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systemic syndrome from the wound itself.3

Eventually, Cannon and then Blalock described our current concept of shock and its attributed

systemic effects. In fact, Blalock was the first to recognize the third-space fluid loss that follows shock

resuscitation that is greater than the quantity of initial blood loss.4 As a result, therapy began to focus

not only on restoring intravascular volume but also on replacing fluid lost to the interstitium with a

balanced salt solution. Investigators then became increasingly intrigued by the fact that, at some point,

shock becomes irreversible and is no longer responsive to further volume resuscitation. As stated more

than 60 years ago by Wiggers, “at a certain stage adequate circulation cannot be restored by merely

filling the system, as one does an automobile radiator.”5 At some point, as had been observed multiple

times previously, the initiating event (e.g., wound, infection, cardiac dysfunction) is no longer the

primary threat. Other “unknown” factors sustain the shock state, blood pressure cannot be restored,

improvements are only transient, and death occurs shortly thereafter due to progressive organ

dysfunction.

The current concept of shock has led to a reclassification into four distinct groups – hypovolemic,

cardiogenic, extracardiac obstructive, and distributive – that may occur independent of each other, or

more characteristically synergistic with each other.6 Early recognition and prompt treatment are

essential to modern treatment. If delayed, uncorrected hypovolemia and critical oxygen delivery deficits

occur that lead to irreversible shock. However, it is believed that future therapies will move beyond

simple recognition and fluid resuscitation. Thus, investigators are increasingly looking to gain an

understanding of the chain of events that occur, which lead to organ damage and irreversibility. This

chapter describes these events, discusses the therapeutic approaches utilized in current management,

and offers a brief perspective on what may lie ahead in the future.

EVALUATION OF SHOCK

Shock is easily recognized by even the most inexperienced caregiver after the compensatory

mechanisms have been overcome (Table 9-1). However, it is more difficult to recognize the patient in

compensated shock, who presents with vital signs that are almost normal. It is critically important to

the patient’s ultimate outcome that recognition and treatment of shock occur before decompensation.

The clinical assessment must be guided by the knowledge that the severity of symptoms and signs of

shock vary between patients and the type of shock present. The patient is evaluated based on clinical

appearance, hemodynamic measurements, physiologic responses, and biochemical analyses.

Early during various shock states, vasoconstriction frequently causes the skin to be cool leading to

poor capillary refill. However, this must be contrasted to shock states induced by either neurogenic or

septic states in which vasodilation is present causing the skin to be warm, with good capillary refill.

Common to the various shock states is the presence of hyperventilation, a compensatory response due

to progressive metabolic acidosis. As shock progresses, mental status changes occur, and decreased

cerebral blood flow and increased catecholamine stimulation may lead to anxiety and restlessness. With

continued shock, lethargy may result. True coma, however, seldom results due to shock alone, unless

coincident complete cardiovascular collapse occurs, and is usually associated with other conditions such

as direct brain injury or severe hypoxia.7 This includes evaluation of the rate and character of the pulse;

the blood pressure; and, in some cases, the central venous pressure (CVP), pulmonary artery pressure,

pulse pressure variation (PPV), and echocardiography.8

The hemodynamic assessment should include evaluation of the rate and character of the pulse; the

blood pressure; and, in some cases, the CVP, pulmonary artery pressure, and PPV.8 Tachycardia is a

normal response to volume loss but also to pain, anxiety, and fear, all of which are commonly present.

Assessment of the pulse may be helpful in determining the proper diagnosis. Because of the body’s

ability to compensate for hypovolemia, changes in blood pressure do not occur reliably until nearly 30%

of blood volume has been lost. However, the pulse pressure usually narrows, even in compensated

shock, because of the effects of vasoconstriction on the diastolic blood pressure. Importantly, the CVP

reflects the adequacy of and not the true blood volume, and the state of the venous tone. Changes in

CVP in response to treatment or from continuing hemorrhage are more revealing than a solitary

measurement. However, this concept remains debatable. Because of the misuse or overuse of pulmonary

artery catheters (PACs), routine placement no longer occurs and has been associated with increased

morbidity.9 As a result, invasive monitoring using PPV, and noninvasive measures such as

echocardiography have become more commonly used.10

An indirect but extremely valuable measure of perfusion and volume status is urine output. A urinary

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catheter should be inserted in every patient being evaluated for shock. Hourly urine output should be

0.5 to 1 mL/kg for adult patients, at least 1 mL/kg for most pediatric patients, and 1 to 2 mL/kg for

patients younger than 2 years of age. Lack of adequate urine output in the setting of previous normal

kidney function should cause the caregiver to be highly concerned about the continued presence of

inadequate perfusion and cellular hypoxia.

Although each of the physical examination components are important in the identification of shock,

used alone these factors can fail to diagnose compensated shock. As a result, biochemical markers are

used as a means to identify shock in its early stages. Biochemical analysis of shock is based on the shift

from aerobic to anaerobic metabolism in underperfused tissues. This shift is marked by the production

of lactate that can, in turn, be measured serially. Resuscitation of shock results in a decrease in serum

lactate levels, and the time required to normalize serum lactate levels appears to be an important

prognostic factor for survival.11–15

Another biochemical marker useful in the resuscitation of shock is the base deficit. This is defined as

the amount of a fixed base (or acid) that must be added to an aliquot of blood to restore the pH to 7.40.

Base deficit values have been categorized as normal (2 to –2), mild (–3 to –5), moderate (–6 to –9), and

severe (>–10). Changes in base deficit toward normal with volume infusion can be used to judge the

efficacy of resuscitation.16–18 Base deficit has been shown to be superior to pH values in assessing the

normalization of acidosis after shock resuscitation, and the time required for normalization of base

deficit has perhaps even greater prognostic significance than that of lactate.16,19

Table 9-1 Shock Recognition

The biochemical changes associated with the hypoperfusion of shock occur even with compensation.

Because of the potential difficulties in diagnosing compensated shock, an arterial and/or venous blood

gas analysis including base deficit and lactate should be obtained for every patient suspected of being in

shock. Additionally, any patient with a lactate of ≥4 mmol/L or base deficit of ≥6 mEq/L should be

considered to be in shock until proven otherwise.17,20,21

Future Measures: Although each of these factors can be used to characterize shock, no single

measurement has been determined to be optimal or when used singly to be always accurate for

identification and treatment of shock. Currently, other measurements are being investigated that

demonstrate promise. These markers include measurements of central and mixed venous oxygen

saturations, end-diastolic cardiac volume indices, and specific noninvasive end-organ tissue oxygen

saturations.22–28

TYPES OF SHOCK

Although several different classifications for shock have been described, the most widely accepted

classification of shock was proposed by Weil and Shubin in 1971.6 This classification divides the shock

syndrome into four distinct categories (Table 9-2). Despite this separation, however, there is

considerable overlap between the categories, with some patients presenting with more than one factor

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at the same time. Given this overlap, it is helpful to evaluate the hemodynamic pattern in order to

elucidate the etiology and manage the patient (Table 9-3).

Hypovolemic Shock

2 Hypovolemic shock is the form of shock most commonly encountered in surgical practice (Table 9-2).

The essential feature is a reduction in intravascular volume to a level that prevents the heart from being

able to pump sufficient blood to vital organ systems. Substantial blood (>20% circulating volume) or

plasma (via soft tissue, enteric sequestration, gastrointestinal, urinary, or other insensible losses) losses

are required to produce this syndrome.

The signs and symptoms of shock vary with both the severity and duration of fluid loss. A review of

the Advanced Trauma Life Support classification system of the American College of Surgeons is useful to

comprehend the manifestations and physiologic changes associated with hemorrhagic shock in adults.29

Blood volume is estimated at 7% of ideal body weight, or approximately 4,900 mL in a 70-kg patient

(Table 9-4).

Class I: Mild hemorrhage, up to 15% of total blood volume. This condition is exemplified by voluntary

blood donation. In the supine position, there are no measurable changes in heart or respiratory rates,

blood pressure, or pulse pressure. Capillary refill is normal. This degree of hemorrhage requires little or

no treatment, and blood volume is restored within 24 hours by transcapillary refill and the other

compensatory methods.

Class II: Loss of 15% to 30% of blood volume (800 to 1,500 mL). Clinical symptoms include

tachycardia and tachypnea. The systolic blood pressure may be only slightly decreased, especially in the

supine position, but the pulse pressure is narrowed (because of the diastolic increase from adrenergic

discharge). Urine output is reduced only slightly (20 to 30 mL/hr). Mental status changes (e.g., anxiety)

are frequently present. Capillary refill is usually delayed. Patients with class II hemorrhage usually can

be resuscitated with crystalloid solutions, but some may require blood transfusion.

Class III: Loss of 30% to 40% of blood volume (up to 2,000 mL). Patients with class III hemorrhage

present with inadequate perfusion that is obvious; marked tachycardia and tachypnea; cool, clammy

extremities with significantly delayed capillary refill; hypotension; and significant changes in mental

status (e.g., confusion, combativeness). Class III hemorrhage represents the smallest volume of blood

loss that consistently produces a decrease in systolic blood pressure. The resuscitation of these patients

frequently requires blood transfusion in addition to administration of crystalloids.

Class IV: Loss of more than 40% of blood volume (more than 2,000 mL), representing life-threatening

hemorrhage. Symptoms include marked tachycardia, a significantly depressed systolic blood pressure,

and narrowed pulse pressure or unobtainable diastolic pressure. The mental status is depressed and the

skin is cold and pale. Urine output is negligible. These patients require immediate transfusion for

resuscitation and frequently require immediate surgical or other (e.g., angiographic embolization)

intervention.

In practice, individual susceptibility to blood loss varies greatly and is affected by age, pregnancy,

pre-existing disease, prescription and nonprescription medications (e.g., beta blockers), adequacy of

compensatory mechanisms, and other factors that are poorly characterized. Presence of these factors

should lead the caregiver to consider early use of invasive monitoring as an adjunct to appropriate fluid

resuscitation.

Hypovolemia due to plasma losses may also lead to hypovolemic shock. The clinical findings of

hemorrhagic shock are typically present, but significant differences do exist. Hemoconcentration,

elevated blood urea nitrogen (BUN) and creatinine, and hypernatremia are typical of acute plasma

and/or free water losses and are not necessarily present in other forms of shock. Appropriate evaluation

of preload and urine output should be followed, with specific considerations for unique electrolyte

abnormalities associated with specific plasma and fluid losses (e.g., gastric vs. colonic losses).

Cardiogenic Shock

3 The clinical definition of cardiogenic shock is decreased cardiac output with tissue hypoperfusion,

despite presence of adequate intravascular volume. It is caused by a primary problem with the cardiac

muscle, electrical conduction system, or valves. The most common cause is anterior wall myocardial

infarction, although in surgical patients it is often precipitated by pulmonary embolus, myocardial

contusion, or pulmonary hypertension.

Distinguishing cardiogenic shock from other shock etiologies is occasionally difficult. It is not

uncommon to see combined cardiogenic and traumatic shock in the elderly patient, with one often being

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