A simplified “plumbing” view of the circulation indicates that failure of cardiac output, and associated transport of oxygen, must be due to inadequate fluid in the system (hypovolemic shock), pump failure (cardiogenic shock), obstruction of flow (obstructive shock), or poor distribution of flow (septic/distributive shock). But shock is not just a plumbing problem so that the associated inflammatory response is considered in the next section. We use cardiac function curves and venous return relations in the following discussion to compare and contrast cardiovascular mechanisms responsible for hypovolemic shock (Fig. 33-3), cardiogenic shock (Fig. 33-4), and septic shock (Fig. 33-5). Obstructive shock (eg, tamponade, pulmonary embolism, abdominal compartment syndrome) is considered with cardiogenic shock because its presentation is often similar to right heart failure.
Cardiovascular mechanics in hypovolemic shock. Abnormalities of systolic and diastolic left ventricular (LV) pressure and volume (ordinate and abscissa, respectively) relations during hypovolemic shock (continuous lines) with normal pressure-volume relations (dashed lines). Lower panel.During hypovolemic shock, the primary abnormality is a decrease in the intravascular volume so that mean systemic pressure decreases as illustrated by a shift of the venous return curves from the normal relation (straight dashed line) leftward (straight continuous line). This hypovolemic venous return curve now intersects the normal cardiac function curve (dashed curvilinear relation) at a much lower end-diastolic pressure so that cardiac output is greatly reduced. Upper panel. The increased sympathetic tone accompanying shock results in a slight increase in contractility, as illustrated by the slight left shift of the left ventricular end-systolic pressure-volume relation (from the dashed straight line to the solid straight line). However, because the slope of the end-systolic pressure-volume relation is normally quite steep, the increase in contractility cannot increase stroke volume or cardiac output much and is therefore an ineffective compensatory mechanism in patients with normal hearts. If volume resuscitation to correct the primary abnormality is delayed for several hours, the diastolic pressure-volume relation shifts from its normal position (dashed curve, upper panel), resulting in increased diastolic stiffness (continuous curve, upper panel). Increased diastolic stiffness results in a decreased stroke volume and therefore a depressed cardiac function curve (continuous curve, lower panel) compared with normal (dashed curve, lower panel). This decrease in cardiac function due to increased diastolic stiffness probably accounts for irreversibility of severe prolonged hypovolemic shock. LV, left ventricular.
Cardiovascular mechanics in cardiogenic shock (axes as labeled as in Fig. 33-3). Upper panel. The primary abnormality is that the end-systolic pressure-volume relation (sloped straight lines) is shifted to the right mainly by a marked reduction in slope (decreased contractility). As a result, at similar or even lower systolic pressures, the ventricle is not able to eject as far, so end-systolic volume is greatly increased and stroke volume is therefore decreased. To compensate for the decrease in stroke volume, the curvilinear diastolic pressure-volume relation shifts to the right, which indicates decreased diastolic stiffness (increased compliance). To maximize stroke volume, diastolic filling increases even further, associated with an increase in end-diastolic pressure. Lower panel. Why end-diastolic pressure increases is determined from the pump function and venous return curves as a plot of cardiac output (ordinate) versus right atrial end-diastolic pressure (abscissa). The decrease in contractility (upper panel) results in a shift of the curvilinear cardiac function curve from its normal position (dashed curve, lower panel) down and to the right (continuous curve, lower panel). Because end-diastolic pressure and cardiac output are determined by the intersection of the cardiac function curve (curvilinear relations, lower panel) with the venous return curve (straight lines, lower panel), the shift of the cardiac function curve immediately results in a decrease in cardiac output and an increase in end-diastolic pressure. Compensatory mechanisms (fluid retention by the kidneys, increased sympathetic tone) act to maintain venous return by increasing mean systemic pressure (venous pressure when cardiac output = 0) from 16 to 25 mm Hg as indicated by the rightward shift from the dashed straight line to the continuous straight line in the lower panel. The effect is that end-diastolic pressure increases so that stroke volume (upper panel) and cardiac output (lower panel) are increased toward normal.
Cardiovascular mechanics in septic shock (axes as labeled as in Fig. 33-3). Septic shock has important independent effects on left ventricular (LV) pressure-volume relations, on the venous return curve, and on arterial vascular resistance. Upper panel. Depressed systolic contractility indicated by a decreased slope of the LV end-systolic pressure-volume relation from normal (dashed sloped line) to sepsis (continuous sloped line) is caused in part by a circulating myocardial depressant factor, but the end-systolic volume remains near normal owing to the reduced afterload. Survivors of septic shock have a large end-diastolic volume even at reduced diastolic pressure associated with dilation of their diastolic ventricles, indicated by a shift of the normal diastolic pressure-volume relation (dashed curve) to the right (right-hand continuous curve). As a result, stroke volume is increased. However, in nonsurvivors, stroke volume decreases because of a leftward shift of the diastolic pressure-volume relation (left-hand continuous curve), indicating increased diastolic stiffness and impaired diastolic filling. Lower panel. The cardiac function curve for survivors is normal (dashed curvilinear relation) or slightly increased (continuous curvilinear relation) owing to reduced afterload. The peripheral circulation during septic shock is often characterized by high flows and low vascular pressures. It follows that the resistance to venous return is decreased as indicated by a steeper venous return curve (continuous straight line) compared with normal (straight dashed lines). This accounts for the high venous return and large end-diastolic volumes and stroke volumes. As with other interventions, resistance to venous return may be decreased in part by redistribution of blood flow to vascular beds with short time constants. However, the nonsurvivors may have significantly depressed cardiac function (downward shifted continuous curve) because of the additive effects of decreased systolic contractility and impaired diastolic filling. Depending on the relative contribution of the abnormalities of ventricular mechanics and peripheral vascular changes, cardiac output is usually normal or high even at relatively normal end-diastolic pressures until diastolic dysfunction limits cardiac output by reducing diastolic volume even at high diastolic pressures.
DECREASED VENOUS RETURN—HYPOVOLEMIC SHOCK
Venous return to the heart when right atrial pressure is not elevated may be inadequate owing to decreased intravascular volume (hypovolemic shock), to decreased tone of the venous capacitance bed so that mean systemic pressure is low (eg, drugs, neurogenic shock), and occasionally to increased resistance to venous return (eg, obstruction of the inferior vena cava by tumor). In the presence of shock, decreased venous return is determined to be a contributor to shock by finding low left and right ventricular diastolic pressures, often in an appropriate clinical setting such as trauma or massive gastrointestinal hemorrhage.
Hypovolemic Shock: Hypovolemia is the most common cause of shock caused by decreased venous return and is illustrated in Figure 33-3. Intravascular volume is decreased, so the venous capacitance bed is not filled, leading to a decreased pressure driving venous return back to the heart. This is seen as a left shift of the venous return curve in Figure 33-3, lower panel, so that cardiac output decreases at a low end-diastolic pressure (intersection of the venous return curve and cardiac function curve). Endogenous catecholamines attempt to compensate by constricting the venous capacitance bed, thereby raising the pressure driving venous return back to the heart, so that 25% reductions in intravascular volume are nearly completely compensated for. Orthostatic decrease in blood pressure by 10 mm Hg or an increase in heart rate of more than 30 beats/min31 may detect this level of intravascular volume reduction. When approximately 40% of the intravascular volume is lost, sympathetic stimulation can no longer maintain mean systemic pressure, resulting in decreased venous return and clinical shock.
After sufficient time (>2 hours) and severity (>40% loss of intravascular volume), patients often cannot be resuscitated from hypovolemic shock.32 This observation highlights the urgency with which patients should be resuscitated. Gut and other organ ischemia with systemic release of inflammatory mediators,33 a “no-reflow” phenomenon in microvascular beds, and increased diastolic stiffness (see Fig. 33-3) contribute to the pathophysiology.34
Shock after trauma is a form of hypovolemic shock in which a significant systemic inflammatory response, in addition to intravascular volume depletion, is present. Intravascular volume may be decreased because of loss of blood and significant redistribution of intravascular volume to other compartments, that is, “third spacing.” Release of inflammatory mediators results in pathophysiologic abnormalities resembling septic shock. Cardiac dysfunction may be depressed from direct damage from myocardial contusion, from increased diastolic stiffness, from right heart failure, or even from circulating myocardial depressant substances. Shock related to burns similarly is multifactorial with a significant component of intravascular hypovolemia and a systemic inflammatory response (see Chap. 123).
Other causes of shock caused by decreased venous return include severe neurologic damage or drug ingestion resulting in hypotension caused by loss of venous tone. As a result of decreased venous tone, mean systemic pressure decreases, thereby reducing the pressure gradient driving blood flow back to the heart so that cardiac output and blood pressure decrease. Obstruction of veins owing to compression, thrombus formation, or tumor invasion increases the resistance to venous return and occasionally may result in shock.
The principal therapy of hypovolemic shock and other forms of shock caused by decreased venous return is rapid initial fluid resuscitation. Warmed crystalloid solutions are readily available. Colloid-containing solutions result in a more sustained increase in intravascular volume but there is currently no convincing evidence of benefit.35 The role of hypertonic saline and other resuscitation solutions is similarly uncertain. Alternatively, transfusion of packed red blood cells increases oxygen-carrying capacity and expands the intravascular volume and is therefore a doubly useful therapy. In an emergency, initial transfusion often begins with type-specific blood before a complete cross-match is available. During initial resuscitation, the Early Goal-Directed Therapy protocol suggests that achieving a hematocrit greater than 30% may be beneficial when is less than 70%. However, after initial resuscitation, maintaining hemoglobin above 90 g/L (9 g/dL) does not appear to be better than maintaining hemoglobin above 70 g/L (7 g/dL).12 After a large stored red blood cell transfusion, clotting factors, platelets, and serum ionized calcium decrease and therefore should be measured and replaced if necessary (see Chap. 89).
Recognizing inadequate venous return as the primary abnormality of hypovolemic shock alerts the physician to several commonly encountered and potentially lethal complications of therapy. Airway intubation and mechanical ventilation increase negative intrathoracic pressures to positive values and thus raise right atrial pressure. The already low pressure gradient driving venous return to the heart worsens, resulting in marked reduction in cardiac output and blood pressure. However, ventilation treats shock by reducing the work of respiratory muscle, so ventilation should be implemented early with adequate volume expansion. Sedatives and analgesics are often administered at the time of airway intubation, resulting in reduced venous tone because of a direct relaxing effect on the venous capacitance bed or because of a decrease in circulating catecholamines. Thus, the pressure gradient driving venous return decreases. Therefore, in the hypovolemic patient, these medications may markedly reduce cardiac output and blood pressure and should be used with caution and with ongoing volume expansion.
DECREASED PUMP FUNCTION—CARDIOGENIC SHOCK
The diagnosis of decreased pump function as the cause of shock is made by finding evidence of inappropriately low output (cardiac output) despite normal or high input (right atrial pressure). Cardiac output is the most important “output” of the heart and is clinically assessed in the same way that perfusion was assessed during the urgent initial examination. Better estimates are later obtained using , by thermodilution measurement of cardiac output, and by echocardiographic examination. Right atrial pressure or CVP is the most easily measured “input” of the whole heart and is initially assessed by examination of jugular veins and, after catheter insertion, by direct measurement. Left and right ventricular dysfunction can be caused by decreased systolic contractility, increased diastolic stiffness, greatly increased afterload (including obstruction), valvular dysfunction, or abnormal heart rate and rhythm.
Left Ventricular Failure: Acute or acute-on-chronic left ventricular failure resulting in shock is the classic example of cardiogenic shock. Clinical findings of low cardiac output and increased left ventricular filling pressures include, in addition to assessment of perfusion, pulmonary crackles in dependent lung regions, a laterally displaced and diffuse precordial apical impulse, elevated jugular veins, and presence of a third heart sound.36 These findings are not always present or unambiguous. Therefore, echocardiography is helpful and often essential in establishing the diagnosis. In some cases pulmonary artery catheterization may assist in titrating therapy. Cardiogenic shock then is usually associated with a cardiac index lower than 2.2 L/m2 per minute when the pulmonary artery occlusion pressure has been raised above 18 mm Hg.37
Systolic Dysfunction As a result of a decrease in contractility, the patient presents with elevated left and right ventricular filling pressures and a low cardiac output. Mixed venous oxygen saturation may be well below 50% because cardiac output is low. The primary abnormality is that the relation of end-systolic pressure to volume is shifted down and to the right (see Fig. 33-4, upper panel) so that, at the same afterload, the ventricle cannot eject as far (decreased contractility). It follows that pump function is also impaired, indicated by a shift down and to the right (see Fig. 33-4, lower panel) so that at similar preloads cardiac output is reduced.
Acute myocardial infarction or ischemia is the most common cause of left ventricular failure leading to shock. The use of fibrinolytic therapy and early angioplasty or surgical revascularization has reduced the incidence of cardiogenic shock to less than 5%.9 Infarction greater than 40% of the myocardium is often associated with cardiogenic shock38; anterior infarction is 20 times more likely to lead to shock than is inferior or posterior infarction.39 Details of the diagnosis and management of ischemic heart disease are discussed in Chap. 37; other causes of decreased left ventricular contractility in critical illness are discussed in more detail in Chap. 35, and each may contribute to shock.
Diastolic Dysfunction Increased left ventricular diastolic chamber stiffness contributing to cardiogenic shock occurs acutely during myocardial ischemia, chronically with ventricular hypertrophy, and in a range of less common disorders (see Table 33-4); all causes of tamponade listed in Table 33-4 need to be considered in a systematic review of causes of diastolic dysfunction.40,41 Stroke volume is decreased by decreased end-diastolic volume caused by increased diastolic chamber stiffness. Conditions resulting in increased diastolic stiffness are particularly detrimental when systolic contractility is decreased because decreased diastolic stiffness (increased compliance; see Fig. 33-4, upper panel) is normally a compensatory mechanism. Increased diastolic chamber stiffness contributing to hypotension in patients with low cardiac output and high ventricular diastolic pressures is best identified echocardiographically by small diastolic volumes.
Causes of and Contributors to Shock
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Causes of and Contributors to Shock
|Decreased pump function of the heart—cardiogenic shock |
| Left ventricular failure |
| Systolic dysfunction—decreased contractility |
| Myocardial infarction |
| Ischemia and global hypoxemia |
| Cardiomyopathy |
| Depressant drugs: β-blockers, calcium channel blockers, antiarrhythmics |
| Myocardial contusion |
| Respiratory acidosis |
| Metabolic derangements: acidosis, hypophosphatemia, hypocalcemia |
| Diastolic dysfunction—increased myocardial diastolic stiffness |
| Ischemia |
| Ventricular hypertrophy |
| Restrictive cardiomyopathy |
| Consequence of prolonged hypovolemic or septic shock |
| Ventricular interdependence |
| External compression (see cardiac tamponade below) |
| Greatly increased afterload |
| Aortic stenosis |
| Hypertrophic cardiomyopathy |
| Dynamic outflow tract obstruction |
| Coarctation of the aorta |
| Malignant hypertension |
| Valve and structural abnormality |
| Mitral stenosis, endocarditis, mitral aortic regurgitation |
| Obstruction owing to atrial myxoma or thrombus |
| Papillary muscle dysfunction or rupture |
| Ruptured septum or free wall |
| Arrhythmias |
| Right ventricular failure |
| Decreased contractility |
| Right ventricular infarction, ischemia, hypoxia, acidosis |
| Greatly increased afterload |
| Pulmonary embolism |
| Pulmonary vascular disease |
| Hypoxic pulmonary vasoconstriction, PEEP, high alveolar pressure |
| Acidosis |
| ARDS, pulmonary fibrosis, sleep disordered breathing, chronic obstructive pulmonary disease |
| Valve and structural abnormality |
| Obstruction due to atrial myxoma, thrombus, endocarditis |
| Arrhythmias |
|Decreased venous return with normal pumping function—hypovolemic shock |
| Cardiac tamponade (increased right atrial pressure—central hypovolemia) |
| Pericardial fluid collection |
| Blood |
| Renal failure |
| Pericarditis with effusion |
| Constrictive pericarditis |
| High intrathoracic pressure |
| Tension pneumothorax |
| Massive pleural effusion |
| Positive-pressure ventilation |
| High intra-abdominal pressure |
| Ascites |
| Massive obesity |
| After extensive intra-abdominal surgery |
| Intravascular hypovolemia (reduced mean systemic pressure) |
| Hemorrhage |
| Gastrointestinal |
| Trauma |
| Aortic dissection and other internal sources |
| Renal losses |
| Diuretics |
| Osmotic diuresis |
| Diabetes (insipidus, mellitus) |
| Gastrointestinal losses |
| Vomiting |
| Diarrhea |
| Gastric suctioning |
| Loss via surgical stomas |
| Redistribution to extravascular space |
| Burns |
| Trauma |
| Postsurgical |
| Sepsis |
| Decreased venous tone (reduced mean systemic pressure) |
| Drugs |
| Sedatives |
| Narcotics |
| Diuretics |
| Anaphylactic shock |
| Neurogenic shock |
| Increased resistance to venous return |
| Tumor compression or invasion |
| Venous thrombosis with obstruction |
| PEEP |
| Pregnancy |
|High cardiac output hypotension |
| Septic shock |
| Sterile endotoxemia with hepatic failure |
| Arteriovenous shunts |
| Dialysis |
| Paget disease |
|Other causes of shock with unique etiologies |
| Thyroid storm |
| Myxedema coma |
| Adrenal insufficiency |
| Hemoglobin and mitochondrial poisons |
| Cyanide |
| Carbon monoxide |
| Iron intoxication |
Treatment of increased diastolic stiffness is approached by first considering the potentially contributing reversible causes. Acute reversible causes include ischemia and the many causes of tamponade physiology listed in Table 33-4. Fluid infusion results in large increases in diastolic pressure without much increase in diastolic volume. Positive inotropic agents and afterload reduction are generally not helpful and may decrease blood pressure further. If conventional therapy of cardiogenic shock aimed at improving systolic function is ineffective, then increased diastolic stiffness should be strongly considered as the cause of decreased pump function. Cardiac output responsiveness to heart rate is another subtle clue suggesting impaired diastolic filling. Heart rate does not normally alter cardiac output (which is normally set by, and equal to, venous return) except at very low heart rates (maximally filled ventricle before end diastole) or at very high heart rates (incomplete ventricular relaxation and filling). However, if diastolic filling is limited by tamponade or a stiff ventricle, then very little further filling occurs late in diastole. In this case, increasing heart rate from 80 to 100 or 110 beats/min may result in a significant increase in cardiac output, which may be therapeutically beneficial and also a diagnostic clue.
Valvular Dysfunction Acute mitral regurgitation, due to chordal or papillary muscle rupture or papillary muscle dysfunction, most commonly is caused by ischemic injury. The characteristic murmur and the presence of large V waves on the pulmonary artery occlusion pressure trace suggest significant mitral regurgitation, which is quantified by echocardiographic examination. Rupture of the ventricular septum with left-to-right shunt is detected by Doppler echocardiographic examination or by observing a step-up in oxygen saturation of blood from the right atrium to the pulmonary artery. Rarely, acute obstruction of the mitral valve by left atrial thrombus or myxoma may also result in cardiogenic shock. These conditions are generally surgical emergencies.
More commonly, valve dysfunction aggravates other primary etiologies of shock. Aortic and mitral regurgitation reduces forward flow and raises LVEDP, and this regurgitation is ameliorated by effective arteriolar dilation and by nitroprusside infusion. Vasodilator therapy can effect large increases in cardiac output without much change in mean blood pressure, pulse pressure, or diastolic pressure, so repeat or cardiac output measurement, or echocardiographic assessment is essential to titrating effective vasodilator doses. In contrast, occasional patients develop decreased blood pressure and cardiac output on inotropic drugs such as dobutamine; in this case, excluding dynamic ventricular outflow tract obstruction by echocardiography or treating it by increasing preload, afterload, and end-systolic volume is essential.
Cardiac Arrhythmias Not infrequently, arrhythmias aggravate hypoperfusion in other shock states. Ventricular tachyarrhythmias are often associated with cardiogenic shock; sinus tachycardia and atrial tachyarrhythmias are often observed with hypovolemic and septic shock. Specific therapy of tachyarrhythmias depends on the specific diagnosis, as discussed in Chap. 36. Inadequately treated pain and unsuspected drug withdrawal should be included in the intensive care unit differential diagnosis of tachyarrhythmias; whatever their etiology, the reduced ventricular filling time can reduce cardiac output and aggravate shock. Bradyarrhythmias contributing to shock may respond acutely to atropine or isoproterenol infusion and then pacing; hypoxia or myocardial infarction as the cause should be sought and treated. Symptomatic hypoperfusion resulting from bradyarrhythmias, even in the absence of myocardial infarction or high-degree atrioventricular block, is an important indication for temporary pacemaker placement that is sometimes overlooked.
Treatment of Left Ventricular Failure After initial resuscitation, which includes consideration of early institution of thrombolytic therapy in acute coronary thrombosis and revascularization or surgical correction of other anatomic abnormalities where appropriate,3 management of patients with cardiogenic shock requires repeated testing of the hypothesis of “too little versus too much.” Clinical examination is not accurate enough; when the response to initial treatment of cardiogenic shock is inadequate, repeated or cardiac output measurement or repeated echocardiographic exam may be required to titrate therapy. Therapy for cardiogenic shock follows from consideration of the pathophysiology illustrated in Figure 33-4 and includes optimizing filling pressures, increasing contractility, and optimizing afterload. Temporary mechanical support using an intra-aortic balloon pump or a ventricular assist device is often extremely useful in cardiogenic shock and should be considered early as a support in patients who may benefit from later surgical therapy.9 Cardiac transplantation and mechanical heart implantation are considered when other therapy fails.
Filling pressures are optimized to improve cardiac output but avoid pulmonary edema. Depending on the initial presentation, cardiogenic shock frequently spans the spectrum of hypovolemia (so fluid infusion helps) to hypervolemia with pulmonary edema (where reduction in intravascular volume results in substantial improvement). If gross fluid overload is not present, then a rapid fluid bolus should be given. In contrast to patients with hypovolemic or septic shock, a smaller bolus (250 mL) of crystalloid solution should be infused as quickly as possible. Immediately after infusion, the patient’s circulatory status should be reassessed. If there is improvement but hypoperfusion persists, then further infusion with repeat examination is indicated to attain an adequate cardiac output and oxygen delivery while seeking the lowest filling pressure needed to accomplish this goal. If there is no improvement in oxygen delivery and evidence of worsened pulmonary edema or gas exchange, then the limit of initial fluid resuscitation has been defined. Crystalloid solutions are used particularly if the initial evaluation is uncertain because crystalloid solutions rapidly distribute to the entire extracellular fluid compartment. Therefore, after a brief period only one-fourth to one-third remains in the intravascular compartment, and evidence of intravascular fluid overload rapidly subsides.
Contractility increases if ischemia can be relieved by decreasing myocardial oxygen demand, by improving myocardial oxygen supply by increasing coronary blood flow (coronary vasodilators, thrombolytic therapy, surgical revascularization, or intra-aortic balloon pump counterpulsation), or by increasing the oxygen content of arterial blood. Inotropic drug infusion attempts to correct the physiologic abnormality by increasing contractility (see Fig. 33-2). However, this occurs at the expense of increased myocardial oxygen demand. Afterload is optimized to maintain arterial pressures high enough to perfuse vital organs (including the heart) but low enough to maximize systolic ejection. When systolic function is reduced, vasodilator therapy may improve systolic ejection and increase perfusion, even to the extent that blood pressure rises.42 In patients with very high blood pressure, end-systolic volume increases considerably so that stroke volume and cardiac output decrease unless LVEDV and LVEDP are greatly increased; this sequence is reversed by judicious afterload reduction.
Right Ventricular Failure—Overlap With Obstructive Shock: Shock presenting as low cardiac output, high venous pressures, and clear or ambiguous (concurrent pulmonary process) breath sounds is an important diagnostic challenge generally requiring urgent echocardiographic examination. This classic presentation of right heart failure must first be distinguished from cardiac tamponade (obstructive shock). Then the cause of right heart failure must be determined. Most commonly the cause is left heart failure contributing to right heart failure, right heart failure due to right ventricular infarction, or right heart failure due to increased right ventricular afterload—pulmonary artery hypertension. Increased right ventricular afterload then needs to be understood as acute, often due to pulmonary embolism (obstructive shock), or acute on chronic where inflammatory mediators, hypoxic pulmonary vasoconstriction, or high ventilator pressures may be the “acute” precipitants or contributors. Echocardiography is fundamental in distinguishing between all of the above scenarios.
Diagnosis and Management of Right Ventricular Failure With the above clinical presentation, due to any of these underlying causes, volume resuscitation is particularly problematic. Volume infusion increases right atrial and, hence, right ventricular diastolic pressure. Excessive change in diastolic pressure gradient between right and left ventricles then shifts the interventricular septum from right to left. Importantly, right-to-left shift of the interventricular septum limits left ventricular filling and induces inefficient and paradoxical septal movement during left ventricular contraction. As a result, stroke volume and cardiac output are reduced. Therefore, volume resuscitation must be judicious and is enabled by repeat echocardiographic examination, specifically examining septal position and motion.
Early recognition of right versus left ventricular infarction as the cause of shock is important so potentially dangerous therapy, including systemic vasodilators, morphine, and β-blockers, are avoided. Right ventricular infarction is found in approximately half of inferior myocardial infarctions and is complicated by shock only 10% to 20% of the time.43 Isolated right ventricular infarction with shock is uncommon and has a mortality rate ∼50% comparable to left ventricular infarction shock.39 Pulmonary crackles are classically absent. Therapy includes infusion of dobutamine and volume expansion, although excessive volume can aggravate shock by shifting the intraventricular septum from right to left.44 Because bradyarrhythmias are common and atrioventricular conduction is frequently abnormal, atrioventricular sequential pacing may preserve right ventricular synchrony and often improves cardiac output and blood pressure in shock caused by right ventricular infarction.44 Afterload reduction using balloon counterpulsation may also be useful,39 as are early fibrinolytic therapy and angioplasty when indicated (see Chap. 37).
Pulmonary artery hypertension may contribute to right ventricular ischemia, with or without coronary artery disease. In shock states systemic arterial pressure is often low, and right ventricular afterload (pulmonary artery pressure) may be high owing to emboli, hypoxemic pulmonary vasoconstriction, acidemic pulmonary vasoconstriction, sepsis, or ARDS. Therefore, right ventricular perfusion pressure is low leading to right ventricular ischemia and decreased contractility, which, in the face of normal or high right ventricular afterload, results in right ventricular dilation with right-to-left septal shift.
Approaches to right heart failure include verifying that pulmonary emboli are present and initiating therapy with anticoagulation, fibrinolytic agents for submassive pulmonary embolism or shock, or surgical embolectomy as necessary.45 Pulmonary vasodilator therapy may be useful in some patients if pulmonary artery pressures can be lowered without significantly lowering systemic arterial pressures. Inhaled nitric oxide, inhaled prostacyclins, sildenafil, and many other agents have been variably successful. Measurements of pulmonary artery pressure, systemic pressure, cardiac output, and oxygen delivery before and after a trial of a specific potential pulmonary vasodilator are essential (see Chap. 38). Hypoxic pulmonary vasoconstriction may be reduced by improving alveolar and mixed venous oxygenation. More aggressive correction of acidemia should be considered in this setting. Adequate right ventricular perfusion pressure is maintained by ensuring that aortic pressure exceeds pulmonary artery pressure.
Compression of the Heart by Surrounding Structures Compression of the heart (cardiac tamponade) limits diastolic filling and can result in shock with inadequate cardiac output despite very high right atrial pressures. Diagnosis of cardiac tamponade can be made physiologically by using pulmonary artery catheterization to demonstrate a low cardiac output in addition to elevated and approximately equal right atrial, right ventricular diastolic, pulmonary artery diastolic, and pulmonary artery occlusion pressures (particularly their waveforms). The diagnosis is often best confirmed anatomically by using echocardiographic examination to demonstrate pericardial fluid, diastolic collapse of the atria and right ventricle, and right-to-left septal shift during inspiration. Septal shift during inspiration and increased afterload that accompany decreased intrathoracic pressure during inspiration account for the clinically observed pulsus paradoxus. Although pericardial tamponade by accumulation of pericardial fluid is the most common cause of cardiac tamponade, other structures surrounding the heart may also produce tamponade. Tension pneumothorax, massive pleural effusion, pneumopericardium (rarely), and greatly elevated abdominal pressures may also impair diastolic filling.
Decreasing the pressure of the tamponading chamber by needle drainage or surgical decompression of the pericardium, pleural space, and peritoneum can rapidly and dramatically improve venous return, blood pressure, and organ system perfusion. Therefore, the goal of therapy is to accomplish this decompression as rapidly and safely as possible under ultrasound guidance. In patients who are hemodynamically stable, fluid infusion is a temporizing therapy that increases mean systemic pressure so that venous return increases even though right atrial pressure is high. Excessive volume resuscitation worsens shock, as discussed above.
HIGH CARDIAC OUTPUT HYPOTENSION—SEPTIC SHOCK
Septic shock is the most common example of shock that may be caused primarily by reduced arterial vascular tone and reactivity, often associated with abnormal distribution of blood flow. Septic shock accompanies severe infection from a wide variety of gram-positive, gram-negative, fungal, and viral pathogens and is a consequence of the endogenous inflammatory response induced by these pathogens. Induction of a similar endogenous inflammatory response by noninfectious tissue injury (eg, pancreatitis, trauma) results in the same shock state, now called distributive shock. Noninfectious distributive shock is, by virtually all measures, the same as septic shock. Classical septic shock is characterized by increased cardiac output with low SVR hypotension, manifested by a high pulse pressure, warm extremities, good nail bed capillary filling, and low diastolic and mean blood pressures. However, septic shock is often initially associated with loss of intravascular volume and therefore presents with combined hypovolemic and septic shock. Additional accompanying clues to a systemic inflammatory response are an abnormal temperature and white blood cell count and differential and an evident site of sepsis.
Several pathophysiologic mechanisms contribute to inadequate organ system perfusion in septic shock. There may be abnormal distribution of blood flow at the organ system level, within individual organs, and even at the capillary bed level. The result is inadequate oxygen delivery in some tissue beds.
The cardiovascular abnormalities of septic shock (see Fig. 33-4) are extensive and include systolic and diastolic abnormalities of the heart, abnormal arterial tone, decreased venous tone, and abnormal distribution of capillary flow leading to regions of tissue hypoxia. In addition, there may be a cellular defect in metabolism so that even cells exposed to adequate oxygen delivery may not maintain normal aerobic metabolism. Depressed systolic contractility illustrated as a rightward shift of the end-systolic pressure-volume relation in Figure 33-5, upper panel, occurs in septic shock46 due to the systemic inflammatory response and an induced intramyocardial inflammatory response.47 Decreased systolic contractility associated with septic shock is reversible over 5 to 10 days as the patient recovers. Systolic and diastolic dysfunctions during sepsis that progress to the point that high cardiac output (hyperdynamic circulation) is no longer maintained (normal or low cardiac output is observed) are associated with poor outcome.46
Decreased arterial resistance is almost always observed in septic shock. Early in septic shock, a high cardiac output state exists with normal or low blood pressure. The low arterial resistance is associated with impaired arterial and precapillary autoregulation and may be due to increased endothelial nitric oxide production and opening of potassium adenosine triphosphate channels on vascular smooth muscle cells. Redistribution of blood flow to low-resistance, short time–constant vascular beds (such as skeletal muscle) results in decreased resistance to venous return, as illustrated in Figure 33-5 (lower panel) by a steeper venous return curve. As a result, cardiac output may be increased even when cardiac function is decreased (see Fig. 33-5, lower panel) because of decreased contractility (see Fig. 33-5, upper panel). Hypovolemia, caused by redistribution of fluid out of the intravascular compartment and to decreased venous tone, can limit venous return during inadequately resuscitated septic shock.
Early institution of appropriate antibiotic therapy and surgical drainage of abscesses or excision of devitalized and infected tissue is central to successful therapy. Many anticytokine and anti-inflammatory therapies and inhibition of nitric oxide production have not been successful in improving outcome.
As detailed in Table 33-4, there are many less common etiologies of shock, and the diagnosis and management of several causes of high right atrial pressure hypotension are discussed elsewhere in this book (see Chaps. 35, 38, and 40). A few other types of hypovolemic shock merit early identification by their characteristic features and lack of response to volume resuscitation including neurogenic shock and adrenal insufficiency. Anaphylactic shock results from the effects of histamine and other mediators of anaphylaxis on the heart, circulation, and the peripheral tissues (see Chap. 128). Despite increased circulating catecholamines and the positive inotropic effect of cardiac H2 receptors, histamine may depress systolic contractility via H1 stimulation and other mediators of anaphylaxis. Marked arterial vasodilation results in hypotension even at normal or increased cardiac output. Like septic shock, blood flow is redistributed to short time–constant vascular beds. The endothelium becomes more permeable, so fluid may shift out of the vascular compartment into the extravascular compartment, resulting in intravascular hypovolemia. Venous tone and therefore venous return are reduced, so the mainstay of therapy of anaphylactic shock is fluid resuscitation of the intravascular compartment and includes epinephrine and antihistamines as adjunctive therapy.48
Neurogenic shock is uncommon. In general, in a patient with neurologic damage that may be extensive, the cause of shock is usually associated with blood loss. Patients with neurogenic shock develop decreased vascular tone, particularly of the venous capacitance bed, which results in pooling of blood in the periphery. Therapy with fluid will increase mean systemic pressure. Catecholamine infusion will also increase mean systemic pressure, and stimulation of α-receptors will increase arterial resistance, but these are rarely needed once circulation volume is repleted.
Several endocrinologic conditions may result in shock. Adrenal insufficiency (Addison disease, adrenal hemorrhage and infarction, Waterhouse-Friderichsen syndrome, adrenal insufficiency of sepsis, and systemic inflammation) or other disorders with inadequate catecholamine response may result in shock or may be important contributors to other forms of shock.22 Whenever inadequate catecholamine response is suspected, diagnosis should be established by measuring serum cortisol and conducting an ACTH stimulation test (see Chap. 102). Hypothyroidism and hyperthyroidism may in extreme cases result in shock; thyroid storm is an emergency requiring urgent therapy with propylthiouracil or other antithyroid drug, steroids, propranolol, fluid resuscitation, and identification of the precipitating cause49 (see Chap. 103). Pheochromocytoma may lead to shock by markedly increasing afterload and by redistributing intravascular volume into extravascular compartments.50 In general, the therapeutic approach involves treating the underlying metabolic abnormality, resuscitating with fluid to produce an adequate cardiac output at the lowest adequate filling pressure, and infusing inotropic drugs, if necessary, to improve ventricular contractility if it is decreased. Details of diagnosis and therapy of shock associated with poisons (carbon monoxide, cyanide) are discussed in Chap. 124.