Diuretics While the complete effects of diuretics are still subjects of clinical research, the common understanding is that they reduce blood pressure by lowering the body’s sodium content, and thereby lowering blood volume. The primary mechanism of action is an increase in urine volume. Diuretics are often effective in treatment of mild to moderate hypertension, reducing blood pressure by an average of 10 to 15 mmHg (Katzung, 2018, p. 177). This course will primarily discuss diuretics based on common administration in the acute hospital setting, and include loop diuretics, thiazides, potassium-sparing diuretics and osmotic diuretics. Loop diuretics are the most commonly employed version of this pharmaceutical class, and are often prescribed in the presence of edema, whether pulmonary or otherwise. They are also useful to reduce potassium levels in the body and increase urine flow in the presence of renal failure, as well as treatment following ingestion of certain toxic compounds. Thiazides prohibit reabsorption of sodium chloride (NaCl); a common example includes hydrochlorothiazide. Primary toxic effects of loop diuretics, as well as thiazides, are caused by excessive influx of sodium into the renal collecting duct, which can lead to hypokalemia and metabolic alkalosis. Potassium- sparing diuretics reduce potassium loss either by antagonizing mineralocorticoid receptors associated with potassium secretion, or by inhibiting sodium influx through the luminal membrane. Common examples include spironolactone and amiloride (Katzung, 2018, p. 265). In contrast, the primary toxic effect of this drug subgroup is acute hyperkalemia, which can be fatal in the presence of chronic renal insufficiency as well as liver failure. Osmotic diuretics, such as mannitol, promote water retention in the proximal tubule and loop of Henle, which in turn promotes water diuresis. Loop agents are often used in combination with thiazides to prevent refractory response, while potassium-sparing diuretics may be prescribed in combination with loop diuretics or thiazides to reduce hypokalemic effects. Diuretics are commonly prescribed for treatment and/or medical management of edema, heart failure, mild renal failure, hepatic cirrhosis, hypertension, nephrolithiasis, hypercalcemia, and diabetes insipidus. While diuretics are effective in mobilizing interstitial edema, application requires continuous monitoring of blood volume as well as blood pressure, often in a hospital setting, to ensure that vital organs remain perfused. By reducing blood volume, diuretics also reduce venous pressure and ventricular preload, which ultimately reduce heart size and improve pump efficiency. The downside of this process is consequent reduction in venous return, which can reduce right ventricular preload (Katzung, 2018, p. 270). In the context of physical therapy, the primary concern for patients received diuretics is the onset of acute hypotension, often as a combined result of pharmaceutical therapy in the setting of medical comorbidities. Vasodilators Pharmaceuticals whose primary action is vasodilation are commonly prescribed in the presence of ischemic heart disease and heart failure. Cardiac ischemia is the result of disparity between the heart’s oxygen requirements and the body’s ability to supply the coronary vessels with oxygen. Myocardial oxygen consumption is determined by physical stress on the myocardial wall, heart rate and contractility. Myocardial wall stress is quantified by intraventricular pressure, ventricular radius and wall thickness (Katzung, 2018, p. 195). Angina is commonly associated with coronary artery disease and presents along a spectrum from stable to unstable; medical care is provided based on relative stability. Stable angina may be mild to moderate, and is often predictable in terms of precursors such as stress and/or physical exertion. Unstable angina is described under the umbrella term of acute coronary syndrome, as chest pain at rest with increase in severity, frequency and duration. Therefore, the goal of pharmaceutical vasodilation in the presence of angina is to either decrease cardiac demand for
oxygen, or to increase oxygen delivery to coronary vessels. In the presence of heart failure, vasodilators can reduce ventricular preload, thereby improving cardiac output and reducing cardiac tissue stress in the presence of compromised tissue. Knowledge pertaining to this pharmaceutical subclass presents valuable information to the physical therapist, for it is almost always a guarantee that treatment will include aerobic activity in some form. The chief vasodilators include nitroglycerin, calcium channel blockers and beta-blockers. Physical therapists must be familiar with these concepts with regards to aerobic exercise prescription, as well as acute medical presentation with respect to clinical setting. Nitroglycerin is administered via sublingual route, or in some cases buccal and/or transdermal routes, to produce widespread smooth muscle relaxation. General bioavailability of nitroglycerin is low. Short-acting sublingual doses are typically less than 5 milligrams, with effects typically lasting less than 60 minutes (Katzung, 2018, p. 202). As well, sublingual administration bypasses the gastrointestinal tract, thereby avoiding the fist- pass effect. In contrast, transdermal patches may be prescribed and worn for periods of up to 12 to 14 hours. Marked points of vascular relaxation lead to increased venous capacitance, decreased ventricular preload and decreased heart size. Decreased preload of the right ventricle leads may also assist the drug in enacting decreases in pulmonary vascular pressure. Of note to the physical therapist, widespread vasodilation in this form may be associated with acute episodes of hypotension and correlated syncope. Thus, it is valuable to employ a subjective exam and record vital signs for patients presenting after nitrate administration, whether associated with an acute or chronic pathological state. Although nitroglycerin is associated with an acute temporary increase in coronary blood flow in patients without coronary artery disease, these effects are negated in the presence of atherosclerotic lesions. However, it has been postulated that nitroglycerin may be associated with redistribution of coronary blood flow, from normal toward ischemic regions, which is of therapeutic benefit for patients presenting with anginal symptoms associated with coronary artery disease (Katzung, 2018, p. 199). As with many pharmaceuticals, patients may develop tolerance to nitroglycerin, which is typically associated with indirect pharmacologic effects such as water and salt retention, as well as reflexive tachycardia and increased cardiac contractility. Nitrates may be employed across the anginal spectrum. Decreases in intraventricular pressure and left ventricular volume can present symptoms of angina associated with physical exertion. Nitrates may relieve variant angina as a general vasodilator that relaxes smooth muscle and alleviates coronary artery spasm. While the pharmacodynamic process is not completely understood, nitrates remain a hallmark of pharmaceutical security for patients with unstable angina. Common theories of therapeutic effect include dilation of epicardial coronary arteries, reduced coronary vascular tone and decreased platelet aggregation. Anti-arrhythmic agents Cardiac arrhythmias are essentially results of disruption to cardiac impulse formation and/or conduction. Cardiac arrhythmias occur in the presence of multiple variables along the physiologic continuum. As well, they may be related to pharmaceutical use and/or toxicity, comorbid states or a combination of the former. The goal of anti-arrhythmic drugs is to decrease activity at the site of ectopic conduction sites outside of the sino-atrial node, as well as to moderate incomplete circuitous depolarization. Primary pharmaceutical therapy for cardiac arrhythmias can be categorized as follows: Sodium channel blockade; blockade of sympathetic autonomic cardiac function (e.g. beta blockers); prolonging refractory periods; and calcium channel blockade (Katzung, 2018, p. 236). While some drugs may enact in the context of one category, the majority of anti-arrhythmics affect the heart by two or more categories, thus depicting broad-spectrum pharmaceutical therapy. For example, one of the most common anti-arrhythmic agents,
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