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- Etiology and Classification
- Symptoms and Signs
- Prognosis and Treatment
- Resources In This Article
Shock is a state of organ hypoperfusion with resultant cellular dysfunction and death. Mechanisms may involve decreased circulating volume, decreased cardiac output, and vasodilation, sometimes with shunting of blood to bypass capillary exchange beds. Symptoms include altered mental status, tachycardia, hypotension, and oliguria. Diagnosis is clinical, including BP measurement and sometimes markers of tissue hypoperfusion (eg, blood lactate, base deficit). Treatment is with fluid resuscitation, including blood products if necessary, correction of the underlying disorder, and sometimes vasopressors.
The fundamental defect in shock is reduced perfusion of vital tissues. Once perfusion declines and O2 delivery to cells is inadequate for aerobic metabolism, cells shift to anaerobic metabolism with increased production of CO2 and accumulation of lactic acid. Cellular function declines, and if shock persists, irreversible cell damage and death occur.
During shock, both the inflammatory and clotting cascades may be triggered in areas of hypoperfusion. Hypoxic vascular endothelial cells activate WBCs, which bind to the endothelium and release directly damaging substances (eg, reactive O2 species, proteolytic enzymes) and inflammatory mediators (eg, cytokines, leukotrienes, tumor necrosis factor [TNF]). Some of these mediators bind to cell surface receptors and activate nuclear factor kappa B (NFκB), which leads to production of additional cytokines and nitric oxide (NO), a potent vasodilator. Septic shock (see Sepsis and Septic Shock) may be more proinflammatory than other forms of shock because of the actions of bacterial toxins, especially endotoxin.
In septic shock, vasodilation of capacitance vessels leads to pooling of blood and hypotension because of “relative” hypovolemia (ie, too much volume to be filled by the existing amount of blood). Localized vasodilation may shunt blood past the capillary exchange beds, causing focal hypoperfusion despite normal cardiac output and BP. Additionally, excess NO is converted to peroxynitrite, a free radical that damages mitochondria and decreases ATP production.
Blood flow to microvessels including capillaries is reduced even though large-vessel blood flow is preserved in settings of septic shock. Mechanical microvascular obstruction may, at least in part, account for such limiting of substrate delivery. Leukocytes and platelets adhere to the endothelium, and the clotting system is activated with fibrin deposition.
Multiple mediators, along with endothelial cell dysfunction, markedly increase microvascular permeability, allowing fluid and sometimes plasma proteins to escape into the interstitial space. In the GI tract, increased permeability possibly allows translocation of the enteric bacteria from the lumen, potentially leading to sepsis or metastatic infection.
Neutrophil apoptosis may be inhibited, enhancing the release of inflammatory mediators. In other cells, apoptosis may be augmented, increasing cell death and thus worsening organ function.
BP is not always low in the early stages of shock (although hypotension eventually occurs if shock is not reversed). Similarly, not all patients with “low” BP have shock. The degree and consequences of hypotension vary with the adequacy of physiologic compensation and the patient’s underlying diseases. Thus, a modest degree of hypotension that is well tolerated by a young, relatively healthy person might result in severe cerebral, cardiac, or renal dysfunction in an older person with significant arteriosclerosis.
Initially, when O2 delivery (DO2) is decreased, tissues compensate by extracting a greater percentage of delivered O2. Low arterial pressure triggers an adrenergic response with sympathetic-mediated vasoconstriction and often increased heart rate. Initially, vasoconstriction is selective, shunting blood to the heart and brain and away from the splanchnic circulation. Circulating β-adrenergic amines (epinephrine, norepinephrine) also increase cardiac contractility and trigger release of corticosteroids from the adrenal gland, renin from the kidneys, and glucose from the liver. Increased glucose may overwhelm ailing mitochondria, causing further lactate production.
The combination of direct and reperfusion injury may cause MODS—the progressive dysfunction of ≥ 2 organs consequent to life-threatening illness or injury. MODS can follow any type of shock but is most common when infection is involved; organ failure is one of the defining features of septic shock (see Sepsis and Septic Shock). MODS also occurs in > 10% of patients with severe traumatic injury and is the primary cause of death in those surviving > 24 h.
Any organ system can be affected, but the most frequent target organ is the lung, in which increased membrane permeability leads to flooding of alveoli and further inflammation. Progressive hypoxia may be increasingly resistant to supplemental O2 therapy. This condition is termed acute lung injury or, if severe, acute respiratory distress syndrome (ARDS—see Acute Hypoxemic Respiratory Failure (AHRF, ARDS)).
The kidneys are injured when renal perfusion is critically reduced, leading to acute tubular necrosis and renal insufficiency manifested by oliguria and progressive rise in serum creatinine.
In the heart, reduced coronary perfusion and increased mediators (including TNF and IL-1) may depress contractility, worsen myocardial compliance, and down-regulate β-receptors. These factors decrease cardiac output, further worsening both myocardial and systemic perfusion and causing a vicious circle often culminating in death. Arrhythmias may occur.
In the GI tract, ileus and submucosal hemorrhage can develop. Liver hypoperfusion can cause focal or extensive hepatocellular necrosis, transaminase and bilirubin elevation, and decreased production of clotting factors.
There are several mechanisms of organ hypoperfusion and shock. Shock may be due to a low circulating volume (hypovolemic shock), vasodilation (distributive shock), a primary decrease in cardiac output (both cardiogenic and obstructive shock), or a combination.
Hypovolemic shock is caused by a critical decrease in intravascular volume. Diminished venous return (preload) results in decreased ventricular filling and reduced stroke volume. Unless compensated for by increased heart rate, cardiac output decreases.
A common cause is bleeding (hemorrhagic shock), typically due to trauma, surgical interventions, peptic ulcer, esophageal varices, or ruptured aortic aneurysm. Bleeding may be overt (eg, hematemesis, melena) or concealed (eg, ruptured ectopic pregnancy).
Hypovolemic shock may also follow increased losses of body fluids other than blood ( Hypovolemic Shock Caused by Body Fluid Loss).
Hypovolemic Shock Caused by Body Fluid Loss
Hypovolemic shock may be due to inadequate fluid intake (with or without increased fluid loss). Water may be unavailable, neurologic disability may impair the thirst mechanism, or physical disability may impair access.
In hospitalized patients, hypovolemia can be compounded if early signs of circulatory insufficiency are incorrectly ascribed to heart failure and fluids are withheld or diuretics are given.
Distributive shock results from a relative inadequacy of intravascular volume caused by arterial or venous vasodilation; circulating blood volume is normal. In some cases, cardiac output (and DO2) is high, but increased blood flow through arteriovenous shunts bypasses capillary beds; this bypass plus uncoupled cellular O2 transport cause cellular hypoperfusion (shown by decreased O2 consumption). In other situations, blood pools in venous capacitance beds and cardiac output falls.
Distributive shock may be caused by anaphylaxis (anaphylactic shock—see Anaphylaxis); bacterial infection with endotoxin release (septic shock—see Sepsis and Septic Shock); severe injury to the spinal cord, usually above T4 (neurogenic shock); and ingestion of certain drugs or poisons, such as nitrates, opioids, and adrenergic blockers. Anaphylactic shock and septic shock often have a component of hypovolemia as well.
Cardiogenic shock is a relative or absolute reduction in cardiac output due to a primary cardiac disorder. Obstructive shock is caused by mechanical factors that interfere with filling or emptying of the heart or great vessels. Causes are listed in Mechanisms of Cardiogenic and Obstructive Shock.
Mechanisms of Cardiogenic and Obstructive Shock
Lethargy, confusion, and somnolence are common. The hands and feet are pale, cool, clammy, and often cyanotic, as are the earlobes, nose, and nail beds. Capillary filling time is prolonged, and, except in distributive shock, the skin appears grayish or dusky and moist. Overt diaphoresis may occur. Peripheral pulses are weak and typically rapid; often, only femoral or carotid pulses are palpable. Tachypnea and hyperventilation may be present. BP tends to be low (< 90 mm Hg systolic) or unobtainable; direct measurement by intra-arterial catheter (see Vascular Access : Procedure), if done, often gives higher and more accurate values. Urine output is low.
Distributive shock causes similar symptoms, except the skin may appear warm or flushed, especially during sepsis. The pulse may be bounding rather than weak. In septic shock, fever, usually preceded by chills, is typically present. Some patients with anaphylactic shock have urticaria or wheezing.
Numerous other symptoms (eg, chest pain, dyspnea, abdominal pain) may be due to the underlying disease or secondary organ failure.
Diagnosis is mostly clinical, based on evidence of insufficient tissue perfusion (obtundation, oliguria, peripheral cyanosis) and signs of compensatory mechanisms (tachycardia, tachypnea, diaphoresis). Specific criteria include obtundation, heart rate > 100, respiratory rate > 22, hypotension (systolic BP < 90 mm Hg) or a 30-mm Hg fall in baseline BP, and urine output < 0.5 mL/kg/h. Laboratory findings that support the diagnosis include lactate > 3 mmol/L, base deficit < −4 mEq/L, and Paco2< 32 mm Hg. However, none of these findings alone is diagnostic, and each is evaluated by its trend (ie, worsening or improving) and in the overall clinical context, including physical signs. Recently, measurement of sublingual PCO2 and near-infrared spectroscopy have been introduced as noninvasive and rapid techniques that may measure the degree of shock; however, these techniques have yet to be validated on a larger scale.
Recognizing the cause of shock is more important than categorizing the type. Often, the cause is obvious or can be recognized quickly based on the history and physical examination, aided by simple testing.
Chest pain (with or without dyspnea) suggests MI, aortic dissection, or pulmonary embolism. A systolic murmur may indicate ventricular septal rupture or mitral insufficiency due to acute MI. A diastolic murmur may indicate aortic regurgitation due to aortic dissection involving the aortic root. Cardiac tamponade is suggested by jugular venous distention, muffled heart sounds, and a paradoxical pulse. Pulmonary embolism severe enough to cause shock typically produces decreased O2 saturation and occurs more often in special settings, including prolonged bed rest and after a surgical procedure. Tests include ECG, troponin I, chest x-ray, ABGs, lung scan, helical CT, and echocardiography.
Abdominal or back pain or a tender abdomen suggests pancreatitis, ruptured abdominal aortic aneurysm, peritonitis, and, in women of childbearing age, ruptured ectopic pregnancy. A pulsatile midline mass suggests ruptured abdominal aortic aneurysm. A tender adnexal mass suggests ectopic pregnancy. Testing typically includes abdominal CT (if the patient is unstable, bedside ultrasound can be helpful), CBC, amylase, lipase, and, for women of childbearing age, urine pregnancy test.
Fever, chills, and focal signs of infection suggest septic shock, particularly in immunocompromised patients. Isolated fever, contingent on history and clinical settings, may point to heatstroke. Tests include chest x-ray; urinalysis; CBC; and cultures of wounds, blood, urine, and other relevant body fluids.
In a few patients, the cause is occult. Patients with no focal symptoms or signs indicative of cause should have ECG, cardiac enzymes, chest x-ray, and ABGs. If results of these tests are normal, the most likely causes include drug overdose, occult infection (including toxic shock), anaphylaxis, and obstructive shock.
If not already done, ECG, chest x-ray, CBC, serum electrolytes, BUN, creatinine, PT, PTT, liver function tests, and fibrinogen and fibrin split products are done to monitor patient status and serve as a baseline. If the patient’s volume status is difficult to determine, monitoring of central venous pressure (CVP) or pulmonary artery occlusion pressure (PAOP) may be useful. CVP < 5 mm Hg (< 7 cm H2O) or PAOP < 8 mm Hg may indicate hypovolemia, although CVP may be greater in hypovolemic patients with preexisting pulmonary hypertension. Rapid bedside echocardiography (done by the treating physician) to assess adequacy of cardiac filling and function is being increasingly used to assess shock.
Untreated shock is usually fatal. Even with treatment, mortality from cardiogenic shock after MI (60 to 65%) and septic shock (30 to 40%) is high. Prognosis depends on the cause, preexisting or complicating illness, time between onset and diagnosis, and promptness and adequacy of therapy.
First aid involves keeping the patient warm. External hemorrhage is controlled, airway and ventilation are checked, and respiratory assistance is given if necessary. Nothing is given by mouth, and the patient’s head is turned to one side to avoid aspiration if emesis occurs.
Treatment begins simultaneously with evaluation. Supplemental O2 by face mask is provided. If shock is severe or if ventilation is inadequate, airway intubation with mechanical ventilation (see Airway Establishment and Control : Tracheal Intubation) is necessary. Two large (14- to 16-gauge) IV catheters are inserted into separate peripheral veins. A central venous line or an intraosseous needle, especially in children, provides an alternative when peripheral veins cannot promptly be accessed (see also Vascular Access : Intraosseous Infusion).
Typically, 1 L (or 20 mL/kg in children) of 0.9% saline is infused over 15 min. In major hemorrhage, Ringer’s lactate is commonly used. Unless clinical parameters return to normal, the infusion is repeated. Smaller volumes (eg, 250 to 500 mL) are used for patients with signs of high right-sided pressure (eg, distention of neck veins) or acute MI. A fluid challenge should probably not be done in a patient with signs of pulmonary edema. Further fluid therapy is based on the underlying condition and may require monitoring of CVP or PAOP. Bedside cardiac ultrasonography to assess contractility and vena caval respiratory variability may help determine the need for additional fluid vs the need for inotropic support.
Patients in shock are critically ill and should be admitted to an ICU. Monitoring includes ECG; systolic, diastolic, and mean BP, preferably by intra-arterial catheter; respiratory rate and depth; pulse oximetry; urine flow by indwelling bladder catheter; body temperature; and clinical status, including sensorium (eg, Glasgow Coma Scale—see Table: Glasgow Coma Scale*), pulse volume, skin temperature, and color. Measurement of CVP, PAOP, and thermodilution cardiac output using a balloon-tipped pulmonary arterial catheter (see Monitoring and Testing the Critical Care Patient : Procedure) may be helpful for diagnosis and initial management of patients with shock of uncertain or mixed etiology or with severe shock, especially when accompanied by oliguria or pulmonary edema. Echocardiography (bedside or transesophageal) is a less invasive alternative. Serial measurements of ABGs, Hct, electrolytes, serum creatinine, and blood lactate are obtained. Sublingual CO2 measurement (see Other Types of Monitoring), if available, is a noninvasive monitor of visceral perfusion. A well-designed flow sheet is helpful.
Because tissue hypoperfusion makes intramuscular absorption unreliable, all parenteral drugs are given IV. Opioids generally are avoided because they may cause vasodilation, but severe pain may be treated with morphine 1 to 4 mg IV given over 2 min and repeated q 10 to 15 min if necessary. Although cerebral hypoperfusion may cause anxiety, sedatives or tranquilizers are not routinely given.
After initial resuscitation, specific treatment is directed at the underlying condition. Additional supportive care is guided by the type of shock.
In hemorrhagic shock, surgical control of bleeding is the first priority. Volume replacement (see also Intravenous Fluid Resuscitation) accompanies rather than precedes surgical control. Blood products and crystalloid solutions are used for resuscitation; however, packed RBCs and plasma are being considered earlier and in a ratio of 1:1 in patients likely to require massive transfusion (see Blood Products). Failure to respond usually indicates insufficient volume administration or unrecognized ongoing hemorrhage. Vasopressor agents are not indicated for treatment of hemorrhagic shock unless cardiogenic, obstructive, or distributive causes are also present.
Distributive shock with profound hypotension after initial fluid replacement with 0.9% saline may be treated with inotropic or vasopressor agents (eg, dopamine, norepinephrine— Inotropic and Vasoactive Catecholamines). Patients with septic shock also receive broad-spectrum antibiotics (see Antibiotics). Patients with anaphylactic shock unresponsive to fluid challenge (especially if accompanied by bronchoconstriction) receive epinephrine 0.05 to 0.1 mg IV, followed by epinephrine infusion of 5 mg in 500 mL 5% D/W at 10 mL/h or 0.02 mcg/kg/min (see also Anaphylaxis).
Inotropic and Vasoactive Catecholamines
In cardiogenic shock, structural disorders (eg, valvular dysfunction, septal rupture) are repaired surgically. Coronary thrombosis is treated either by percutaneous interventions (angioplasty, stenting), coronary artery bypass surgery, or thrombolysis (see also Overview of Coronary Artery Disease). Tachydysrhythmia (eg, rapid atrial fibrillation, ventricular tachycardia) is slowed by cardioversion or with drugs. Bradycardia is treated with a transcutaneous or transvenous pacemaker; atropine 0.5 mg IV up to 4 doses q 5 min may be given pending pacemaker placement. Isoproterenol (2 mg/500 mL 5% D/W at 1 to 4 mcg/min [0.25 to 1 mL/min]) is occasionally useful if atropine is ineffective, but it is not advised in patients with myocardial ischemia due to coronary artery disease.
Shock after acute MI is treated with volume expansion if PAOP is low or normal; 15 to 18 mm Hg is considered optimal. If a pulmonary artery catheter is not in place, cautious volume infusion (250- to 500-mL bolus of 0.9% saline) may be tried while auscultating the chest frequently for signs of fluid overload. Shock after right ventricular MI usually responds partially to volume expansion; however, vasopressor agents may be needed. Bedside cardiac ultrasonography to assess contractility and vena caval respiratory variability can help determine the need for additional fluid vs vasopressors; inotropic support is a better approach for patients with normal or above-normal filling.
If hypotension is moderate (eg, mean arterial pressure [MAP] 70 to 90 mm Hg), dobutamine infusion may be used to improve cardiac output and reduce left ventricular filling pressure. Tachycardia and arrhythmias occasionally occur during dobutamine administration, particularly at higher doses, necessitating dose reduction. Vasodilators (eg, nitroprusside, nitroglycerin), which increase venous capacitance or lower systemic vascular resistance, reduce the workload on the damaged myocardium and may increase cardiac output in patients without severe hypotension. Combination therapy (eg, dopamine or dobutamine with nitroprusside or nitroglycerin) may be particularly useful but requires close ECG and pulmonary and systemic hemodynamic monitoring.
For more serious hypotension (MAP < 70 mm Hg), norepinephrine or dopamine may be given, with a target systolic pressure of 80 to 90 mm Hg (and not > 110 mm Hg). Intra-aortic balloon counterpulsation is valuable for temporarily reversing shock in patients with acute MI. This procedure should be considered as a bridge to permit cardiac catheterization and coronary angiography before possible surgical intervention in patients with acute MI complicated by ventricular septal rupture or severe acute mitral regurgitation who require vasopressor support for > 30 min.
In obstructive shock, nontraumatic cardiac tamponade requires immediate pericardiocentesis, which can be done at the bedside. Trauma-related cardiac tamponade requires surgical decompression and repair. Tension pneumothorax should be immediately decompressed with a catheter inserted into the 2nd intercostal space, midclavicular line; a chest tube is then inserted. Massive pulmonary embolism resulting in shock is treated with anticoagulation and thrombolysis, surgical embolectomy, or extracorporeal membrane oxygenation in select cases.
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