Shock, a common condition necessitating ICU admission or occurring in the course of critical care, 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 with accompanying lactic acidosis. Since the MAP is the product of cardiac output and systemic vascular resistance (SVR), reductions in blood pressure can be caused by decreases in cardiac output and/or SVR. Accordingly, once shock is contemplated, the initial evaluation of a hypotensive patient should include an early bedside assessment of the adequacy of cardiac output (Fig. 293-2). Clinical evidence of diminished cardiac output includes a narrow pulse pressure (systolic BP minus diastolic BP)—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, it can be inferred that the reduced blood pressure is from decreased SVR.
Approach to the patient in shock. JVP, jugular venous pressure.
In hypotensive patients with signs of reduced cardiac output, an assessment of intravascular 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). Although evidence of a reduced jugular venous pressure (JVP) is often sought, static measures of right atrial pressure do not predict fluid responsiveness reliably; the change in right atrial pressure as a function of spontaneous respiration is a better predictor of fluid responsiveness (Fig. 293-3). Patients with fluid-responsive (i.e., hypovolemic) shock also may manifest large changes in pulse pressure as a function of respiration during mechanical ventilation (Fig. 293-4). A hypotensive patient with increased intravascular volume 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. 298).
Right atrial pressure change during spontaneous respiration in a patient with shock whose cardiac output will increase 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 whose cardiac output will increase 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. 297). Other causes include liver failure, severe pancreatitis, burns, trauma, 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 more than one category can occur simultaneously (e.g., hypovolemic and septic shock).
The initial assessment of a patient in shock should take only a few minutes. It is important that aggressive resuscitation is instituted on the basis of the initial assessment, particularly since early resuscitation from septic and cardiogenic shock may improve survival (see below). If the initial bedside assessment yields equivocal or confounding data, more objective assessments such as ultrasound/echocardiography may be useful. In spontaneously breathing patients, inferior vena cava collapse seen on ultrasound predicts a fluid responsive state. Increasingly, ultrasound of the thorax and abdomen is used by intensivists as an extension of the physical examination to assess rapidly imputed filling volumes, adequacy of cardiac performance, and for indices of other specific conditions (e.g., pericardial tamponade, pulmonary embolus, pulmonary edema, pneumothorax). The goal of aggressive resuscitation is to reestablish adequate tissue perfusion and thus to prevent or minimize end-organ injury.
MECHANICAL VENTILATORY SUPPORT
(See also Chap. 295) During the initial resuscitation of patients in shock, principles of advanced cardiac life support should be followed. As such patients may be obtunded and unable to protect the airway, an early assessment of the airway is mandatory. 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. 298) as well as in those who are in septic shock with pneumonia or acute respiratory distress syndrome (ARDS) (Chaps. 294 and 297). Ventilatory failure often occurs as a consequence of an increased load on the respiratory system in the form of acute metabolic (often lactic) acidosis or decreased lung compliance due to 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, the percentage of cardiac output dedicated to respiratory muscles may increase by tenfold or more. Lactic acid production from inefficient respiratory muscle activity presents an additional ventilatory load.
Mechanical ventilation may relieve the work of breathing and allow redistribution of a limited cardiac output to other vital organs. Patients demonstrate respiratory distress by an 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 due to exhaustion. When patients with shock are treated with mechanical ventilation, a major goal is for the ventilator to assume all or the majority of the 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 include impeded venous return from 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., propofol, opiates). Patients with right heart dysfunction or preexiting pulmonary hypertension may also have diminished cardiac output related to the increases in right ventricular afterload resulting from positive pressure ventilation. Accordingly, hypotension should be anticipated during and following endotracheal intubation. Because many of these patients may be fluid responsive, IV volume administration should be considered. Figure 293-2 summarizes the diagnosis and treatment of different types of shock. For further discussion of individual forms of shock, see Chaps. 296, 297, and 298.