Causes, Pathogenesis, Clinical Manifestations, And Nursing Management Of Left-Sided Heart Failure

What is Left-Sided Heart Failure?

Mrs. Brown have represented several clinical manifestations including severe dyspnoea, i.e. difficulties in breathing, high respiratory rate, i.e. 24 breaths per minutes, low oxygen saturation level on room air, i.e. SpO2 85 %, high BP, 170/95 mmHg, high HR, i.e. 120 beats per minutes, auscultation of lungs identifies bilateral basal crackles. When she was connected to ECG monitor, atrial fibrillation was found, which is a sign of acute exacerbation of chronic left-sided heart failure. In this context, the pathogenesis of left sided heart failure is related to the reduced ability of heart’s left chambers to pump oxygen rich blood throughout the body. As the left side of the heart reduces its workability, the lack of oxygen throughout the body causes fatigue, which is one of the symptoms represented by Mrs. Brown (Konstam et al., 2011). On the other hand, as the flow of blood through the left-sided chambers of the heart decreases, the pressure in veins of lung enhances, which causes fluid accumulation in lung, resulting in the shortness of breath along with pulmonary oedema. In case of Mrs. Brown, she has represented the symptoms of breathing shortness since the morning; she was admitted in the emergency department of hospital (Allen et al., 2012).

The heart failure occurs, when the heart becomes unable to provide sufficient cardiac output in order to satisfy the metabolic needs of the body. It occurs due to the impairment of heart structure or function is detected. Left heart failure is the result of the damage to heart tissue. The left heart failure compromises aortic flow to the brain and throughout the body. Left ventricular failure is a life threatening condition (Thenappan et al., 2011). There are several reasons behind the left heart failure condition development, like drinking too much alcohol, high blood pressure, fluid volume overload, systemic hypertension, hypothyroidism, leaking or narrow heart valves or poor functioning of the left sided heart chambers due to prior hear attacks.

With time, the left sided heart failure increases in workload will produce changes to the heart structure and function. For instance, the changes in cellular apoptosis occur, which causes increased fibrous tissue damage. As a result, the contractility or ability to contract frequently is reduced, as a result of overloading of ventricle (Vachiery et al., 2013). Due to the decreased ability of cross-linking actin and myosin filaments in the over-stretched heart muscle, the ventricle is loaded with blood to such a level, which hinders the efficiency of heart muscle contraction. Stroke volume is reduced as the result of failure of systole, diastole or both. When the compliance of the ventricle falls, impaired ventricular filling leads to the decreased end diastolic volume. On the other hand, due to reduced contractility, the systolic volume is usually increased.

Another physical manifestation of the condition is hypertrophy, which is referred to the condition, when the size of myocardium is increased, which the result of an attempt for improving contractility. It ultimately caused by increased size of terminally differentiated heart muscle fibres. The resultant consequences may include increased stiffness and reduced ability of relaxing at the time of diastole. The common effect is reduced cardiac output and enhanced strain on the heart; thereby enhancing the risk of cardiac arrest (Daubert et al., 2012).

Causes and Pathogenesis of Left-Sided Heart Failure

The clinical manifestation of the condition includes fatigue, breathing shortness, waking up due to breathing shortness, rapid pulse, fluid retention and weakness. All of these symptoms are clinically manifested by Mrs. Brown, confirming her condition of left sided heart failure.

Two high priority nursing strategies for Mrs. Brown’s management and rationales are demonstrated below.

1. a) Ms. Brown was administered with two medications, i.e. IV furosemide and sublingual glyceryl trinitrate. The IV furosemide is a diuretic group of medication, which helps the body to eliminate the unnecessary water and salt through urine. As a result, it is easy for the heart to carry out its function, while controlling the blood pressure. It is used for treating fluid build up and high blood pressure due to left sided heart failure (Fitzgerald et al., 2011). Like other loop diuretics, it inhibits NKCC2, which is the luminal N-K-Cl cotransporter situated n the thick ascending limb of the Henle’s loop; although it does not hinder the action of carbonic anhydrase or aldosterone. It can block the negative and positive free water clearance, while abolishing the corticomedullary osmotic gradient. It is also a noncompetitive subtype specific GABA-A receptor blocker (McKelvie et al., 2013). At very low concentration, furosamide is able to antagonize GABA-evoked α₆β₂γ₂ As a result of the wide range of NaCl absorption capacity of Henle’s loop, the process of dieresis is not limited via the procedure of developing acidosis, because it is related with the carbonic anhydrase inhibitors, which are not affected by these diuretics.

On the other hand, glyceryl trinitrate is used as a vasodilator, which can reduce the ventricular filling pressure in very small doses, whereas in high doses it reduces systematic vascular resistance. Its principle action is to relax the vascular smooth muscle, leading to dilation of the post capillary beds. Dilation of post capillary beds reduces venous return to the heart, which ultimately reduce left ventricular and end diastolic pressure (Bui, Horwich & Fonarow, 2011).

1. b) While administering GTN, it should not be mixed with other drugs, for eliminating the chance of drug reaction. Administration should prefer central routes, with a strict monitoring of BP, CVP, HR, capillary refill, fluid intake and output (Felker et al., 2011). Side effects for Mrs. Brown may include tachycardia, hypotension, bradycardia, decreased PaO2 etc. While administering furosemide, it should be administered though intramascular or intravenous way It should be used with caution, when combined with corticosteroids. It should not be used with anesthesics, as it can interact with these drugs (Heidenreich et al., 2013). Side effects for Mrs. Brown should be monitored properly, which include dehydration and electrolyte imbalance. Dosage should be maintained as overdose can lead to kidney damage or collapse.

Reference List

Allen, L. A., Stevenson, L. W., Grady, K. L., Goldstein, N. E., Matlock, D. D., Arnold, R. M., … & Havranek, E. P. (2012). Decision making in advanced heart failure. Circulation, 125(15), 1928-1952.

Bui, A. L., Horwich, T. B., & Fonarow, G. C. (2011). Epidemiology and risk profile of heart failure. Nature Reviews Cardiology, 8(1), 30-41.

Daubert, J. C., Saxon, L., Adamson, P. B., Auricchio, A., Berger, R. D., Beshai, J. F., … & Dickstein, K. (2012). 2012 EHRA/HRS expert consensus statement on cardiac resynchronization therapy in heart failure: implant and follow-up recommendations and management. Heart rhythm, 9(9), 1524-1576.

Felker, G. M., Lee, K. L., Bull, D. A., Redfield, M. M., Stevenson, L. W., Goldsmith, S. R., … & Anstrom, K. J. (2011). Diuretic strategies in patients with acute decompensated heart failure. New England Journal of Medicine, 364(9), 797-805.

Fitzgerald, A. A., Powers, J. D., Ho, P. M., Maddox, T. M., Peterson, P. N., Allen, L. A., … & Havranek, E. P. (2011). Impact of medication nonadherence on hospitalizations and mortality in heart failure. Journal of cardiac failure, 17(8), 664-669.

Gheorghiade, M., Vaduganathan, M., Fonarow, G. C., & Bonow, R. O. (2013). Rehospitalization for heart failure: problems and perspectives. Journal of the American College of Cardiology, 61(4), 391-403.

Heidenreich, P. A., Albert, N. M., Allen, L. A., Bluemke, D. A., Butler, J., Fonarow, G. C., … & Nichol, G. (2013). Forecasting the impact of heart failure in the United States. Circulation: Heart Failure, 6(3), 606-619.

Konstam, M. A., Kramer, D. G., Patel, A. R., Maron, M. S., & Udelson, J. E. (2011). Left ventricular remodeling in heart failure. JACC: Cardiovascular Imaging, 4(1), 98-108.

McKelvie, R. S., Moe, G. W., Ezekowitz, J. A., Heckman, G. A., Costigan, J., Ducharme, A., … & Howlett, J. G. (2013). The 2012 Canadian Cardiovascular Society heart failure management guidelines update: focus on acute and chronic heart failure. Canadian Journal of Cardiology, 29(2), 168-181.

Schwartzenberg, S., Redfield, M. M., From, A. M., Sorajja, P., Nishimura, R. A., & Borlaug, B. A. (2012). Effects of vasodilation in heart failure with preserved or reduced ejection fraction: implications of distinct pathophysiologies on response to therapy. Journal of the American College of Cardiology, 59(5), 442-451.

Thenappan, T., Shah, S. J., Gomberg-Maitland, M., Collander, B., Vallakati, A., Shroff, P., & Rich, S. (2011). Clinical characteristics of pulmonary hypertension in patients with heart failure and preserved ejection fraction. Circulation: Heart Failure, CIRCHEARTFAILURE-110.

Vachiery, J. L., Adir, Y., Barberà, J. A., Champion, H., Coghlan, J. G., Cottin, V., … & Martinez, F. (2013). Pulmonary hypertension due to left heart diseases. Journal of the American College of Cardiology, 62(25), D100-D108.

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