Review Note

Last Update: 01/29/2025 02:42 PM

Current Deck: PHYSIOLOGY::exam one

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Commit #272784

Marvin Zimmerman is a 52 manager, significantly overweight, eats rich diet (red meats, desserts), several beers each evening. Experiences occasional angina, relieved by nitroglycerin.

Marvin goes to bed early not feeling well, wakes at 2am with crushing chest pressure, pain radiating down left arm. No relief from nitroglycerin, nauseated, sweating, dyspnea, especially when recumbent (orthopnea). Breathing “noisy”. Paramedics called, transported to hospital.

In ER, bp was 105/80, inspiratory rales present (pulmonary edema), skin cold and clammy. Electrocardiograms and serum cardiac enzymes suggest left ventricular wall myocardial infarction. Pullmonary capillary wedge pressure was 30mmHg (normal is 5 mmHg), ejection fraction is .35 (normal is .55).

Pt transferred to coronary ICU, treated with thrombolytic agent, digitalis (positive inotropic agent), and furosemide (loop diuretic). After 7 days, sent home on low-fat, low-Na diet.

Question: Marvin had left ventricular wall infarction secondary to myocardial ischemia. Left ventricle could no longer generate enough pressure to eject blood normally. What will happen to the Frank-Starling relationship, and what are consequences to stroke volume and cardiac output?

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Commit #272784

In ventricular failure, contractility decreases and intrinsic ability of the myocardial fibers to produce tension is impaired; thus for a given end-diastolic volume, stroke volume and cardiac output are decreased