Discuss about the Health Variation for Left Heart Failure.
This case study is regarding Mrs. Brown who is 78 years old and has been admitted to the Emergency department at 6 am after waking up with severe breathlessness. The patient has a history of heart failure, which was diagnosed two years ago. On physical examination, she was diagnosed with atrial fibrillation, which suggested acute exacerbation of left heart failure.
The inefficient pumping of the heart for maintaining the blood flow in the body leads to congestive left heart failure. The clinical manifestations of this disease include pulmonary edema, fatigue, shortness of breath and swelling feet and ankles. The patient also had severe dyspnoea that was apparent by the elevated respiratory rate of 24 breaths/ min and had an abnormal pulse rate of 110 beats/minute. It is essential to know the pathogenesis of this condition, which is leading towards these manifestations of the patient (Rosenkranz et al., 2015).
The cause of heart failure is due to the inefficiency of the muscles of the heart along with other conditions such as cardiac amyloidosis. For the patients like Mrs. Brown, the normal Frank-starling mechanism fails and due to this, the contraction of muscles become difficult and leads to a decreased cardiac output. The changes in neurohumoral status, blood volume and vascular function arise due to cardiac dysfunctions (Park et al., 2012). The vascular and cardiac changes associated with left heart failure are the following:
Reduced ejection fraction in case of systolic dysfunction and ventricular dilation impaired filling in the case of diastolic dysfunction
Increase in diastolic pressure and decrease in cardiac output
Vascular alterations comprise impaired arterial pressure and increased volume of blood (Steinberg et al., 2012).
In the patients with heart failure, a decreased output is seen due to the reduction in the stroke volume because of either diastolic or systolic dysfunction. In the case of diastolic dysfunction, stiffening of ventricle occurs along with the impairing of normal ventricular filling. High ventricular end-pressure and decreased ejection of blood results due to reduced ventricular filling. On the other hand, systolic dysfunction results due to the loss of contractility followed by acute myocardial infarction. This compensatory mechanism is initiated by using the Frank-Starling mechanism for increasing stroke volume (Reil et al., 2013).
The volume of blood in left heart failure is enhanced due to the reduced renal perfusion, which leads to the more fluid retention and reduced output of urine. In addition, the activation of rennin-angiotensin system augments the secretion of aldosterone. The outcome is enhanced in the renal absorption of sodium and other fluids. The increased volume of blood helps in maintaining the cardiac output leads to an increase in the venous pressure resulting in systemic and pulmonary edema. For understanding this mechanism, there is a need to understand the cause of clinical manifestation of the patient in the present case study of the patient and plan treatment in order to reduce the volume of blood. The patient is also having a crackle sound at the base of each lung also suggest that she is experiencing pulmonary edema due to which she is not able to breathe properly (Rosenkranz et al., 2015).
The neurohumoral response in the heart of the patients like Mrs. Brown takes place due to heart failure. It is concerned with the activation of the sympathetic nerves together with the release of atrial peptides and vasopressin. It results in venous constriction, vasoconstriction and increased volume of blood (Bath et al., 2016). All of these are the compensatory mechanisms for increasing ventricular filling and, but it frequently deteriorates the condition by enhancing the ventricular load and results in pulmonary congestion and edema. Hence, it is necessary to know the pathophysiology of heart failure for finding the rationale for every therapeutic intervention (Schwartzenberg et al., 2012).
Strategy for relieving pulmonary and dyspnoea: in order to manage acute shortness of breath, the nurse for providing relief from the symptoms of dyspnoea can administer diuretics. It will also be necessary to monitor closely the renal function, fluid balance and urine output in the patient. The output of urine can be assessed by indwelling urinary catheter but is should be restricted very soon as it results in infections of the urinary tract (McMurray et al., 2012).
Strategy for managing the decreased cardiac output: As the patient is experiencing irregular rhythm of pulse along with an altered heart rate, it is essential to plan intervention that will help to reduce the workload of the heart and provide the patient hemodynamic stability. At first the nurses will assess the sounds of the heart and lungs. They will also monitor the blood pressure and perform diagnostic test. For improving the cardiac output, they will administer the cardiac glycoside agents. They will teach the patient to assume those positions, which will better expansion of the chest and along with improved pulmonary capacity. It is necessary to provide education to the patient regarding the pathophysiology of disease for managing the disease in a proper way (McHugh & Ma, 2013).
a loop diuretic pill helps in the prevention of reabsorption of water in the kidney by blocking potassium-chloride cotransporter. On the chloride binding site, competitive inhibition prevents the transport of sodium and reduces osmotic gradient for reabsorption of water throughout the nephron (Ali et al., 2014).
Glyceryl trinitrate: It leads to the activation of guanylate cyclase enzyme and helps in stimulating the release of cyclic guanosine 3’ 5’monophospate. It results in protein kinase dependent phosphorylation in the smoothy muscles and leads to dephosphorylation of of myosin chain of the smooth muscle (Viefhues et al., 2012).
b) After giving Furosemide to the patient, the signs of allergic responses towards drugs will such as nausea, selling of face, kidney problem and jaundice will be will be checked by the nurse. As this drug is utilized for preventing the body to absorb excess salt, it might also result in electrolyte imbalance. Therefore, the nurses should check the signs of muscle cramp, dry mouth and thirst (Ali et al., 2014).
Glyceryl trinitrate is used for the treatment of heart failure and angina. The nurses should take precautions prior to giving it to the patients having glaucoma, anaemia and low blood pressure. The nurses should also monitor the side effect of this drug in the patients having rapid heartbeat, rashes, dizziness, vomiting and swelling (Viefhues et al., 2012).
C) The evaluation of therapeutic effect of the drug will be carried out by checking whether the symptoms of swelling and breathlessness have reduced or not. It will diminish the likelihood of heart attack.
Glyceral nitrate is a vasodilator, and its therapeutic effects will be evaluated by checking if the patients are relived from the symptoms of heart failure (Viefhues et al., 2012).
References
Ali, Y., Parekh, A. M., Rao, R. K., & Baig, M. R. (2014). Furosemide Induced Electrolyte Imbalance: A Real Danger of Overdiuresis in Patients with Heart Failure. Journal of International Translational Medicine, 2(4), 482-484.
Bath, P. M., Woodhouse, L., Krishnan, K., Anderson, C., Berge, E., Ford, G. A., … & in Acute Stroke Collaboration. (2016). Effect of Treatment Delay, Stroke Type, and Thrombolysis on the Effect of Glyceryl Trinitrate, a Nitric Oxide Donor, on Outcome after Acute Stroke: A Systematic Review and Meta-Analysis of Individual Patient from Randomised Trials. Stroke research and treatment, 2016.
Guazzi, M. (2014). Pulmonary hypertension in heart failure preserved ejection fraction prevalence, pathophysiology, and clinical perspectives.Circulation: Heart Failure, 7(2), 367-377.
McHugh, M. D., & Ma, C. (2013). Hospital nursing and 30-day readmissions among Medicare patients with heart failure, acute myocardial infarction, and pneumonia. Medical care, 51(1), 52.
McMurray, J. J., Adamopoulos, S., Anker, S. D., Auricchio, A., Böhm, M., Dickstein, K., … & Jaarsma, T. (2012). ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012. European journal of heart failure, 14(8), 803-869.
Park, S. J., Milano, C. A., Tatooles, A. J., Rogers, J. G., Adamson, R. M., Steidley, D. E., … & Slaughter, M. S. (2012). Outcomes in advanced heart failure patients with left ventricular assist devices for destination therapy.Circulation: Heart Failure, 5(2), 241-248.
Reil, J. C., Hohl, M., Reil, G. H., Granzier, H. L., Kratz, M. T., Kazakov, A., … & Gräber, S. (2013). Heart rate reduction by If-inhibition improves vascular stiffness and left ventricular systolic and diastolic function in a mouse model of heart failure with preserved ejection fraction. European heart journal,34(36), 2839-2849.
Rosenkranz, S., Gibbs, J. S. R., Wachter, R., De Marco, T., Vonk-Noordegraaf, A., & Vachiéry, J. L. (2015). Left ventricular heart failure and pulmonary hypertension. European heart journal, ehv512.
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.
Steinberg, B. A., Zhao, X., Heidenreich, P. A., Peterson, E. D., Bhatt, D. L., Cannon, C. P., … & Fonarow, G. C. (2012). Trends in Patients Hospitalized with Heart Failure and Preserved Left Ventricular Ejection Fraction-Prevalence, Therapies, and Outcomes. Circulation, CIRCULATIONAHA-111.
Tanai, E., & Frantz, S. (2014). Pathophysiology of heart failure.Comprehensive Physiology
Viefhues, H., Schoene, W., Rychlik, R., Kimchi, A., Lewis, B. S., & Weiss, M. (Eds.). (2012). Chronic Heart Failure: I. Quality of Life II. Nitrate Therapy. Springer Science & Business Media.
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