Objectives
Identify the four main categories of shock.
Discuss the goals of resuscitation in shock.
Summarize the general principles of shock management.
Describe the physiologic effects of vasoactive and inotropic agents.
Discuss the differential diagnosis of oliguria.
Case Study
A 25-year-old woman presents to the emergency department complaining of a cough productive of tenacious greenish yellow mucus. Vital signs are temperature 101.8°F (38.8°C), heart rate 129/min, respiratory rate 27/min, and blood pressure 112/68 mm Hg.
– What information is needed to determine if this patient has shock?
– What initial interventions are needed to stabilize the patient?
I. INTRODUCTION
Shock is a syndrome of impaired tissue oxygenation and perfusion due to a variety of etiologies.
Prompt recognition of shock and early, effective intervention is needed to prevent irreversible injury, organ dysfunction, and death. Inadequate tissue oxygenation and perfusion may result from one or more of the following mechanisms:
An absolute or relative decrease in systemic oxygen delivery (inadequate cardiac output, low
blood oxygen content)
Ineffective tissue perfusion (maldistribution of blood flow to tissues or inadequate perfusion pressure)
Impaired utilization of delivered oxygen (cellular or mitochondrial dysfunction)
Shock results when the oxygen balance is disturbed and demand exceeds supply. Shock is not defined by hypotension, although hypotension is frequently associated with shock. In some patients with shock, the blood pressure initially may be normal even though it has significantly dropped from baseline, or it may be preserved due to compensatory sympathetic responses. Management of shock should be directed toward correcting the oxygen balance and hypoperfusion as the primary end points.
II. CLINICAL ALTERATIONS IN SHOCK
The presentation of patients with shock may be subtle (mild confusion, tachycardia) or easily
identifiable (profound hypotension, anuria). Shock may be the initial manifestation of an underlying condition or it may develop as the condition progresses. A strong index of suspicion and vigilant clinical assessment are needed to identify the early signs and initiate appropriate treatment. The clinical manifestations of shock result from inadequate tissue oxygenation and perfusion,
compensatory responses, and the specific etiology of shock. Hypoperfusion of end organs may result in hypotension, altered mental status, oliguria/anuria, and other organ dysfunction. In addition,
hypoperfusion is associated with some degree of inflammatory response that may contribute to organ injury. Direct and indirect effects of hypoperfusion may be reflected in laboratory findings of
abnormal oxygenation, blood urea nitrogen, creatinine, bilirubin, hepatic transaminases, and coagulation parameters. An anion gap metabolic acidosis is one of the most common findings of hypoperfusion. Acidosis is often associated with an elevated lactate concentration. Although neither sensitive nor specific for the diagnosis of shock, the lactate concentration is an indicator of
hypoperfusion and a relevant monitoring tool for assessment of therapeutic interventions.
Compensatory mechanisms in shock involve complex neuroendocrine responses that attempt to increase tissue perfusion and oxygenation. In many forms of shock, sympathetic vasoconstriction redirects blood flow from low-oxygen-requiring organs (eg, skin) toward oxygen-dependent organs (eg, brain and heart). Compensatory vasoconstriction can maintain blood pressure early in shock and
lead to an increase in the diastolic pressure and a narrowing of the pulse pressure. Intense
vasoconstriction correlates with cold, clammy extremities and contributes to organ hypoperfusion.
Hypothermia also may be a manifestation of severe vasoconstriction. Patients with distributive shock (see next section) often have vasodilation and warm extremities, but other signs of hypoperfusion are usually present. Tachycardia, mediated by the sympathetic response, reflects an attempt to increase cardiac output in shock. Tachypnea may be a compensatory response to metabolic acidosis, a response to lung injury, or a reaction to direct stimulation of the respiratory center.
The increased systemic vascular resistance present in cardiogenic, hemorrhagic, and obstructive shock is the body’s attempt to maintain blood pressure (perfusion pressure).
Additional changes in shock alter oxygenation at the tissue level. As discussed in Chapter 6,
hemoglobin releases more oxygen as it traverses the capillaries in order to meet tissue demands. A rightward shift of the oxyhemoglobin saturation curve due to acidosis or increased temperature
facilitates release of hemoglobin-bound oxygen. The greater extraction of oxygen is reflected in lower venous oxyhemoglobin saturation (SVO2) or central venous oxyhemoglobin saturation (ScVO2)
measurements in many forms of shock (Chapter 6). However, a normal value of SVO2 does not imply that tissue oxygenation is adequate because some forms of shock (eg, septic shock) may lead to
impaired tissue or cellular utilization of oxygen or result in maldistribution of blood flow.
III. CLASSIFICATION OF SHOCK
There are four main categories of shock based on cardiovascular characteristics: hypovolemic, distributive, cardiogenic, and obstructive (Table 7-1). A careful history and a physical examination often provide information that is helpful in determining the likely cause of shock. However, many patients will have components of more than one type (mixed shock). Septic shock is a form of distributive shock, but it may have a hypovolemic component before fluid resuscitation. Likewise, myocardial dysfunction may be present in septic shock and hypovolemic shock.
Table 7-1: Classifications of Shock
Knowledge of the expected hemodynamic profiles associated with different types of shock is helpful in determining appropriate therapy, even when specific measurements are not available. Table 7-2 presents the usual hemodynamic profiles for more common forms of shock, but variations occur depending on the patient’s specific etiology, cardiac function, and resuscitation status.
Table 7-2: Hemodynamic Profiles of Shock
Abbreviations: SVO2, mixed venous oxyhemoglobin saturation; N, normal; ScVO2, central venous oxyhemoglobin saturation aMay be decreased prior to or early in resuscitation.
bLeft ventricular filling pressures may be normal or low in massive pulmonary embolism.
A. Hypovolemic Shock
Hypovolemic shock occurs when intravascular volume is depleted relative to the vascular capacity as a result of hemorrhage, gastrointestinal or urinary fluid losses, dehydration, or third-space fluid
losses. Third-space fluid losses resulting from interstitial fluid redistribution may be prominent in burn injury, trauma, pancreatitis, and any severe form of shock. The hemodynamic findings in
hypovolemic shock are decreased cardiac output, decreased right and left ventricular filling pressures (preload), and an increased afterload (systemic vascular resistance [SVR]) due to compensatory
vasoconstriction. The SVO2 or ScVO2 is decreased as a result of decreased cardiac output with
unchanged or increased tissue oxygen demands and potentially decreased hemoglobin concentration (hemorrhage). In addition to the usual clinical findings, patients with hypovolemic shock have flat, nondistended jugular veins.
B. Distributive Shock
Distributive shock is characterized by loss of peripheral vascular tone (vasodilation). However, these patients often have components of hypovolemic shock and cardiogenic shock. The most common form of distributive shock is septic shock, with neurogenic shock and anaphylactic shock being much less common. The hemodynamic profile usually includes a normal or increased cardiac output with a low SVR and low to normal ventricular filling pressures. A consistent finding is increased pulse pressure. A decreased cardiac output may result if intravascular volume is not optimized. ScVO2 or SVO2 may be normal or increased due to shunting of blood in the microvasculature or the inability of tissue to utilize oxygen. In contrast to other forms of shock, the vasodilation of fluid-resuscitated distributive shock results in warm extremities, decreased diastolic pressure, and increased pulse pressure. Neurogenic shock may be associated with bradycardia rather than tachycardia. Fever may be present in septic shock and adrenal crisis.
C. Cardiogenic Shock
In cardiogenic shock, forward blood flow is inadequate because of cardiac pump failure due to loss of functional myocardium (ischemia, cardiomyopathy), a mechanical or structural defect (valvular failure, septal defect), or arrhythmias. Most commonly, cardiogenic shock results from acute
myocardial infarction or a subsequent complication. Cardiogenic shock is the most severe form of heart failure and is distinguished from less severe chronic heart failure by the presence of
hypoperfusion, hypotension, and the need for different therapeutic interventions (Chapter 10). The typical hemodynamic characteristics are decreased cardiac output, elevated ventricular filling pressures, and increased afterload (SVR). When cardiac output is low, the SVO2 or ScVO2 declines due to increased extraction of oxygen from hemoglobin at the tissue level. Clinical manifestations associated with cardiogenic shock may include distended jugular veins, pulmonary edema, and S3 gallop.
Anterior myocardial infarctions are more likely to lead to cardiogenic shock.
D. Obstructive Shock
The common features in obstructive shock are obstruction to flow due to impaired cardiac filling and excessive afterload. Cardiac tamponade and constrictive pericarditis impair diastolic filling of the right ventricle, while tension pneumothorax limits right ventricular filling by obstruction of venous return. Massive pulmonary emboli increase right ventricular afterload. The hemodynamic profile is characterized by decreased cardiac output, increased afterload, and variable left ventricular filling pressures, depending on the etiology. In cardiac tamponade, the pressures of the right heart chambers, the pulmonary artery, and the left heart chambers equilibrate in diastole. A drop of >10 mm Hg in systolic blood pressure during inspiration (pulsus paradoxus) is an important clinical finding in patients with suspected cardiac tamponade. Distended jugular veins may be seen, depending on the time course of development and intravascular volume status.