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Pathogenesis, diagnosis and management of heart failure


Question one: Pathogenesis of heart failure

Heart failure is a chronic clinical syndrome that develops when the heart fails to pump blood at a rate that is required to meet metabolic requirements of the body tissues or if it does that at an elevated diastolic pressure. The cause maybe failure of the heart muscles to pump at the required strength or can be caused by high demand for cardiac function. Heart failure causes of the circulatory failure whereby the blood circulation to tissues is not at the required optimum. Therefore, to maintain heart functions, compensatory mechanisms from subcellular level to organ level such as increase in blood volume, expansion of heart muscle mass, increase in heart rate and cardiac filling pressure occur. However, despite the compensatory mechanisms, progressive decline in functioning of the heart results to exacerbation of heart failure (Craft, Gordon, Huether, McCance, & Brashers, 2015; Kemp & Conte, 2012).

Circulatory failure arising from heart failure affects the purpose of blood circulation to the tissues especially the supply of oxygen. Due to poor circulation of blood, vital organs and the peripheral tissues would not get optimum oxygen saturation. That is why Mrs. Brown presented with SPO2 85% when it should be 100% in a normal person. The vital organs affected by reduced oxygen saturation are the brain and the heart itself. When tissues sense decreased oxygen circulation, the neural endocrine system is triggered to reverse the situation (Craft et al., 2015; Kemp & Conte, 2012).

For example, the respiratory centre is triggered to increase the rate of breathing as a means of improving oxygen saturation in the blood and tissues. Additionally, the heart rate is increased to increase pumping and distribution of oxygen to the tissues (Huether & McCance, 2015). Therefore, patients with heart failure presents with rapid respiratory rate and tachycardia symptoms like Mrs. Brown.

The body responds to inadequate cardiac output by initiating compensatory mechanisms. Among the compensatory mechanisms is the release of norepinephrine to augment contraction of heart muscles. Norepinephrine activates the Renin-Angiotensin-aldosterone system (RAAS) which in addition to vasoconstriction caused by vasopressin, increase pressure of blood in the arteries and improve supply to vital organs in addition to vasoconstriction caused by release of vasopressin. Hence the patients presents with high blood pressure like Mrs. Brown (Aitken, Marshall, & Chaboyer, 2016; Mosterd & Hoes, 2007).

Moreover, activation of the RAAS to compensate cardiac output causes other harmful effects and worsens heart failure. RAAS reduces excretion of salt and water leading to their retention. Water retention in the circulatory system and tissues further overloads the heart and impairs functioning of the lungs. It causes retention of fluids the lungs that manifests as crackles and dyspnoea (Aitken et al., 2016; Mosterd & Hoes, 2007).

Besides vasoconstriction, vasopressin increases cytosolic calcium entry, which augments contractility of heart muscles but impairs relaxation of heart muscle subsequently leading to arrhythmias and risk of sudden death. Increased contraction of heart muscles leads to increased energy expenditure, which is a precursor to myocardial cell death and exacerbated reduction in cardiac functions. The heart is a self-renewing organ. It regenerates to increase its ability contraction power against the increasing pressure in the blood vessels. However, during heart failure the imbalance of hypertrophying and the rate of myocyte loss is higher than the regeneration thereby causing exacerbations of heart failure (Kemp & Conte, 2012).

Question two: Priority nursing strategies in management of heart failure

The first nursing strategy will aim at promoting her comfort, which will reduce the metabolic activity, and increasing his oxygen saturation. This strategy will involve providing a bed rest to Mrs. Brown in a cardiac bed that is elevated 45%. Bed rest is known reduce oxygen consumption and breathlessness. A cardiac patient bed is elevated to 45o to improve functioning ability of the heart. Additional measures will include reassuring her and explaining to her the plan of care to alleviate anxiety. This strategy will be complimented with monitoring of vital signs. She will require self care assistance such as bathing (Aitken et al., 2016; Wagner, Hardin-Pearce, Brenner, & Krenzer, 2014).

The next strategy will be focusing to alleviate fluid overload through administration of diuretics such as furosemide. Diuretics relieve dyspnoea and oedema. The patient will be put on low-salt diet, and drinking of water should be minimized. Salt increases retention of water. To relieve oedema on the limbs, legs will be elevated when sitting out. Physiotherapy will also be provided to improve venous return. Mrs. Brown be put on a urinary catheter to help in strict monitoring of input and out. Other measures to monitor fluid overload will include daily weighing and measurement of jugular venous pressure (Aitken et al., 2016; Mosterd & Hoes, 2007)..

Question three: Pharmacological and nursing management of heart failure

Furosemide is a fast acting but short lasting loop diuretic that prevents reabsorption of water and salt at the loop of Henle and at the renal tubes. Furosemide blocks chloride binding cotransport system thus countering the effect of RAAS compensatory system in salt and water regulation. Therefore, furosemide is able to reduce oedema, fluid overload and the associated dyspnoea and breathlessness. Reduced fluid overload will reduce the preload, which reduces energy expenditure and oxygen demand of the heart muscles (Allen et al., 2010; McMurray et al., 2012; Wagner et al., 2014).

Glyceryl Trinitrite is a vasodilator which is used a first line agent to counter vasoconstriction. It increases myocardia inotropic activity. When in the body, Glyceryl Trinitrite is denitrified to Nitric Oxide (NO), which causes vasodilation through relaxation of the smooth muscle cells. The resulting systemic vasodilation reduces both the preload and the afterload, leading the reduced myocardial oxygen demand (Butler, 2012; Elliott, Aitken, & Chaboyer, 2011).

Furosemide has an ability to cause excessive diuresis, which poses a high risk for hypotension and electrolyte imbalances. Therefore, a complete blood count, serum electrolytes, Blood Urea Nitrogen, carbon dioxide saturation, and magnesium should be monitored prior to administration of furosemide and should be repeated periodically. Additionally, daily weight monitoring, regular observation of vital signs particularly blood pressure and heart rate as well as observation of poor skin turgor and cracked mucous membranes are essential for monitoring adverse effects of furosemide. Such adverse effects can be countered by stopping or reducing furosemide dosage. Glyceryl Trinitrite can lead to hypotension, which can be monitored through regular blood pressure measurements and symptoms of feeling light-headedness, flushing and anxiety. The dosage should be reduced if the adverse effects are unbearable (Allen et al., 2010; McMurray et al., 2012; Wagner et al., 2014).

Therapeutic effects of these drugs will be evaluated by stabilization of diastolic pressure to 60-90mmHg and systolic pressure 100-140mmHg, heartrate ranging 60-100beats per minutes, SPO2 of 100%, respiratory rate of 12-20 beats per minute and absence of crackles on auscultation of the lungs (Wagner et al., 2014).


Aitken, L., Marshall, A., & Chaboyer, W. (2016). ACCCN’s Critical Care Nursing. Elsevier Health Sciences. Retrieved from

Allen, L. A., Turer, A. T., DeWald, T., Stough, W. G., Cotter, G., & O’Connor, C. M. (2010). Continuous versus bolus dosing of furosemide for patients hospitalized for heart failure. The American Journal of Cardiology, 105(12), 1794–1797.

Butler, J. (2012). An overview of chronic heart failure management. Retrieved August 2, 2016, from

Craft, J., Gordon, C., Huether, S. E., McCance, K. L., & Brashers, V. L. (2015). Understanding pathophysiology-ANZ adaptation. Elsevier Health Sciences.

Elliott, D., Aitken, L., & Chaboyer, W. (2011). ACCCN’s critical care nursing. Elsevier Australia. Retrieved from

Huether, S. E., & McCance, K. L. (2015). Understanding pathophysiology. Elsevier Health Sciences.

Kemp, C. D., & Conte, J. V. (2012). The pathophysiology of heart failure. Cardiovascular Pathology: The Official Journal of the Society for Cardiovascular Pathology, 21(5), 365–371.

McMurray, J. J., Adamopoulos, S., Anker, S. D., Auricchio, A., Böhm, M., Dickstein, K., … others. (2012). ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012. European Journal of Heart Failure, 14(8), 803–869.

Mosterd, A., & Hoes, A. W. (2007). Clinical epidemiology of heart failure. Heart, 93(9), 1137–1146.

Wagner, K. D., Hardin-Pearce, M. G., Brenner, Z. R., & Krenzer, M. (2014). High-acuity nursing. 6th edition. Upper Saddle River, New Jersey: Pearson, c2014. xii, 960 p.: illustrations (chiefly color); 28 cm. Retrieved from