Shock

Chapter 6


Shock




Perspective


In philosophic terms, shock can be viewed as a transition between life and death. Whether shock results from hemorrhage, sepsis, or cardiac failure, mortality rates exceed 20%.1,2 In scientific lexicon, shock results from the widespread failure of the circulatory system to oxygenate and nourish the body adequately. In the laboratory the scientist defines the metabolic effect of shock quantitatively, by examining the mechanisms by which shock alters mitochondrial energy transfer, evokes the production of toxic chemicals, and reduces their removal. At the bedside, however, the clinician identifies shock by linking the clinical impression, synthesized from the patient’s history of present illness, age, underlying health status, and general appearance, to quantitative data, including vital signs, blood chemistry, urine output, and direct measurements of oxygenation. When the clinical impression and the quantitative data suggest widespread organ hypoperfusion, emergent resuscitation is used to restore normal tissue oxygenation and substrate delivery to prevent deterioration into systemic inflammation, organ dysfunction, and death.


At the subcellular level, shock first affects the mitochondria. Mitochondria function at the lowest oxygen tension in the body, but paradoxically, they consume almost all the oxygen used by the body. More than 95% of aerobic chemical energy comes from mitochondrial combustion of fuel substrates (fats, carbohydrates, ketones) plus oxygen into carbon dioxide (CO2) and water. Mitochondria therefore have been referred to as the “canaries in the coal mine” because they are affected first in conditions of inadequate tissue perfusion.3,4 When mitochondria have inadequate oxygen, the cell catabolizes fuels to lactate, which inexorably accumulates and diffuses into the blood.



Classification


For years, shock has been classified into four broad categories based on Blalock’s 1934 description: hematologic, neurologic, vasogenic, and cardiogenic. This basic organization scheme remains useful today. Box 6-1 outlines five categories of shock that generally have specific mechanisms and treatments.



BOX 6-1   Categories of Shock According to Primary Treatment









Specific Causes



Hemorrhagic Shock


Hemorrhagic shock results from a rapid reduction in blood volume, which causes baroreceptor activation and leads to vasoconstriction, increased strength of cardiac contraction, and increased heart rate (HR). Cardiovascular response to hemorrhage can vary with underlying cardiopulmonary status, age, and presence of ingested drugs. Responses of HR and BP are notoriously variable in hemorrhage, so no firm conclusion can be made at the bedside about the presence or absence of hemorrhagic shock simply by evaluating HR and BP. In general, hemorrhage first increases pulse and cardiac contraction, then increases vasoconstriction. Blood loss causes an elevated pulse rate with a slight increase in the diastolic BP, causing the pulse pressure (difference between systolic and diastolic BP) to narrow. As blood loss continues, ventricular filling decreases and cardiac output drops, followed by a reduction in systolic BP. Before the total cardiac output begins to decrease, blood flow to noncritical organs and tissues begins to decrease, and their cells produce and release lactic acid.


Consequently, acidemia will often precede any significant decrease in cardiac output with hemorrhage. However, the blood contains bicarbonate ions that buffer the blood pH, keeping it near neutral, even as lactic acid accumulates in blood. The base deficit—the amount of strong base that would have to be added to a liter of blood to normalize the pH—represents an index of how far the bloodstream has dipped into its reserve of bicarbonate buffer. A normal base deficit is more positive than −2 mEq/L. Accordingly, the arterial and venous blood base deficit can become more negative early in hemorrhage even while blood pH and BP remain in the normal range. The base deficit, therefore, crudely represents the physiologic endpoint that distinguishes trivial blood loss from clinically significant hemorrhage. In addition to chemical buffering, the body responds to small reductions in arterial pH by activating brainstem chemoreceptors, which increase minute ventilation, leading to reduced partial pressure of carbon dioxide in the arterial blood (PaCO2).


After approximately one third of the total blood volume has been acutely lost, cardiovascular reflexes can no longer sustain adequate filling of the arterial circuit and frank hypotension supervenes. Arterial hypotension is generally and arbitrarily defined as an arterial BP below 90 mm Hg. Usually coincident with the development of hypotension, bicarbonate buffers become overwhelmed, and increased alveolar ventilation becomes ineffective, culminating in reduced arterial pH. Hemorrhagic shock causes an activation of the hypothalamic-pituitary-adrenomedullary axis, with release of stress hormones that cause glycogenolysis, lipolysis, and mild hypokalemia. Therefore in the ED, patients who have sustained traumatic hemorrhage generally have an arterial lactate concentration greater than 4.0 mmol/L, a PaCO2 less than 35 mm Hg, and mild hyperglycemia (150-170 mg/dL) and hypokalemia (3.5-3.7 mEq/L). Although hemorrhagic hypotension reduces lung perfusion, arterial hypoxemia should not be attributed simply to blood loss, but instead should prompt investigation for aspiration, airway obstruction, alveolar consolidation, or lung injury.


The second phase of organ injury from hemorrhagic shock occurs during resuscitation. It has been said that the acute phase of hemorrhage “cocks the gun” by initiating the inflammatory cascade, and resuscitation “pulls the trigger” by accentuating the inflammation-induced organ injury from hemorrhagic shock. During resuscitation, neutrophils become most aggressive, binding to the lung endothelium and causing capillary leaks that characterize acute respiratory distress syndrome (ARDS). Inflammatory cytokines are liberated during resuscitation, and membrane injury occurs in many cells. In the liver, damage from inflammation and reactive oxygen species from neutrophils is compounded by persistent microischemia. During resuscitation from hemorrhagic shock, the normal balance of vasodilation by nitric oxide (NO) versus vasoconstriction by endothelins becomes distorted, producing patchy centrilobular ischemic damage in the liver, which may produce an immediate rise in blood transaminase levels. A growing body of evidence suggests that resuscitation from hemorrhage exerts greater injury on the heart than the actual hypotensive insult.6 Depending on the degree of hypotensive insult, the kidney may manifest acute spasm of the preglomerular arterioles, causing acute tubular necrosis. Systemic metabolic changes can impair fuel delivery to the heart and brain, secondary to depressed hepatic glucose output, impaired hepatic ketone production, and inhibited peripheral lipolysis.



Septic Shock


Septic shock can be produced by infection with any microbe, although in one half or more of cases of septic shock, no organism is identified. One of the most well-studied mediators of sepsis is lipopolysaccharide, contained in the outer cell membrane of gram-negative bacteria. Infusion of lipopolysaccharide into humans or animals will produce cardiovascular, immunologic, and inflammatory changes identical to those observed with microbial infection. In recent years, multicenter trials of sepsis have suggested the emergence of gram-positive organisms as the chief cause of sepsis in hospitalized patients. Two lines of reasoning suggest that gram-positive sepsis will continue to increase in prevalence:



Septic shock often causes three major effects that must be addressed during resuscitation: relative hypovolemia, cardiovascular depression, and induction of systemic inflammation. Septic shock produces relative hypovolemia from increased venous capacitance, which reduces right ventricular filling. Septic shock often causes absolute hypovolemia from gastrointestinal volume losses, tachypnea, sweating, and decreased ability to drink during development of the illness. Sepsis also induces capillary leak, which leads to relative loss of intravascular volume into third spaces. Recent evidence has shown that septic shock causes myocardial depression simultaneously with vasodepression and capillary leak. Direct measurements of cardiac contractility have shown that cardiac mechanical function becomes impaired early in the course of septic shock, even in the hyperdynamic stages. Multiple mechanisms may explain depressed heart function in sepsis, including actions of specific cytokines (most notably tumor necrosis factor alpha [TNF-α] and interleukin 1 beta [IL-1β]), overproduction of NO by nitric oxide synthase (iNOS),7 and possibly impairment in mitochondrial oxidative phosphorylation coincident with reduced mechanical efficiency.8,9 Evidence indicates that circulating mediators, myocardial cellular injury from inflammation, and deranged metabolism interact synergistically to injure the heart during septic shock. Systemic inflammation causes capillary leak in the lung, which may cause alveolar infiltration characteristic of ARDS early in the treatment of septic shock in up to 40% of patients. With the potential for early development of ARDS, more profound ventilation-perfusion (image) mismatching, and pneumonia or pulmonary aspiration, hypoxemia is more severe with septic shock than hemorrhagic shock.




Clinical Features


Patients in the ED frequently are in shock with no obvious cause. Rapid recognition of shock requires the integration of information from immediate history and physical examination, and shock can be strongly supported by the presence of a worsening base deficit or lactic acidosis. In general, patients with shock exhibit a stress response: they are ill appearing, asthenic, pale, often sweating, and usually tachypneic or grunting, and often have a weak and rapid pulse (Box 6-2). HR can be normal or low in shock, especially in cases complicated by prescribed drugs that depress HR or by profound hypoxemia. BP initially can be normal because of adrenergic reflexes. Although arterial BP as a sole measurement remains an unreliable marker of circulatory status, the finding of a single systolic BP less than 100 mm Hg in the ED is associated with a threefold increase in in-hospital mortality and a tenfold increase in sudden and unexpected death.5 The HR/systolic BP ratio may provide a better marker of shock than either measurement alone; a normal ratio is less than 0.8. Urine output provides an excellent indicator of organ perfusion and is readily available with insertion of a Foley catheter into the bladder. Measurement of urine output, however, requires 30 minutes to 1 hour for accurate determination of whether output is normal (>1.0 mL/kg/hr), reduced (0.5-1.0 mL/kg/hr), or severely reduced (<0.5 mL/kg/hr). Point measurements of the arterial or venous lactate concentration and the base deficit can be rapidly performed and provide accurate assessment of global perfusion status. A lactate concentration greater than 4.0 mM or a base deficit more negative than −4 mEq/L predicts the presence of circulatory insufficiency severe enough to cause subsequent multiple organ failure.11,12 Once the empirical criteria for circulatory shock have been discovered, the next step is to consider the cause of the shock. Figure 6-1 shows a potential sequence of decisions to help arrive at a diagnosis in a patient with undifferentiated shock.



BOX 6-2   Empirical Criteria for Diagnosis of Circulatory Shock*




*Regardless of cause. Four criteria should be met.



The history, vital signs, and physical examination documented by prehospital providers afford valuable insight into a patient’s physiologic status before any medical intervention and can be useful in ED management. Studies suggest that both medical and trauma patients with prehospital hypotension have a threefold to fourfold higher in-hospital mortality rate than patients without hypotension.13,14


On physical examination, dry mucous membranes suggest dehydration, whereas distended jugular veins suggest cardiac failure or obstruction from pulmonary embolism (PE) or cardiac tamponade. Muffled heart sounds suggest cardiac tamponade, whereas a loud machine-like systolic murmur indicates acute rupture of a papillary muscle or rupture of the interventricular septum. Bilateral pulmonary rales in a patient with a normal rectal temperature help to define presence of primary left ventricular failure. Wheezing suggests bronchospasm from anaphylaxis or, less likely, cardiac failure or PE. Abdominal tenderness may indicate peritoneal inflammation or occult trauma. Rectal examination may disclose occult gastrointestinal hemorrhage. Rectal temperature is the preferred method for measuring temperature and in general should be performed as early as is reasonable on every patient with suspected shock.


Neurologic examination documents responsiveness, cognition, and the presence of any focal deficits. In children, documentation should include level of alertness, response to parents, appropriateness of crying, pupillary function, symmetry of grimace, symmetry of extremity movements, and motor tone in infants.


Laboratory, radiographic, and other ancillary data should be ordered to assess tissue and vital organ perfusion and to diagnose injury from trauma, find the source of infection with sepsis, or identify the cause of cardiac failure. A chest radiograph, electrocardiogram, finger-stick glucose measurement, complete blood count (CBC), urinalysis, serum electrolytes, and kidney and liver function tests are all indicated in the ED assessment. Arterial blood gases are ordered for a base deficit calculation and to correlate arterial gas tensions (oxygen [PaO2] and PaCO2) with those measured by pulse oximetry and capnography. Serum lactate measurement should be performed as early as possible in patients with suspected shock. Either venous or arterial lactate concentrations can be used.15,16 If peripheral venous lactate is used, the effect of time, storage temperature, and tourniquet use have no significant effect on in vitro lactate production by erythrocytes if the measurement is done within 15 minutes after the sample has been obtained.17 Cardiac and abdominal bedside ultrasound scanning can screen for inadequate central venous volume, occult hemoperitoneum, abdominal aortic aneurysm, left ventricular failure, and cardiac tamponade.18 A systematic ultrasound protocol can significantly improve the physician’s ability to accurately diagnose the cause of undifferentiated shock in ED patients, and the finding of hyperdynamic left ventricular function in patients with undifferentiated shock strongly suggests sepsis as the cause.19,20


Consensus definitions of shock show the spectrum of hypoperfusion for the following three common causes of shock (Box 6-3):



BOX 6-3   Definitions and Criteria for Septic, Hemorrhagic, and Cardiogenic Shock


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Jul 26, 2016 | Posted by in ANESTHESIA | Comments Off on Shock

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