Alden H. Harken, MD and Brian C. George, MD
A new patient arrives by private vehicle to the ER. The nurse runs over from triage and says to you: “Doctor, this patient doesn’t look so good.”
You bring him back to the trauma bay and check his vital signs: his blood pressure is 60/—and his heart rate is 140.
1. Is this patient in shock?
2. What is the first thing you would do to treat his hypotension?
SHOCK
Answers
1. Given the information in the case, we can’t actually tell. Remember, “shock” is not just “looking bad” and is not just a low blood pressure. And shock is not just decreased peripheral perfusion. And shock is not just reduced systemic oxygen delivery. Ultimately, shock is decreased end-organ tissue respiration. Stated differently, “shock” is suboptimal oxygen consumption and carbon dioxide excretion at the cellular level.
The most practical method of diagnosing shock is to look at end-organ function. The organs most sensitive to hypoperfusion are the brain and the kidneys. A confused or anxious patient should be a source of concern, just as oliguria should trigger you to investigate further. Perfusion of the skin and extremities can also be sensitive indicators of shock, as the body preferentially shunts blood to the core when cardiac output is compromised. This is why surgeons will often feel the big toe as a quick and dirty measure of cardiac output. Other organ systems can of course also be hypoperfused, but evidence of, for example, cardiac or hepatic dysfunction is usually a late sign.
Another method of diagnosing shock is to look for systemic signs of decreased end-organ tissue respiration. This is most easily done by measuring the pH of the blood. While arterial blood gases are traditionally used, venous blood gases can also be of huge practical clinical value when a patient is really sick. Venous gases reflect arterial acid/base status with useful precision. Just add 0.05 to the venous pH and you will get the arterial pH. Subtract 5 from the arterial PCO2 and you get arterial PCO2. So you don’t need to repeatedly stick the artery (see Table 12-1).
Table 12-1. How to Interpret Venous Blood Gases
A little bit like sorting your socks, some surgeons are more comfortable “classifying” shock—all the while acknowledging that it is the cardiovascular response to a stressor (blood loss/myocardial ischemia) that dictates the danger. Class I (fully compensated) shock is how a young healthy patient presents following a 2-U (750 mL) bleed. This young person can vasoconstrict, diverting blood flow away from his extremities in a manner that preserves completely normal coronary and carotid flow. The problem, of course, is that the same 2-U bleed in a Supreme Court justice may prove lethal.
On the other end of the clinical spectrum, class IV shock represents a near-death state that is seen with severe blood loss (eg, 6 U, or 2000 mL). If the patient is still alive, there will almost certainly be severe organ dysfunction, including coma and/or stroke, renal failure, and myocardial ischemia (see Table 12-2).
Table 12-2. Classification of Shock
2. “Shock” may be treated in a logically sequential fashion that is the same for all patients. So, when a chubby, cigar-chomping, sixtyish personal injury lawyer presents hypotensive with a big GI bleed, or with crushing chest pain, or with a sigmoid perforation, you should activate the following steps in order:
A. Optimize volume status: Give the patient volume until an increase in the right-sided central venous pressure (CVP) and/or left-sided pulmonary capillary wedge pressure (PCWP) confers no additional benefit to either blood pressure or cardiac output. This is strictly Starling law. It doesn’t make any difference how good the engine is, if there is no gas in the tank. You want your patient’s ventricles working at the top of this Starling curve (Figure 12-1). In the absence of a Swan catheter it can sometimes be difficult to precisely measure the cardiac output—in those cases, you can also target a CVP of 8 to 12.
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 H2O. 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 β2 vasodilation may actively drop his blood pressure, but hoping that the β1 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 H2O. 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 O2 saturation is 80%! Using mixed venous O2 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 O2 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.