Shock is a common condition necessitating admission to the ICU or occurring in the course of critical care. Shock is defined by the presence of multisystem end organ hypoperfusion. Clinical indicators include reduced mean arterial pressure (MAP), tachycardia, tachypnea, cool skin and extremities, acute altered mental status, and oliguria. Hypotension is usually, though not always, present. The end result of multiorgan hypoperfusion is tissue hypoxia, often clinically manifested by lactic acidosis. Since the MAP is the product of cardiac output and systemic vascular resistance (SVR), reductions in blood pressure can be caused by decreased cardiac output and/or decreased SVR. Accordingly, the initial evaluation of a hypotensive patient should include an assessment of the adequacy of cardiac output; this should be part of the earliest assessment of the patient by the clinician at the bedside once shock is contemplated (Fig. 267-2). Clinical evidence of diminished cardiac output includes a narrow pulse pressure—a marker that correlates with stroke volume—and cool extremities with delayed capillary refill. Signs of increased cardiac output include a widened pulse pressure (particularly with a reduced diastolic pressure), warm extremities with bounding pulses, and rapid capillary refill. If a hypotensive patient has clinical signs of increased cardiac output, one can infer that the reduced blood pressure is a result of decreased SVR.
Approach to patient in shock. EGDT, early goal-directed therapy; JVP, jugular venous pulse.
In hypotensive patients with signs of a reduced cardiac output, an assessment of intravascular and cardiac volume status is appropriate. A hypotensive patient with decreased intravascular volume status may have a history suggesting hemorrhage or other volume losses (e.g., vomiting, diarrhea, polyuria). The jugular venous pressure (JVP) may be reduced in such a patient, although the change in right atrial pressure as a function of spontaneous respiration is a better predictor of fluid responsiveness (Fig. 267-3). Patients with fluid-responsive (i.e., hypovolemic) shock also may manifest large changes in pulse pressure as a function of respiration during positive-pressure mechanical ventilation (Fig. 267-4). A hypotensive patient with increased intravascular volume status and cardiac dysfunction may have S3 and/or S4 gallops on examination, increased JVP, extremity edema, and crackles on lung auscultation. The chest x-ray may show cardiomegaly, widening of the vascular pedicle, Kerley B lines, and pulmonary edema. Chest pain and electrocardiographic changes consistent with ischemia may be noted (Chap. 272).
Right atrial pressure change during spontaneous respiration in a patient with shock who will increase cardiac output in response to intravenous fluid administration. The right atrial pressure decreases from 7 mmHg to 4 mmHg. The horizontal bar marks the time of spontaneous inspiration.
Pulse pressure change during mechanical ventilation in a patient with shock who will increase cardiac output in response to intravenous fluid administration. The pulse pressure (systolic minus diastolic blood pressure) changes during mechanical ventilation in a patient with septic shock.
In hypotensive patients with clinical evidence of increased cardiac output, a search for causes of decreased SVR is appropriate. The most common cause of high cardiac output hypotension is sepsis (Chap. 271). Other causes of high cardiac output hypotension include liver failure, severe pancreatitis, burns and other trauma that elicit the systemic inflammatory response syndrome (SIRS), anaphylaxis, thyrotoxicosis, and peripheral arteriovenous shunts.
In summary, the most common categories of shock are hypovolemic, cardiogenic, and high cardiac output with decreased SVR (high-output hypotension). Certainly these categories may overlap and occur simultaneously (e.g., hypovolemic and septic shock).
The initial assessment of a patient in shock as outlined above should take only a few minutes. It is important that aggressive, early resuscitation is instituted based on the initial assessment, particularly since early resuscitation of septic and cardiogenic shock may improve survival (see below). If the initial bedside assessment yields equivocal or confounding data, more objective assessments such as echocardiography and/or invasive vascular monitoring may be useful. The goal of early resuscitation is to reestablish adequate tissue perfusion to prevent or minimize end organ injury.
Mechanical Ventilatory Support
(See also Chap. 269) During the initial resuscitation of patients in shock, principles of advanced cardiac life support should be followed. Since patients in shock may be obtunded and unable to protect the airway, an early assessment of the patients airway is mandatory during resuscitation from shock. Early intubation and mechanical ventilation often are required. Reasons for the institution of endotracheal intubation and mechanical ventilation include acute hypoxemic respiratory failure and ventilatory failure, which frequently accompany shock. Acute hypoxemic respiratory failure may occur in patients with cardiogenic shock and pulmonary edema (Chap. 272) as well as in those in septic shock with pneumonia or acute respiratory distress syndrome (ARDS) (Chaps. 268 and 271). Ventilatory failure often occurs as a result of an increased load on the respiratory system. This load may present in the form of acute metabolic acidosis (often lactic acidosis) or decreased compliance of the lungs ("stiff" lungs) as a result of pulmonary edema. Inadequate perfusion to respiratory muscles in the setting of shock may be another reason for early intubation and mechanical ventilation. Normally, the respiratory muscles receive a very small percentage of the cardiac output. However, in patients who are in shock with respiratory distress for the reasons listed above, the percentage of cardiac output dedicated to respiratory muscles may increase tenfold or more. Lactic acid production from inefficient respiratory muscle activity presents an additional ventilatory load.
Mechanical ventilation may relieve the patient of the work of breathing and allow redistribution of a limited cardiac output to other vital organs, often with an improvement in lactic acidosis. Patients demonstrate signs of respiratory distress with a number of clinical signs, including inability to speak full sentences, accessory use of respiratory muscles, paradoxical abdominal muscle activity, extreme tachypnea (>40 breaths/min), and decreasing respiratory rate despite an increasing drive to breathe. When patients with shock are treated with mechanical ventilation, a major goal of ventilator settings is to assume all or the majority of work of breathing, facilitating a state of minimal respiratory muscle work. With the institution of mechanical ventilation for shock, further declines in MAP are frequently seen. The reasons for this include impeded venous return with positive-pressure ventilation, reduced endogenous catecholamine secretion once the stress associated with respiratory failure abates, and the actions of drugs used to facilitate endotracheal intubation (e.g., barbiturates, benzodiazepines, opiates), all of which may result in hypotension. Accordingly, hypotension should be anticipated after endotracheal intubation and positive-pressure ventilation. Many of these patients have a component of hypovolemia, which may respond to IV volume administration. Fig. 267-2 summarizes the diagnosis and treatment of different types of shock. For further discussion of individual forms of shock, see Chaps. 270, 271, and 272.