ACE Inhibitor

Situation: Two patients in their 70s present to the office at different times today, each with documented heart failure: one diastolic and the other systolic, and both are hypertensive. First, discuss the difference between systolic and diastolic heart failure, providing appropriate pathophysiology. ACEI/ARBs are the only medications prescribed for CHF that have been found to prolong life and improve the quality of that life. EXPLAIN the mechanism of action of ACEI/ARBs and how they affect morbidity and mortality in CHF. Be specific. Diuretics must be used very carefully in diastolic ventricular dysfunction. EXPLAIN this statement using appropriate physiology. Now considering all of the above, describe an appropriate comprehensive plan of

ACE inhibitors are important and useful in the medication and treatment for KH due to their effectiveness in treating hypertension. ACE inhibitors will help treat KH by slowing the angiotensin converting enzyme (ACE). Angiotensin II is produced by the body that can cause vasoconstriction of the blood vessels. Angiotensin II is made from Angiotensin I by the ACE. If the production of Angiotensin II is slowed by the ACE inhibitor, the blood vessels will be able to dilate, and blood pressure is able to be lowered (Copstead and Banasik). Thus, it is important for KH to stay on the ACE inhibitors due to his blood pressure readings. KH’s blood pressure is 135/96. His systolic blood pressure is in the pre-hypertensive range, however, his diastolic blood pressure is in the hypertensive range and therefore, his blood pressure is hypertensive. Since his blood pressure is high, it is important for KH to remain taking the

Possible side effects: “dry mouth, sedation, blurred vision (disturbance of accommodation, increased intra-ocular pressure), constipation, nausea, difficulty with micturition; cardiovascular side-effects (such as ECG changes, arrhythmias, postural hypotension, tachycardia, syncope, particularly with high doses); sweating, tremor, rashes and hypersensitivity reactions (including urticaria, photosensitivity), behavioural disturbances (particularly children), hypomania or mania, confusion or delirium (particularly elderly), headache, interference with sexual function, blood sugar changes; increased appetite and weight gain (occasionally weight loss); endocrine side-effects such as testicular enlargement, gynaecomastia, galactorrhoea; also convulsions (see also Cautions), movement disorders and dyskinesias, dysarthria, paraesthesia, taste disturbances, tinnitus, fever, agranulocytosis, leucopenia, eosinophilia, purpura, thrombocytopenia, hyponatraemia

The concern regarding the use of anti-hypertensive medication as a treatment procedure for hypertension has mainly been centered on the optimal choice of these agents. The other factors include the side effects of these drugs on a hypertensive patient, especially coughing. While three categories of these drugs are linked with cough as a side effect, they have varying casual explanations though angiotensin-converting enzyme (ACE) inhibitors play a crucial role (Van Amburgh, 2011). The main objective for the use of anti-hypertensives in dialysis patients is to obtain and sustain an optimal blood pressure or lessen it by the least intrusive measures possible. While this is not

Pharmacological treatments with diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers or aldosterone antagonist, and beta-blockers are essential for the treatment of heart failure and are effective in improving symptoms of heart failure and patient well-being. Diuretics are administered to help get rid of the excess fluid that helps improve breathing associated with shortness of breath, at rest or on exertion. Diuretics provide relief from symptoms and signs of pulmonary and venous congestion by promotion of fluid loss through the kidneys. Diuretics, for example, Furosemide helps improve breathing status, but monitoring patients for dehydration and kidney problems is crucial. Patient education is essential to ensuring medication adherence and early identification of adverse effects and potential for drug interactions.

The first drug of this subclass and prototype is called Nifedipine. Nifedipine works in at peripheral arterioles inhibiting calcium to enter and in turn promoting smooth muscle relaxation and vasodilation, results in a decrease of blood pressure and activates baroreceptor reflex, but no or very little blockade of Ca+ at the heart. Also increases coronary perfusion because of blockades formed at cardiac arteries/arterioles, and helps with angina pectoris (Lehne, 2007). The stimulation of the baroreceptor reflex occurs only as a result of a fast decline of blood pressure and in turn this indirectly promotes an increase in heart rate and contractile force (Lehne,

Alpha-adrenergic agonists. These reduce the production of aqueous humor and increase outflow of the fluid in the eye. Examples include apraclonidine (Iopidine) and brimonidine (Alphagan). Possible side effects include an irregular heart rate; high blood pressure; fatigue; red, itchy or swollen eyes; and dry mouth.

ACE inhibitors have an increasing role in the management of cardiovascular risk. Examples of these drugs include enalapril, captopril, fosinopril, perindopril, lisinopril, ramipril and quinapril. The reduction in blood pressure that follows ACE inhibition is greatest after

The cleaved residues will be classified as angiotensin 1 and will be converted by ACE into angiotensin 2 (Casas et al., 2005; Mechanisms and Robertson, 2010) Angiotensin is the active form that will stimulate the adrenal glands to release aldosterone. The role of ACE inhibitors in this system will be the blockage of the conversion of angiotensin 1 to angiotensin 2. All of this inhibition occurs in the kidney, blood vessels, the brain, adrenal glands as well as the heart (Casas et al., 2005; Mechanisms and Robertson, 2010). As a result it is identified that there will be an increase in the amount of sodium and urine excreted from the body as well as a decrease resistance of blood vessels in the kidney, decrease in cardiac output and volume (Mechanisms and Robertson, 2010; (Myles et al., 2009). There will also be an increase in venous capacity (Mechanisms and Robertson, 2010; (Myles et al.,

Selective α1 antagonists work on the post-synaptic α1 adrenoreceptors predominantly found in vascular smooth muscle. These receptors are normally bound by norepinephrine or epinephrine to mediate regulation of the cardiovascular system by the sympathetic nervous system. As can be seen in Figure 1, these receptors are bound to Gq-proteins which have two signal transduction pathways. One of the pathways forms IP3 (Inositol triphosphate) which then stimulates the release of Calcium from the sarcoplasmic reticulum in a cardiac monocyte (Klabunde, R.E., 2013). The release of calcium then stimulates contraction in the heart. By selectively inhibiting these adrenoceptors, vasodilation occurs which in turn causes a decrease in arterial pressure (Rang and Dale).

Carvedilol provides benefits through a balance in blocking beta receptors, which as a result on one hand reduce cardiac work and on other produce peripheral vasodilation. This drug ensures cardiovascular protection through their anti-proliferative, anti-atherogenic, anti-ischemic, anti-hypertrophic and antiarrhythmic actions. These actions are a consequence of their potent antioxidant effects, decreased lipid metabolism, glucose, insulin sensitivity, modulating neurohormones factors and modulation of cardiac electrophysiological properties (Andersson et al., 2014). By reducing the heart rate, the myocardial metabolism is decreased, the ventricular diastole filling is prolonged, and thus the infusion time, increase coronary flow, and also streamlines

Very common: Bradycardia Common: Myocardial ischaemia or infarction, tachycardia Uncommon: Atrioventricular block first degree, cardiac output decreased Vascular disorders: Very common: Hypotension, hypertension Respiratory, thoracic and mediastinal disorders Common: Respiratory depression Uncommon: Dyspnoea, apnoea Gastrointestinal disorders Common: Nausea, vomiting, dry mouth Uncommon: Abdominal distension General disorders and administration site conditions

Atacand HCT (Candesartan celexetil-hydrochlorothiazide) was developed for patients who were unsuccessfully treated with single antihypertensive agents. The proposed benefit is elicited by the drugs action on angiotensin II receptor antagonists, the agent that causes vasoconstriction. Additionally the second ingredient hydrochlorothiazide a diuretic reduces blood pressure by improving the kidneys ability to eliminate salt and fluid from the body (www.centerwatch.com).

Throughout this paper, I will state the cardiovascular system’s role in the body and define the elements that compose blood pressure. As well as emphasize the risk factors, pathophysiology, and management of hypertension.

Other side effects include cloudy urine, proteinuria, irregular heartbeats, and chest pain. Angioedema involving the extremities, face, lips, mucous membranes, tongue, glottis or larynx has been seen in patients treated with ACE inhibitors, including captopril (Capoten, 2014). If these effects happen nurses should be ready to administer epinephrine to reduce swelling. Other adverse effect according to Karch (2014) include, “CV: Tachycardia, angina pectoris, heart failure, MI, Raynouds syndrome, hypotension in salt-or volume depleted patients.”