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Answered 2016-04-29 23:09:12

Sympathetic activation almost always speeds up any system. In this case breathing rate.

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During an asthma attack, a person's respiratory passages become narrowed and inflamed


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your hart would stop and you would die


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The pathophysiology of acute myocardial infarction is complex. Loss of viable myocardium impairs global cardiac function, which can lead to reduced cardiac output, and if damage is severe, to cardiogenic shock. Systolic and diastolic dysfunction are associated with ischemic myocardium. If left ventricular function is significantly impaired, pulmonary congestion and edema can occur. Ischemia can also precipitate abnormal cardiac rhythms and conduction blocks that can further impair function and become life-threatening in some cases. Reduced cardiac output and arterial pressure can elicit baroreceptor reflexes that lead to activation of neurohumoral compensatory mechanisms (e.g., activation of sympathetic nerves and the renin-angiotensin-aldosterone system) similar to what occurs during heart failure. The pain and anxiety associated with myocardial infarction further activates the sympathetic nervous system, which causes systemic vasoconstriction and cardiac stimulation (this explains why some patients become hypertensive and have tachycardia). While sympathetic activation helps to maintain arterial pressure, it also leads to a large increase in myocardial oxygen demand that can lead to greater myocardial hypoxia, enlarge the infarcted region, precipitate arrhythmias, and further impair cardiac function. Sympathetic activation is responsible for the diaphoresis (sweating) experienced by the patient. Renal hypoperfusion and sympathetic activation stimulate renin release, which leads to increased plasma levels of angiotensin II and aldosterone that enhance renal retention of sodium and water.



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