Chapter 103. Decreased Perfusion and Circulatory Shock

Systemic perfusion can be reduced by a wide variety of processes and diseases that affect the infant and child. If the poor perfusion is not promptly recognized and appropriate intervention taken, there can be rapid progression to circulatory shock, a life-threatening state. While the regulatory mechanisms that control circulatory function are similar at all ages, some developmental features render the infant and young child vulnerable to shock: (1) the infant’s high surface-to-mass ratio causes excessively high insensible water loss when there is fever, hypermetabolism, or a dry environment; (2) the lack of free access to fluids limits the infant’s ability to restore a fluid-volume deficit; (3) the exposure to certain pathogens and susceptibility to overwhelming infection predispose the young infant to septicemia; and (4) the perinatal closure of the ductus arteriosus can precipitate a severely reduced systemic perfusion in the presence of aortic stenosis or coarctation. The clinician who examines the child with poor perfusion must thoroughly, rigorously, and quickly assess the extent of the impairment to determine the most likely mechanism(s) contributing to the circulatory disturbance and to initiate therapy to restore circulation.

Reduced systemic perfusion provokes some physical manifestations that are nonspecific and some that reveal valuable information about the cause of the particular disturbance. Any of these signs should serve as a prompt for medical attention. Nonspecific signs (eg, lassitude, hypotension, delayed capillary refill, pallor) provide information about the severity of the dysfunction but are not unique to a specific circulatory disturbance. Other, more specific signs (eg, crackles, gallop rhythm, peripheral edema, and hepatosplenomegaly) are not found in all patients, because they result from the physiological alterations produced by particular circulatory disturbances; these often provide valuable clues about the cause or mechanism of the derangement.

In considering both nonspecific and specific manifestations, it is useful to start by clarifying some terms. Impaired perfusion describes any state in which blood flow to the tissues is appreciably decreased. It encompasses a wide range of problems, from mild decreases in the circulating blood volume to cardiovascular collapse. Shock is the extreme form of impaired perfusion in which systemic blood flow is insufficient to sustain vital functions. An essential component of shock is that it is an unstable state; if left untreated, and possibly even if treated, it causes progressive dysfunction of multiple organs, signs of severe tissue ischemia (eg, lactic acidemia), and death. Congestive heart or circulatory failure (see Chapter 497) is another form of impaired perfusion in which the compensatory mechanisms of the cardiovascular system maintain vital functions but cause the patient to suffer complications from the adaptations (eg, peripheral and pulmonary edema, azotemia). Congestive circulatory failure is a more stable state than shock.

Understanding how disease can alter the normal mechanisms that maintain and regulate tissue perfusion greatly facilitates assessing the child with impaired systemic blood flow.

Blood flow and the supply of nutrients are normally in great excess of metabolic demands. At rest, nearly 75% of the oxygen transported in arterial blood is returned to the right side of the heart. This large reserve permits maintenance of metabolic balance even when there is a moderate decrease in cardiac output or increase in metabolic demands1,2(see Fig. 103-1). However, when systemic blood flow is decreased relative to the tissues’ needs, a variety of compensatory mechanisms are usually activated to redistribute the circulation and to maximize the extraction of oxygen and other nutrients from the blood. In the process, there are substantial changes in the perfusion and function of organs. As stated earlier, these changes provide important signs of an impaired circulation. The ability to acclimate to an imbalance between metabolic demands and tissue perfusion depends on how quickly the disturbance begins and the presence of intact adaptive responses, some of which may be disturbed by the illness or injury.

In general, blood flow is distributed to match the metabolic needs of an organ, and blood pressure is tightly regulated so that organs such as the brain and heart remain well perfused when posture or activity change.3,4 Some organs, such as the skin and kidneys, receive blood flow well in excess of their nutritive needs, because they perform heat exchange and filtration, respectively, which necessitate high perfusion rates. When cardiac output is reduced, there are both local and systemic responses that sustain perfusion to metabolically active organs and that serve to maintain blood pressure. The redistribution of blood flow away from organs, such as the skin, gut, and kidneys, produces some characteristic changes in the physical examination that commonly help identify the child with a compromised circulation.

To understand the nature of these changes, we will briefly review the mechanisms by which blood pressure and regional blood flow are regulated. Blood pressure provides the driving force to perfuse the organs and tissues. Because there is virtually no pressure decrease from the aorta to the large arteries, most organs receive blood at the same perfusion pressure. However, there are large intraorgan differences in the resistance that regulates the distribution of blood flow so that perfusion to individual organs varies widely despite the relative uniformity of perfusion pressure; this is analogous to parallel pipes with faucets or parallel electrical circuits with resistors (see Fig. 103-2). Blood pressure is modulated by both neural and humoral influences, which serve to sustain perfusion pressure to organs throughout a wide range of cardiac output.5 For this reason, mean blood pressure is an insensitive measure of circulatory dysfunction and can be normal (or even increased) despite a marked reduction in cardiac output. This is well demonstrated by considering the relationship between pressure (P), flow (F), and resistance (R): F × R = P. When flow, or cardiac output, is reduced, the host of neural and humoral responses that increase resistance sustain mean blood pressure near normal (↓ F × ↑R = near-normal P), although pulse pressure diminishes. However, some processes such as sepsis, which interfere with vasoconstriction, can produce hypotension despite near-normal or even increased cardiac output.6

When intravascular volume, and thereby venous return, is reduced, homeostatic mechanisms are rapidly activated to increase the flow of systemic venous blood from the peripheral tissues back to the heart, restoring arterial blood pressure.7,8 The initial responses to volume depletion include venous and arterial constriction (mediated by the sympathetic nervous system) and tachycardia (from increased circulating epinephrine and reduction of the tonic vagal tone). Whenever arterial blood pressure is reduced, there is a rapid (within seconds) reflex constriction of most veins and arteries mediated by the sympathetic nervous system. Intravascular volume is sensed by low-pressure stretch receptors located in the atria and pulmonary vessels, and arterial blood pressure is sensed by carotid sinus and aortic baroreceptors. Although the venoconstriction can transiently increase venous return, it also raises venous resistance, so it is necessary for other responses to raise the driving pressure for blood to return to the right side of the heart. Some of the increase in pressure is accomplished by transcapillary refill, or autotransfusion, a process by which arteriolar constriction transiently lowers capillary hydrostatic pressure, which promotes absorption of interstitial fluid into the capillaries.9 This is why hematocrit decreases over time following hemorrhage.

In addition to the rapid responses to decreased blood pressure or volume, sympathetic stimulation of the adrenal gland causes the release of epinephrine and norepinephrine. These neural and humoral responses constrict renal afferent arterioles and stimulate renin release because of the decreased perfusion of the macula densa. Renin metabolizes angiotensinogen to angiotensin I, which is then hydrolyzed to angiotensin II by angiotensin-converting enzyme, an enzyme on the lumenal surface of endothelial cells. The angiotensin II stimulates release of aldosterone and antidiuretic hormone; each of these hormones is a potent vasoconstrictor that raises blood pressure. Furthermore, antidiuretic hormone and aldosterone promote water and sodium reabsorption, respectively, which helps restore intravascular volume. Thus, the humoral responses complement the neural reflexes and provide long-range regulation of the circulation (see Fig. 103-3). It is also important to realize that these sympathetic responses might persist when intravascular volume is restored if cardiac output is not adequate.

Perfusion to Individual Organs

Even when arterial blood pressure decreases and many arteries constrict in response, some organs maintain blood flow by local vasodilation. In several organs (eg, brain, kidney, heart), a change in perfusion pressure causes the tone of the conducting vessels to change, such that blood flow stays constant (autoregulation).10,11 Autoregulation opposes the neural and humoral stimulation by the sympathoadrenal system and the release of vasoactive peptides that tend to cause vasoconstriction when cardiac output is decreased. How much a given organ responds to the vasodilatory or the vasoconstrictive influences depends on the inherent capacity to autoregulate, the α-adrenergic innervation (causing constriction), and the density and nature of the vascular receptors. Local metabolism also influences blood flow such that arteries perfusing active tissue (eg, working muscle) dilate and maintain blood flow even in the presence of neurohumoral stimulation. Therefore, when cardiac output is decreased, organs that are usually active metabolically or have little autonomic innervation (eg, brain or heart) preserve their perfusion, whereas organs that have a low metabolic rate (eg, skin) or that have rich autonomic innervation (eg, kidney or gut) have intense vasoconstriction and reduced blood flow. These overall responses improve matching of blood flow to metabolism and, by increasing total vascular resistance, raise blood pressure.

Perfusion Within Individual Organs

Even when perfusion to an organ or tissue is reduced, local responses, including opening of previously closed capillaries and reduction in hemoglobin O2 affinity, can serve to maximize the extraction of oxygen and other nutrients from arterial blood. The increased capillary density increases vascular surface area, increases the (transit) time for exchange, and reduces the distance for diffusion of these nutrients. The local decrease in pH decreases the affinity of O2 for hemoglobin (right shift of the hemoglobin O2 dissociation curve) and permits more oxygen to be released at any given venous PO2. If extraction of O2 is not sufficient to sustain oxidative metabolism, the tissue produces excess H+ and lactate, the metabolic rate declines, and the function of that tissue is reduced.12Thus, when there is compromised perfusion to tissues, such as the skin, the cooler temperature (less perfusion with warm blood, less metabolism), prolonged capillary refill time (less perfusion), bluish or cyanotic discoloration (increased oxygen extraction and lower capillary and venous oxygen saturation), and diminished pulsation of the artery serving that tissue (vasoconstriction) all signal the impaired perfusion. For this reason, a pulse oximeter can register a very low saturation or is unable to detect a pulse in a patient with very poor perfusion (an event that should be dismissed as equipment malfunction). It is also essential to feel the pulse and evaluate perfusion whenever the oximeter has an erratic or unexpectedly low reading for saturation or heart rate.

In addition to redistributing the limited blood flow, humoral responses serve to augment cardiac output by three mechanisms. First, the heart rate is increased (response to epinephrine and reduced vagal tone). Thus, sinus tachycardia is an expected adaptive response in any child with compromised perfusion unless there is also impaired responsiveness to catecholamines. The sinus tachycardia is an essential response, because cardiac output is quite dependent on heart rate in young children. Furthermore, sinus tachycardia is a sensitive barometer for the state of perfusion, because it is expected to abate as perfusion improves. Second, contractility will also be increased by the catecholamine stimulation (norepinephrine and epinephrine); the effectiveness of this adaptation depends on the capacity of the myocardium to respond and on whether there is adequate cardiac filling. And third, venous return will be increased by the venous and arterial constriction and by the mechanisms that promote fluid retention.

Impaired perfusion arises when cardiac output to the tissues cannot keep pace with the demands for blood flow imposed by the body’s metabolism. Because cardiac output is the product of stroke volume and heart rate, it depends directly on three factors: end-diastolic or filling volume, ejection fraction, and heart rate. If any of these decrease, a decline in systemic blood flow would be expected, unless adaptive responses compensate. Alternatively, if metabolic demands were extraordinarily increased, perfusion might be insufficient, even if systemic blood flow were within the normal range. Mechanisms for low cardiac output are shown in Figure 103-4, and examples of disturbances that decrease systemic perfusion are shown in Table 103-1.

Reduced cardiac filling occurs with intravascular volume depletion, an increase in vascular capacity, or an impedance to venous return. It is important to note that end-diastolic volume of the heart cannot be assessed by physical examination. However, as end-diastolic volume changes, end-diastolic pressure of the ventricle (and atrial pressure) generally changes in parallel. Thus, the physical correlates of the atrial pressures reflect these changes in volume: on the right side of the circulatory system, jugular venous pressure, liver size, and fullness of the fontanel in the young infant change in accord with the central venous pressure; on the left side of the circulatory system, the signs are less precise, but interstitial pulmonary edema, tachypnea, and wheezing are often indications of high atrial pressure. However, there are also important conditions when atrial and venous pressure can be quite high but atrial volume is reduced; these are typified by pericardial tamponade (see Fig. 103-4A), in which pressure outside of the heart restricts volume inflow but raises atrial pressure.

Whereas loss of intravascular volume from the body is usually apparent from history and measurement of body weight, a shift from the vascular space to another body compartment can be subtle and recognized only by careful physical examination, especially when fluid has leaked into the interstitial space, bowel lumen, or peritoneum. Increased vascular (predominantly venous) capacity is also a particularly difficult problem to detect, because the blood remains in the vascular space, and there is no sign of vascular congestion or weight loss. Finally, impedance to venous return or tamponade dramatically reduces end-diastolic volume of the heart but produces signs of increased systemic venous pressure (hepatic enlargement, jugular venous distention, fullness of the fontanel). Thus, the difference between collapsed veins and small cardiac silhouette with volume depletion or increased vascular capacity, and venous engorgement with increased impedance to venous return is an important distinction in the physical examination.

Reduced ejection fraction results from poor contractile function or increased impedance (resistance) to outflow from the heart. With impaired contractile function, there is often a gallop rhythm and signs of systemic and pulmonary venous congestion. It is very important to recognize that the respiratory distressæ including tachypnea, wheezing, air trapping, or alveolar collapseæfrom the congested and edematous lungs may mimic a primary pulmonary disease and obscure the diagnosis of cardiac dysfunction; a useful finding that implicates cardiac rather than respiratory disease is the presence of cardiomegaly. An increased afterload, the pressure against which the ventricle must pump during ejection, can also depress cardiac ejection, especially when the process is precipitous—for example, infants with aortic stenosis or coarctation in whom the ductus arteriosus closes or narrows. With an increased afterload, there are also signs of systemic or pulmonary venous congestion, depending on which ventricle(s) is predominantly affected. However, circulatory shock can be the first obvious sign of the disturbance if the load on the heart rises abruptly before compensatory responses (eg, hypertrophy) can occur.

Although a slow heart rate is uncommon as a primary problem in children, it can occur in response to hypoxia or asphyxia, or when a patient is in extremis. Bradycardia can also aggravate other causes of poor perfusion, because tachycardia is the expected adaptive response.

With any of these physiological disturbances, the adequacy of the circulation can be further confounded by factors that increase the demands for blood flow, such as anemia, hypoxemia, fever, and excessive respiratory work. Recognizing and treating such factors may significantly improve the balance between blood flow and metabolic demands.

The first goal of assessment is to determine whether the child’s perfusion is adequate to sustain vital functions or whether the circulatory disturbance is uncompensated. The physical findings of the child with poor perfusion reflect both the changes that occur primarily from the decrease in blood flow and those changes that occur in response to the adaptations. Superimposed on this picture may also be factors that relate to the underlying illness or injury that has disturbed the perfusion. For example, the child with dehydration will have decreased peripheral arterial pulses, cold and cyanotic extremities, and decreased capillary refill, whereas a child with sepsis might have warm extremities, edema, and easily felt peripheral pulses, even though there is acidosis and signs of organ dysfunction (see Chapters 115 and 223). With these general principles in mind, Table 103-2 gives an overview of the physical examination of the child with reduced systemic perfusion. These signs are sensitive to the degree of circulatory compromise but are not specific for a particular cause of poor perfusion. And, as shown, certain signs are particularly suggestive that the child may be in a state of uncompensated shock. Agitation, confusion, or apathy; undetectable peripheral pulses; cold extremities; and hypotension are symptoms that should be treated immediately.

In all patients with potentially impaired perfusion, vital signs should be measured and put in perspective with other physical findings. It is important to consider whether the findings are internally consistent or whether more information is needed. Both systolic and diastolic blood pressure should be measured, because with peripheral vasoconstriction, systolic blood pressure can be normal but pulse pressure will be narrow. Recall that neural and humoral responses preserve systolic blood pressure over a wide range of cardiac output. Blood pressure should be measured in an upper- (preferably right arm) and lower-body extremity in an infant because of the possibility of aortic coarctation. Currently, the PALS (Pediatric Advanced Life Support) manual recommends using the quick reference formulae to estimate 50th and 5th percentile systolic blood pressures for children ages 1 to 10: (1) Fiftieth percentile systolic BP = 90 mm Hg + (2 × age in years); (2) fifth percentile systolic BP (below this is considered hypotensive) = 70 mm Hg + (2 × age in years).13

Certain signs are valuable, because they yield insight into the nature or site of the specific disturbance. In particular, findings that locate disruption in cardiac function are useful. Pulmonary venous congestion and edema might be detected by tachypnea, crackles, wheezing, or grunting respiration and might be seen as pulmonary edema on chest radiograph. Tachypnea results from activation of stretch receptors in the lung with interstitial pulmonary edema. Wheezing, sometimes referred to as cardiac asthma, arises from congestion of the small airways and may be associated with gas trapping on radiography. Grunting, which may appear as a weak cry, is typically a response to reduced functional residual capacity of the lung. Interestingly, grunting can also be seen with low-perfusion states even when there is no primary or secondary pulmonary involvement. It is also worth noting that when the lungs are congested, the response to the metabolic acidosis is tachypnea, whereas when the lungs are relatively normal, hyperpnea is expected (see Chapter 102).

Systemic venous congestion might be detected by hepatomegaly, jugular venous distention, or peripheral edema. (Peripheral edema without other signs of venous distention often indicates injured capillary endothelium, as is common in sepsis or other inflammatory processes.) In the presence of these congestive findings, the cardiothymic silhouette should usually be enlarged on the radiograph, although hyperinflated lungs, alveolar collapse, or pulmonary edema might obscure the detection of this enlargement. Murmurs help locate a site of turbulence, which suggests either excess flow through or a narrowing of an orifice. A gallop rhythm suggests that the particular ventricle has diminished compliance. An active precordium is found when there is a large stroke volume, as with anemia, fever, or a patent ductus arteriosus. A quiet precordium might suggest a reduced stroke volume or a cushion of fluid or air between the chest wall and the heart, as with tamponade. These findings could help the clinician establish a mechanism for the impaired circulation.

Some patients with apparently poor organ function and hypotension but with relatively brisk flow to the skin are often described as having distributive shock. These individuals may have signs of reduced extraction of oxygen by the tissues, which can be assessed from mixed venous blood as demonstrated by eFigure 103.1. They also often manifest clinical signs consistent with inflammation (eg, fever, flushed skin, leukocytosis) and impairment of many somatic functions (eg, uremia, ileus). A cursory examination may dismiss the findings as having little significance and lead to a misdiagnosis.

After it is established that perfusion is impaired, data should be sought to determine the primary factors interfering with perfusion and to find a rational approach to reestablish adequate circulation (see Fig. 103-5). To determine the cause(s) of the poor perfusion, it is particularly useful to assess whether intravascular volume is expanded or depleted by examining the size of the liver and fullness of the anterior fontanel or of the jugular veins. When possible, it is also valuable to weigh the patient. Laboratory data are usually not needed to decide whether perfusion is adequate but are quite useful in determining how long perfusion has been disturbed and by what mechanism. An electrocardiogram (to determine whether there is the expected sinus tachycardia, a dysrhythmia, or ventricular hypertrophy), a radiograph of the chest (to determine whether the pulmonary circulation is engorged or depleted and whether the cardiothymic silhouette is large or small), and a measure of acid/base status to determine the adequacy of metabolic compensation and whether asphyxia has contributed to myocardial dysfunction are generally of value.

The arterial and central venous lactate concentration reflects the balance between lactate production and use. The lactate concentration rises in seriously ill or injured patients when metabolic acidosis is present and falls when adequate perfusion is restored and metabolic acidosis is corrected.14Measuring hemoglobin concentration or hematocrit and blood electrolyte, glucose (particularly in the infant or the child who has been ill for a while), creatinine, and urea nitrogen concentration are helpful to discern the etiology of the circulatory disturbance and to determine which fluid composition will be most appropriate after the initial treatment. Because the serum creatinine rises progressively when renal perfusion is impaired, it can yield inference about the duration of the circulatory disturbance.

Certain monitoring should also be initiated to assist with the assessment and to judge the adequacy of the response to treatment. This should include frequent measurements of blood pressure, continuous display of the heart rate or ECG and arterial O2 saturation, and measurement of urine output (consider inserting a bladder catheter). Ultrasound imaging and Doppler flow analysis are exceptionally valuable for evaluating and monitoring myocardial contractile function and cardiac filling volume and for detecting a pericardial effusion.

When it is clear that the patient needs restoration of perfusion, vascular access must be established (see Chapter 107). The route of catheter placement is dictated by the urgency for care. It is often quite difficult to place a percutaneous catheter in a peripheral vein when the patient’s intravascular volume is decreased, so alternative approaches may be needed. Techniques such as intraosseous cannulation, percutaneous cannulation (Seldinger technique) of a large central vein, or venisection are appropriate when the patient is in shock and there is no means for fluid and medication administration.

Supplemental oxygen should be provided (by face mask, nasal cannulae, or head box in the infant) to maximize oxygen delivery and to keep the lungs filled with oxygen, even if arterial oxygen saturation is normal. If, however, oxygen administration worsens the patient’s perfusion, as can occur in the infant with critical left-heart obstruction in whom the ductus arteriosus constricts, then it should be stopped immediately (as with any other drug that causes an adverse outcome).

Improvement of Cardiac Output

Physical assessment should identify factors—heart rate, cardiac ejection, or cardiac filling—responsible for poor perfusion, and therapy should be targeted accordingly. With prolonged or severe shock, it is likely that circulatory function is impaired by more than one of these factors. For example, with sepsis, a child can have poor contractile function, diminished intravascular volume, vasodilation, maldistribution of blood flow, and increased metabolic demands. However, in any child with poor perfusion, it is essential to start restoring circulatory function before there is further deterioration. If there are no signs of venous congestion (ie, liver not enlarged or jugular veins distended), perfusion will likely improve with rapid and repetitive infusion of crystalloid fluid in an isotonic mixture (eg, isotonic saline or Ringer’s lactate) in aliquots of 5 to 20 mL/kg over 5 to 20 minutes. The precise amount in an aliquot is less important than the need for continued reassessment of the intervention’s effect.

After assessing serum glucose concentration, glucose should be given with the initial fluid if there is hypoglycemia. Routine glucose administration is not indicated, as hyperglycemia has been associated with worse outcomes following resuscitation from traumatic shock and cardiac arrest. Although there is a long-standing and unresolved controversy about the merits of colloid versus crystalloid in resuscitation, crystalloid remains a practical initial therapy.15,16 Following initial attempts at restoring perfusion with crystalloid, the subsequent choice of fluid should be based on the type of deficits and specific problems identified. For example, if there is anemia or hemorrhage, packed red blood cells are needed.

The quantity of fluid required for restoring perfusion might be quite large and can exceed normal blood volume, which is 70 to 80 mL/kg. Often, the fluid volume has been lost over an extended period of time, such that the interstitial or cellular compartments are also likely to be depleted. Much of the isotonic fluid will leave the intravascular compartment and distribute rapidly into extravascular spaces during the resuscitation. In addition, when capillary integrity is damaged, fluid may readily extravasate from the plasma into the interstitium, even though the effective circulating plasma volume is inadequate. For these reasons, some clinicians prefer to use colloid-containing fluid, although it, too, can extravasate rapidly from the vascular compartment if there is capillary injury.

If, during the course of fluid infusion, venous congestion develops before perfusion is near normal, then impaired ejection of blood or impedance to filling of the heart is likely. Inotropic support should be provided whenever there is direct evidence of depressed myocardial function (eg, venous congestion, cardiomegaly in the presence of a gallop rhythm) or when there is a progressive increase in venous engorgement without improvement in perfusion during fluid administration. Even with the risks of venous congestion, when myocardial function is depressed, it is appropriate to provide sufficient intravascular volume so that inotropic medications will be effective in increasing stroke volume (for any given ejection fraction, the stroke volume will increase when the filling of the heart is increased). Although peripheral edema is unsightly, it is unlikely to compromise the patient’s vital functions. Pulmonary edema, on the other hand, will increase the work of breathing and can impair gas exchange, thereby necessitating tracheal intubation and assisted ventilation.

The inotropic drugs that are most appropriate are given by intravenous route and are rapidly metabolized, and the dose can be adjusted as conditions change. The most commonly used drugs (see Table 103-3) are the direct- and indirect-acting β agonists, including epinephrine, isoproterenol, dopamine, and dobutamine, and phosphodiesterase inhibitors such as milrinone. Because these drugs also have important effects on the peripheral vasculature, it is worth considering whether some degree of vasoconstriction is needed to increase blood pressure (eg, dopamine, epinephrine) or whether vasodilation would be beneficial (eg, dobutamine, milrinone, amrinone, isoproterenol). Generally, the former group of drugs is most useful initially until it is clear whether blood pressure is sufficient to support perfusion. More invasive approaches to supporting circulation, such as left-ventricular assist devices and balloon counterpulsation, are not widely available and are appropriate only in specialized settings (see Chapter 109).

If the heart rate is not appropriately increased, there should be immediate concern that there is severe hypoxemia or asphyxia or that the myocardium is intrinsically injured. In this circumstance, oxygen should be given immediately, cardiac rhythm should be checked closely, and use of an inotropic drug with chronotropic properties or use of a pacemaker if the rhythm is not sinus should be considered. In addition, chest compressions should be started if severe bradycardia is associated with poor perfusion.

The response to therapy must be evaluated with repetitive physical examinations and measurements of vital signs. In particular, if cardiac output is improving, one should expect to find a decreasing heart rate, enhanced peripheral perfusion, and possibly increasing blood pressure or pulse pressure as the circulation is improved, as well as warming extremities. If, on the other hand, signs of pulmonary congestion or edema (eg, tachypnea, crackles, wheezing, retractions) develop or worsen, or signs of systemic venous congestion (eg, enlarged liver or fontanel) develop without appropriate restoration of peripheral perfusion, it is necessary to consider more invasive monitoring and more extensive evaluation of cardiac function by echocardiography. Placement of a central venous catheter can be useful for measuring the filling pressure of the right side of the heart and for monitoring oxygen extraction. When there is reason to believe that the right and left ventricles have markedly different filling pressures or disparate function, a balloon flotation catheter can be passed into the pulmonary artery to measure wedge pressure and cardiac output and to assist in evaluating cardiac function and response to therapy.

Reduction in Demands and Adjuncts to Treatment

When shock is present, the goal of therapy is to maximize oxygen delivery and minimize demand for oxygen and blood flow. Anemia, hypoxemia, and fever should be corrected whenever possible. It is important to recognize, however, that fever may not abate until perfusion is restored, because the vasoconstriction interferes with heat dissipation. This is in keeping with a common finding of an increased core temperature in the presence of cold extremities.

An important adjunct to therapy can be using positive-pressure ventilation in the patient with shock, even when there are no overt signs of respiratory distress. Supplanting the work of breathing can decrease overall metabolic rate and can divert blood flow from respiratory muscles to other vital tissues.17 Tracheal intubation and initiation of assisted ventilation is not without risk, so it should be performed in a controlled environment with appropriate personnel; tube placement should always be verified using physical examination and, if possible a confirmation device (eg, exhaled CO2 detector) at the time of insertion, when the patient is moved, and whenever the intubated patient deteriorates. Positive-pressure ventilation can reduce venous return and decrease cardiac output.18Therefore, it is important to be prepared to restore cardiac filling if this occurs.

There are some special considerations related to the neonate with left-heart obstruction, coarctation, aortic stenosis, or atresia that merit discussion because of the frequency with which these conditions occur and the potential for improvement with infusion of prostaglandin E1 (see Chapters 56, 60, and 483). These conditions commonly produce circulatory shock within the first week after birth; there will be little, if any, improvement in perfusion by using the conventional approaches described above, but dilation of a constricted ductus arteriosus after the administration of a prostaglandin can provide a dramatic increase in perfusion until more definitive therapy is initiated.

After therapy for poor perfusion begins, it is incumbent to search for an underlying etiology to treat (eg, antibiotics for suspected sepsis), to consider additional strategies for improving circulatory function, and to plan a transfer to a facility that can provide extended monitoring and management. eFigure 103.2 summarizes many of the manifestations of circulatory shock described in this chapter, including hypotension, marked vasoconstriction, the inability to dissipate heat, the decline in metabolic rate, the increase in O2 extraction, the increase in lactate concentration, and progressive acidosis. It also shows the types of responses expected as the circulation is restored.14