HMH2007 Person Centred Care: Left Sided Heart Failure

ous exchange.          Severe shortness of breath consequently occurs. 

Management

Goals of managing left sided heart failure

• Minimizing symptoms
• Reducing stress of the heart,
• Treating the infection that is causing heart failure  
• Preventing death.

Treatments might include:

• Pharmacotherapyis the first form of treatment for left-sided heart failure.
• The drugs are diuretics are ACE, aldosterone antagonists, beta blockers, digoxin and hydralazine hydrochloride. (Inamdar & Inamdar, 2016)
• Surgery to unclog blocked heart arteries.

Prognosis

• Leads to early death.
• Chances of full recovery are minimal.
• Patients remain stable with medication

Diagnostic procedures

Physical examination

• Disclose a rapid or irregular heartbeat.
• Detecting unusual heart motion

Laboratory Tests

• Electrocardiogram (ECG)
• Chest x-ray
• Coronary angiography
• Heart stress test
• Echocardiogram (ultrasound of the heart)
• Blood tests to examine kidney and liver function
• An MRI

Course

• Stage A:Detecting heart failure at this stage is difficult. It is primarily linked to individuals with a history of heart failure. The initial level in which a person faces frequent fatigue.
• Stage B: The individual faces shortness of breath and blood pressure starts to rise. The ventricular walls starts to weakening
• Stage C: Signs of heart failure are evident and in this stage the individual might experience heart attack.

Prevention

• Regular exercises
• Losing weight
• Low salt diet
• Reducing alcohol intake
• Quitting smoking
• Eating low fat foods
• Getting sufficient sleep
• Avoiding stressful events

Left Sided Heart Failure: Questions

1: Pathogenesis

Mrs. Brown presented with acute dyspnoea, rapid pulse rate, high blood pressure, increased breath rate and auscultation of lungs characterized by bilateral basal crackles. Left heart sided failure can be diastolic or systolic. Left sided heart failure occurs due to an ineffective left ventricular contractile function (Craft, Gordon, Huether, McCance, Brashers, & Rote, 2015). Right-heart failure or right-sided heart disease might also cause left-sided heart failure. A decrease in right ventricular output diminishes blood return to the left ventricular, which causes left ventricular stroke volume to decrease (Lilly, 2012). Oxygenated blood is received in the left atrium from the lugs before it is pumped by the left ventricular into the systemic circulation.

Thus, when the capacity of the left side of the heart to pump blood to all the body parts is incapacitated, the body gets insufficient oxygen (Andrade, Khairy, Dobrev, & Nattel, 2014). As a result, pressure builds up in the pulmonary vein. Congestion of the pulmonary vein occur leading to the accumulation of fluid in the lungs. Accumulation of fluid in the lung can lead to pulmonary embolism (Wagner, Hardin-Pearce, Brenner, & Krenzer, 2014). Shortness of breath, a rapid heart rate, and chest pain are the common symptoms of this condition which were evident in Mrs. Brown.

Left-sided heart failure causes a substantial burden for patients and is thus a life threatening condition. As pressure mounts on the left ventricle of the heart, the myocardium weakens progressively. Myocardium in the left side of the heart loses the ability to pump adequate oxygenated blood out of the left ventricle (Marieb & Hoehn, 2016). This condition escalates to a level where the heart muscles are completely unable to pump oxygenated blood from the left ventricle. As a result, vital body organs like the brain fail to receive oxygenated blood. Mrs. Brown’s condition worsened to a point where body parts were unable to receive oxygenated blood. She began to face drowsiness and acute shortness of breath. In an effort to compensate the inadequate flow of blood from the left ventricle, the pressure receptors on the aorta are activated leading to the stimulation of the Sympathetic Nervous System. In turn, the Sympathetic Nervous System prompts a sequence of reactions resulting in the production of hormones like the noradrenaline and catecholamine that trigger myocardial contractility (Marieb & Hoehn, 2016).

The secreted hormones lead to vasoconstriction which, in turn, raises the pressure in the arteries and veins. This clinical manifestation was evident in Mrs. Brown. Her pulse rate was 120 beats per minute while the blood pressure was 170/95 mmHg. An adult has a normal blood pressure and pulse rate of 100/120 mmHg and 60 to 100 beats per minute respectively (Satpathy & Mishra, 2015). Thus, Mrs. Brown’s blood pressure and pulse rate were very high. This symptom occurs in conjunction with strain to preserve high amounts of fluid, which impedes gaseous exchange in the alveoli. The retention of fluid in the lungs and the area around the heart undermines the competence of the lungs in conducting gaseous exchange by minimizing the surface area for effective gaseous exchange. This mechanism was responsible for the auscultation of the lungs which led to crackles at the lower parts of the lungs in the case of Mrs. Brown (Andrade, Khairy, Dobrev, & Nattel, 2014).

2. Nursing Strategies

The primary intervention for chronic heart failure entails pharmacotherapy, lifestyle modification and administration of multidisciplinary health failure programs (Krum & Driscoll, 2013). As explained in the case study, Mrs. Brown has a history of heart failure. Thus, the nursing priority is to promote systemic perfusion and the contractility of the heart muscles. Physical activity has a positive effect on patients with chronic heart failure (Klompstra, Jaarsma, & Stromberg, 2015). The primary nursing intervention that should be undertaken to manage Mrs. Brown’s condition is to enhance activity tolerance. Exercising for 30 minutes each day will be a great intervention for Mrs. Brown. Exercise tolerance can improve the outcome of patients with heart failure (Intwala & Balady, 2015).

Additionally, nurses can prioritize the reduction of the fluid that might be accumulating in the patient’s body. Nurses can start monitoring Mrs. Brown to determine her lung condition and prevent possible edema of the lungs that might occur due to the accumulation of fluid (McMurray, et al., 2012). Besides, the patient should be advised to embrace a low sodium diet. Sodium has been found to trigger the accumulation of fluid and thus reducing the patient’s sodium levels would result in low fluid accumulation in the lungs (Lemone & Burke, 2014).

3 (a). Mechanism of drug action

Furosemide is a primary loop diuretic for heart failure patient and is used for the management of volume overload (Mentz, et al., 2015). Furosemide is administered intravenously assist in reducing fluid retention as well as accumulation in the body. It hinders the re-absorption of sodium chloride (NaCl) as well as water back into the blood at the loop of Henle in the kidney (Marieb & Hoehn, 2016). This medicine inhibits re-absorption by obstructing the osmotic gradient of the fluid flowing in the loop of Henle (Lemone & Burke, 2014). Consequently, sodium is excreted from the blood and reabsorbed before the filtered fluid is eliminated as urine. Diuresis occurs whereby the patient experiences a significant increase of urine. After injection, the onset of action of the IV furosemide is two hours.

Glyceryl trinitrate is the active ingredient in sublingual glyceryl trinitrate. This drug is administered orally and assists the heart to function seamlessly. After administration, the drug is converted into a chemical compound known as nitric oxide (Lemone & Burke, 2014). Nitric oxide is an endothelia smooth muscle relaxant (Aitken, Marshall, & Chaboyer, 2015). The impact of this chemical is triggering vasodilation. As the blood vessels widen, they provide low resistance to blood flow, and thus the heart can effortlessly pump blood into them. Evidently, the drug helps to minimize the pressure and strain that is experienced by the left side of the heart while pumping blood into constricted veins and arteries (McMurray, et al., 2012).

3 (b). Nursing implication

The nurse examining and attending to Mrs. Brown should closely monitor the administration of these drugs to prevent adverse outcomes. The IV furosemide leads to diuresis, and if not carefully tracked, the level of sodium chloride in the blood might be lowered to threatening levels (Dempsey, French, Hillege, & Wilson, 2014). Excessive diuresis might result in dehydration of the body, which would impact gaseous exchange in the lungs because gaseous exchange in the lungs is only practical when there is adequate moisture. Conversely, the glyceryl trinitrate might lead to low blood pressure if prescribed in high dosages (Lemone & Burke, 2014). Hence, the nurse should make sure that the blood pressure of Mrs. Brown is carefully monitored to make sure that the medicine does not result in adverse outcomes. 

References

Aitken, L., Marshall, A., & Chaboyer, W. (2015). ACCCN’s critical care nursing. Chatswood, NSW: Elsevier Australia.

Andrade, J., Khairy, P., Dobrev, D., & Nattel, S. (2014). The clinical profile and pathophysiology of atrial fibrillation. Circulation Research , 114 (9), 1453-1468.

Craft, A., Gordon, C. J., Huether, S. E., McCance, K. L., Brashers, V. L., & Rote, N. E. (2015). Understanding pathophysiology – ANZ adaptation. Chatswood, NSW: Elsevier Australia.

Dempsey, J., French, J., Hillege, S., & Wilson, V. (2014). Fundamentals of nursing and midwifery: A person-centred approach to care. Broadway, NSW: Lippincott Williams & Wilkins.

Inamdar, A. A., & Inamdar, A. C. (2016). Heart Failure: Diagnosis, Management and Utilization. J Clin Med , 5 (7), 62.

Intwala, S., & Balady, G. J. (2015). Physical Activity in the Prevention of Heart Failure. Circulation , 136 (5), 1777-1779.

Kemp, C. D., & Conte, J. V. (2012). The pathophysiology of heart failure. Cardiovasc Pathol , 21 (5), 365-371.

Klompstra, L., Jaarsma, T., & Stromberg, A. (2015). Physical activity in patients with heart failure: barriers and motivations with special focus on sex differences. Patient preference and adherence , 9, 1603-1610.

Krum, H., & Driscoll, A. (2013). Management of heart failure. Med J Aust , 199 (5), 334-339.

Lemone, P., & Burke, K. (2014). Medical-surgical nursing: Critical thinking in client care (2nd Australian ed.). Frenchs Forest, NSW: Pearson Australia.

Lilly, L. S. (2012). Pathophysiology of heart disease: a collaborative project of medical students and faculty. Lippincott Williams & Wilkins.

Marieb, E. N., & Hoehn, K. (2016). Human anatomy and physiology. Boston, MA: Pearson.

McMurray, J. J., Adamopoulos, S., Anker, S. D., Auricchio, A., Bohm, M., Dickstein, K., et al. (2012). ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012. European journal of heart failure , 14 (8), 803-869.

Mentz, R. J., Buggey, J., Fiuzat, M., Ersboll, M. K., Schulte, P. J., DeVore, A. D., et al. (2015). Torsemide versus furosemide in heart failure patients: insights from Duke University Hospital. Journal of cardiovascular pharmacology , 65 (5), 438-443.

Pazos-López, P., Peteiro-Vázquez, J., Carcía-Campos, A., García-Bueno, L., Torres, J. P., & Castro-Beiras, A. (2012). The causes, consequences, and treatment of left or right heart failure. Vasc Health Risk Manag , 7, 237-254.

Satpathy, M., & Mishra, R. B. (2015). Clinical diagnosis of congenital heart disease. JP Medical Ltd.

Wagner, K. D., Hardin-Pearce, M. G., Brenner, Z. R., & Krenzer, M. (2014). High acuity nursing (6^thed.). Upper Saddler River, New Jersey.