Review Note
Last Update: 01/29/2025 02:45 PM
Current Deck: PHYSIOLOGY::exam one
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Front
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: Why treat with digitalis (Na-K ATPase inhibitor)? Why a diuretic?
Back
Inhibiting the Na-K ATPase will
increase intracellular Na. This in turn
depresses the Na-Ca antiporter by reducing the Na gradient which
drives the antiporter.
The end result is increased Ca2+ concentration,
which will increase muscle contractility, and thus increase stroke volume.
The diuretic is used to help the pt
shed fluids, and thereby reduce venous blood
volume. This is important to address the
pulmonary edema.
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