Resident Readiness General Surgery (16 page)

Figure 12-1.
The relationship between preload and cardiac output. There is a point at which there is too much preload and cardiac output actually falls—this is what is happening when a patient develops heart failure from volume overload.

B.
Augment cardiac performance
: If the blood pressure, cardiac output, and tissue perfusion remain inadequate despite optimal volume resuscitation, your patient has a pump problem (cardiogenic shock). You should infuse cardiac inotropic drugs up to the point of toxicity (typically ventricular ectopy). Start with dobutamine 5 μg/kg/min or epinephrine 0.05 μg/kg/min, and go up.

C.
Assess for peripheral vascular collapse
: Occasionally, a patient will present with a surprisingly high cardiac output (warm big toe) and a paradoxically low blood pressure. This unusual loss of peripheral vascular autoregulatory control is associated typically, but not always, with sepsis. In this instance, you should infuse norepinephrine 0.4 μg/kg/min or vasopressin (ADH) 0.04 U/min to achieve the desired blood pressure. But remember you are playing with Ohm’s law. As you increase systemic resistance, you will most likely reduce cardiac output.

To illustrate these concepts, let’s examine 3 patients who come in with the exact same heart rate and blood pressure.

Case 1: Hypovolemic Shock

A sixtyish man just arrived with stab wounds in the RUQ and just below his left nipple. He is covered in blood. Blood pressure is 60/—and heart rate 140. The guy says his name is Duncan. He states that he’s a king. He was visiting his friend’s castle when his host came into his bedroom in the middle of the night and stabbed him.

You aren’t terribly sure of the accuracy of this patient’s story, but the fact that he can tell you one means that he is perfusing his brain.

You start 2 large-bore IVs and complete your primary survey. Following 500 mL of crystalloid, your patient is still hypotensive. You should follow the goal-directed therapy (GDT) protocol (first outlined by Rivers et al) for patients in septic shock. Continue infusing crystalloid up to a CVP of 12 mm Hg. This patient suffered an isolated liver laceration, and with fluid resuscitation, he became hemo-dynamically stable. Two days later he was able to return to the castle—where he was able to make peace with his despondent host.

Case 2: Cardiogenic Shock

Another pudgy, pale, sixtyish male arrives, stating his name is Polonius. He claims to be the Lord Chamberlain of Elsinore and his story is that he was standing behind a hanging tapestry, “minding my own business” (an activity that, in
most trauma centers, is a robust predictor of trouble) when, for no apparent reason, a young man enters the room and stabs him right through the tapestry with a sword. This patient’s blood pressure is also 60/—, with a heart rate of 140. You are reassured that this patient is also talking and therefore perfusing his brain. You start 2 large-bore IVs and complete your primary survey. The patient has a single RUQ laceration and after 500 mL LR × 3, his blood pressure has increased to 80/50 with a heart rate of 120. Again, following GDT protocol, you place a central venous line, and it is already 16 cm H
₂
O. So, his tank is full. He has a pump problem. Castle life, for a favored courtier, has permitted a high-fat diet and open access to the wine cellar—so, he has ample reason for both an ischemic and an alcoholic cardiomyopathy. You start dobutamine 5 μg/kg/min, acknowledging that the β
₂
vasodilation may actively drop his blood pressure, but hoping that the β
₁
inotropic stimulation will more than compensate. This patient had both a hypovolemic and a cardiogenic component to his initial “shock” presentation. He also resolves his liver laceration and you are able to shepherd him through his inadequate cardiovascular response to this massive stress. He returns to Elsinore in time to provide his son some sage advice as he departs for college.

Case 3: Peripheral Vascular Collapse Shock

You are cleaning things up when another patient arrives. Unlike the first 2, this patient is a young, healthy-appearing athlete. He says his name is Laertes, and he claims he was pierced in the RUQ by a poisoned sword during a duel. To your surprise, his blood pressure is also 60/—and heart rate 140, and during your otherwise negative primary survey, you are surprised that his feet are warm. Wow, he is perfusing both his brain and his feet with a systolic of 60 mm Hg! Using the same logically sequential (GDT) therapeutic response to shock, you infuse 500 mL LR × 2 and this patient’s blood pressure does increase to 90/—with a heart rate of 130. Again, using goal-directed principles, you place a central venous line. The CVP is still 3 cm H
₂
O. After 4 more 500 mL boluses of LR this patient’s blood pressure is 80/50 with a heart rate of 100 beats/min. This guy has received a lot of fluid; so 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