● Atria : Decreased heart rate, contractile strength and conduction velocity. ● Blood vessels : Arteries and veins; dilation and/or constriction. ● Lung : Bronchial muscle and glands; bronchoconstriction and mucus secretion. ● Gastrointestinal tract : Increased motility, sphincter relaxation, secretion stimulant. ● Urinary bladder : Detrusor contraction, trigone and sphincter relaxation. ● Glands : Salivary, lacrimal, sweat, nasopharyngeal; secretion. With regards to physical movement, cholinomimetics are effective in prolonging the presence and intensifying the effects of acetylcholine by inhibiting acetylcholinesterase. This pharmacodynamic action can increase muscular contraction force and induce muscular fibrillation at higher doses (Katzung, 2018, p. 119). Cholinomimetics are a primary pharmacologic intervention in the presence of myasthenia gravis. Primary effects of this autoimmune pathology include breakdown of the post-synaptic membrane, binding of pathologic antibodies to nicotinic receptors and cross-linking receptors. Symptoms of the pathology often include muscular weakness, ptosis, diplopia, and trouble speaking and swallowing. Common therapeutic pharmaceuticals include pyridostigmine and neostigmine. These drugs may also be employed to reverse the effects of non- depolarizing agents, which may be employed during surgical procedures and induce acute post-surgical paralysis. In contrast, choline receptor-blocking agents block the effects of parasympathetic autonomic discharge and are primarily employed to block muscarinic receptors. Atropine is the most well-known cholinoreceptor-blocking agent. Termed antimuscarinic compounds , this class of pharmaceuticals causes CNS stimulation, tachycardia and bronchodilation (Katzung, 2018, p. 130). Atropine once served as the sole drug therapy to treat Parkinson’s disease, prior to the development of levodopa. Scopolamine is another popular antimuscarinic drug, used to treat motion sickness. Adrenoreceptor agonists bind either directly to epinephrine and norepinephrine receptors, or augment the actions of endogenous catecholamines, thereby initiating sympathetic neural responses. Termed sympathomimetic drugs, this pharmaceutical class generally initiates localized “fight or flight”
responses at various sites of action. When applied to cardiac function, they are said to have a positive chronotropic effect, meaning they can increase heart rate by affecting the sinoatrial electrical node conduction rate. In addition, adrenoreceptor agonists generally increase cardiac muscle contractile force, vascular smooth muscle contraction, renal blood vessel dilation, bronchodilation, and urinary sphincter contraction. Common examples include direct application of epinephrine in the presence of cardiac arrest and/or anaphylaxis, and dobutamine to induce controlled cardiac stress testing (Katzung, 2018, p. 152). Adrenoreceptor antagonist drugs bind to alpha- and beta- receptors, primarily outside the CNS, preventing their activation by catecholamines and/or similar agonists. The most well-known effect of alpha-receptor antagonists is reducing peripheral vascular resistance and blood pressure. Alpha-receptor antagonists may be reversible or irreversible with regards to receptor binding (Katzung, 2018, p. 156). Reversible alpha- receptor antagonists may be disassociated with elevated agonist concentrations though remains primarily dependent upon the chemical signature half-life. In contrast, irreversible alpha-receptor antagonist effects require production of new receptors, which often requires a period of days. In contrast, beta-receptor antagonists may be partial or full antagonists. Beta-receptor antagonists are also commonly associated with reducing hypertension and are often termed “beta-blockers.” Beta-blockers are commonly associated with decreasing frequency of cardiac angina, especially with regards to cardiac stress-associated with exercise. Despite colloquial prescription, the mechanism of action for beta-receptor antagonists is less understood when compared to alpha-receptor antagonists. Cardiovascular effects of this drug class are postulated to involve inhibition of renin release in the CNS. Common side effects of beta-blockers may include bronchial smooth muscle spasm. Thus, applying these drugs in the presence of chronic obstructive pulmonary disease is often contraindicated and/or managed carefully depending on the therapeutic net value. In addition, beta-receptor blockers restrict sympathetic nervous system stimulation of lipolysis, and may be employed to treat acute hypoglycemia, an example of which is glucagon (Katzung, 2018, p. 165).
ANTI-HYPERTENSIVE PHARMACEUTICALS
Hypertension is more often than not a multi-factorial pathology. Contributing factors may be genetic, environmental, dietary and/or psychological. Common considerations include smoking, obesity, diabetes and emotional stress, as well as pathologies such as Cushing’s disease. Current research has also associated hypertension with daily consumption of red meat. Primary hypertension indicates that no clear-cut etiology exists for a patient, while secondary hypertension can be attributed to a specific cause and is diagnosed in roughly 10 to 15 percent of patients (Katzung, 2018, p. 175). Blood pressure is the physiologic product of cardiac output against peripheral vascular resistance. In the absence of pathological conditions, blood pressure is regulated on a moment-to-moment basis in the heart, arterioles and postcapillary venules. The kidney provides additional chronic pressure regulation in the form of intravascular fluid management. Nephrotic blood volume control is achieved by varying reabsorption rates of blood and water. Dynamic blood pressure adaptation occurs in the form of baroreflexes. Baroreceptors in the carotid sinus and aortic arch initiate inhibitory autonomic sympathetic responses to increases in arterial wall pressure. This process is reduced in the presence
of reduced arterial wall pressure, commonly observed in the presence of positional changes from lying down to sitting up and/or acute vasodilation. Four categories of anti-hypertensive drugs include diuretics, sympathoplegic agents, direct vasodilators, and angiotensin blocking agents. Hypertension is managed across inpatient and outpatient medical settings. Primary conservative measures are non- pharmacologic and may include reduced dietary salt intake, prescribed exercise and weight loss. This increases the value of physical therapy to compliment treatment of hypertension. While pharmaceutical management of mild hypertension may include prescription of a single drug, more severe presentations lead to prescriptions of two or more. Physical therapy thus requires clinical application that accounts for the pathophysiology of hypertension and associated comorbidities. While physical therapists treating patients with hypertensive urgency in the acute hospital setting follow up with examination and treatment of patients who have been medically optimized, therapists in outpatient settings must be familiar with a patient’s prescription for antihypertensive agents and prepare for potential adverse effects during prescribed exercise by recording blood pressure in variable positions and activities.
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