Shock is the clinical syndrome that results from inadequate tissue perfusion. Irrespective of cause, the hypoperfusion-induced imbalance between the delivery of and requirements for oxygen and substrate leads to cellular dysfunction. The cellular injury created by the inadequate delivery of oxygen and substrates also induces the production and release of inflammatory mediators that further compromise perfusion through functional and structural changes within the microvasculature. This leads to a vicious circle in which impaired perfusion is responsible for cellular injury, which causes maldistribution of blood flow, further compromising cellular perfusion; the latter causes multiple organ failure and, if the process is not interrupted, leads to death. The clinical manifestations of shock are the result, in part, of autonomic neuroendocrine responses to hypoperfusion as well as the breakdown in organ function induced by severe cellular dysfunction (Fig. 264-1).
When very severe and/or persistent, inadequate oxygen delivery leads to irreversible cell injury; thus, only rapid restoration of oxygen delivery can reverse the progression of the shock state. The fundamental approach to management, therefore, is to recognize overt and impending shock in a timely fashion and to intervene emergently to restore perfusion. This often requires the expansion or reexpansion of intravascular blood volume. Control of any inciting pathologic process, e.g., continued hemorrhage, impairment of cardiac function, or infection, must occur simultaneously.
Clinical shock is usually accompanied by hypotension, i.e., a mean arterial pressure less than 60 mmHg in previously normotensive persons. Multiple classification schemes have been developed in an attempt to synthesize the seemingly dissimilar processes leading to shock. Strict adherence to a classification scheme may be difficult from a clinical standpoint because of the frequent combination of two or more causes of shock in any individual patient, but the classification shown in Table 264-1 provides a useful reference point from which to discuss and further delineate the underlying processes.
Pathogenesis and Organ Response
Normally when cardiac output falls, systemic vascular resistance rises to maintain a level of systemic pressure that is adequate for perfusion of the heart and brain at the expense of other tissues such as muscle, skin, and especially the gastrointestinal tract. Systemic vascular resistance is determined primarily by the luminal diameter of arterioles. The metabolic rates of the heart and brain are high, and their stores of energy substrate are low. These organs are critically dependent on a continuous supply of oxygen and nutrients, and neither tolerates severe ischemia for more than brief periods. Autoregulation, i.e., the maintenance of blood flow over a wide range of perfusion pressures, is critical in sustaining cerebral and coronary perfusion despite significant hypotension. However, when mean arterial pressure drops to 60 mmHg, flow to these organs falls, and their function deteriorates.
Arteriolar vascular smooth muscle has both - and -adrenergic receptors. The 1 receptors mediate vasoconstriction, while the 2 receptors mediate vasodilation. Efferent sympathetic fibers release norepinephrine, which acts primarily on 1 receptors in one of the most fundamental compensatory responses to reduced perfusion pressure. Other constrictor substances that are increased in most forms of shock include angiotensin II, vasopressin, endothelin 1, and thromboxane A2. Both norepinephrine and epinephrine are released by the adrenal medulla, and the concentrations of these catecholamines in the bloodstream rise. Circulating vasodilators in shock include prostacyclin [prostaglandin (PG) I2], nitric oxide (NO), and, importantly, products of local metabolism such as adenosine that match flow to the tissue's metabolic needs. The balance between these various vasoconstrictor and vasodilator influences acting upon the microcirculation determines local perfusion.
Transport to cells depends on microcirculatory flow; capillary permeability; the diffusion of oxygen, carbon dioxide, nutrients, and products of metabolism through the interstitium; and the exchange of these products across cell membranes. Impairment of the microcirculation, which is central to the pathophysiologic responses in the late stages of all forms of shock, results in the derangement of cellular metabolism, which is ultimately responsible for organ failure.
The endogenous response to mild or moderate hypovolemia is an attempt at restitution of intravascular volume through alterations in hydrostatic pressure and osmolarity. Constriction of arterioles leads to reductions in both the capillary hydrostatic pressure and the number of capillary beds perfused, thereby limiting the capillary surface area across which filtration occurs. When filtration is reduced while intravascular oncotic pressure remains constant or rises, there is net reabsorption of fluid into the vascular bed, in accord with Starling's law of capillary-interstitial liquid exchange. Metabolic changes (including hyperglycemia and elevations in the products of glycolysis, lipolysis, and proteolysis) raise extracellular osmolarity, leading to an osmotic gradient between cells and interstitium that increases interstitial and intravascular volume at the expense of intracellular volume.
Interstitial transport of nutrients is impaired in shock, leading to a decline of intracellular high-energy phosphate stores. Mitochondrial dysfunction and uncoupling of oxidative phosphorylation are the most likely causes for decreased amounts of ATP. As a consequence, there is an accumulation of hydrogen ions, lactate, and other products of anaerobic metabolism. As shock progresses, these vasodilator metabolites override vasomotor tone, causing further hypotension and hypoperfusion. Dysfunction of cell membranes is thought to represent a common end-stage pathophysiologic pathway in the various forms of shock. Normal cellular transmembrane potential falls, and there is an associated increase in intracellular sodium and water, leading to cell swelling, which interferes further with microvascular perfusion. In a preterminal event, homeostasis of calcium via membrane channels is lost with flooding of calcium intracellularly and a concomitant extracellular hypocalcemia. There is also increasing evidence for a widespread but selective apoptotic loss of cells, contributing to organ and immune failure.
Hypovolemia, hypotension, and hypoxia are sensed by baroreceptors and chemoreceptors, which contribute to an autonomic response that attempts to restore blood volume, maintain central perfusion, and mobilize metabolic substrates. Hypotension disinhibits the vasomotor center, resulting in increased adrenergic output and reduced vagal activity. Release of norepinephrine from adrenergic neurons induces peripheral and splanchnic vasoconstriction, a major contributor to the maintenance of central organ perfusion, while reduced vagal activity increases the heart rate and cardiac output. Vagal tone is also recognized to downregulate the innate immunity inflammatory response. The effects of circulating epinephrine released by the adrenal medulla in shock are largely metabolic, causing increased glycogenolysis and gluconeogenesis and reduced pancreatic insulin release. Epinephrine also inhibits production and release of inflammatory mediators through stimulation of -adrenergic receptors on innate immune cells.
Severe pain and other severe stress cause the hypothalamic release of adrenocorticotropic hormone (ACTH). This stimulates cortisol secretion, which contributes to decreased peripheral uptake of glucose and amino acids, enhances lipolysis, and increases gluconeogenesis. Increased pancreatic secretion of glucagon during stress accelerates hepatic gluconeogenesis and further elevates blood glucose concentration. These hormonal actions act synergistically to increase blood glucose in the maintenance of blood volume. Many critically ill patients have recently been shown to exhibit low plasma cortisol levels and an impaired response to ACTH stimulation. Low levels of cortisol in response to stimulation are linked to a decrease in survival. The importance of the cortisol response to stress is illustrated by the profound circulatory collapse that occurs in patients with adrenal cortical insufficiency .
Renin release is increased in response to adrenergic discharge and reduced perfusion of the juxtaglomerular apparatus in the kidney. Renin induces the formation of angiotensin I, which is then converted to angiotensin II, an extremely potent vasoconstrictor and stimulator of aldosterone release by the adrenal cortex and of vasopressin by the posterior pituitary. Aldosterone contributes to the maintenance of intravascular volume by enhancing renal tubular reabsorption of sodium, resulting in the excretion of a low-volume, concentrated, sodium-free urine. Vasopressin has a direct action on vascular smooth muscle, contributing to vasoconstriction, and acts on the distal renal tubules to enhance water reabsorption.
Three variables—ventricular filling (preload), the resistance to ventricular ejection (afterload), and myocardial contractility—are paramount in controlling stroke volume. Cardiac output, the major determinant of tissue perfusion, is the product of stroke volume and heart rate. Hypovolemia leads to decreased ventricular preload, which in turn reduces the stroke volume. An increase in heart rate is a useful but limited compensatory mechanism to maintain cardiac output. A shock-induced reduction in myocardial compliance is frequent, reducing ventricular end-diastolic volume and hence stroke volume at any given ventricular filling pressure. Restoration of intravascular volume may return stroke volume to normal but only at elevated filling pressures. Increased filling pressures also stimulate release of brain natriuretic peptide (BNP) to secrete sodium and volume to relieve the pressure on the heart. Levels of BNP correlate with outcome following severe stress. In addition, sepsis, ischemia, myocardial infarction, severe tissue trauma, hypothermia, general anesthesia, prolonged hypotension, and acidemia may all impair myocardial contractility and also reduce the stroke volume at any given ventricular end-diastolic volume. The resistance to ventricular ejection is significantly influenced by the systemic vascular resistance, which is elevated in most forms of shock. However, resistance is depressed in the early hyperdynamic stage of septic shock, thereby initially allowing the cardiac output to be maintained or elevated.
The venous system contains nearly two-thirds of the total circulating blood volume, most in the small veins, and serves as a dynamic reservoir for autoinfusion of blood. Active venoconstriction as a consequence of -adrenergic activity is an important compensatory mechanism for the maintenance of venous return and therefore of ventricular filling during shock. On the other hand, venous dilatation, as occurs in neurogenic shock, reduces ventricular filling and hence stroke volume and cardiac output (see below).
The response of the pulmonary vascular bed to shock parallels that of the systemic vascular bed, and the relative increase in pulmonary vascular resistance, particularly in septic shock, may exceed that of the systemic vascular resistance. Shock-induced tachypnea reduces tidal volume and increases both dead space and minute ventilation. Relative hypoxia and the subsequent tachypnea induce a respiratory alkalosis. Recumbency and involuntary restriction of ventilation secondary to pain reduce functional residual capacity and may lead to atelectasis. Shock is recognized as a major cause of acute lung injury and subsequent acute respiratory distress syndrome (ARDS). These disorders are characterized by noncardiogenic pulmonary edema secondary to diffuse pulmonary capillary endothelial and alveolar epithelial injury, hypoxemia, and bilateral diffuse pulmonary infiltrates. Hypoxemia results from perfusion of underventilated and nonventilated alveoli. Loss of surfactant and lung volume in combination with increased interstitial and alveolar edema reduces lung compliance. The work of breathing and the oxygen requirements of respiratory muscles increase.
Acute renal failure, a serious complication of shock and hypoperfusion, occurs less frequently than heretofore because of early aggressive volume repletion. Acute tubular necrosis is now more frequently seen as a result of the interactions of shock, sepsis, the administration of nephrotoxic agents (such as aminoglycosides and angiographic contrast media), and rhabdomyolysis; the latter may be particularly severe in skeletal muscle trauma. The physiologic response of the kidney to hypoperfusion is to conserve salt and water. In addition to decreased renal blood flow, increased afferent arteriolar resistance accounts for diminished glomerular filtration rate, which together with increased aldosterone and vasopressin is responsible for reduced urine formation. Toxic injury causes necrosis of tubular epithelium and tubular obstruction by cellular debris with back-leak of filtrate. The depletion of renal ATP stores that occurs with prolonged renal hypoperfusion contributes to subsequent impairment of renal function.
During shock, there is disruption of the normal cycles of carbohydrate, lipid, and protein metabolism. Through the citric acid cycle, alanine in conjunction with lactate (which is converted from pyruvate in the periphery in the presence of oxygen deprivation) enhances the hepatic production of glucose. With reduced availability of oxygen, the breakdown of glucose to pyruvate and ultimately lactate represents an inefficient cycling of substrate with minimal net energy production. An elevated plasma lactate/pyruvate ratio is consistent with anaerobic metabolism and reflects inadequate tissue perfusion. Decreased clearance of exogenous triglycerides coupled with increased hepatic lipogenesis causes a significant rise in serum triglyceride concentrations. There is increased protein catabolism, a negative nitrogen balance, and, if the process is prolonged, severe muscle wasting.
Activation of an extensive network of proinflammatory mediator systems plays a significant role in the progression of shock and contributes importantly to the development of organ injury and failure (Fig. 264-2). In those surviving the acute insult, there is a delayed endogenous counterregulatory response to "turn off" the excessive proinflammatory response. If balance is restored, the patient does well. If the immunosuppressive response is excessive, the patient is highly susceptible to secondary nosocomial infections, which can then drive the inflammatory response and lead to delayed multiple organ failure.
Multiple humoral mediators are activated during shock and tissue injury. The complement cascade, activated through both the classic and alternate pathways, generates the anaphylatoxins C3a and C5a. Direct complement fixation to injured tissues can progress to the C5-C9 attack complex, causing further cell damage. Activation of the coagulation cascade causes microvascular thrombosis, with subsequent fibrinolysis leading to repeated episodes of ischemia and reperfusion. Components of the coagulation system, such as thrombin, are potent proinflammatory mediators that cause expression of adhesion molecules on endothelial cells and activation of neutrophils, leading to microvascular injury. Coagulation also activates the kallikrein-kininogen cascade, contributing to hypotension.
Eicosanoids are vasoactive and immunomodulatory products of arachidonic acid metabolism that include cyclooxygenase-derived PGs and thromboxane A2 as well as lipoxygenase-derived leukotrienes and lipoxins. Thromboxane A2 is a potent vasoconstrictor that contributes to the pulmonary hypertension and acute tubular necrosis of shock. PGI2 and PGE2 are potent vasodilators that enhance capillary permeability and edema formation. The cysteinyl leukotrienes LTC4 and LTD4 are pivotal mediators of the vascular sequelae of anaphylaxis as well as of shock states resulting from sepsis or tissue injury. LTB4 is a potent neutrophil chemoattractant and secretagogue that stimulates the formation of reactive oxygen species. Platelet-activating factor, an ether-linked, arachidonyl-containing phospholipid mediator, causes pulmonary vasoconstriction, bronchoconstriction, systemic vasodilation, increased capillary permeability, and the priming of macrophages and neutrophils to produce enhanced levels of inflammatory mediators.
Tumor necrosis factor (TNF-), produced by activated macrophages, reproduces many components of the shock state, including hypotension, lactic acidosis, and respiratory failure. Interleukin 1 (IL-1), produced by tissue-fixed macrophages, is critical to the inflammatory response. Both are significantly elevated immediately following trauma and shock. IL-6, also produced predominantly by the macrophage, has a slightly delayed peak response but is the best predictor of prolonged recovery and development of multiple organ failure following shock. Chemokines such as IL-8 are potent neutrophil chemoattractants and activators that upregulate adhesion molecules on the neutrophil to enhance aggregation, adherence, and damage to the vascular endothelium. While the endothelium normally produces NO, the inflammatory response stimulates the inducible isoform of NO synthase (iNOS), which is overexpressed and produces toxic nitrosyl- and oxygen-derived free radicals that contribute to the hyperdynamic cardiovascular response in sepsis.
Multiple inflammatory cells, including neutrophils, macrophages, and platelets, are a major contributor to inflammation-induced injury. Margination of activated neutrophils in the microcirculation is a common pathologic finding in shock, causing secondary injury due to the release of toxic oxygen radicals, lipases, and proteases. Tissue-fixed macrophages produce virtually all major components of the inflammatory response and orchestrate the progression and duration of the inflammatory response. A major source of activation of the monocyte/macrophage is through the highly conserved membrane Toll-like receptors (TLRs), which recognize damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) released following tissue injury and by pathogenic microbial organisms, respectively. TLRs also appear important for the chronic inflammation seen in Crohn's disease, ulcerative colitis, and transplant rejection
Approach to the Patient: Shock
Patients in shock require care in an intensive care unit. Careful and continuous assessment of the physiologic status is necessary. Arterial pressure through an indwelling line, pulse, and respiratory rate should be monitored continuously; a Foley catheter should be inserted to follow urine flow; and mental status should be assessed frequently. Sedated patients should be allowed to awaken ("drug holiday") daily to assess their neurologic status and to shorten duration of ventilator support.
There is ongoing debate as to the indications for using the flow-directed pulmonary artery catheter (PAC, Swan-Ganz catheter). Most patients in the intensive care unit can be safely managed without the use of a PAC. However, in patients with significant ongoing blood loss, fluid shifts, and underlying cardiac dysfunction, a PAC may be useful. The PAC is placed percutaneously via the subclavian or jugular vein through the central venous circulation and right heart into the pulmonary artery. There are ports both proximal in the right atrium and distal in the pulmonary artery to provide access for infusions and for cardiac output measurements. Right atrial and pulmonary artery pressures are measured, and the pulmonary capillary wedge pressure (PCWP) serves as an approximation of the left atrial pressure. Normal hemodynamic parameters are shown in Table 223-1 and Table 264-2.
Note: HR, heart rate; BSA, body surface area; MAP, mean arterial pressure; RAP, right atrial pressure; PAPm, pulmonary artery pressure—mean; PCWP, pulmonary capillary wedge pressure.
Cardiac output is determined by the thermodilution technique, and high-resolution thermistors can also be used to determine right ventricular end-diastolic volume to monitor further the response of the right heart to fluid resuscitation. A PAC with an oximeter port offers the additional advantage of on-line monitoring of the mixed venous oxygen saturation, an important index of tissue perfusion. Systemic and pulmonary vascular resistances are calculated as the ratio of the pressure drop across these vascular beds to the cardiac output . Determinations of oxygen content in arterial and venous blood, together with cardiac output and hemoglobin concentration, allow calculation of oxygen delivery, oxygen consumption, and oxygen-extraction ratio (Table 264-3). The hemodynamic patterns associated with the various forms of shock are shown in Table 264-4.
Note: PO2, partial pressure of oxygen; SaO2, saturation of hemoglobin with O2 in arterial blood; PaO2, partial pressure of O2 in arterial blood; SvO2, saturation of hemoglobin with O2 in venous blood; PvO2, partial pressure of O2 in venous blood; CO, cardiac output; BSA, body surface area.
Note: CVP, central venous pressure; PCWP, pulmonary capillary wedge pressure.
In resuscitation from shock, it is critical to restore tissue perfusion and optimize oxygen delivery, hemodynamics, and cardiac function rapidly. A reasonable goal of therapy is to achieve normal mixed venous oxygen saturation and arteriovenous oxygen-extraction ratio. To enhance oxygen delivery, red cell mass, arterial oxygen saturation, and cardiac output may be augmented singly or simultaneously. An increase in oxygen delivery not accompanied by an increase in oxygen consumption implies that oxygen availability is adequate and that oxygen consumption is not flow-dependent. Conversely, an elevation of oxygen consumption with increased cardiac output implies that the oxygen supply was inadequate. A reduction in systemic vascular resistance accompanying an increase in cardiac output indicates that compensatory vasoconstriction is reversing due to improved tissue perfusion. The determination of stepwise expansion of blood volume on cardiac performance allows identification of the optimum preload (Starling's law). An algorithm for the resuscitation of the patient in shock is shown in Fig. 264-3.
This most common form of shock results either from the loss of red blood cell mass and plasma from hemorrhage or from the loss of plasma volume alone arising from extravascular fluid sequestration or gastrointestinal, urinary, and insensible losses. The signs and symptoms of nonhemorrhagic hypovolemic shock are the same as those of hemorrhagic shock, although they may have a more insidious onset. The normal physiologic response to hypovolemia is to maintain perfusion of the brain and heart while restoring an effective circulating blood volume. There is an increase in sympathetic activity, hyperventilation, collapse of venous capacitance vessels, release of stress hormones, and an attempt to limit the loss of intravascular volume through the recruitment of interstitial and intracellular fluid and reduction of urine output.
Mild hypovolemia (20% of the blood volume) generates mild tachycardia but relatively few external signs, especially in a supine resting young patient (Table 264-5). With moderate hypovolemia (~20–40% of the blood volume), the patient becomes increasingly anxious and tachycardic; although normal blood pressure may be maintained in the supine position, there may be significant postural hypotension and tachycardia. If hypovolemia is severe (40% of the blood volume), the classic signs of shock appear; the blood pressure declines and becomes unstable even in the supine position, and the patient develops marked tachycardia, oliguria, and agitation or confusion. Perfusion of the central nervous system is well maintained until shock becomes severe. Hence, mental obtundation is an ominous clinical sign. The transition from mild to severe hypovolemic shock can be insidious or extremely rapid. If severe shock is not reversed rapidly, especially in elderly patients and those with comorbid illnesses, death is imminent. A very narrow time frame separates the derangements found in severe shock that can be reversed with aggressive resuscitation from those of progressive decompensation and irreversible cell injury.
Hypovolemic shock is readily diagnosed when there are signs of hemodynamic instability and the source of volume loss is obvious. The diagnosis is more difficult when the source of blood loss is occult, as into the gastrointestinal tract, or when plasma volume alone is depleted. After acute hemorrhage, hemoglobin and hematocrit values do not change until compensatory fluid shifts have occurred or exogenous fluid is administered. Thus, an initial normal hematocrit does not disprove the presence of significant blood loss. Plasma losses cause hemoconcentration, and free water loss leads to hypernatremia. These findings should suggest the presence of hypovolemia.
It is essential to distinguish between hypovolemic and cardiogenic shock because definitive therapy differs significantly. Both forms are associated with a reduced cardiac output and a compensatory sympathetic mediated response characterized by tachycardia and elevated systemic vascular resistance. However, the findings in cardiogenic shock of jugular venous distention, rales, and an S3 gallop distinguish it from hypovolemic shock and signify that ongoing volume expansion is undesirable.
Hypovolemic Shock: Treatment
Initial resuscitation requires rapid reexpansion of the circulating intravascular blood volume along with interventions to control ongoing losses. In accordance with Starling's law, stroke volume and cardiac output rise with the increase in preload. After resuscitation, the compliance of the ventricles may remain reduced due to increased interstitial fluid in the myocardium. Therefore elevated filling pressures are required to maintain adequate ventricular performance.
Volume resuscitation is initiated with the rapid infusion of isotonic saline (although care must be taken to avoid hyperchloremic acidosis from loss of bicarbonate buffering capacity and replacement with excess chloride) or a balanced salt solution such as Ringer's lactate through large-bore intravenous lines. No distinct benefit from the use of colloid has been demonstrated, and in trauma patients it is associated with a higher mortality, particularly in patients with traumatic brain injury. The infusion of 2–3 L of salt solution over 20–30 min should restore normal hemodynamic parameters. Continued hemodynamic instability implies that shock has not been reversed and/or that there are significant ongoing blood or volume losses. Continuing blood loss, with hemoglobin concentrations declining to 100 g/L (10 g/dL), should initiate blood transfusion, preferably as fully cross-matched blood. In extreme emergencies, type-specific or O-negative packed red cells may be transfused. In the presence of severe and/or prolonged hypovolemia, inotropic support with dopamine, vasopressin, or dobutamine may be required to maintain adequate ventricular performance after blood volume has been restored. Infusion of norepinephrine to increase arterial pressure by raising peripheral resistance is inappropriate, other than as a temporizing measure in severe shock while blood volume is reexpanded. Once hemorrhage is controlled and the patient has stabilized, blood transfusions should not be continued unless the hemoglobin is less than ~7g/dL. Studies have demonstrated an increased survival in patients treated with this restrictive blood transfusion protocol.
Successful resuscitation also requires support of respiratory function. Supplemental oxygen should be provided, and endotracheal intubation may be necessary to maintain arterial oxygenation. Following resuscitation from isolated hemorrhagic shock, end-organ damage is frequently less than following septic or traumatic shock. This may be due to the absence of the massive activation of inflammatory mediator response systems and the consequent nonspecific organ injury seen in the latter conditions.
Shock following trauma is, in large measure, due to hypovolemia. However, even when hemorrhage has been controlled, patients can continue to suffer loss of plasma volume into the interstitium of injured tissues. These fluid losses are compounded by injury-induced inflammatory responses, which contribute to the secondary microcirculatory injury. Recent evidence demonstrates release of mediators induced by DAMPs from injured tissue that are recognized by the highly conserved membrane receptors of the TLR family (see "Inflammatory Responses," above). These receptors on the cells of the innate immune system, particularly the circulating monocyte, tissue-fixed macrophage, and dendritic cell, are potent activators of an excessive proinflammatory phenotype in response to cellular injury. This causes secondary tissue injury and maldistribution of blood flow, intensifying tissue ischemia and leading to multiple organ system failure. In addition, direct trauma to the heart, chest, or head can also contribute to the shock. For example, pericardial tamponade or tension pneumothorax impairs ventricular filling, while myocardial contusion depresses myocardial contractility.
Traumatic Shock: Treatment
Inability of the patient to maintain a systolic blood pressure 90 mmHg after trauma-induced hypovolemia is associated with a mortality rate of ~50%. To prevent decompensation of homeostatic mechanisms, therapy must be promptly administered.
The initial management of the seriously injured patient requires attention to the "ABCs" of resuscitation: assurance of an airway (A), adequate ventilation (breathing, B), and establishment of an adequate blood volume to support the circulation (C). Control of ongoing hemorrhage requires immediate attention. Early stabilization of fractures, debridement of devitalized or contaminated tissues, and evacuation of hematomata all reduce the subsequent inflammatory response to the initial insult and minimize subsequent diffuse organ injury. Supplementation of depleted endogenous antioxidants also reduces subsequent organ failure and mortality.
Compressive Cardiogenic Shock
With compression, the heart and surrounding structures are less compliant, and thus normal filling pressures generate inadequate diastolic filling. Blood or fluid within the poorly distensible pericardial sac may cause tamponade. Any cause of increased intrathoracic pressure, such as tension pneumothorax, herniation of abdominal viscera through a diaphragmatic hernia, or excessive positive pressure ventilation to support pulmonary function, can also cause compressive cardiogenic shock while simultaneously impeding venous return. Although initially responsive to increased filling pressures produced by volume expansion, as compression increases, cardiogenic shock recurs. The window of opportunity gained by volume loading may be very brief until irreversible shock recurs. Diagnosis and intervention must occur urgently.
The diagnosis of compressive cardiogenic shock is most frequently based on clinical findings, the chest radiograph, and an echocardiogram. The diagnosis of compressive cardiac shock may be more difficult to establish in the setting of trauma when hypovolemia and cardiac compression are present simultaneously. The classic findings of pericardial tamponade include the triad of hypotension, neck vein distention, and muffled heart sounds. Pulsus paradoxus, i.e., an inspiratory reduction in systolic pressure >10 mmHg, may also be noted. The diagnosis is confirmed by echocardiography, and treatment consists of immediate pericardiocentesis. A tension pneumothorax produces ipsilateral decreased breath sounds, tracheal deviation away from the affected thorax, and jugular venous distention. Radiographic findings include increased intrathoracic volume, depression of the diaphragm of the affected hemithorax, and shifting of the mediastinum to the contralateral side. Chest decompression must be carried out immediately. Release of air and restoration of normal cardiovascular dynamics are both diagnostic and therapeutic.
Interruption of sympathetic vasomotor input after a high cervical spinal cord injury, inadvertent cephalad migration of spinal anesthesia, or devastating head injury may result in neurogenic shock. In addition to arteriolar dilatation, venodilation causes pooling in the venous system, which decreases venous return and cardiac output. The extremities are often warm, in contrast to the usual vasoconstriction-induced coolness in hypovolemic or cardiogenic shock. Treatment involves a simultaneous approach to the relative hypovolemia and to the loss of vasomotor tone. Excessive volumes of fluid may be required to restore normal hemodynamics if given alone. Once hemorrhage has been ruled out, norepinephrine or a pure -adrenergic agent (phenylephrine) may be necessary to augment vascular resistance and maintain an adequate mean arterial pressure.
The normal host response to the stress of illness, operation, or trauma requires that the adrenal glands hypersecrete cortisol in excess of that normally required. Hypoadrenal shock occurs in settings in which unrecognized adrenal insufficiency complicates the host response to the stress induced by acute illness or major surgery. Adrenocortical insufficiency may occur as a consequence of the chronic administration of high doses of exogenous glucocorticoids. In addition, recent studies have shown that critical illness, including trauma and sepsis, may also induce a relative hypoadrenal state. Other, less common causes include adrenal insufficiency secondary to idiopathic atrophy, tuberculosis, metastatic disease, bilateral hemorrhage, and amyloidosis. The shock produced by adrenal insufficiency is characterized by loss of homeostasis with reductions in systemic vascular resistance, hypovolemia, and reduced cardiac output. The diagnosis of adrenal insufficiency may be established by means of an ACTH stimulation test.
Hypoadrenal Shock: Treatment
In the persistently hemodynamically unstable patient, dexamethasone sodium phosphate, 4 mg, should be given intravenously. This agent is preferred if empiric therapy is required because, unlike hydrocortisone, it does not interfere with the ACTH stimulation test. If the diagnosis of absolute or relative adrenal insufficiency is established as shown by nonresponse to corticotropin stimulation (cortisol 9 g/dL change poststimulation), the patient has a reduced risk of death if treated with hydrocortisone, 100 mg every 6–8 h, and tapered as the patient achieves hemodynamic stability. Simultaneous volume resuscitation and pressor support are required. The need for simultaneous mineralocoid is unclear.
The sympathomimetic amines dobutamine, dopamine, and norepinephrine are widely used in the treatment of all forms of shock. Dobutamine is inotropic with simultaneous afterload reduction, thus minimizing cardiac-oxygen consumption increases as cardiac output increases. Dopamine is an inotropic and chronotropic agent that also supports vascular resistance in those whose blood pressure will not tolerate peripheral vascular dilation. Norepinephrine primarily supports blood pressure through vasoconstriction and increases myocardial oxygen consumption while placing marginally perfused tissues, such as extremities and splanchnic organs, at risk for necrosis, but it is also inotropic without chronotropy. Arginine-vasopressin (antidiuretic hormone) is also being used increasingly and may better protect vital organ blood flow and prevent pathologic vasodilation.
Positioning of the patient may be a valuable adjunct in the initial treatment of hypovolemic shock. Elevating the foot of the bed (i.e., placing it on "shock blocks") and assumption of the Trendelenburg position without flexion at the knees are effective but may increase work of breathing and risk for aspiration. Simply elevating both legs may be the optimal approach.
Pneumatic Antishock Garment (PASG)
The PASG and the military antishock trousers (MAST) are inflatable external compression devices that can be wrapped around the legs and abdomen and have been widely used in the prehospital setting as a means of providing temporary support of central hemodynamics in shock. However, they cause a significant increase in systemic vascular resistance and blood pressure by arterial compression, without causing a significant change in cardiac output or tissue perfusion. The most appropriate use appears to be as a means to tamponade and to prevent ongoing bleeding and augment hemostasis. Inflation of the suit provides splinting of fractures of the pelvis and lower extremities and helps to arrest hemorrhage.
Hypothermia is a potential adverse consequence of massive volume resuscitation. The infusion of large volumes of refrigerated blood products and room-temperature crystalloid solutions can rapidly drop core temperatures if fluid is not run through warming devices. Hypothermia may depress cardiac contractility and thereby further impair cardiac output and oxygen delivery. Hypothermia, particularly temperatures less than 35°C, directly impairs the coagulation pathway, sometimes causing a significant coagulopathy. Rapid rewarming to more than 35°C significantly decreases the requirement for blood products and produces an improvement in cardiac function. The most effective method for rewarming is endovascular countercurrent warmers through femoral vein cannulation. This process does not require a pump and can rewarm from 30° to 35°C in less tahn 30 min.