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Heart failure and ACE inhibitors

Abstract

This report will give a brief overview of heart failure and ACE inhibitors. The purpose of this assignment is to highlight the mechanism and functioning of the heart and responsible factors for heart failure. The homeostasis denotes the body’s capability to uphold a steady interior setting (controlling hormones, body temperature, liquid equilibrium).  Upholding homeostasis needs the body unceasingly control its interior settings. The report will describe the key pathophysiology of heart failure and decreasing effectiveness of the heart muscle. The pharmacology of heart failure will give a brief idea of the cure to prevent heart failure mainly considered here is Angiotensin-Converting Enzyme (ACE) inhibitors an essential drugs for handling heart catastrophe. Also discussing its mechanism in preventing the heart failure, certain chronic kidney diseases, heart attacks and coronary artery disease. The adverse effects of ACE inhibitors are dry cough, rash, fever, altered taste, hyperkalemia, headache and dizziness. The treatment with ACE inhibitors must be given with care to patients suffering from dehydration or hypovolemia and damaged renal function. In order to avoid heart failure and the related problem, it has been mentioned below about the medications like Beta-blockers (carvedilol, metoprolol, bisoprilol), Combination medicines (Entresto, or sacubitril/valsartan) and Digoxin (Lanoxin). Altogether with improvement in personal lifestyle like, stop smoking, weight management, restricting alcohol, restricting caffeine and physical fitness. Also, there is a clinical treatment in the context of nursing in hospitals while taking care of cardiovascular issues. The key finding through this report aiming at the patients within the age group of 60-65 years suffering from heart-related problems are the good care of the cardiology section in hospitals, effective communication and complete care of the patients.

Overview

The Physiology of Heart

The heart is a beefy tissue approximately the scope of a locked fist. It is located inside the chest, more towards the left concerning the centre. The blood is pumped throughout the body when the heart contracts. It moves de-oxygenated blood into the lungs to refuel it with oxygen and discharge carbon dioxide, a byproduct of breakdown. The blood, blood vessels, and heart altogether are denoted as “circulatory system” of a body. On average, a human carries approx. 5 litres (8 pints) of blood, that is continuously propelled inside the body (Ouwerkerk et al. 2017). 

The heart constitutes of 4 chambers, 2 ventricles and 2 atria. Deoxygenated blood comes back to the right flank of the heart through the veins flow. The blood is pushed into the right ventricle and going in the lungs where carbon dioxide is discharged and oxygen is absorbed. The oxygenated blood then moves to the left part of the heart in to the left atria, going in to the left ventricle after which it is propelled in to the aorta and arterial circulation (Fonarow 2019).

image showing the physiology of Human Heart

Figure 1: Physiology of Human Heart

The pressure created in the arteries by the contraction of the left ventricle is the systolic blood pressure. Once the left ventricle has completely contracted it starts to relax and top-up by blood as of the left atria. When the ventricle refills the pressure in the arteries drops and is termed as “diastolic blood pressure” (Gujral, Lloyd and Bhattacharyya 2018). The atrioventricular septum entirely splits the 2 parts of the heart. The 2 parts of the heart not ever straightly converse, except there is a septal defect. Blood journeys from the right side to the left side through the lungs. Though the chambers self-function the 2 atria contract concurrently, and the 2 ventricles contract concurrently.

Homeostasis

Homeostasis denotes to the body’s capability to uphold a steady interior setting (controlling hormones, body temperature, liquid equilibrium).  Upholding homeostasis needs the body unceasingly control its interior settings like the body pressure to blood temperature to amounts of definite nutrients and respective physiological illness has a specific “Set Point”. A “Set Point” is the physiological rate about the usual limits fluctuations. A standard limit is the limited set of standards which are effectively nutritious and steady. For Example the “Set Point” for a typical human body’s temperature is roughly 37 °C (98.6°F). Physiological constraints, like body temperature and blood pressure, incline to vary inside a usual limit, a slight degree up or down. Control hubs in the brain act parts in controlling physiological constraints and ensuring it under a usual limit. The body acts to sustain homeostasis, some major abnormality as of the usual limit must be countered and homeostasis returned via a procedure termed as “feedback loop” (Van Der Meulen et al. 2018).

Any feedback loop has 3 elementary modules. A sensor, termed as the receptor, is a module of a response mechanism which observers the physiological rate.  It is accountable for sensing any variation in the body. If the variation is found in values, it is conveyed to the control hub. The control hub is a module in response mechanism which matches the values to the standard limit. If the values differ very considerably from the “set point”, then the control hub triggers an “effector”. An effector is a module in a response mechanism which sources a modification to inverse the condition and set the values to the standard limit.  Any effectors are either a muscle or gland (McMurray et al. 2016).

Pathophysiology of Heart Failure

The key pathophysiology of heart failure is decreasing effectiveness of the heart muscle, via harm or congestion. Intrinsically, there are many factors responsible for it, comprising myocardial infarction (a situation where the heart muscle is depleting in oxygen levels and then eventually expire), hypertension (a situation where the heart contraction is too high to pump the blood) and amyloidosis (a situation where misfolded proteins that are settled down in the heart muscle, triggering it to thicken). During the period an increase in workload results in producing fluctuations to the heart itself.

Any human with heart failure could have a lessen power of contraction because of congestion of the ventricles. Comparing it with fit heart, the improved filling of the ventricles outcomes in amplified contraction power (Frank-Starling law of the heart) and therefore a growth in cardiac yield (Edelmann et al. 2018). This system flops during heart failure, as the ventricles are overloaded by blood to an extent that the heart muscle contraction turns out to be not so effective. The reason is the decreased capability to cross-link actin and myosin filaments in excessively strained heart muscles.

Pharmacology of Heart Failure

Ace Inhibitors

Angiotensin-Converting Enzyme (ACE) inhibitors are the most essential drugs for handling heart catastrophe. They soothe the blood vessels and decrease blood pressure. Resulting in better blood flow. Examples of Ace Inhibitors are Enalapril, Lisinopril, Quinapril and Ramipril. ACE inhibitors are consumed orally and are inconsistently engrossed (Ricci et al. 2016).

Mechanism of action

In the case of heart failures, the heart cannot pump well enough, therefore uncluttering the blood vessels and dropping the blood pressure becomes necessary. This decreases the hardworking of the heart. This might aid to retain blood from backtrack in the heart and lungs. ACE inhibitors snag the process of proteins (enzymes) which prevents blood vessels to constrict. Consequently, blood vessels to soothe and broaden. This drops blood pressure and facilitates the heart to propel blood (Milfred-LaForest et al. 2017).

image showing Function of Angiotensin-Converting Enzyme (ACE)  Inhibitors

Figure 2: Function of Angiotensin-Converting Enzyme (ACE)  Inhibitors

ACE inhibitors are used to prevent or cure the symptoms of heart failure, certain chronic kidney diseases, heart attacks and coronary artery disease. The adverse impact of ACE inhibitors are dry cough, rash, fever, altered taste, hyperkalemia, headache and dizziness. The ACE inhibitors are avoided in patients suffering from, former angioedema related to ACE inhibitor treatment. The ACE inhibitors should be given with care to patients suffering from dehydration or hypovolemia and damaged renal function. Some important drugs for the medication for heart failure are, Beta-blockers (carvedilol, metoprolol, bisoprilol), Combination medicines (Entresto, or sacubitril/valsartan) and Digoxin (Lanoxin) (Rincon-Choles 2019).

The individuals with potential heart failure must consider several other options like,

1. Stop Smoking: The puffs taken from cigarettes momentarily elevates the heart rate and blood pressure and also decrease the amount of oxygen levels in the blood throughout the body. Too much smoking causes blood to stick and clot the vessels that are connected with the heart.

2. Weight Management: Abrupt weight increase or decrease could be symptoms of increasing the chances of heart failure or there is a potential chance of heart failure. Checking up the weight every day and consulting with physicians about it.

3. Restricting Alcohol: Avoiding overconsumption of alcohol as it impacts on the liver and increases the chances for heart failure. 

4. Restricting Caffeine:  The consumption of coffee must be limited with 1 to 2 cups a day.

5. Physical Fitness: Is important for the entire body and one must consider to be physically active and develop some kind of exercise in their lifestyle (Ohlsson et al. 2016).

The key clinical practice for heart failure patients between the age of 60-65 years are:

1. Creating an adequate environment for secure clinical maintenance like cardiology wards, medical wards, OPDs and coronary care units.

2. Keeping track of changing symptoms of the patients’ treatment. Significantly recognizing the variation in the health of the patient.

3. Patient’s concerns must be resolved with effective communication and show clear information to the patient and family.

This level of care is recognized in global advice for nursing in cardiovascular problems. The emphases on the administration of heart failure had directed to emphasize on the involvement given by nurses to the complete heart failure period and their parts in refining patient result and giving of valuable care (Fonarow 2019).

Conclusion

This report has briefly discussed the aspects of heart failure and ACE inhibitors. The  “Homeostasis” is a mechanism termed for one's body’s capability to maintain interior environment like the blood pressure, moisture, heart rate, fluidity and many more. The physiology of the heart describes its mechanism and functions it performs within the body. The heart constitutes of 4 chambers, 2 ventricles and 2 atria. Deoxygenated blood comes back to the right flank of the heart through the veins flow and reoxygenated blood pumps into the body via the lungs from the left side of the heart. The pathophysiology of heart failure describes the heart’s inability to pump blood because of continuous abuse and harm to the heart’s muscle. The pharmacology of heart failure gives a solution and care to decrease the chances of heart failure i.e Angiotensin-Converting Enzyme (ACE) inhibitors are given to patients to soothe their blood vessels. The ACE inhibitors snag the process of proteins (enzymes) which prevents blood vessels to constrict. To decrease the chances of heart failure one must improve their lifestyle by adding discipline in consumption and being physically active.   

References

Edelmann, F. et al. 2018. Chronic heart failure. Deutsches Ärzteblatt International, 115(8), pp. 124-154.

Fonarow, G. C. 2019. Heart failure: recent advances in prevention and treatment. Reviews in cardiovascular medicine, 1(1), pp. 25-33.

Gujral, D. M. Lloyd, G. and Bhattacharyya, S. 2018. Effect of prophylactic beta-blocker or ACE inhibitor on cardiac dysfunction & heart failure during anthracycline chemotherapy±trastuzumab. The Breast, 37(10), pp. 64-71.

McMurray, J. J. et al. 2016. Aliskiren, enalapril, or aliskiren and enalapril in heart failure. New England Journal of Medicine, 374(16), pp. 1521-1532.

Milfred-LaForest, S. K. et al. 2017. Heart failure transitions of care: a pharmacist-led post-discharge pilot experience. Progress in cardiovascular diseases, 60(2), pp. 249-258.

Ohlsson, A. Lindahl, B. Hanning, M. and Westerling, R., 2016. Inequity of access to ACE inhibitors in Swedish heart failure patients: a register-based study. J Epidemiol Community Health, 70(1), pp. 97-103.

Ouwerkerk, W. et al. 2017. Determinants and clinical outcome of uptitration of ACE-inhibitors and beta-blockers in patients with heart failure: a prospective European study. European heart journal, 38(24), pp. 1883-1890.

Ricci, F. Di Castelnuovo, A. Savarese, G. Filardi, P. P. and De Caterina, R. 2016. ACE-inhibitors versus angiotensin receptor blockers for prevention of events in cardiovascular patients without heart failure—a network meta-analysis. International journal of cardiology, 217(8), pp. 128-134.

Rincon-Choles, H. 2019. ACE inhibitor and ARB therapy: Practical recommendations. Cleveland Clinic journal of medicine, 86(9), pp. 609-701.

Van Der Meulen, M. et al. 2018. Question 1: How safe are ACE inhibitors for heart failure in children?. Archives of Disease in Childhood, 103(1), pp. 106-109.

 

 

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