Anaphylaxis can precipitate acute myocardial infarction in susceptible individuals: in patients with ischemic heart disease, the number and density of cardiac mast cells is increased, including in the atherosclerotic plaques. Mediators released during anaphylaxis contribute to vasoconstriction and coronary artery spasm. Epinephrine is not contraindicated in the treatment of anaphylaxis in patients with known or suspected cardiovascular disease, or in middle-aged or elderly patients without any history of coronary artery disease who are at increased risk of ACS only because of their age. Through its beta-1 adrenergic effects, epinephrine actually increases coronary artery blood flow because of an increase in myocardial contractility and in the duration of diastole relative to systole. Glucagon has noncatecholamine-dependent inotropic and chronotropic cardiac effects, and is sometimes needed in patients taking a beta-adrenergic blocker who have hypotension and bradycardia and who do not respond optimally to epinephrine. Anticholinergic agents are sometimes needed in beta-blocked patients, for example, atropine in those with persistent bradycardia or ipratropium in those with epinephrine-resistant bronchospasm.
In the pressure-volume loop below, cardiac work is best represented by: the area of the curve the slope of the line from points C to D the distance of the line from points C to D the slope of a line from points A to D .. .. ... .... ... .... .... .... In the pressure-volume loop below, cardiac work is best represented by: the area of the curve Cardiac work is the product of pressure and volume and is linearly related to myocardial oxygen consumption. Cardiac work is best represented by the area of the curve of a pressure-volume loop.
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