tic 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 con- tinuum. 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 phar- maceutical therapy for cardiac arrhythmias can be categorized as follows: Sodium channel blockade; blockade of sympathetic autonomic cardiac function (e.g. beta blockers); prolonging re- fractory periods; and calcium channel blockade (Katzung, 2018, p. 236). While some drugs may enact in the context of one cat- egory, 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, particularly in the acute care hospital setting. Amioda- rone is applied orally and/or intravenously in the setting of criti- cal arrhythmias, and acts by prolonging cardiac action potential and refractory period. However, amiodarone is known to block inactivated sodium channels and produce weak calcium-channel blocking actions (Katzung, 2018, p. 243). The broad-spectrum effects of amiodarone also lower heart rate and atrioventricular node conduction speed. Although pharmaceuticals are often suc- cessful in containing abnormal cardiac pacing and depolarization while maintaining normal electrical activity, increasing dosages can dampen conduction in unaffected cardiac tissue, leading to drug-induced arrhythmias. In addition to recognizing common anti-arrhythmic pharmaceuticals and associated pathologies, the physical therapist should gather information related to duration of cardiac arrhythmic conditions. This portion of an individual medi - cal history will supply data with which to appropriate the plan of care. Calcium channel blockers act as a blockade to the cardiac calcium current, reducing action potential conduction primarily at the si- noatrial and atrioventricular nodes. These fundamental cardiac re - gions require calcium channel influx to enact depolarization (Kat- zung, 2018, p. 236). Common calcium channel blockers include verapamil, diltiazem, amlodipine and nicardipine. Additional ef- fects of this drug subgroup include reduced tone and contraction of smooth muscle, as well as anti-hypertensive effects. Calcium channel blockers may be utilized in the hospital setting to reduce cerebral vasospasm following cerebral vascular accident, with specific respect to thromboembolic stroke and/or subarachnoid hemorrhage. Anti-asthmatic pharmaceuticals The pathophysiology for bronchial hyperreactivity and constriction associated with asthma attacks is not appropriately understood. Anti-asthmatic pharmaceuticals are most often administrated via inhalation of a microaerosol form. Current pharmaceutical therapy for asthma includes application of sympathomimetics, adrenore - ceptor agonists and corticosteroids. As previously mentioned, sympathomimetics and adrenoreceptor agonist subgroups are associated with smooth muscle relaxation, in this case applied to bronchial region. When administered via inhalation, beta 2 selec- tive sympathomimetic agents, such as albuterol, can reach maxi- mum bronchodilation within 15 minutes, with continued results over periods of three to four hours. Additional pharmaceutical de - velopment has led to 12-hour duration of action pharmaceuticals such as salmeterol and formoterol (Katzung, 2018, p. 351). Corticosteroids are used to reduce airway hyperreactivity present in asthmatic lungs. Corticosteroids are associated with reduced inflammatory response; specifically reduced lymphocyte and mast cell infiltration. These drugs are not associated with airway smooth muscle relaxation. Due to potential toxic effects, corticosteroids are administered via inhalation; oral and/or parenteral administra- tion is reserved for severe exacerbations. Corticosteroid adminis-
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, of - ten as a combined result of pharmaceutical therapy in the setting of medical comorbidities. Vasodilators Pharmaceuticals whose primary action is vasodilation are com - monly 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 consump- tion is determined by physical stress on the myocardial wall, heart rate and contractility. Myocardial wall stress is quantified by in- traventricular pressure, ventricular radius and wall thickness (Kat- zung, 2018, p. 195). Angina is commonly associated with coronary artery disease and presents along a spectrum from stable to un- stable; medical care is provided based on relative stability. Sta- ble angina may be mild to moderate, and is often predictable in terms of precursors such as stress and/or physical exertion. Unsta- ble 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 infor- mation to the physical therapist, for it is almost always a guaran- tee 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 mil- ligrams, with effects typically lasting less than 60 minutes (Kat- zung, 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 relax- ation 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 valu - able to employ a subjective exam and record vital signs for pa- tients 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 re- distribution 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 associ- ated 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 spec- trum. 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 vaso- dilator 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 therapeu-
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