Cardiac Failure Review Discussion
Cardiac Failure Review Discussion Essay
Cardiac Failure Review Discussion Essay
for this assignment, you will write a paper on the pharmacological management of the disease. The paper should include a review of the: Select a disease process that is of interest to you. Pathophysiology of the disease state. Review of the pharmacological agents used for treatment and important information related to advanced practice nurse. clearly write a title for this topic: For examples, “Pharmacological Effects of Anti-Hypertensive Medications in the Management of Hypertension”.
Congestive Heart Failure (CHF) affects close to 6 million Americans with approximately 670,000 new incidences diagnosed annually (Savarese & Lund, 2017). CHF is the number one cause of hospitalization amongst persons that are 65 years or above (Savarese & Lund, 2017). The disease is characterized by a chronic progression that inhibits the heart muscles’ power to pump blood. While CHF is oftentimes also referred to as ‘heart failure,’ it particularly refers to the stage where fluid build-up occurs around the heart and which results in its inefficiency to pump blood. Cardiac Failure Review Discussion Essay
The heart has two atria in its upper part while the lower half has the two ventricles. The atria receive blood from the body while the ventricles pump blood from the heart to the rest of the body tissues and organs. Carthon et al., (2015), note that CHF occurs when the heart ventricles are unable to effectively pump sufficient volume of blood to the rest of the body. This results in blood as well as other body fluids, to back up and accumulate in the lower body, liver, abdomen, and lungs. CHF is life-threatening and a person who exhibits symptoms of the same ought to seek immediate medical attention (Carthon et al., 2015). This paper will give a brief review and pathophysiology of CHF. The pharmacological agents used in the treatment of CHF will also be discussed while highlighting the important information that an Advanced Practice Nurse needs to be aware of when dealing with a CHF patient.
Review of Congestive Heart Failure
CHF can occur for many reasons as it is a major clinical manifestation in various disease states (Nicholson, 2014). CHF can be due to arrhythmia, right heart failure, valvular heart disease, high output CHF (that is, critical arteriovenous malformations and anemia), diastolic dysfunction characterized by filling or relaxation abnormality, and systolic dysfunction due to a reduction in ejection fraction (Nicholson, 2014). The American Heart Association has categorized heart failure into four stages (Yancy et al., 2017, for the American Heart Association). The first stage A is where a patient is at risk but is yet to develop any structural heart changes. This stage includes patient with diabetes as well as those that have the coronary disease but have no prior infarct. The second stage B refers to patients who have structural heart disease. This category of patients exhibits chamber enlargement, left ventricle hypertrophy, and reduced ejection fraction. Stage B patients do not have heart failure symptoms. Clinical heart failure is developed in Stage C while patients in Stage D have refractory heart failure that necessitates advanced care intervention such as transplantation, left ventricle assistive device, and biventricular pacemakers.
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Pathophysiology of CHF- Systolic
CHF results from the several compensatory mechanisms’ activation in the heart’s attempt to increase its blood output. However, these work for a short period while the long term effects are negatively effective to the heart because of negative remodeling (Kober et al., 2016). The main mechanisms which are referred to as the neurohormonal response, constitute two actions the first being the sympathetic nervous system activation while the second is the renin-angiotensin-aldosterone system activation (Kober et al., 2016). The current pharmacological interventions aimed at reducing these two systems’ activities. Additionally, a compensatory third response that takes place through the natriuretic peptide as well as the A-type natriuretic peptide. The diagram below summarizes the pathophysiology of a CHF. Cardiac Failure Review Discussion Essay
Pathophysiology of CHF. Source: Munzel et al., (2015)
When low blood pressure is sensed by the carotid baroreceptors, one of the responses is the SNS activation. This action increases norepinephrine and epinephrine levels that elevate contractility, the heart rate, as well as the afterload through peripheral vasoconstriction (Munzel et al, 2015). This works in the short term to enhance cardiac muscle output and thus relieve the symptoms of HF. However, this short term activation has deleterious outcomes and can result in a further decline in the left ventricular systolic. This SNS action is mitigated by beta-blockers as the main therapy (Munzel et al., 2015).
When there is a decrease in renal perfusion, hypoyolemia is assumed by the kidney although this does not always happen because a cardiac output that is low can reduce renal perfusion (Munzel et al., 2015). The compensatory and inherent mechanism that retains water and sodium is the renin-angiotensin-aldosterone system activation. The afterload is increased by angiotensin through the peripheral vasoconstriction which in turn results and increase in blood pressure. The RAAS activation is known to negatively contribute to heart remodeling thus, causing elevated worsening of the cardiac functioning. Angiotensin-Converting Enzyme inhibitors can block the RAAS and so too the antidiuretic hormone antagonists, aldosterone antagonists, and angiotensin receptor blockers (Munzel et al., 2015).
McCullough, Omland & Maisel (2019), point out that both the A-type and B-type natriuretic peptides are beneficial concerning CHF hemodynamic effects and are another natural form of causing symptom relief. The two are released first in the atrium following atrial myocytes stretching that is caused by increased cardiac pressures. They act by causing sodium excretion following vasodilatation which results in natriuresis. CHF can be treated using an analog of B-Type natriuretic peptide referred to as Nesiritide (McCullough, Omland, & Maisel, 2019). Also, endothelin negatively affects vasoconstriction and heart remodeling. The endothelin inhibitors’ clinical trials show no benefits hence, the role is still unclear.
Review of Pharmacological Agents used in CHF Treatment and Implications for APNs
Beta-blockers are the main CHF pharmacological management drugs of choice (Wiysonge et al., 2017). The drugs decrease the excess SNS activity which is a key CHF characteristic. Increased SNS activity is a neurohormonal compensation that involves the renin-angiotensin system occurring in CHF patients which enhances cardiac output as well as maintain blood pressure in a heart that is failing (Wiysonge et al., 2017). Although it is beneficial at the onset, it eventually causes heart damage to a stressful degree. The beta-blockers bind to the myocardial beta-adrenergic consequently blocking the epinephrine and norepinephrine effects (Wiysonge et al., 2017). This way, beta-blockers reduce angina, cardiac contraction force, and heart rate reduction through the normalization of the SNS activity. These are referred to as the beta-1 cardioselective blockers. Beta-2 blockers do not provide valid clinical value as they are bronchoconstrictors (Wiysonge et al., 2017).
Carvedilol and Metoprolol are the widely used beta-blockers approved by FDA, among other drugs. Carvedilol is taken in doses of between 3.125mg-50mg twice a day. Metoprolol dosages range between 12.5-25mg and are taken once a day and can be doubled to a maximum of 200mg per day (Wiysonge et al., 2017)
The main potential side effect of taking beta-blockers is that they cause an abnormal heart rate that is slow or bradycardia. This may worsen the capability of the failing heart to pump sufficient volumes of blood. Also, a patient with CHF may experience dizziness, weakness, and fatigue (Wiysinge et al., 2017).
An Advanced Practice Nurse (APN) should prescribe physiotherapy with extreme caution and monitor a CHF patient closely. This is because although beta-blockers may allow patients to get involved in physiotherapy programs with reduced heart stress and that are less restricted by angina; beta-blockers can mislead the therapist. This is because beta-blockers decrease the heart rate of a CHF patient thus rendering inappropriate, the aerobic workload conventional guidelines. Frequent monitoring of heart rate and blood pressure should be conducted with the patient assessed for weakness, dizziness, and fatigue before the therapy session commences and monitoring should be continuous as well. Cardiac Failure Review Discussion Essay
Angiotensin-Converting Enzyme (ACE) Inhibitors
ACE inhibitors are also used in CHF treatment and work by decreasing heart workload and increasing vasodilatation (Ouwerkerk et al., 2017). The ACE suppresses the angiotensin-converting enzyme thus preventing vasoconstriction as well as preventing the conversion of angiotensin I to angiotensin II. Conversion of the latter from the former is enabled by the angiotensin-converting enzyme which also causes vasoconstriction (Ouwerkerk et al., 2017). Additionally, it is responsible for aldosterone secretion and vascular tissue hypertrophy. Vascular tissue hypertrophy causes narrowing of vessels which in turn causes increased heart workload. Water retention, on the other hand, is caused by aldosterone secretion which results in the increasing volume of vascular fluid and consequently the heart workload. Hence angiotensin II inhibition decreases heart pressure as well as the heart workload. Another ACE inhibitors’ benefit is the increase of blood bradykinin levels (that cause vasodilatation resulting from a decrease in their breakdown).
The most common ACE inhibitors for CHF patients include Benazepril and Fosinopril (Peng et al., 2015). Either of the two drugs can be prescribed and are taken once a day at a dose of 10mg and increased gradually to a dose of 20-40mg. The initial dose for this drug when given alongside a diuretic is 5mg. Captopril, another ACE inhibitor drug, is taken thrice a day at a dose of 25mg.
According to Flather et al., (2016), the main side effects though rare and minor, include renal failure and hypotension because excretion of ACE inhibitors occurs through the kidneys. When the dosage is adjusted, this can resolve minor side effects such as dizziness, GI discomfort, rashes, and angioedema (swelling in the lower skin layer and tissue in the mucous membrane or the skin).
An APN needs to be aware that ACE inhibitors result in blood pressure reduction along with the hypotension that occurs naturally post-exercise and this can result in blood pressure excessive reduction. This, as noted by Townsend (2016), can cause a CHF patient to become dizzy or syncope in rare cases. An APN should give education to a post-exercise patient on ACE inhibitors, on adherence to a cool-down that is gradual after every exercise session. A cool-down regimen will prevent the said symptoms as well as enhance the venous return and prevent skeletal muscle blood pooling. Additionally, CHF patients should have a gradual cool-down post-exercise as this allows for the body to attain homeostasis while preventing excessive blood pressure reductions.
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In conclusion, patients with CHF have to take extra precautions and medication for a lifetime. An APN can help a patient with CHF to have a better quality of life by ensuring that such a patient adheres to the prescribed medication and a regular, frequently monitored exercise regimen. Some patients require a combination of drugs for treating the different symptoms, the APN along with the patient should work at when, how often, and the dosage levels should be taken. The desired effects for each drug should be discussed by the APN with the patient and so too, the side effects. Proper use of drugs will save a patient’s life, prolong it, and improve the functioning of the heart.
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