When the heart stops beating (see Fig. 20-1), pressure equalizes throughout the vascular system, and its new value is the Pms (10 to 15 mm Hg). This pressure is much lower than the arterial pressure and is closer to the Pra. When flow stops, blood drains from the high-pressure, low-volume arterial system into the high-volume, low-pressure venous system, which accommodates the displaced volume with little change in pressure. When the heart begins to beat again, the left heart pumps blood from the central circulation into the systemic circuit, thus increasing pressure there. At the same time, the right heart pumps blood into the lungs, thereby decreasing its pressure (Pra) with respect to Pms, so blood flows from the venous reservoir into the right atrium. Pressure on the venous side decreases slightly below Pms, whereas pressure on the arterial side increases considerably above Pms with succeeding heartbeats. This continues until a steady state is reached, when arterial pressure has increased enough to drive the whole SV of each succeeding heartbeat through the high arterial resistance into the venous reservoir. The Pms does not change between the state of no flow and the new state of steady flow because neither the vascular volume nor the compliance of the vessels has changed. What has changed is the distribution of the vascular volume from the compliant veins to the stiff arteries; this volume shift creates the pressure difference driving flow through the circuit.1,2,17,18
Pms is the driving pressure for VR to the right atrium when circulation resumes. It can be increased to increase VR by increasing the vascular volume or by decreasing the unstressed volume and compliance of the vessels.17,18 The latter two mechanisms are mediated by baroreceptor reflexes responding to hypotension by increasing venous tone and usually occur together. The unstressed volume also may be reduced by raising the legs of a supine patient or applying military antishock trousers; both methods return a portion of the unstressed vascular volume from the large veins in the legs to the stressed volume, thereby increasing Pms and VR. When the heart has an improvement in inotropic state or a reduction in afterload, blood is shifted from the central compartment to the stressed volume of the systemic circuit, thereby increasing Pms and VR;18 moreover, improved ventricular pumping function decreases Pra to increase VR further (see below).
Venous Return and Cardiac Function Curves
Before the heart was started in the discussion above, Pra was equal to the pressure throughout the vascular system, Pms. With each succeeding heartbeat, Pra decreases below Pms and VR increases. This sequence is repeated in a more controlled, steady state by replacing the heart with a pump set to keep Pra at a given value while VR is measured.17,18 Typical data are plotted in Fig. 20-6. As Pra is decreased from 12 to 0 mm Hg (indicated by the thin continuous line), VR is progressively increased with the driving pressure (Pms − Pra). The slope of the relation between VR and Pms − Pra is the resistance to VR (RVR = Δ[Pms − Pra]/ΔVR). When Pra falls below zero, VR does not increase further because flow becomes limited while entering the thorax. This occurs when the pressure in these collapsible great veins decreases below the atmospheric pressure outside the veins. Further decreases in Pra and CVP are associated with progressive collapse of the veins rather than with an increase in VR.
Control of cardiac output by systemic vessels. Venous return (VR) or cardiac output (Q̇T) is plotted on the ordinate against right atrial pressure (Pra) on the abscissa. A, B. The thin continuous VR curve shows that VR increases as Pra decreases below Pra equal to mean systemic pressure (Pms; where VR = 0), so the inverse of the slope of this VR curve ([Pms − Pra]/VR) is the resistance to VR (RVR). The thick continuous cardiac function curve shows that Q̇T increases as Pra increases because ventricular end-diastolic volume increases. The intersection (shown in A) marks the unique value of Pra where VR equals Q̇T in A and B. When this value of Q̇T is insufficient, VR can be increased by increasing Pms without changing RVR, indicated by the interrupted VR curve intersecting the unchanged cardiac function curve at a higher Q̇T and Pra (shown in B, left panel). In the right panel, VR is increased from point A to point B by increased cardiac function (see interrupted cardiac function curve intersecting the original VR curve at point B). Accordingly, inotropic agents that increase contractility (dobutamine) can produce modest increases in VR by lowering Pra, but further increases in VR are limited by compression of the great veins at lower values of Pra (right panel); such an enhanced cardiac function displaces central blood volume into the peripheral circulation, tending to increase Pms and thus promote further increases in VR (left panel). Often, other inotropic agents (dopamine, epinephrine) also raise Pms and VR by venoconstriction.
For a given stressed vascular volume and compliance, Pms is set and RVR is relatively constant. In the absence of pulmonary hypertension or right heart dysfunction, LV function will determine Pra and, hence, VR to the right heart, which must equal the Q̇T from the left heart. Q̇T is described by the cardiac function curve, drawn as a thick continuous line relating Pra (abscissa) to Q̇T (ordinate), in Fig. 20-6. The heart is able to eject a larger SV and Q̇T when the end-DP is greater because more distended ventricles eject to about the same end-systolic volume as less distended ventricles do. Accordingly, as Pra decreases, Q̇T decreases along the cardiac function curve. However, VR increases as Pra decreases until VR equals Q̇T at a unique value of Pra, indicated by the intersection of the cardiac function and VR curves in Fig. 20-6 (see point A in both panels).
When Q̇T is insufficient, VR can be increased in several ways. A new steady state of increased VR is achieved by increasing Pms with no change in RVR, indicated by the interrupted VR curve in the left panel of Fig. 20-6. This new VR curve intersects the same cardiac function curve at a higher value of Q̇T at point B. This method of increasing VR is associated with an increase in Pra. Due to the steep slope of the cardiac function curve in normal hearts, large increases in VR occur with only small increases in Pra. Alternatively, VR can be increased by enhanced cardiac function by increasing contractility or decreasing afterload of the heart. This is depicted as an upward shift of the cardiac function curve, as in the right panel of Fig. 20-6, such that greater Q̇T occurs at each Pra. The increase on each VR curve by this mechanism is associated with a reduction in Pra. Further, in the normal heart, only a small change in VR is possible (from point A to point B in the right panel), and greater reductions in Pra do not increase Q̇T further because VR becomes flow limited as Pra decreases to below zero. This explains why inotropic agents that enhance contractility are ineffective in hypovolemic shock.
When cardiac pumping function is depressed, as depicted by the interrupted line in Fig. 20-7, VR is decreased from point A to point B for the same value of Pms as Pra increases. The patient must then retain fluid or initiate cardiac reflexes to increase Pms toward the new value required to maintain adequate Q̇T, as in chronic congestive heart failure. This is associated with a large increase in Pra from point B to point C, which in turn causes jugular venous distention, hepatomegaly, and peripheral edema. Diuretic reduction of vascular volumes will correct these cosmetic abnormalities at the expense of decreasing Pms and VR. In contrast, inotropic and vasodilator drugs, which improve depressed cardiac function by shifting the interrupted cardiac function curve upward, increase Q̇T and decrease Pra more effectively than in patients with normal cardiac function.
Reduced cardiac function (interrupted curve BC) decreases steady-state venous return from A to B because right atrial pressure (Pra) increases along the normal venous return curve (continuous line AB). In response, baroreceptor reflexes and/or vascular volume retention increase mean systemic pressure such that the new interrupted venous return curve intersects the depressed cardiac function curve at C, whereby caridac output has returned to normal at increased Pra. The new steady state can be produced by systolic or diastolic dysfunction of the left or right ventricle. For further discussion, see text.
Effects of Pressure Outside the Heart on Cardiac Output
In the figures cited and the preceding discussions, values of Pms and Pra were expressed relative to atmospheric pressure. However, the transmural pressure of the right atrium exceeds the Pra by the subatmospheric value (about −4 mm Hg) of the Ppl surrounding the heart. Consider the effect of opening the thorax, which raises Ppl from −4 to 0 mm Hg: VR decreases from point A to point B in Fig. 20-8 because Pra increases.19 This is indicated by the interrupted cardiac function curve shifted to the right by the increase in pressure outside the heart but parallel to the normal cardiac function curve (continuous line through point A). Normal VR can be restored (point B to point C) by increasing Pms by an amount equal to the increase in Ppl and Pra induced by thoracotomy. Then transmural Pra will be the same as at point A, and Pra will have increased from point A to point C at the same Q̇T.
Schematic showing effects of increased pleural pressure (Ppl) on venous return (VR) and cardiac output (Q̇T). Compared with the normal steady state (continuous VR and cardiac function curves), increasing Ppl and right atrial pressure (Pra) by 4 mm Hg shifts the normal cardiac function curves to the right (interrupted cardiac function curve BC) so that venous return decreases from A to B. This accounts for the decrease in Q̇T when thoracotomy exposes the right atrium to atmospheric pressure; similarly, the increase in Ppl and Pra when positive end-expiratory pressure (PEEP) is applied to a patient with an intact thorax decreases Q̇T. In both cases, baroreceptor reflexes or iatrogenic expansion of vascular volume increase Pms to allow the new interrupted VR curve to intersect the displaced cardiac function curve at C, thereby returning Q̇T to normal. A much larger increase in PEEP increases Ppl and Pra even more so that the displaced normal cardiac function curve (dotted curve DE) intersects the normal VR curves at a very low value (E) required by a larger increase in mean systemic pressure to allow the new interrupted VR curve to intersect the dotted function curve at E. For further discussion, see text.
This mechanism for the decrease in Q̇T with thoracotomy also partly explains the decrease in Q̇T with PEEP. The Ppl within an intact thorax increases with passive positive-pressure ventilation, thereby increasing Pra and decreasing VR.4,5,8,9,20 When 8 mm Hg of PEEP (10 cm H2O) is added to the ventilator, the end-expiratory value of Ppl increases by about half that amount, e.g., from −4 to 0 mm Hg. Accordingly, VR decreases with PEEP from point A to point B in Fig. 20-8, with no change in cardiac function or Pms. Q̇T is returned to normal by volume infusion or vascular reflexes that increase Pms by an amount equal to the increases in Ppl and Pra. Greater PEEP (20 cm H2O, as in the dotted line shown in Fig. 20-8) decreases VR further (from point A to point D) and requires greater increases in Pms to return it to normal (from point D to point E). Alternatively, Pms increases as much as Pra when PEEP is added, so the decrease in VR must be due to an increase in RVR with PEEP.20 In either event, VR can be restored on PEEP by increasing Pms.
Q̇T is much less susceptible to the deleterious effects of PEEP when Pms is high. In patients with reduced circulatory volume, vascular reflexes are already operating to maintain VR and Pms by reducing unstressed volume or vascular compliance. Such patients have little vascular reflex reserve and poorly tolerate intubation and positive-pressure ventilation without considerable intravenous infusion to increase vascular stressed volume. In contrast, well-hydrated or overhydrated patients may tolerate even large amounts of PEEP with no reduction in Q̇T because their previously inactive vascular reflexes can increase Pms in well-filled systemic vessels by the amount that Ppl increases with PEEP. These considerations allow the physician to anticipate and treat the hypotension induced by ventilator therapy; the concept should not be interpreted as an indication for maintaining high circulatory volume in critically ill patients on ventilators because this often increases lung edema and provides even more Q̇T than was already deemed sufficient. Further, pressure outside the heart can be increased by a variety of other concomitant conditions and complications of critical illness; all these actions increase pressures measured in the heart chambers and decrease heart volume and, as a consequence, are often interpreted as diastolic dysfunction (see Table 20-1).
How much is the pressure outside the heart increased by PEEP, and is there a practical approach to relating the transmural wedge pressure to SV and Q̇T? When PEEP increases end-expired lung volume, the inflated lungs push the thorax to an increased volume through greater pleural pressure, and this change in Ppl (ΔPpl) with PEEP is approximately equal to the change in pressure outside the right and left ventricles.8 During mechanical ventilation, the ratio of ΔPpl to the change in static elastic pressure across the lung and chest wall (ΔPel) for each breath is given by the ratio of respiratory system compliance (Crs) to the compliance of the chest wall (Cw); that is, ΔPpl/ΔPel = Crs/Cw (assuming no alveolar recruitment). When lung compliance (CL) is normal, CL = Cw, so ΔPpl/ΔPel = 0.5. When the lungs lose compliance in acute hypoxemic respiratory failure (AHRF), ΔPel increases because Crs decreases, but ΔPpl changes little (at constant tidal volume) because Cw is unaffected by the lung disease, and ΔPpl becomes much less than half of ΔPel. To the extent that the increase in lung volume (ΔVL) with PEEP is determined by Crs, ΔPpl/PEEP = Crs/Cw, and a decrease in Crs with AHRF would decrease Ppl for a given amount of PEEP well below the normal value of 0.5. However, ΔVL with PEEP is much greater than that predicted by Crs in AHRF because PEEP recruits many previously flooded airspaces,21,22 so ΔPpl/PEEP is as great after acute lung injury as before4 (Fig. 20-9). Accordingly, the ΔPpl with PEEP is difficult to measure and hard to predict, so many approaches have been tested to estimate the transmural pressure of heart chambers on PEEP.23 Because PEEP is used most often to decrease shunt in pulmonary edema and because accurate knowledge of transmural Pla shows that the value associated with an adequate Q̇T can differ between patients by 20 mm Hg according to the extent of LV dysfunction, a better approach is to seek the lowest pulmonary wedge pressure (Ppw) that provides adequate output on each level of PEEP. In this way, therapy to decrease Ppw and edema and maintain Q̇T is not confounded by erroneous estimates of transmural Ppw on PEEP.24,25
Relations between lung volume (percent total lung capacity, TLC; ordinate) and pressure across the respiratory system (pressure airway opening [cm H2O], Pao; abscissa). The thin continuous line represents the inflation volume-pressure (V-P) relation of the normal respiratory system, showing an end-expired lung volume (Pao = 0) of 50% TLC and inflation compliance (V-P) during a tidal volume of about 10% TLC (thick part of line). In contrast, the interrupted line shows the inflation V-P curve after pulmonary edema floods many lung units, thereby decreasing end-expired lung volume to about 30% TLC; then a tidal inflation of the same volume causes a much larger increase in Pao because there are many fewer airspaces to accommodate the tidal volume. Adding 15 cm H2O positive end-expiratory pressure (PEEP) might be expected to produce a much smaller increase in end-expired lung volume in edematous lungs than in a normal respiratory system; however, when PEEP is effective in reducing shunted fraction of total pulmonary blood flow by redistributing alveolar edema, the increase in end-expired lung volume (and, hence, pleural pressure) is as large after pulmonary edema as in the normal respiratory system (table at right of graph). (Reproduced with permission from Prewitt and Wood4 and Hall and Wood.24)
An Approach to Hypoperfusion States
A hypoperfusion state, or shock, is almost always signaled by systemic hypotension; commonly associated clinical features of multiple organ system hypoperfusion are tachycardia, tachypnea, prerenal oliguria (urine flow < 20 mL/h, urine Na+ > 20 mEq/L, urine K+ > 20 mEq/L, urine-specific gravity > 1.020), abnormalities of mentation and consciousness, and metabolic acidosis. The mean BP is determined by the product of Q̇T and SVR. A conceptual framework for the initial diagnosis and management of the hypotensive patient is outlined in Table 20-2. Utilization of this approach aims to categorize the patient's symptoms into one of the three common causes of shock (septic, cardiogenic, or hypovolemic) and to initiate early appropriate therapy of the presumed diagnosis (see Chap. 21). Response to the therapeutic intervention tests the accuracy of the initial diagnosis, so the hemodynamic response is reevaluated within 30 minutes. The diagnostic decision is aided by collating clinical data from the medical history, physical examination, and routine laboratory tests to answer three questions in sequence.
Table 20–2. Initial Approach to the Diagnosis and Management of the Hypotensive Patient ||Download (.pdf)
Table 20–2. Initial Approach to the Diagnosis and Management of the Hypotensive Patient
|Blood pressure (BP) = Cardiac output (Q̇t) × systematic vascular resistance (SVR)|
|IS Q̇t REDUCED?|
|BP||90/70 mm Hg||90/40 mm Hg|
|Skin||Cool, blue||Warm, pink|
|Nail bed return||Slow||Rapid|
|History/lab||Hypervolemic or cardiogenic etiology||↓ or ↑ WBC and/or temperature|
|Source of infection|
|Severe liver disease|
|Working diagnosis||See next question||Septic shock/endotoxemia|
|IS THE HEART TOO FULL?|
|Presentation||Angina, dyspnea||Hemorrhage, dehydration|
|Signs||Cardiomegaly||Dry mucous membranes|
|Extra heart sounds||↓ tissue turgor|
|↑ JVP||Stool, gastric blood|
|Lab||ECG, x-ray||↓ hematocrit|
|Working diagnosis||Cardiogenic shock||Hypovolemic shock|
|WHAT DOES NOT FIT?|
|Acute pulmonary hypertension||Spinal shock|
|Right ventricular infarction||Adrenal insufficiency|
|Overlapping multiple etiologies|
Is BP decreased because Q̇T is decreased? If not, SVR must be reduced, a condition almost always related to sepsis or sterile endotoxemia associated with severe liver disease. As indicated in Table 20-2 (right column), a low BP is often characterized by a large PP because the SV is large and by a very low DP because each SV has a rapid peripheral runoff through dilated peripheral arterioles (see Fig. 20-3). This produces warm, pink skin with rapid return of color to the nail bed and crisp heart sounds. As in other types of shock, tachycardia is evident due in part to baroreceptor reflex response to hypotension, but the arterial vasoconstriction response to reflex sympathetic tone is blocked by relaxation of arteriolar smooth muscle induced by endothelium-derived relaxing factor (or nitric oxide). The combination of tachycardia and large PP indicates a large Q̇T that is almost always present early unless concurrent hypovolemia or myocardial dysfunction precludes the hyperdynamic circulatory state of sepsis.
Initial therapy starts with appropriate broad-spectrum antibiotics (see Chap. 46) and expands the circulating volume by intravenous infusion of fluids to treat associated hypovolemia, which is due to venodilation decreasing Pms and VR lower than needed to maintain adequate perfusion pressure of vital organs. The end point of volume infusion is obscure because Q̇T and oxygen delivery (DO2) are already increased, and although Q̇T usually increases further with intravenous infusions, BP increases little with increased Q̇T. Further, the need for an even greater Q̇T to increase DO2 is questionable because the lactic acidosis of septic shock may not be due to anaerobic metabolism.26–28 Accordingly, septic patients in whom Q̇T is maximized do not have improved survival.29,30 Conversely, pulmonary vascular pressures always increase with volume infusion, thus increasing pulmonary edema when the septic process increases the permeability of lung vessels.25,31–33 This coincidence of the acute respiratory distress syndrome (ARDS) and septic shock has created an apparent dilemma concerning fluid therapy and cardiovascular management of these conditions. My approach is to ensure resuscitation from septic shock as the first priority by ensuring a large Q̇T with a Ppw that does not exceed 15 mmHg and add dobutamine to increase Q̇T and BP as necessary.25 When early ARDS is not associated with septic shock, I seek the lowest circulating volume to provide adequate Q̇T.25
The septic myocardium does not function normally,34,35 but this dysfunction is often associated with SV values larger than 100 mL at normal values of LVEDP. Accordingly, it seems unlikely that systolic dysfunction contributes substantially to the shock, but infusion of dobutamine does increase Q̇T for a given high-normal LVEDP without increasing O2 uptake or correcting lactic acidosis in septic shock.36 Even when Q̇T and DO2 are made adequate with fluid and dobutamine infusions, the perfusion pressure for vital organs such as the brain and heart may still be too low in some septic patients. In this case, norepinephrine infusion increases BP and splanchnic blood flow37,38 without compromising renal function;39 in contrast, dopamine and epinephrine infusions cause splanchnic hypoperfusion in septic shock.37,38,40 Tachypnea and respiratory distress may be severe, so initial supportive therapy includes consideration of early intubation and mechanical ventilation and correction of hyperthermia with antipyretics, paralysis, and cooling (see Table 21-4). This prevents catastrophic respiratory muscle fatigue, respiratory acidosis, and the complications of emergent intubation and may improve tissue oxygenation by reducing O2 requirements in patients with limited DO2.41,42
In contrast to septic shock, low Q̇T is signaled by low PP indicating low SV (see Fig. 20-3), signs of increased systemic vascular resistance (e.g., cold, blue, damp extremities and poor return of color to the nail bed), and a history or presentation including features suggesting a cardiogenic or hypovolemic cause of hypotension. If Q̇T is reduced in the hypotensive patient, then the heart may be too full.
A heart that is too full (see Table 20-2) is often signaled by symptoms of ischemic heart disease or arrhythmia, signs of cardiomegaly, the third and fourth sounds or gallop rhythm of heart failure, new murmurs of valvular dysfunction, increased jugular or CVP, and laboratory tests suggesting ischemia (e.g., electrocardiogram [ECG] or creatine phosphokinase determination) or ventricular dysfunction (e.g., chest x-ray suggesting cardiomegaly, a widened vascular pedicle, or cardiogenic edema or echocardiogram showing regional or global systolic dyskinesia). The most common cause of hypotension associated with a circulation that is too full on initial evaluation is cardiogenic shock due to myocardial ischemia (see Chaps. 22 and 25). Initial therapy treats this presumptive diagnosis with inotropic drug therapy (dobutamine 3 to 10 μg/kg per minute) to assist the ejecting function of the ischemic heart. Such therapy does not directly address the coronary insufficiency and may increase the myocardial O2 demand, especially if it causes tachycardia. Concurrent sublingual, dermal, or intravenous nitroglycerin ameliorates elements of coronary vasospasm to increase blood flow and reduces preload to decrease myocardial O2 consumption. Morphine also decreases pain, anxiety, and preload.43
In this situation, even a cautious volume challenge (250 mL 0.9% NaCl over 20 minutes) may be risky because ventricular function and Q̇T are decreased as often as they are increased by this intervention, and the risk of pulmonary edema is increased. When signs of pulmonary edema are present on clinical and radiologic examinations of the thorax, diuretics, morphine, and nitroglycerin often reduce preload by relaxing the capacitance veins, associated with an increase in LV systolic performance. However, about 10% of patients with myocardial ischemia present with significant hypovolemia. Accordingly, the clinical assessment of hemodynamics should be supplemented as soon as possible with other means to exclude hypovolemia (e.g., right heart catheterization, empiric volume challenge, echocardiography, or dynamic tests of the adequacy of circulating volume) so that appropriate volume infusion or reduction can be titrated. When these measures are addressed adequately but the hypoperfusion state persists, early movement toward arteriolar vasodilator therapy or a balloon-assist device is indicated to reduce LV afterload and preserve coronary perfusion pressure (see Chap. 25). These latter interventions are not relegated to the last resort but are considered early in this initial stabilization of cardiogenic shock. Similarly, early elective intubation and mechanical ventilation allow effective sedation and reduce O2 consumption,41 and PEEP improves arterial oxygenation, often without reducing VR and with improvement of pumping function in the damaged left ventricle by reducing preload and afterload.44
Beyond the absence of clinical features suggesting that the heart is too full in the hypotensive patient who is presenting reduced Q̇T (see Table 20-2), hypovolemic shock is distinguished from cardiogenic shock by several positive clinical features. Often there is an obvious source of external bleeding (e.g., multiple trauma, hemoptysis, hematemesis, hematochezia, or melena); internal bleeding is often signaled by blood aspirated from the nasogastric tube or on rectal examination, by increasing abdominal girth, or by clinical and radiologic examinations of the thoracic cavity for pleural, alveolar, retroperitoneal, or periaortic blood. Each of these signals is often associated with a new reduction in the hematocrit. Nonhemorrhagic hypovolemia often presents with recognizable excess gastrointestinal fluid losses (e.g., vomiting, diarrhea, suctioning, and stomas), excess renal losses (e.g., osmotic or drug diuresis and diabetes insipidus), or third-space losses as in extensive burns. Physical examination shows dry mucous membranes with decreased tissue turgor, and routine laboratory tests often show increased serum urea nitrogen out of proportion to a relatively normal creatinine level and increased hematocrit due to hemoconcentration.
The initial management of patients with presumed hypovolemic shock necessitates early vascular access with two large-bore (14-gauge) peripheral intravenous catheters for rapid infusion of large volumes of warmed blood and fluids for hemorrhagic shock and the appropriate crystalloid solution for dehydration. Central venous access ensures adequate volume resuscitation and allows early measurement of CVP. An immediate response of increased BP and pulse volume supports the presumed diagnosis, whereas no improvement in these hemodynamic measurements necessitates emergent repair of the site of blood loss or a reevaluation of the working diagnosis. Achieving hemostasis in hemorrhagic shock is a prerequisite for adequate volume resuscitation: urgent and simultaneous pursuit of hemostasis and fluid resuscitation is encouraged.45 Vasoconstricting drugs such as norepinephrine should be used only as short-term antihypotensives to mobilize endogenous unstressed volume or enhance arteriolar vasoconstriction until the circulating volume is restored by transfusion; prolonged use of these drugs confounds the physician's assessment of the end point of volume resuscitation. Early endotracheal intubation and mechanical ventilation reduce the patient's work of breathing and allow respiratory compensation for lactic acidosis during volume resuscitation; warming the fluids and covering the patient with warm dry blankets prevent the complication of hypothermia, including cold coagulopathy and further bleeding (see Table 21-4).
Other Common Causes of Shock: A Short Differential Diagnosis
The purpose of this initial schema is to formulate a working diagnosis for the most common presentations of shock so that early and rapid therapy can be initiated. The response to the initial therapy confirms or challenges the working diagnosis. When features of the initial clinical presentation or the response of the patient to appropriate management challenges the working diagnosis, early acquisition of more objective hemodynamic data is appropriate. In the interim, other features of the clinical presentation often suggest a cause of shock that falls outside this simplistic schema, or the possibility of overlapping or concurrent causes expands. This section briefly reviews several important differential diagnostic conditions for cardiogenic shock (e.g., tamponade or acute right heart syndromes) and hypovolemic shock (e.g., anaphylactic, neurogenic, or adrenal shock; (see Table 20-2, what does not fit?).
Pericardial effusion is often suggested early by the clinical setting (e.g., renal failure, malignancy, or chest pain), physical examination (e.g., elevated neck veins, systolic BP that decreases >10 mm Hg on inspiration, or distant heart sounds), or routine investigations (e.g., chest radiograph with “water bottle” heart, low voltage on the ECG, or electrical alternans). Such a constellation of clinical data requires early echocardiographic confirmation of pericardial effusion, and tamponade is signaled by right ventricular and right atrial collapse that worsens with inspiration, with a relatively small left ventricle (see Chap. 28). Tamponade requires urgent pericardiocentesis or operative drainage by pericardiostomy. While deciding on definitive treatment, one should remember that intravenous expansion of the circulating volume may produce small increases in BP, whereas reductions in circulating volume (e.g., diuretics, nitroglycerin, morphine, or intercurrent hemodialysis) are often associated with catastrophic reduction in Q̇T by reducing the venous tone and volume necessary to maintain the Pms required to drive VR back to high Pra.
Right heart catheterization typically shows a Pra increased to about 16 to 20 mm Hg and equal to pulmonary arterial DP and the arterial Pwp; Q̇T and SV are much reduced (see Chap. 28). This hemodynamic subset resembles that of cardiogenic shock (high Ppw and low SV). However, in the case of pericardial tamponade, Ppw is increased because pericardial pressure is increased, so the transmural pressure of the left ventricle approaches zero, a value consistent with the very low LVEDV accounting for the low SV. Other etiologies of hypotension associated with high cardiac pressures and small ventricular volumes include constrictive pericarditis, tension pneumothorax, massive pleural effusion, positive-pressure ventilation with high PEEP, and very high intraabdominal pressure (see Table 21-1). Up to 33% of patients presenting with cardiac tamponade have increased BP despite low Q̇T; this subset of patients has a high incidence of hypertension preceding the onset of tamponade.46
Right Ventricular Overload and Infarction
Another clinical presentation that may fall outside the simplest scheme presented in Table 20-2 is the hypotension associated with acute or acute-on-chronic pulmonary hypertension. Shock after acute pulmonary embolism is often signaled by the clinical setting including risk factors (e.g., perioperative, immobilized, thrombophilia, or prior pulmonary embolisms); symptoms of acute dyspnea, chest pain, or hemoptysis; physical examination showing a loud P2 with a widened and fixed split of the second heart sound; new hypoxemia without obvious radiologic explanation; and acute right heart strain on the ECG (see Chap. 27). Noninvasive Doppler studies of the veins in the lower extremities and helical computed tomographic angiography confirm the diagnosis. Anticoagulation or placement of a filter in the inferior vena cava reduces the incidence of subsequent emboli, and there may be some success with thrombolytic therapy (or, in some centers, surgical removal of the embolus) in patients with shock due to pulmonary embolism. Acute-on-chronic pulmonary hypertension causes shock in the setting of prior primary pulmonary hypertension, recurrent pulmonary emboli, progression of collagen vascular disease, or chronic respiratory failure (e.g., chronic obstructive pulmonary disease or pulmonary fibrosis) aggravated in part by hypoxic pulmonary vasoconstriction. In these circumstances, O2 therapy and pulmonary vasodilator therapy combine to decrease pulmonary hypertension and increase Q̇T in a small but significant proportion of patients (see Chap. 27).
Right heart catheterization shows a unique hemodynamic profile: a very high mean pulmonary artery pressure, pulmonary arterial DP considerably greater than the Pwp, and reduced Q̇T and SV. Not uncommonly, arterial Pwp is normal or increased despite a small LVEDV on echocardiographic examination, which also shows a right-to-left shift of the interventricular septum; presumably, this causes stiffening of the diastolic V-P curve of the left ventricle. A complication of pulmonary vasodilator therapy is hypotension due to systemic arterial dilation unaccompanied by increased right heart output. Such effects aggravate the hypoperfusion state, perhaps by reducing coronary blood flow to the hypertrophied, dilated right ventricle. Some evidence suggests that shock associated with pulmonary hypertension is ameliorated by α-agonist therapy (e.g., norepinephrine or phenylephrine), which acts as a predominant systemic arteriolar constrictor to increase BP sufficiently to maintain right ventricular perfusion.47,48
Right ventricular infarction causes low pulmonary artery pressures and normal LV filling pressures because the dilated, injured right ventricle is unable to maintain adequate flow to the left heart.49 Elevated neck veins and Pra tend to decrease with dobutamine infusion, perhaps because the enhanced contractility of the left ventricle improves systolic function of the mechanically interdependent right ventricle.45,46 Volume expansion often aggravates right ventricular dysfunction, and systemic vasoconstriction may preserve right ventricular perfusion.50
Anaphylactic, Neurogenic, and Adrenal Shock
Other etiologies of shock having unique clinical presentations that usually lead to early diagnosis are anaphylactic shock and neurogenic shock. Beyond identifying the etiology early through their association with triggering agents and trauma, respectively, the physician should note that the pathophysiology of each is a dilated venous bed with greatly increased unstressed volume of the circulation leading to hypovolemic shock. Accordingly, the mainstay of therapy for both conditions is adequate volume infusion; adjunctive therapy for anaphylaxis includes antihistamines, steroids, and epinephrine to antagonize the mediators released in the anaphylactic reaction (see Chap. 106), whereas a careful search for sources of blood loss and hemorrhagic shock is part of the early resuscitation of spinal shock in the traumatized patient (see Chap. 94).
Not uncommonly, the presentation of patients with nonhemorrhagic hypovolemic shock raises the concern of acute adrenal cortical insufficiency. When this possibility is not obviously excluded, it is appropriate to draw a serum cortisol level, provide adequate circulating steroids with dexamethasone, and conduct a corticotropin stimulation test to confirm or refute the diagnosis. Characteristically, hypotension and hypoperfusion in such patients will not respond to adequate vascular volume expansion until dexamethasone is administered (see Chap. 79).
Multiple Etiologies of Shock
With this differential diagnosis and management evaluation in mind, the initial approach to patients with hypoperfusion states should be completed in less time than it takes to read about it. The target is to distinguish among patients with septic shock, cardiogenic shock, and hypovolemic shock and to initiate an appropriate therapeutic challenge—antibiotics, inotropic agents, or a volume challenge—within 30 minutes of presentation. By the response, the diagnosis is confirmed or challenged, with special regard to equivocal responses to therapy or to several other diagnostic categories of shock. Sorting out the primary etiology of the hypoperfusion state often requires considerable additional data. This process is rendered more complex by concurrent etiologies contributing to the shock, for example, the patient with septic shock unable to increase Q̇T due to intercurrent myocardial dysfunction, the patient with acute myocardial infarction who is hypovolemic, or the patient with hemorrhagic shock who becomes septic. Other combinations of these major categories overlap with confounding effects of tamponade, positive-pressure ventilation, pneumothorax, and pulmonary hypertension—all to challenge ongoing diagnostic and management approaches.