This blog is intended for students in the health sciences and other students with an interest in cardiovascular, pulmonary and renal physiology and pathophysiology. It is a compilation of original contributions as well as notes I have taken during lectures on these topics and clinical lectures. At the bottom of each post is a box for comments that you are invited to use. Steve Wood, PhD, swood60@gmail.com teaching website: http://www.cvpulmrenal.com
Friday, May 3, 2013
Wednesday, May 1, 2013
World Record Metabolic Acidosis
A 44-year-old woman drank approximately 720 ml of ethylene glycol in the form of antifreeze. She had previously attempted suicide by injecting the same substance into her buttocks. When admitted to the hospital, the patient was unresponsive and incontinent and was receiving ventilation. Her temperature was 37.1 °C (98.7 °F), her pulse 110 per minute, and her blood pressure 130/70 mm Hg. Her pupils were fixed and dilated, and she had no corneal, gag, or deep-tendon reflexes. The serum sodium level was 140 mmol per liter, the potassium level 6.6 mmol per liter, the chloride level 110 mmol per liter, and the bicarbonate level 1 mmol per liter (anion gap, 29 mmol per liter). The serum creatinine concentration was 2.8 mg per deciliter (248 μmol per liter), and the lactate concentration 10.1 mmol per liter. The osmolar gap (the difference between the measured value and the predicted value) was 84 mOsm per kilogram. Urinalysis revealed calcium oxalate crystals. The serum concentration of ethylene glycol was 2600 mg per liter; no other toxins were detected. Serial arterial-blood gas values are shown
Two hours after admission, hemodialysis was begun and continued intermittently for 48 hours. To reduce the conversion of ethylene glycol to its acid metabolites, ethanol was added to the dialysate1 and then given by gavage in a dose of 600 mg per kilogram of body weight, followed by intragastric infusion at a rate of 200 mg per kilogram per hour for 37 hours. Renal failure did not develop, and the patient recovered completely.
Although the arterial-blood pH of normal subjects may fall to 6.80 after extreme exertion,2 in a clinical setting such a level is usually fatal. Arterial-blood pH values of 6.78, 6.57, and 6.49 have been reported in patients who survived poisoning with ammonium chloride3 and strychnine4 and isoniazid overdose,5 respectively.
85-YO male in ED
good article on medical response to Boston Marathon bombing
Drs. Voyles, Busby, Spaulding
85-YO male in ED
Diagnosis of COPD should be supported by objective data (e.g., PFT)
unable to assess CVP by JVD in obese patients
Cold upper and lower extremities; slight mottling of lower extremities = vasoconstriction
2/6 early SEM at the base only - could be due to turbulence from tachycardia, anemia, sclerotic valve leaflets
gallop uncertain - hard to tell at high heart rates S3 and S4 may blend with shortened diastolic period. also hard to hear due to low pitch. S4 occurs with atrial kick and LV hypertrophy from chronic HTN
Shallow respirations and decreased breath sounds in both bases; coarse rhonchi in all lung fields; scattered expiratory wheezes; no rales - rhonci = gunk in airways; shallow sounds = low volume breaths; expiratory wheezing could be airway sounds or "cardiac asthma" where edema in lymphatics constricts airways = wheezing. no rales or crackles could be due to shallow breaths and no opening of collapsed airways. may become audible if pt. sits up and takes a big breath.
not making urine - maybe he voided in ambulance or is not making urine. BPH may contribute. ??? not making urine vs. not voiding. hypotension responsible?
Place Foley catheter and maybe bedside bladder scan.
Echocardiograms hard to obtain with morbidly obese pts. transesophageal echo is a way around this.
don't give nl saline and furosemide at the same time. need more data; e.g., blood pressure (via arterial line with pressure transducer in obese pts. since cuffs aren't accurate) saline may increase
BP BUT worsen pulmonary edema.
Flank pain presenting complaint - don't drift far from this; e.g., AAA
no abdominal tenderness since abdominal pain is peritoneal and AA is in peritoneal space.
CT scan problematic with high Cr. Do it anyway if suspicion is AAA.
PE vs. AAA - in one case heparinize not in AAA (would kill him)
Calcification occurs with smoking, obesity, and HTN
PE does not present with back and flank discomfort but AAA that ruptures does.
Tests for AAA
Drs. Voyles, Busby, Spaulding
85-YO male in ED
Diagnosis of COPD should be supported by objective data (e.g., PFT)
unable to assess CVP by JVD in obese patients
Cold upper and lower extremities; slight mottling of lower extremities = vasoconstriction
2/6 early SEM at the base only - could be due to turbulence from tachycardia, anemia, sclerotic valve leaflets
gallop uncertain - hard to tell at high heart rates S3 and S4 may blend with shortened diastolic period. also hard to hear due to low pitch. S4 occurs with atrial kick and LV hypertrophy from chronic HTN
Shallow respirations and decreased breath sounds in both bases; coarse rhonchi in all lung fields; scattered expiratory wheezes; no rales - rhonci = gunk in airways; shallow sounds = low volume breaths; expiratory wheezing could be airway sounds or "cardiac asthma" where edema in lymphatics constricts airways = wheezing. no rales or crackles could be due to shallow breaths and no opening of collapsed airways. may become audible if pt. sits up and takes a big breath.
not making urine - maybe he voided in ambulance or is not making urine. BPH may contribute. ??? not making urine vs. not voiding. hypotension responsible?
Place Foley catheter and maybe bedside bladder scan.
Echocardiograms hard to obtain with morbidly obese pts. transesophageal echo is a way around this.
don't give nl saline and furosemide at the same time. need more data; e.g., blood pressure (via arterial line with pressure transducer in obese pts. since cuffs aren't accurate) saline may increase
BP BUT worsen pulmonary edema.
Flank pain presenting complaint - don't drift far from this; e.g., AAA
no abdominal tenderness since abdominal pain is peritoneal and AA is in peritoneal space.
CT scan problematic with high Cr. Do it anyway if suspicion is AAA.
PE vs. AAA - in one case heparinize not in AAA (would kill him)
Calcification occurs with smoking, obesity, and HTN
PE does not present with back and flank discomfort but AAA that ruptures does.
Tests for AAA
- KUB xray
- aortagram
- CT scan -
AAA can create ATN if renal arteries are involved.
Huge surgical risks with this pt. (not a candidate for a haircut)
option = endovascular repair
pt. died on operating table with refractory shock.
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