had in her childhood- represents a more
common aetiology in women than men (Kemp & Conte, 2012).
Furthermore, idiopathic dilated cardiomyopathy presents another major cause of systolic
dysfunction that is commonly encountered. This condition represents 15-20% of reported cases
of heart failure globally. The syndrome can be accelerated by a previous or ongoing excessive
consumption of alcohol. Mrs. X enjoyed 5-6 beers a day, which in part is to blame for her state
deterioration. What is not clear is the relationship between diabetes and the systolic and diastolic
dysfunction, literature has, however, pointed to a higher susceptibility to heart failure as a result
of diabetes (Gardner, McDonagh, & Walker, 2014). Correspondingly, her non-compliance to
treat diabetes put her at this risk of heart failure.
Incredibly, as the heart fails the body in response develops specific adaptation
mechanisms referred to as the compensatory mechanisms (Peacock, 2017). These occur in an
attempt to restore the heart performing its adequate function of supplying oxygen-rich blood.
These compensatory mechanisms include Frank-Starling mechanism which aims to have the
cardiac output increased, ventricular remodeling has the objective of increasing ventricular
volume, and activation of neurohormonal systems ensures tissue perfusion (Maclver & Dayer,

CASE STUDY 4
2012). Initially, these mechanisms help restore the heart’s purpose, but with time they lead to a
vicious cycle of failing the left ventricular even further (Peacock, 2017).
In the case of chronic heart failure, continued attempt to use the compensatory
mechanisms leads to sodium and water retention. Mrs. X registers higher than normal levels of
Sodium in the U&E test and also exhibits a moist cough showing signs of retained sodium and
water (Blankesteijn & Altara, 2015). The adaptations also lead to extraordinarily high pulmonary
capillary and artery pressures resulting in the shortness of breath experienced by the patient.
Also, sodium and water retained in the vascular walls lead to arterial constriction and stiffening.
In turn, this increases the afterload eventually causing the damaged left ventricle to fail further.
Most of the symptoms exhibited by patients of heart failure are due to the compensatory
mechanisms (Blankesteijn & Altara, 2015).
Investigations
The condition of heart failure could be a result of any abnormality ranging from electrical
activity or mechanical function. Each of these failures would require a different kind of
treatment, though they would display similar signs and symptoms. It is always advisable that
before putting a heart failure patient to treatment, to first investigate the aetiology of the failure
to have the right diagnosis (McMurray, Komajda, Anker, & Gardner, 2015). Patients may
display similar symptoms of heart failure but require different treatments due to the difference in
the underlying causes of heart failure. For correct administration of medication; it is crucial to
carry sufficient trials on a patient suspected of heart failure to establish the root cause (Cowan,
2017).

CASE STUDY 5
In addition to the trials recommended by the medical expert in the case of Mrs. X, the
following is a list of important additional investigations: exercise testing, electrocardiogram,
Doppler echocardiography, invasive examination, and pulmonary function testing. For this paper
the focus of the additional investigation is on electrocardiogram and Doppler echocardiography.
These two provide relevant information that would otherwise not be available from the other
tests ordered by the medical expert. The additional information from these two tests is very vital
for diagnosis and the determination of the treatment to be administered to a patient (Harris &
Kuppurao, 2016).
Electrocardiogram test is a measure of the heart’s electrical activity. It’s also referred to
as 12-lead ECG as it investigates and records information from 12 parts of the heart. Its
significance is to check the heart for any problems and monitor its status under different
situations (Cowan, 2017). 12-lead ECG checks for irregularities in the heart rhythm, narrowed or
blocked arteries, structural issues of the heart, and signs of myocardial infarction. The test
objective is to investigate any abnormality of the heart that would call for immediate action.
Presence of inconsistent waves is a confirmation of suspected heart failure (Jonas, 2018). This
test doesn’t only provide information on abnormalities; it also points to the specific heart
problem and the location in the region of the heart.
Information from this test is useful in diagnosing a patient and helps provide prognostic
direction. Deviation from the standard ECG readings indicates heart failure. A normal ECG
reading doesn’t have a trace of left ventricular systolic dysfunction. Abnormalities in this test
include inconsistent Q waves, presence of left bundle branch block, and other conduction
disturbances. Increase in size of the left ventricular suggests a specific aetiology. The detection

CASE STUDY 6
of a branch block in a patient with a left ventricular systolic dysfunction indicates a worse
prognosis (Cowan, 2017).
Doppler echocardiography better known as ultrasound is another test that investigates the
heart condition. Echocardiography is a widely available, fast, non-invasive and safe technique of
examining heart failure (Gardner, McDonagh, & Walker, 2014). It provides extensive
information on chamber dimension, wall thickness, and a useful tool for determining diastolic
and systolic dysfunction. Determination of LVEF is an essential determinant in the establishment
of ventricular systolic function. Readings of LVEF of the Doppler echocardiography test of
<0.4O indicates systolic dysfunction (Gardner, McDonagh, & Walker, 2014).
In the determination of diastolic dysfunction; several abnormalities that include impaired
relaxation, restrictive and pseudonormal filling patterns. The restrictive filling pattern is marked
by an exaggeration in E wave velocity which results in an increased E: A ratio; this marks a
severe diastolic dysfunction. Impaired relaxation, on the other hand, is characterized by E: A rate
less than one as a result of sharp decline in the E-wave velocity coupled by a rise in A-wave
velocity (Harris & Kuppurao, 2016). Finally, the pseudonormal filling pattern is marked by an
atrial pressure rise in more advanced heart failure. Of the three abnormalities, restrictive filling
scores the most vital as the prognostic information is of poor outcome (Gardner, McDonagh, &
Walker, 2014).
Pharmacology
Medication of Renal Impairment
Renal impairment is declared when the kidneys cannot perform the task of purifying
blood. Symptoms of kidney failure include shortness of breath, nausea, loss of appetite, edema

CASE STUDY 7
due to fluid retention, and chest pains. The standard creatinine levels for women are 55-100
μmol/L while that of urine is in the range of 2.5-8 mmol/L. The tests results for urine and
creatinine in our case study for Mrs. X were Creatinine 250μmol/L Urea 15mmol/L. A rise in
both urea and creatinine suggests renal dysfunction (McMurray, Komajda, Anker, & Gardner,
2015).
Since during her childhood Mrs. X was diagnosed with hypertension and diabetes, the
best cause of action would be to administer angiotensin-converting enzyme inhibitors. Lisinopril
and captopril are the only ACE inhibitors that do not require activation (DeBrue, 2009). This
activation occurs in the liver; hence in the case of Mrs. X, it would be appropriate to use either of
the two as she has shown signs of hepatic failure.
Mechanism of the medication
Angiotensin II is responsible for the following: creates vasoconstriction by binding of
arteries and veins to AT1 receptors on the smooth muscle, prevents reuptake of norepinephrine
by adrenergic nerves, reduces urinary excretion of sodium and water, and promotes production
and discharge of aldosterone (Gamperl, Gillis, Farrell, & Brauner, 2017). ACE inhibitors stop
angiotensin converting enzyme from facilitating the conversion of angiotensin I to angiotensin II.
ACE inhibitors also protect the degradation of bradykinin- a peptide that causes vasodilation,
which helps reduce arterial pressure on the heart (Gamperl, Gillis, Farrell, & Brauner, 2017).
Adverse effects of the medication
One of the harmful effects of using ACE inhibitors is that patients are likely to develop a
dry, nonproductive cough. There have also been reported cases of angioedema that can occur in
any part of the body including intestine. Most concerning, however, is the edema of the tongue

CASE STUDY 8
that can cause airway obstruction (DeBrue, 2009). Furthermore, some patients have experienced
life-threatening anaphylactoid reactions as a result of the medication. Additionally, cholestatic
jaundice represents another adverse effect; it can proceed to hepatic necrosis if not well
managed. As is the case with any treatment that lowers blood pressure, ACE inhibitors lead to
hypotension. Finally, ACE inhibitors can result in hyperkalemia (Gamperl, Gillis, Farrell, &
Brauner, 2017).
Management of Pulmonary Oedema
The underlying principle of pulmonary oedema management is; to reduce the symptoms,
to improve oxygenation, maintain perfusion of vital organs, while ultimately limiting cardiac and
renal damage. The cornerstone of pulmonary oedema (PO) management is the use of
vasodilators, nitrates in particular (Graham, 2009). Also of importance is the use of diuretics.
Significantly, the administration of intravenous IV vasodilators provides the best mechanism of
satisfying these principles. A study by ADHERE reported higher mortality in cases of patients
treated with inotropes compared to patients treated with vasodilators. Relying on this report,
Peacock, demonstrated that early administration of nitrate therapy resulted in improved results
for patients; avoiding unnecessary ICU admission in some cases (Peacock, 2017).
Nitrates can be classified into two: those with the ability to discharge nitric oxide (NO)
immediately such as sodium nitroprusside and others that depend upon an enzymatic activation
to release NO such as nitroglycerine (Levy, et al., 2007). Upon administration of nitrate therapy,
nitric oxide stimulates the formation of cGMP from the enzymatic activation of soluble
guanylate cyclase (sGC). This increase of cGMP ensures a reduction in the entry of calcium into

CASE STUDY 9
the cell. Consequently, the decline in the concentration of calcium in the cells allows room for
relaxation and arterial vasodilation. Also, NO activates K+ channels that lead to
hyperpolarization and relaxation (Graham, 2009). When administered to patients, vasodilation
generates a notable fall in biventricular filling pressure. Furthermore, vasodilation ensures a
reduction of pulmonary vascular resistance and a systemic fall of arterial blood pressure.
Incredibly, optimal results of nitrate therapy are registered when administering a high
dosage of nitrate. Cases of adverse effects in hypertensive patients undergoing high-dose nitrate
therapy are low compared to those who received standard treatment (Hsieh, Lee, Kao, Hsu, &
Chong, 2018). A low dosage of organic nitrates only induces a venous dilation. In contrast, a
high dosage of the nitrates dilates not only the arteries but also the coronary arteries. A high
dosage, in turn, results in equilibria vasodilation of the left and right ventricles.

CASE STUDY 10
References
Blankesteijn, M., & Altara, R. (2015). Inflammation in heart failure. Amsterdam: Academic
Press.
Cowan, M. (2017). 12-lead electrocardiogram for nurses and allied professionals. New York:
New York: Page Publishing.
DeBrue, A. N. (2009). Angiotensin Converting Enzyme Inhibitors. Nova Science Publishers, Inc.
Gamperl, A. K., Gillis, T. E., Farrell, A. P., & Brauner, C. J. (2017). he Cardiovascular System:
Morphology, Control and Function. Cambridge: Academic Press.
Gardner, R. S., McDonagh, T. A., & Walker, N. L. (2014). Heart Failure. New York City:
Oxford University Press.
Graham, C. A. (2009). Pharmacological therapy of acute cardiogenic pulmonary oedema in the
emergency department. Emergency Medicine Australiasia, 47-54.
Harris, P., & Kuppurao, L. (2016). Quantitative Doppler echocardiography. Bja Education, 46-
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Hsieh, Y.-T., Lee, T.-Y., Kao, J.-S., Hsu, H.-L., & Chong, C.-F. (2018). Treating acute
hypertensive cardiogenic pulmonary edema with high-dose nitroglycerin. Turkish
Journal of Emergency Medicine, 34-36. Retrieved from
https://doi.org/10.1016/j.tjem.2018.01.004.
BJonas, D. (2018). Screening for cardiovascular disease risk with electrocardiography: An
evidence review for the U.S. Preventive Services Task Force. Rockville: Agency for
Healthcare Research and Quality.

CASE STUDY 11
Kemp, C. D., & Conte, J. V. (2012). The pathophysiology of heart failure. Cardiovascular
Pathology, 365-371.
Levy, P., Compton, S., Welch, R., Delgado, G., Jennet, A., Penugonda, N., Zalenski, R. (2007).
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Smiseth, O. A., & Tendera, M. (2008). Diastolic heart failure. London: Springer.
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