The information needed to diagnose angina is a through health history (Arcangelo and Peterson, 2006).The chief complaint in detail and any other symptoms the patient experiences. Asking the patient where the pain is located, any radiation, type of pain, what precipitated the pain, duration of the pain and shortness of breath. Also confirm whether the patient has symptoms for; nausea, vomiting, diaphoresis and chest palpitations. Medications that can be taken at home include nitroglycerin and aspirin therapy (Arcangelo and Peterson, 2006). Arcangelo and Peterson state that most often examination of the patient may not be feasible during acute angina episodes, therefore, concentration of the overt physical findings such as obesity, tachycardia, tachypnea, hypertension, edema, murmurs, and heart sound, 12-lead electrocardiogram and echocardiogram. Troponin levels and cardiac enzymes are initial diagnostic methods.
What is the connection between cocaine use and angina?
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Cocaine use results from the alpha and beta receptor sites being triggered by the catecholamine levels. Cocaine blocks the "presynaptic reuptake of norepinephrine causing an increase of catecholamine at the post-synaptic receptor site" (Keller & Lemberg, 2003, p. 563). As a result of this increase in catecholamines, alpha receptors are triggered that result to peripheral vasoconstriction occurring resulting in hypertension. Cocaine also stimulates the beta receptors which cause an increase in chronotrope and inotrope and what occurs as a result of this is increase oxygen demand (Keller & Lemberg, 2003). According to Keller and Lemberg, (2003), cocaine results in production of endothelin, an extremely powerful vasoconstrictor that reduces nitric oxide (a vasodilator). Keller and Lemberg (2003) further note that once cocaine is used, there are reductions in the diameter of several of the coronary arteries. Cocaine also results in platelet aggregation that results in increased thrombus formation (Keller & Lemberg, 2003). Cocaine is believed to alter calcium of the myocytes and blocks sodium channels that result in dysrhythmias (Lapasota, 1991). The use of cocaine is a double edged sword as it increases myocardial oxygen demand, but at the same time reduces oxygen supply through vasoconstriction. Regardless which side of the sword the patients is, on the end result is ischemia and eventual MI.
List Specific goals of treatment for E.H.
- Relief of chest pain and prevent heart attack-Use of nitroglycerin to alleviate angina caused by cocaine induced vasospasm (Keller & Lemberg, 2003).
- Beta blocker therapy-To decrease myocardial oxygen demand (Arcangelo and Peterson, 2006).
- Blood pressure reduction-Use benzodiazepines (Lingle, 2009)).
- Reduce tachycardia-Can use benzodiapzepines (Lingle, 2009).
- Improvement of long term prognosis.
- Maintain hemodynamic stability such as hypertension and tachycardias that increases myocardial oxygen consumption.
- Prevent platelet aggregation that occurs with cocaine abuse with antithrombotic therapy (Keller & Lemberg, 2003).
- Prevent recurrent ischemia and dysrhythmias using beta blocker therapy (Keller & Lemberg, 2009).
- Assessment of future indicator for ischemia and MI through stress test and if positive, a coronary angiography for significant symptoms or positive stress test