Review Note
Last Update: 01/29/2025 02:45 PM
Current Deck: PHYSIOLOGY::exam one
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Commit #272790Marvin
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 did pulmonary edema develop? Why is pulmonary edema so dangerous?
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Commit #272790Decreased left ventricular ejection
fraction caused blood to back-up in the left side of the heart, increasing left
ventricular and left atrial pressures.
This leads to increase in pulmonary venous pressure, causing fluids to
filter from plasma to the interstitial space.
Pulmonary edema is extremely
dangerous because it interferes with gas exchange. The mechanism is an increase in the diffusion
distance O2 has
to travel at the level of the
alveoli. The result is impaired
oxygenation of blood and hypoxia
