The paper focuses on analyzing evidence based treatment of heart failure disease. Heart failure (HF) refers to a complex medical syndrome in which the heart fails to uphold cardiac output (CO), which is enough to address metabolic needs and handle venous return. According to Kemp and Conte (2012), there are numerous etiologies resulting to this last common medical pathway, that causes a mortality rate of 50% of all kids, aged five and which is accountable for more than 33.3% of all cardiovascular caused deaths in the United States (Kemp & Conte, 2012). There are about 500000 new heart failure cases in the United State every year and about two million cases in the globe (Kemp and Conte, 2012). Heart failure is initiated by a loss of crucial quantity of operational myocardial cells after heart injury due to various causes. Some of these causes include diabetes, hypertension, and heart disease.
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The heart failure symptoms and signs which include wheezing, cough and dyspnea are as result of lack of enough venous return, and the medical insufficient CO sequelae (McKelvie et al., 2013). Some of the pathophysiology characteristics include complex neurohormonal pattern changes, sympathetic nervous system stimulation, and abnormalities of renal, skeletal muscles, and cardiac function. The condition is normally handled by a combination of drugs that include hydralazine/nitrates, ACEI (Ace Inhibitors), Digitalis Antiarrhythmic drugs, ARB (angiotensin receptor blocker), Alddosterone Antagonist, Beta Blockers and Diuretics (McKelvie et al., 2013). The paper focuses more on heart failure pharmacology where evidence based practices are highly considered.
In normal circumstances, the total volume of blood that the heart pumps over a certain period of time is referred to as cardiac output. This results to the stroke volume (SV) and heart rate (HR) product and is characteristically 4-8L/min (Adebayo, Olunuga, Durodola & Ogha, 2017). Moreover, other aspects that include valvular competence, ventricular wall integrity, and synergistic ventricular concentration all impact CO. SV is regarded as the volume of blood driven out by the ventricle in every heartbeat, and is normally 1cc/kg or about 60-100 cc (Adebayo, Olunuga, Durodola & Ogha, 2017). SV is influenced by three main aspects that include preload that is the quantity of myocardial fiber stretch at the diastole end; afterload, that is the resistance, which have to be astounded so that the blood can be ejected by the ventricle, and contractility that is the inotropic heart state that is independent of the afterload or the preload (Kemp & Conte, 2012).
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The prime non-valvar heart failure abnormality is left ventricular function impairment, resulting to reduction in cardiac output. The dysfunction of left ventricular can be grouped into two classes known as diastolic dysfunction and systolic dysfunction. However, systolic dysfunction is the main cause of heart failure in the left ventricular accounting to 70% of all cases, compared to diastolic that only accounts for 30% of all cases (McKelvie et al., 2013). Right ventricular dysfunction is another form of heart failure which is normally initiated by left ventricular failure. However, they both show increase in the ventricle blood volume (McKelvie et al., 2013). Cardiac output reduction results to activation of various compensatory mechanism ofneurohormon aimed at enhancing the heart mechanical environment (MuMurray, Komajda, Anker & Gardner, 2015). The sympathetic system activation, for instance, attempts to uphold cardiac output, with increased catecholamines or peripheral vasoconstriction, augmented myocardial contractility increase, and augmented heartrate. Renin-angiotensin aldosterone system (RAAS) activation also yields in blood volume increase and vasoconstriction (angiotenin), with water and salt retention (aldosterone). Natriuretic peptides and vasopressin concentrations increase. There might also cause cardiac structure alterations or advancing cardiac dilation or both (Adebayo, Olunuga, Durodola & Ogha, 2017).
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Chronic heart failure is related to automatic control alterations and neurohormonal activation. Even though these compensatory mechanismsof neurohormonal offer valuable heart support in normal physiological situations, they also contain an essential role in the chronic heart failure development and later progression (Adebayo, Olunuga, Durodola & Ogha, 2017). Renin-angiotensin-aldosterone system stimulation results to increased aldosterone, plasma angiotension II andrenin concentrations. Angiotensin II contains significant impacts on cardiac myocytes, and might add to the endothelia dysfunction, which is witnessed in chronic heart failure (Deedwani & Carbajal, 2012).
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Heart failure also activate sympathetic nervous system through high and low pressure baroreceptors, as an initialcompensatory mechanism that gives inotropic support and upholds cardiac output. Activation of chronic sympathetic, nevertheless, contains deleterious impacts, resulting to further cardiac function deterioration (Steinberg et al., 2017). The earliest sympathetic activity increase is noticed in the heart, and this appears to precede the rise in sympathetic outflow to the kidneys and skeletal muscle, which is identified in progressive heart failure. The RAASand other neurohormones are activated by persistent sympathetic stimulation (McKelvie et al., 2013). This results to increased arterial and venous tone, oedema, increased concentrations of plasma noradrenaline, and water and salt progressive retention. Excessive activity of sympathetic is also related to focal myocardial necrosis, hypertrophy, and cardiac myocyte (Adebayo, Olunuga, Durodola & Ogha, 2017).
Drug Classification, Discussion and Contradiction
Heart failure is controlled by a combination of drugs. Some of the drugs class ACEI (Ace Inhibitors), ARB (angiotensin receptor blocker), Beta Blockers, Diuretics, Alddosterone Antagonist, Digitalis, antiarrhythmic drugs (amiodarone) and Hydralazine/nitrates.
This is one of the classes of drugs used to manage heart failure. They are form of vasodilator, which is a drug which broadens blood vessels to reduce blood pressure, decrease heart workload, and improve the flow of blood (Steinberg et al., 2012). ACEIs slow the cardiovascular disease progression through multiple pleiotropic effects that include antithrombotic effects, antiproliferative impacts on monocytes, neutrophils, and smooth muscles cells, and enhanced endothelial function. Meta-analyses demonstrate mortality reduction by 23%, and combination end point reduction of hospitalizations and mortality rate by 35% for heart failure patients, who are treated using ACEIs (Reed & Sueta, 2015). There are various forms of ACE inhibitor include captopril, lisinopril, and enalapril block the angiotensin I to angiotensin II conversion that lower the RAAS activation (McKelvie et al., 2013).
Beta Blockers are used to reduce blood pressure, slow heart rate and to reverse or limit heart damages caused by systolic heart failure (McKelvie et al., 2013). Beta Blockers regulate the density of Beta-1 receptor upward, mitigate deleterious cytokines production that include tumor necrosis factor α, and blunt renin and norepinephrine production. Large-scale medical trials revealed a 35% mortality rate reduction in Beta Blocker treated patients, above the ACEIs benefits (Kemp & Conte, 2012). Beta Blocking agents that include metoprolol and carvedilol are employed to safeguard the vasculature and heart from the overstimulation deleterious effects of the SNS and to assist slow the heart down, to permit for the effective contraction.
These are drugs used to increase contractions strength of the heart muscle. The drug also reduces the heartbeat, and systolic heart failure symptoms. They are commonly administered to patient with heart rhythm issues (Adebayo, Olunuga, Durodola & Ogha, 2017).
Hydralazine lowers afterloads, inhibits nitrate tolerance, and exhibits antioxidant impacts. Nitrates on the other hand inhibit remodeling, lower afterload and preload, and they contain anti-ischemic effects (Reed & Sueta, 2015). Nitrate and hydralazine therapy enhances survival; improve heart failure symptoms, and lower hospitalizations. The therapy needs to be at lower dosage (Reed & Sueta, 2015).
Amiodarone is among the most in effect agent for upholding normal sinus rhythm with no increasing in patient mortality, with heart failure and atrial fibrillation (Reed & Sueta, 2015). In addition, Amiodarone is among the best drugs for ventricular arrhythmias, among the heart failure patients. However, the drug shows possible toxicities, pulmonary function, liver, and thyroid should be determined periodically and baseline (Reed & Sueta, 2015).
Intravenous and oral diuretics are early mainstay therapy given to handle acute heart failure. Intravenous drugs used to initiate regular urination to avoid fluid collection in the body. These drugs also reduce lungs fluid to enhance the breathing process (Reed & Sueta, 2015). This initiates reduction in pulmonary edema, cardiac filling pressure, and peripheral congestion. Their probable side effect is reduction in magnesium and potassium. They include furosemide (McKelvie et al., 2013).
Angiotensin Receptor Blocker (ARB)
These are drugs that are normally administered in critical cases of systolic heart failure. They offer direct angiotensin II type I receptors blockade. They have been utilized to counteract angiotension II developed by the different pathways (Reed & Sueta, 2015). The ARBs use yields to the effective obstruction of hypothetically harmful angiotensin II effects on tissues irrespective of the angiotensin II site of origin. ARBs have shown positive hemodynamic effect in long- and short-term administration. Moreover, randomized medical trials contrasting ACEIs with ARBs have generally demonstrated enhanced or equivalent benefits (Deedwania & Carbajal, 2012). The category includes epleronone and spironolactone, which are potassium-sparing diuretics. Angiotensin receptors that include candesartan, losartan, and valsartan are employed in patients that cannot stand ACE inhibitor therapy. They also work directly on the receptors angiotensin, which is the last RAAS downstream target pathway (Reed & Sueta, 2015).
The process will involve four stages that include stage A to B. The first stage will involve the identification of the condition. Some of the identifiable signs include wheezing, cough, and dyspnea which result from augmented pressure in the pulmonary capillary bed, because of unproductive forward left ventricle flow. This should also involve the identification of those with high risk factors. Some of these individuals include those with hypertension, obesity, atherosclerotic disease and metabolic syndrome. The main aim in this case will be to enhance treat hypertension, control metabolic syndrome, encourage smoking cessation, discourage illicit drug use and alcohol intake, and treat lipid disorders. The second stage will involve the assessment of the structural heart disease though without symptoms or signs of heart failure. The identifiable structural heart disease include patient with MI, asymptomatic valvular disease, and previous MI. The main goal would be to enhance treatment of condition define above. Some of the possible drugs to use to fight heart failure include Beta Blockers in suitable patient, and ARB or ACR in suitable patients.
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The third stage will involve the assessment of individual structural heart disease with current or prior heart failure disease. This stage will involve the identification of known structural heart disease and fatigue and breathe shortness, and lowered exercise tolerance. The therapy includes dietary salt restriction. The drugs in this stage include ACEI, ARBs, Aldosterone antagonist, Beta-blockers, hydralazine/nitrates, digitalis. The last stage will involve the refractory heart failure needing specialized interventions. This stage entails identifying patients that have showed symptoms irrespective of maximum medical therapy. The main goal in this case is to ensure suitable care for the patient. This ensures end-of-life compassionate care. Extensive measures that involve effective treatment include experimental drugs or surgery, permanent mechanical support, heart transplant, and chronic inotropes. Order Unique Answer Now