particularly in the acute care hospital setting. Amiodarone is applied orally and/or intravenously in the setting of critical 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 successful 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 medical 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 sinoatrial and atrioventricular nodes. These fundamental cardiac regions require calcium channel influx to enact depolarization (Katzung, 2018, p. 236). Common calcium channel blockers include verapamil, diltiazem, amlodipine and nicardipine. Additional effects 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, adrenoreceptor 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 selective sympathomimetic agents, such as albuterol, can reach maximum bronchodilation within 15 minutes, with continued results over periods of three to four hours. Additional pharmaceutical development 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 administration is reserved for severe exacerbations. Corticosteroid administration for asthma is gradually tapered to prevent and/or limit toxic effects. Common inhaled corticosteroids used to treat asthma include fluticasone, beclomethasone, budesonide, ciclesonide, flunisolide and mometasone (Katzung, 2018, p. 355). With regards to physical therapy, distinction between sympathomimetic/adrenoreceptor agonist versus corticosteroid treatment of asthma is the key to formulating an appropriate plan of care for this patient population. Patients commonly present for physical therapy across multiple settings (inpatient <> outpatient) with chronic prescription of albuterol to treat bronchospasm. As such, aerobic intervention for these patients is indicated, provided graded examination has been completed, and parameters of perceived exertion have been established. In contrast, patients presenting with acute prescriptions for corticosteroids should be regarded with the understanding that they pose higher risk of inflammatory onset, and will likely be in a period of relative recovery. As such, aerobic intervention for these patients should be limited to required activities of daily living as tolerated. Patients taking corticosteroids for an acute asthmatic flare up may also benefit and/or require physical therapy treatment targeted toward breathing efficacy, and may include education/review of pursed-lip breathing techniques as well as active cycle breathing training.
CENTRAL NERVOUS SYSTEM PHARMACOLOGY
To review, the central nervous system (CNS) includes the brain and spinal cord. Thus, drugs that act on the CNS impose alterations on chemical synaptic transmission, either at the pre-synaptic or post-synaptic regions. CNS drugs include sedatives, general anesthetics, local anesthetics, drugs used in Parkinsonism and other movement disorders, antidepressants and opioids. Sedative-hypnotics Sedative-hypnotic pharmaceuticals include benzodiazepines, barbiturates and specific hypnotics. Drugs within this pharmaceutical subgroup are used to promote sedation and/ or sleep. In turn, this class of drugs is used for sedation during medical and surgical procedures, treatment of seizures/epilepsy, control of sedative-hypnotic and ethanol withdrawal states (detox), and muscle relaxation in the presence of neuromuscular disorders (Katzung, 2018, p. 390). While their use is appropriated in acute hospital settings, this class of drugs is highly associated with chronic development of physiologic tolerance, as well as compulsive abuse due to perceived euphoria, anxiety relief, disinhibition and sleep promotion. Common sedative- hypnotics include alprazolam, buspirone, diazepam, lorazepam, phenobarbital and temazepam. General anesthetics General anesthetics reduce central nervous system activity to produce states of variable sedation by inducing immobility, amnesia and decreased consciousness. Despite clinical application for more than 170 years, the precise mechanism of action for general anesthetics is unknown. Inhaled anesthetics enter the blood stream via gas exchange within pulmonary alveoli, leading to systemic distribution, bypassing first-
pass metabolism. The rate of pharmakinetic uptake can be quantified and controlled in terms of alveolar-venous partial pressure difference. Anesthesiologists may adjust anesthetic concentration as well as alveolar ventilation rate. Recovery from inhaled general anesthetic administration depends primarily on duration of administration, and is based on elimination of the drug from the brain. Following discontinuation of inhaled anesthetic administration, alveolar concentration diminishes rapidly primarily via pulmonary ventilation, though with some respect to systemic metabolism depending upon the state of solubility. Common inhaled anesthetics include nitrous oxide, halothane, enflurane, isoflurane and sevoflurane (Katzung, 2018, p. 441). Intravenous anesthetic administration induces rapid onset of anesthesia, and is the current preferred method of clinically induced anesthesia. Propofol is the most frequently administered pharmaceutical for induction of anesthesia. Propofol is commonly applied for deep, as well as conscious, sedation in a variety of surgical and non-surgical settings, producing general reduction in CNS activity that includes decreased cerebral blood flow and peripheral vasodilation (Katzung, 2018, p. 451). In addition to administration during surgical intervention, intravenous general anesthetics such as dexmedetomidine (aka precedex) are commonly applied for patients requiring intensive/ critical care due to respiratory failure and/or systemic shock, as they can be precisely administered and titrated alongside patient medical presentation. Modern medicine has developed general anesthesia into a dynamic process termed balanced anesthesia , which generally employs multiple pharmaceuticals including inhaled general
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