Alan E. Jones and Jeffrey A. Kline

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.

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.

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.