Hypovolemic shock is the most common form of shock. Almost all forms include some component of hypovolemia as a result of decreased intravascular volume or “preload.” The sympathetic response to reduced preload is arterial vasoconstriction, diverting blood from the splanchnic viscera, skin, and skeletal muscle. Physical findings include cold clammy skin, tachypnea, tachycardia, and low urinary output, all a result of either hypovolemia or compensatory mechanisms.

Hypovolemic shock is stratified into four classes based on the degree of circulating volume loss (Table 157.1). It is important to recognize that significant blood volume may be lost in the absence of any clinical signs. Compensatory mechanisms allow systemic blood pressure to be maintained and a well-compensated patient may display tachycardia as the only objective clinical abnormality, even with a blood volume loss of up to 30%. Hypovolemic shock may be further subclassified as either hemorrhagic or nonhemorrhagic. Hemorrhagic shock may be visibly apparent (external blood loss from traumatic injury) or occult (chronic gastrointestinal hemorrhage). Emphasis on hemorrhage control rather than simply volume replacement is an essential difference in the management of hemorrhagic shock [11,12]. Nonhemorrhagic hypovolemic shock is seen in a number of pathologic states and may be caused by absolute loss of total body fluid volume and/or migration of acellular fluid from the intravascular to the interstitial compartment (third spacing). Third spacing of fluid occurs predictably in severe illnesses such as pancreatitis, small bowel obstruction, and burns. Volume depletion may also occur as a consequence of uncompensated gastrointestinal, urinary, or evaporative losses. It is imperative that the intensivists focus on resuscitation of the patient’s intravascular volume as opposed to total body volume. Failure to do so will uniformly result in under-resuscitation and poor patient outcome.

Obstructive forms of shock are those in which the underlying pathology is a mechanical obstruction to normal cardiac output (CO) with a resulting diminution in systemic perfusion. Cardiac tamponade is an example of obstructive shock. A small amount of fluid (usually less than 200 mL) within a noncompliant pericardium may produce significant myocardial compression [13]. Clinical signs of tamponade include jugular venous distention and a central venous pressure (CVP) waveform
demonstrating a rapid “x” descent and a blunted “y” descent due to inability of the heart to fill during diastole. Pulsus paradoxus, an exaggerated fluctuation in arterial pressure caused by changes in intrathoracic pressure during respiration, may be present. Formal echocardiography is helpful in making the diagnosis although recent advances in the use of bedside ultrasonography by noncardiologists have demonstrated excellent sensitivity and rapid performance of the examination [14].

Pulmonary venous thromboembolism is another example of obstructive shock and may present as profound circulatory collapse. CO is restricted either by mechanical obstruction of the pulmonary arterial tree or by pulmonary hypertension induced by release of secondary mediators. Additional findings include elevated CVP and pulmonary hypertension, but normal pulmonary artery occlusion pressure (PAOP). Through similar mechanisms, venous air embolism can completely obstruct pulmonary arterial blood flow, with ensuing cardiac arrest. Central hemodynamics mimic those of pulmonary embolism. Although numerous causes exist, of greatest concern are the placement and removal of central venous catheters and surgical procedures in which the operative site is more than 5 cm above the right atrium [15]. Venous air embolism is diagnosed by auscultation of the classic “mill wheel” heart murmur. Immediate placement of the patient in a head-down, left lateral decubitus position is advocated, as are attempts to aspirate air from the right ventricle through a central venous catheter.

Finally, tension pneumothorax may cause shock through obstruction of venous return. Elevated intrapleural pressure collapses intrathoracic veins resulting in inadequate venous filling. Tension pneumothorax should be diagnosed by physical examination and not by radiography. Needle decompression often restores venous filling sufficiently until a thoracostomy tube can be placed.

In cardiogenic shock, the underlying defect is primary ventricular pump failure, the most common cause of coronary artery disease related mortality. The foundations of ventricular failure include (a) myocardial infarction with loss of myocardium, (b) reduced contractility (cardiomyopathy), (c) ventricular outflow obstruction (aortic stenosis or dissection), (d) ventricular filling anomalies (atrial myxoma, mitral stenosis), (e) acute valvular failure (aortic or mitral regurgitation), (f) cardiac dysrhythmias, and (g) ventriculoseptal defects. Most often, cardiogenic shock is a direct or indirect consequence of acute myocardial infarction.

Cardiogenic shock due to left ventricular infarction suggests that more than 40% of the left ventricle is involved [16]. On physical examination, signs of peripheral vasoconstriction are evident and oliguria is common. The typical hemodynamic profile includes systemic hypotension with decreased CO and elevated PAOP. Physical examination findings of pulmonary and peripheral edema as well as hepatomegaly may suggest volume overload, but are commonly due to third spacing of fluid due to shock with relative intravascular volume depletion being present. In such situations, hemodynamic monitoring using echocardiography or a volumetric pulmonary artery catheter may provide additional diagnostic information clarifying the patient’s true volume status.

Right ventricular dysfunction as a consequence of inferior wall myocardial infarction carries a better prognosis than left-sided failure. Diagnosis may be suggested by elevated right ventricular diastolic pressure with decreased pulmonary artery pressure [17]. Hypotension caused by right-sided heart failure must be distinguished from left-sided failure because of the significant differences in their management. Shock from right-sided failure is corrected by volume resuscitation to maintain right ventricular preload while left-sided failure is treated by volume restriction to reduce myocardial work. If inotropes are indicated, agents that do not increase pulmonary vascular resistance should be chosen [18].

Dysrhythmias are another source of cardiogenic shock. In addition to malignant dysrhythmias, such as ventricular fibrillation, atrial dysrhythmias such as atrial fibrillation or flutter as well as supraventricular tachycardia are common in the critically ill and may result in shortened diastolic filling time with a profound decrease in CO.

The classic hemodynamic profile of septic shock (high CO and systemic hypotension) has prompted some clinicians to institute antimicrobial therapy and search for an infectious source in any patient who exhibits these cardiac parameters. Such hyperdynamic patterns, however, are seen in non-infectious conditions as well including anaphylaxis, spinal cord injury, and severe liver dysfunction. The term distributive shock, rather than septic shock, is therefore used to account for these dissimilar diseases with a common hemodynamic picture.

The management of septic shock remains a major challenge to the intensivist [1,2,3]. A milieu of inflammatory cytokines, bacterial factors, and complement and coagulation activation combine to induce the complex hemodynamic pattern characteristic of septic shock. In most forms of shock, illness leads to a low CO state with elevated systemic vascular resistance (SVR) and reduced mixed venous oxygen saturation (SvO₂). Early septic shock, however, is manifested by normal-to-low cardiac filling pressures, increased CO, decreased SVR, and increased SvO₂ [19]. Despite elevated systemic blood flow and oxygen delivery (DO₂), abnormalities exist in tissue oxygen extraction at the cellular level, perhaps through disruption of normal mitochondrial metabolic pathways [20,21]. Sepsis-induced myocardial depression may be demonstrated through decreased ejection fraction, right ventricular dysfunction, and left ventricular dilation. In the later stages of septic shock, cardiac function deteriorates with the patient’s hemodynamic status mimicking that of cardiogenic shock with decreased CO and increased SVR [22].

Anaphylaxis represents another form of distributive shock in which histamine-mediated vasodilatation occurs. The most common causes are medications, insect envenomations, blood products, radiographic contrast media, and food allergies [23]. Reactions severe enough to result in shock occur shortly after exposure to the offending agent. Physical findings include a dermatologic reaction (erythema, urticaria) and obstructive respiratory processes. Occasionally, the reaction is severe enough to produce shock through myocardial depression.

Neurogenic shock, another form of distributive shock, occurs as a result of upper thoracic spinal cord injury with hypotension, bradycardia, and warm, dry skin due to loss of sympathetic vascular tone. Although euvolemic, patients demonstrate relative hypovolemia due to vasodilatation of the intravascular space. If hypotension does not respond to volume resuscitation, it may be treated with vasopressors and any bradycardia may be corrected with atropine. In the trauma patient, hemorrhage should always be excluded before attributing shock to a neurogenic source [24].

Over the last decade, endocrine insufficiency as a result of critical illness has been recognized as an underappreciated cause of distributive shock. This relative adrenal insufficiency may worsen the impact of the various shock states as the patient is unable to respond appropriately to the stress of their critical illness [25,26]. Corticosteroid supplementation in such
patients can significantly improve systemic perfusion as well as reduce the patient’s requirement for vasopressor support.

The diagnosis of shock was originally based on abnormalities in a patient’s vital signs. Until the late 1960s, the presence of tachycardia and hypotension was considered synonymous with shock. Over time, it became apparent that normalization of heart rate, blood pressure, temperature, and urinary output was not necessarily sufficient to reverse a patient’s shock state. Critically ill patients continued to have a high incidence of multiple organ failure and mortality despite seemingly adequate resuscitation based on restoration of vital signs to “normal.” Shock is therefore defined by the adequacy of end-organ perfusion rather than derangements in vital signs alone. Nevertheless, these physiologic parameters remain the foundation for the initial recognition that shock is present.

In 1970, Swan and Ganz introduced the flow-directed pulmonary artery catheter, allowing clinicians to measure pulmonary artery pressures at the bedside [34]. In 1972, addition of a temperature thermistor provided the ability to calculate CO. These advancements provided clinicians with the ability to assess a variety of new hemodynamic parameters evaluating patient preload, contractility, and afterload. In the 1980s, continuous mixed venous oximetry was added as the importance of DO₂, [V with dot above]O₂, and oxygen transport balance in the diagnosis and management of the shock states became clear. By the early 1990s, catheters capable of calculating right ventricular volumes became available, further improving preload assessment. Current pulmonary artery catheters continuously assess hemodynamic and oxygen transport variables providing the clinician with minute-by-minute assessments of cardiopulmonary function by which to guide resuscitation. Although pulmonary artery catheterization is performed with much less frequency than in years past, it remains an important
monitoring technology for the most critically ill patients with shock and has recently been demonstrated to improve patient outcome when used in a goal-directed fashion [35,36]. A variety of other hemodynamic monitoring techniques have been developed including arterial pressure wave contour analysis, esophageal Doppler, and transesophageal echocardiography among others. Regardless of the method by which hemodynamic data is obtained, a thorough understanding of the available hemodynamic and oxygenation variables is essential if resuscitative therapy is to improve patient outcome from shock (Tables 157.2 and 157.3) [37].