Shock

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rate to 35, and a change in mental status. Despite 3 L of 0.9% normal saline intravenous fluid (IVF) resuscitation, hypotension and tachycardia persist.

Introduction

Shock, by definition, is a clinical syndrome that develops due to inadequate tissue perfusion. Hypoperfusion results in insufficient delivery of oxygen and nutrients for metabolism, leading to severe vital organ dysfunction. Organ dysfunction, combined with the body’s sympathetic and neuroendocrine response to oxygen and nutrient deficiency, characterizes the shock state. Several classification profiles have been proposed to categorize shock syndromes. It should be emphasized that these categories of shock are not absolute, and significant overlap may be observed. Traumatic shock, for example, may include components of each of the other primary categories. Septic shock often demonstrates hypovolemia, myocardial depression, and distributive abnormalities.

This chapter discusses the various types of shock: definitions, the diagnostic workups, and management.

Types of Shock

Hypovolemic Shock (see Algorithm 7.1)

Hypovolemia is the most common cause of shock, and hemorrhage is the most common cause of hypovolemic shock. Table 7.1 presents the physical findings in hemorrhagic shock by class of hemorrhage. Class I hemorrhage represents a loss of 10% to 15% of the blood volume and results in a minimal change in the patient’s vital signs. A patient with class II hemorrhage (15–30% blood volume loss) manifests tachycardia, a decreased pulse pressure, and delayed capillary refill. The patient may be mildly anxious and have decreased urine output. Larger volume losses result in the classic presentation of hemorrhagic shock. Class III (30–40% blood volume loss) hemorrhage presents with hypotension, tachycardia, tachypnea, and mental confusion progressing to lethargy. Greater than 40% blood volume loss (>2000 mL in a 70-kg patient, class IV) presents with obtundation, profound hypotension, and anuria. Compensated hemorrhagic shock (class I and II) may progress rapidly to class IV (Case 1), especially in the pediatric population. In Case 1, the initial vital signs are normal at the scene of the accident. However, rapid transition to class IV shock is evident upon arrival at the emergency department. Recognition of the early stages of shock and appropriate early intervention are the keys to management.

Other important etiologies of hypovolemic shock are losses via the gastrointestinal or urinary tracts and extravascular fluid sequestration or “third space” fluid loss. Ongoing fluid losses through these routes may not be diagnosed as readily as is hemorrhage, and, therefore they require a higher index of suspicion. For example, severely

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Hypovolemic

shock

History and physical exam

Trauma, surgery

Hypotension

Tachycardia

Tachypnea

Adequate perfusion

Lab:

Hb/Hct

Electrolytes

ABG

CXR

Large-bore IV access

Fluid challenge Improvement (2 L)

No improvement

Central venous access

Look for ongoing blood loss

Algorithm 7.1. Algorithm for treating hypovolemic shock. ABG, arterial blood gas; CXR, chest x-ray.

burned patients require large-volume fluid replacement due to extravascular sequestration or “third space” fluid loss. Subsequent burn wound infections in such a patient could result in septic shock, adding to the complexity of management in these patients. Furthermore, a component of inhalation injury likely would add to further resuscitative fluid requirements. Processes such as peritonitis commonly lead to large-volume retroperitoneal or intraabdominal fluid sequestration. In Case 2, peritonitis secondary to perforated appen-

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dicitis with abscess formation leads to intraabdominal fluid sequestration, and, despite aggressive fluid resuscitation, shock persists. Septic shock, a form of severe sepsis, is evident when an infectious source is confirmed or suspected, coupled with hypoperfusion despite adequate volume resuscitation. The treatment of septic shock involves adequate fluid resuscitation, point source control of the infectious source (such as drainage of appendicial abscess in Case 2), and other supportive measures, such as nutritional support, ventilation, and renal replacement.

Shock following traumatic injury frequently combines aspects of several shock categories. Hypovolemia due to hemorrhage combined with tissue injury and/or bone fractures evokes a potentially more destructive proinflammatory response than hypovolemia alone. Neurogenic shock may compound a spinal cord injury. Cardiogenic shock may accompany traumatic cardiac injury, tension pneumothorax, pericardial tamponade, or myocardial contusion. There are multiple contributors to the systemic inflammatory reaction stimulated by tissue injury. Devitalized tissue, bacterial contamination, ischemiareperfusion injury, and hemorrhage act together to place the traumatized patient at risk for hypermetabolism, multiorgan dysfunction, and death. Therefore, the treatment of traumatic shock is aimed at quickly diagnosing the areas of injury, controlling hemorrhage, restoring circulating intravascular volume, preventing hypoxia, and limiting the extent of secondary damage introduced by inflammation and infection. In Case 1, the progression to class IV shock may be due to several etiologies, including direct hemorrhagic sources, such as a ruptured spleen or liver with intraabdominal blood loss. Exclusion of intraabdominal sources of hemorrhage must be done expeditiously because such injuries require immediate surgical treatment in the operating room. Further sources of hemorrhage include aortic injury with hemorrhage into the chest cavity. A

Table 7.1. Physical findings in hemorrhagic shock.a

a Alcohol or drugs (e.g., b-blockers) may alter physical signs.

Source: Adapted from American College of Surgeons. Shock. In: Advanced Trauma Life Support Manual. Chicago: American College of Surgeons, 1997:87–107, with permission. Reprinted from Nathens AB, Maier RV. Shock and resuscitation. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.

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nonhemorrhagic source in this patient could be a myocardial contusion with subsequent impairment of cardiac output resulting in cardiogenic shock. This may be diagnosed by echocardiography and treated with supportive measures such as inotropes.

Treatment of hypovolemic shock, regardless of the etiology, involves restoration of circulating blood volume and control of ongoing volume loss. In patients with clear evidence of shock, aggressive fluid resuscitation is of great importance. For hemorrhagic shock especially, caregivers should follow a systematic approach to resuscitation, including the airway, breathing, circulation, and disability assessment as outlined in the Advanced Trauma Life Support course. This approach may be both diagnostic and therapeutic and increases the likelihood of recognizing sources of hemorrhage.

Fluid resuscitation should be initiated with two large-bore (16 gauge or larger) catheters in the antecubital fossae and connected to the widest administration tubing available to allow for rapid volume infusion. The choice of route for vascular access (peripheral vs. central) is determined by the skill level of the practitioner and the availability of catheters required. Patient assessment for placement of intravenous catheters should take into consideration the location of fractures, open wounds, burns, and areas of potential vascular disruption. These areas should be avoided.

The choice of fluid for resuscitation begins with the most efficacious and cost effective. Rapid infusion (less than 15 minutes) of 2 L of isotonic saline or a balanced salt solution should restore adequate intravascular volume. If blood pressure and heart rate do not improve following this intervention, suspect hemorrhage in excess of 1500 cc or ongoing blood loss. Blood transfusion should follow, using O-positive or O-negative blood in the most critical circumstance or type-specific or fully crossmatched blood if time allows. As a general caveat, no time should be wasted with crossmatching if the patient has a clear source of continuing hemorrhage and remains severely unstable despite crystalloid administration.

As a conventional approach to fluid resuscitation, crystalloid and blood product infusions are standard for patients with hemorrhagic or hypovolemic shock. There are alternate solutions, however, that include hypertonic saline, several colloid formulations, and blood substitutes (Fig. 7.1). Hypertonic saline (7.5% NaCl) has been studied extensively in animal models and humans with hemorrhagic shock. The hypertonic component draws water out of the intracellular space into the extracellular space in a type of “autotransfusion.” This may result in significant improvement in blood pressure and cardiac output. Some formulations add 6% dextran to hypertonic saline in order to increase intravascular oncotic pressure. The beneficial effects of hypertonic saline in improving survival have not been clearly apparent in human clinical trials, with the exception of the subset of patients in shock with traumatic brain injury. (For further discussion, see Chapter 15, “Shock and Resuscitation,” by A. B. Nathens and R. V. Maier, in Surgery: Basic Science and Clinical Evidence, edited by J. A. Norton et al, published by Springer-Verlag, 2001.)

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Figure 7.1. Total fluid requirements in patients with hypovolemic shock receiving either a synthetic colloid (hetastarch), 5% albumin, or 0.9% saline. Synthetic colloids have a far greater volume-expanding effect than crystalloid solutions, roughly equal to that of 5% albumin. LVEDP, left ventricular end-diastolic pressure. (Adapted from Rackow EC, Falk JL, Fein IA, et al. Fluid resuscitation in circulatory shock: a comparison of albumin, hetastarch and saline solutions in patients with hypovolemic and septic shock. Crit Care Med 1983;11:839–850. With the permission of Lippincott Williams & Wilkins. Reprinted from Nathens AB, Maier RV. Shock and resuscitation. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: SpringerVerlag, 2001, with permission.)

The colloid versus crystalloid debate in fluid resuscitation recently has been addressed in two meta-analyses.1 Although no single study clearly showed survival benefit in hypovolemic patients receiving crystalloid versus colloid, the meta-analyses concluded that patients resuscitated with colloid products (albumin, plasma protein products, synthetic colloids) have increased mortality. The mechanism by which albumin resuscitation leads to worse outcome has not been clarified. However, there is evidence to suggest that exogenous albumin may decrease sodium and water excretion, worsen renal failure, and impair pulmonary gas exchange.

Synthetic colloids, such as hetastarch (6% hydroxyethyl starch solution) and pentastarch, possess significant volume expansion capability. Hetastarch has a high average molecular weight and tends to remain within the intravascular space, where it can exert an oncotic effect that lasts up to 24 hours. Pentastarch has a lower average molecular weight than hetastarch, is more easily cleared in the plasma and excreted in the urine, and may cause fewer anaphylactic reactions than hetastarch. In addition, the oncotic effects of pentastarch last for approximately 12 hours and may require smaller volume infusions for similar effects on plasma expansion.

1 Reviewers CIGA. Human albumin administration in critically ill patient: systemic review of randomized controlled trials. Br Med J 1998;317:235–240.

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otic regimens, and critical care management. Bacteremia occurs in 40% to 60% of septic patients, and patients may be bacteremic without display of sepsis. Gram-positive, viral, fungal, and protozoal organisms may induce a septic response that previously was attributed only to gram-negative organisms. Bacterial products stimulate the release of proinflammatory cytokines from endothelial cells and macrophages. These mediators also contribute to the myocardial depression, vascular dilatation, hypercoagulability, impared fibrinolysis, and decreased oxygen utilization observed in severe sepsis. In Case 2, despite 3 L of IVF resuscitation, the patient remains hypotensive, tachycardic, and with evidence of impaired end-organ perfusion (oliguria and mental status changes). Persistent hypotension despite resuscitation could represent myocardial depression seen in sepsis, vasomotor dilatation due to inflammatory mediators, or the need for further fluid resuscitation if intravascular volume deficits were underestimated.

The symptoms of sepsis may present with varying degrees of severity. Tachypnea, tachycardia, oliguria, and mental status changes are common clinical findings in early sepsis, often preceding fever and leukocytosis (Case 2). Laboratory findings of hyperbilirubinemia, lactic acidosis, coagulopathy, and increased serum creatinine signal hypoperfusion and end-organ ischemia. Septic decompensation is signaled by leukopenia, hypothermia, acute respiratory distress syndrome, and shock. Patients often require large-volume fluid resuscitation for hypotension due to systemic vasodilatation and increased microvascular permeability. Vasopressor support is frequently necessary as an adjunct to volume infusion, but pressors should not be used in the place of fluid. The risk of organ damage secondary to the infusion of pressors without fluid outweighs the potential benefit of minimizing pulmonary edema by limiting volume resuscitation. For patients with renal or cardiac disease and for patients not responding to initial efforts at resuscitation, a pulmonary artery catheter may be useful to guide management.

Treatment of septic shock depends on eradication of the infectious focus as early as possible. Blood, urine, and sputum specimens should be sent for culture, along with fluid from any catheter drainage sites. Indwelling catheter sites should be examined, and catheters should be either removed or changed, as necessary. All surgical or traumatic wounds should be examined; all devitalized or infected tissue should be cultured and aggressively debrided. Computed tomography is an indispensable diagnostic tool if intraabdominal or intrathoracic infections are suspected. Abscess cavities should be percutaneously or surgically drained, whichever is appropriate. Surgical control of any ongoing contamination is mandatory. Empirical treatment with broadspectrum antibiotics is required if the organism or site is unknown. Strong emphasis should be placed on the correct choice of antibiotic, as this has been shown to have a clinically significant impact on mortality reduction.2 In Case 2, the patient has symptoms of sepsis. Given

2 Leibovici L, Drucker M, et al. Septic shock in bacteremic patients: risk factors, features, and prognosis. Scand J Infect Dis 1997;29:71–75.

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the prior history of appendiceal abscess drainage, recurrent intraabdominal infection (recurrent abscess) is likely. However, blood-, urine-, sputum-, wound-, and catheter-related infection should be considered. A repeat CT scan of the abdomen would be the diagnostic modality to exclude recurrent intraabdominal abcess. Broad-spectrum antibiotics should be initiated pending the results of the diagnostic workup.

Cardiogenic Shock (see Algorithm 7.3)

Cardiogenic shock may be difficult, at least initially, to distinguish from hypovolemic shock. Both forms of shock are associated with decreased cardiac output and compensatory upregulation of the sympathetic response. Both entities also respond initially to fluid resuscitation. The syndrome of cardiogenic shock is defined as the inability of the heart to deliver sufficient blood flow to meet metabolic demands. The etiology of cardiogenic shock may be intrinsic or extrinsic. In Case 1, the development of class IV shock may be due to hemorrhage, such as an aortic injury, or may be cardiogenic, such as a myocardial contusion from blunt injury to the chest. Echocardiography would evaluate the possibility of intrinsic (infarction/contusion) or extrinsic (cardiac tamponade) myocardial dysfunction.

Intrinsic causes of cardiogenic shock include myocardial infarction, valvular disease, contusion from thoracic trauma, and arrhythmias. For patients with myocardial infarction, cardiogenic shock is associated with loss of greater than 40% of left ventricular myocardium. The normal physiologic compensation for cardiogenic shock actually results in progressively greater myocardial energy demand that, without intervention, results in the death of the patient (Fig. 7.2). A decrease in blood pressure activates an adrenergic response that leads to increased sympathetic tone, stimulates renin-angiotensin- aldosterone feedback, and potentiates antidiuretic hormone secretion. These mechanisms serve to increase vasomotor tone and retain salt and water. The resultant increase in systemic vascular resistance and in left ventricular end-diastolic pressure leads to increased myocardial oxygen demand in the face of decreased oxygen delivery. This, in turn, results in worsening left ventricular function, a perceived reduction in circulating blood volume, and repetition of the cycle.

Compressive cardiogenic shock occurs due to extrinsic pressure on the heart, which reduces diastolic filling, thereby impairing cardiac output. Pericardial tamponade, tension pneumothorax, diaphragmatic hernia, mediastinal hematoma, and excessive intraabdominal compartment pressure can lead to compressive (obstructive) cardiogenic shock. Pericardial tamponade is signaled by jugular venous distention, muffled heart tones, and hypotension—Beck’s triad. Pulsus paradoxus, an inspiratory drop in systolic BP of, at least 10 mm Hg, may not be observed in patients on mechanical ventilation. Similarly, equalization of diastolic pressures may not be apparent when the right atrium is being compressed by clot. Both these scenarios complicate the diagnosis of tamponade in the post–cardiopulmonary bypass period.

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Antidiuretic hormone

Figure 7.2. The reduction in cardiac output associated with left-ventricular dysfunction results in a series of compensatory responses that function to maintain blood pressure at the expense of aggravating any disparity in myocardial oxygen demand and supply. This imbalance increases left-ventricular dysfunction and sets up a vicious cycle. (Reprinted from Nathens AB, Maier RV. Shock and resuscitation. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.)

Diagnosing cardiogenic shock involves utilizing the physical exam to look for jugular venous distention, pulmonary edema, an S3 gallop, and evidence of perfusion abnormalities. Clinical and laboratory data suggesting end-organ hypoperfusion include mottled extremities, lactic acidosis, elevation in blood urea nitrogen and creatinine, and oliguria. An immediate electrocardiogram should be obtained, and cardiac enzymes should be drawn to make the diagnosis of myocardial infarction. A chest x-ray gives information regarding the existence of pulmonary edema; arterial blood gas measurement helps determine oxygenation and acid–base status. Echocardiography is invaluable as a noninvasive method for determining ventricular function, wall motion abnormalities, valvular function, and the presence or absence of pericardial fluid. Pulmonary artery catheter placement is useful for ongoing measurement of cardiac function and to gauge the resuscitation.

The therapeutic objective in managing intrinsic cardiogenic shock is to perform general supportive measures (oxygenation/ventilation, electrolyte, and arrhythmia correction) while expediting a diagnostic workup. Intravenous fluid can improve perfusion in the hypovolemic patient. Vasodilators should be used with caution, as they may serve to reduce afterload in cardiogenic shock but also may exacerbate

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hypotension. Inotropes (dobutamine) or pressors (dopamine, norepinephrine) are required in the hemodynamically unstable following or concurrent with volume resuscitation. These medications are administered with the understanding that they also increase myocardial oxygen demand as contractility and systemic vascular resistance are increased. There is no evidence that survival is improved with the use of inotropes or pressors, which are considered only as temporizing measures until a definitive intervention can occur.

An important adjunct to therapy for patients with intrinsic cardiogenic shock is the use of the intraaortic balloon pump (IABP). The IABP device is placed in the thoracic aorta via the femoral artery. It serves to decrease myocardial oxygen demand by augmenting diastolic pressure, improving coronary blood flow, and reducing afterload. The IABP is a means of temporary support for the failing heart while definitive measures are planned.

Treatment of extrinsic cardiogenic shock is directed at relief of the underlying cause: decompression of a tension pneumothorax, repair of a diaphragmatic hernia, evacuation of the mediastinal hematoma, or drainage of the pericardial effusion. Early, rapid diagnosis of the condition leading to compressive cardiogenic shock is imperative in order to decrease morbidity and mortality. Echocardiography is the most sensitive, rapidly available modality to demonstrate pericardial fluid and the need for surgical intervention. In the patient at risk for extrinsic cardiac compression, an echocardiogram should be requested early in the diagnostic workup.

Neurogenic Shock (see Algorithm 7.4)

Neurogenic shock must be differentiated from spinal shock. The former comprises a group of clinical features including bradycardia and hypotension following acute cervical or high thoracic spinal cord injury. The latter term, spinal shock, refers to loss of spinal cord reflexes below the level of cord injury. Neurogenic shock occurs after acute spinal cord transection and is characterized by loss of sympathetic tone, leading to arterial and venous dilatation and hypotension. Persistent, unopposed vagal tone results in severe bradycardia. The patient is generally warm and perfused. In a patient who presents with spinal cord injury and concomitant hypotension, a bleeding source must be ruled out before the symptom complex can be attributed solely to neurologic sources. Pressor support frequently is required in these patients. Continuous infusions of dopamine or epinephrine provide both a- and b-adrenergic support to counteract the bradycardia and hypotension.

Diagnostic and Therapeutic Adjuncts

Pulmonary Artery Catheter

If the cause of the shock state is unclear or if it is multifactorial, the use of a pulmonary artery catheter (PAC) can be useful to help differen-

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Table 7.2. Differential diagnosis of shock states based on hemodynamic parameters.

CVP, central venous pressure; PCWP, pulmonary capillary wedge pressure.

Source: Reprinted from Nathens AB, Maier RV. Shock and resuscitation. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.

further fluid resuscitation if needed or guide the clinician toward other therapies, such as inotropic support. In this scenario, information gained from pulmonary artery catheterization can help guide the use of fluid, inotropes, and pressors.

Other patient groups have been shown to benefit from the use of the PAC. A frequently cited example is the traumatized elderly patient with multiple comorbidities who may have myocardial ischemia or dysfunction either preceding or secondary to the traumatic event. There is compelling evidence that the earlier invasive monitoring can be established in this high-risk patient population, the greater likelihood of improved functional outcome or reduction in morbidity.4 Even young traumatized patients may have a complex clinical picture for which more information is required in order to direct the treatment plan.5 Use of PACs in the critical care setting remains controversial, as there have been questions raised as to the indications for use of invasive monitoring,6 and there have been many reports of associated complications. A meta-analysis of 16 randomized controlled trials of pulmonary artery catheterization found the greatest risk-reduction in surgical patients undergoing PAC-guided therapy.7 Significant design flaws may have created limitations in the collection and analysis of the data in these studies; these flaws will need to be addressed in future trials using PACs. Established indications for use of invasive monitoring are summarized in Table 7.3.

4 McMahon D, Schwab C, et al. Comorbidity and the elderly trauma patient. World J Surg 1996;20:1113–1120; Scalea T, Simon H, et al. Geriatric blunt multitrauma: improved survival with early invasive monitoring. J Trauma 1990;30(2):129–134.

5 Abou-Khalil B, Scalea T, et al. Hemodynamic responses to shock in young trauma patients: the need for invasive monitoring. Crit Care Med 1994;22(4):633–639.

6 Leibowitz A, Beilin Y. Pulmonary artery catheters and outcome in the perioperative period. New Horizons 1997;5(3):214–221.

7 Ivanov R, Allen J, et al. Pulmonary artery catheterization: a narrative and systematic critique of randomized controlled trials and recommendations for the future. New Horizons 1997;5(3):268–276.

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Table 7.3. Indications for invasive monitoring.*

Unresponsive hemodynamic instability Elderly patient

Multiple-trauma patient Suspicion of sepsis

Previous organ dysfunction Cardiac

Pulmonary Renal Hypertensive

High-risk surgery

Use of high levels (10 cm H2O) of peak endexpiratory pressure (PEEP)

* Established indications for the use of arterial lines and Swan-Ganz pulmonary artery catheters. These criteria are met in approximately 15% of patients in a surgical ICU, indicating that most patients can be monitored with less invasive technology.

Source: Reprinted from Livingston D, Machiedo GW. Shock. In: Polk HC Jr, Gardner B, Stone HH, eds. Basic Surgery, 5th ed. St. Louis: Quality Medical Publishing, Inc. 1995, with permission.

Inotropes and Pressors

Under most circumstances of shock, optimal fluid resuscitation should precede the use of pharmacologic agents. Proper management of shock requires optimization of preload, afterload, and myocardial contractility. Inotropic and/or pressor support may be a necessary adjunct in the resuscitation of the patient in shock (Table 7.4).

Dopamine is a biosynthetic precursor of epinephrine that, at low doses (1–3 mg/kg/min), may increase renal blood flow, diuresis, and natriuresis. At higher doses (3–5 mg/kg/min), stimulation of cardiac beta receptors leads to increases in contractility, cardiac output, and, later (5–10 mg/kg/min), heart rate. Above 10 mg/kg/min, alpha activity, with peripheral vasoconstriction, is most prominent.

Dobutamine is a synthetic catecholamine whose predominant effect is to stimulate an increase in cardiac contractility with little increase in heart rate. b2-receptor activation also leads to peripheral vasodilatation. This combination of attributes leads to improved left-ventricular emptying and a reduction in pulmonary capillary wedge pressure. In Case 1, hemorrhagic/hypovolemic shock is excluded, and echocardiography confirms ventricular dysfunction due to myocardial contusion. Dobutamine may be indicated to improve left ventricular function and improve blood pressure.

Epinephrine is both a strong b-adrenergic and an a-receptor stimulant. At lower infusion rates, beta responses lead to increased heart rate and contractility. At higher rates of infusion, alpha effects predominate, resulting in elevation of blood pressure and systemic vascular resistance. Use of epinephrine is limited by its arrhythmogenic properties and its capability to stimulate increased myocardial oxygen requirements.

Norepinephrine exerts both a- and b-adrenergic effects. Beta effects, stimulating myocardial contractility, occur at lower doses, while alpha

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vasoconstrictor effects are noted at higher doses. Norepinephrine is becoming an earlier choice as a pressor agent used for septic shock, once adequate intravascular volume has been restored. In Case 2, despite adequate fluid resuscitation guided by pulmonary artery, broad-spectrum antibiotics, and surgical drainage of appendiceal abscess, the patient remains hypoperfused. Norepinephrine infusion could be initiated for persistent shock.

Multiorgan Dysfunction Syndrome

Shock is the most common precursor to multiorgan dysfunction syndrome (MODS), which is recognized as part of a continuum ranging from systemic inflammatory response syndrome (SIRS) to multiorgan dysfunction, culminating in multiple system organ failure (MSOF) and death. The process may occur with or without a known infectious source. Uncontrolled systemic inflammation plays a significant role in the development of MODS. Extensive microvascular endothelial damage leads to liberation of inflammatory mediators, with subsequent microvascular ischemia, increased permeability, decreased intravascular volume, and hypoperfusion. Without intervention, the process escalates to cause end-organ damage. Mortality ranges from 30% to 50% with single organ failure and increases to 80% with three-organ dysfunction. Mortality is nearly 100% with four dysfunctional organ systems.

Recently, activated protein C (Xigris, Eli Lilly) has been approved for the treatment of severe sepsis. It is the first agent to demonstrate a mortality reduction in patients with severe sepsis. Activated protein C modulates coagulation, fibrinolysis, and inflammation, thus reinstating homeostasis between the major processes driving sepsis. In certain patient populations, risk of bleeding is elevated, and careful attention to patient selection should be given.

There is no specific treatment for MODS. Therapy is directed toward minimizing any stimulus of ongoing infection, ischemia, necrosis, fracture, or other tissue injury. Supportive care includes ensuring adequate oxygenation, ensuring organ perfusion, and reducing the duration of shock. Monitoring the patient for response

Table 7.5. Criteria of adequate perfusion.

Normal mental status

Normal pulse rate (no beta-blockade)

Adequate urine output

Warm, pink skin

No core/extremity temperature gradient

Normal systemic vascular resistance

No lactic acidosis

Normal oxygen extraction ratio

Source: Reprinted from Livingston D, Machiedo GW. Shock. In: Polk HC Jr, Gardner B, Stone HH, eds. Basic Surgery, 5th ed. St. Louis: Quality Medical Publishing, Inc., 1995, with permission.

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to intervention is a crucial part of management. Generally accepted criteria of adequate perfusion—end points of resuscitation—are summarized in Table 7.5.

Summary

Shock, by definition, is a clinical syndrome that develops due to inadequate tissue perfusion. Hypoperfusion results in insufficient delivery of oxygen and nutrients for metabolism, leading to severe vital organ dysfunction. Untreated or undertreated shock may result in multiple organ failure and death. Patients enter into the shock state due to hypovolemia, trauma, sepsis, cardiac dysfunction, or severe neurologic compromise. The physician’s role in patient management is to ensure adequate hemodynamic support first (airway, breathing, circulation), followed by an aggressive search for the etiology of shock. With few exceptions, the first inotrope, the first pressor, should be fluid.

Selected Readings

Abou Khalil B, Scalea T, et al. Hemodynamic responses to shock in young trauma patients: the need for invasive monitoring. Crit Care Med 1994; 22(4):633–639.

Cobb J, Perren. Critical care: a system-oriented approach. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001.

Ivanov R, Allen J, et al. Pumonary artery catheterization: narrative and systematic critique of randomized controlled trials and recommendations for the future. New Horizons 1997;5(3):268–276.

Leibovici L, Drucker M, et al. Septic shock in bacteremic patients: risk factors, features and prognosis. Scand J Infect Dis 1997;20:71–75.

Leibowitz A, Beilin Y. Pulmonary artery catheters and outcome in the perioperative period. New Horizons 1997;5(3):214–221.

McMahon D, Schwab C, et al. Comorbidity and the elderly trauma patient. World J Surg 1996;20:1113–1120.

Nathens AB, Maier RV. Shock and resuscitation. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001.

Parker M, Peruzzi W. Pulmonary artery catheters in sepsis/septic shock. New Horizons 1997;5(3):228–232.

Reviewers CIGA. Human albumin administration in critically ill patient: systematic review of randomized controlled trials. Br Med J 1998;317:235–240.

Scalea T, Simon H, et al. Geriatric blunt multitrauma: improved survival with early invasive monitoring. J Trauma 1990;30(2):129–134.