Free Resident Readiness General Surgery by Debra Klamen, Brian George, Alden Harken, Debra Darosa Page A

following GDT guidelines, you obtain a mixed venous oxygen saturation through the central line. Venous O 2 saturation is 80%! Using mixed venous O 2 saturation as a surrogate for cardiac output, you reason that this patient must have a colossal cardiac output because he is extracting relatively little oxygen peripherally. The poison (like endotoxin) on the venomous sword must be a potent vasodilator. You infuse norepinephrine 0.4 μg/kg/min or vasopressin 0.04 U/min until your patient’s systolic pressure clears 100 mm Hg systolic. Two days later, he has metabolized the poison and is hemodynamically stable again. He returns to the castle, makes amends with his old friend, and both of them conspire to “. . . outwit the divinity that shapes our ends.”
    A savvy surgical resident, using GDT strategies, could have capably resuscitated many of the victims of Shakespeare’s tragedies, transforming these “tragedies” into much more comfortable “histories.”
    TIPS TO REMEMBER
All shock will respond to logically sequential GDT principles:
First optimize volume.
If you’re still in trouble, infuse cardiotonic drugs.
If you’re still in trouble, search for a septic focus and document a high mixed venous O 2 saturation prior to infusing vasoconstrictive drugs.
The Surviving Sepsis Campaign has focused a lot of high-octane light on septic shock recovery. In the absence of an obvious septic focus, most shock is still hypovolemic, cardiogenic, or both.
Infusing a vasoconstrictive agent is a form of instant gratification. Remember, though, that you are playing with Ohm’s law. An increase in systemic vascular resistance does increase the blood pressure while it invariably decreases cardiac output.
    COMPREHENSION QUESTIONS
1. For a previously healthy young trauma patient involved in a high-speed motor vehicle crash, which of the following findings enables you to diagnose shock?
A. Venous blood gas of 7.25/45/100
B. Blood pressure of 75/55
C. Heart rate of 170
D. Lethargy
2. How much volume should you give a patient whom you suspect is in shock?
A. Enough to normalize the blood pressure
B. 2 L
C. Until oxygenation is compromised due to pulmonary edema
D. Until there is no additional effect on blood pressure or cardiac output
3. A trauma patient remains hypotensive despite adequate volume resuscitation. Adding pressors will do which of the following?
A. Increase end-organ perfusion
B. Decrease end-organ perfusion
    Answers
1. A . If we convert the VBG to an ABG, we can see that this patient has a metabolic acidosis. This reflects anaerobic metabolism, that is, end-organ hypoperfusion. Lethargy, while sensitive for cerebral hypoperfusion, is not specific—it could also be due to head trauma. Blood pressure and heart rate alone are not diagnostic unless they are associated with end-organ hypoperfusion.
2. D . You give volume until you are convinced the patient is at the peak of the Starling curve, based on blood pressure and/or cardiac output. Sometimes you will be able to normalize the blood pressure with volume alone, but you can imagine a scenario with a septic patient who cannot constrict his arterioles and might therefore remain hypotensive even if you’ve given him 50 L (and caused him to go into congestive heart failure).
3. B . It is counterintuitive, but this patient is not hypotensive for lack of arterial vasoconstriction. The patient is hypotensive because the heart cannot produce enough output. Increasing the afterload with pressors will reduce the already inadequate cardiac output by increasing the systemic vascular resistance that, in turn, decreases the stroke volume. The only time pressors might be indicated for a patient in shock is if there is peripheral vascular collapse from, say, sepsis or anaphylaxis.
    SUGGESTED READING
Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med . 2001;345(19):1368–1377.

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