Shock:

A great slide show of the different types of shock and their effects: shock

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Dobutamine nurse web site

A good site for dopamine

Good overall web site for cardiogenic shock

New test released to detect heart attack: MI

A product that measures ischmeia: albumin binding test

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TABLE 204-3. INOTROPIC CATECHOLAMINES

TABLE 204-1. LOSS OF BODY FLUID IN HYPOVOLEMIC SHOCK

Shock may be due to hypovolemia, vasodilation, or cardiogenic causes (poor cardiac output) or a combination. The fundamental defect in shock is reduced perfusion of vital tissues due (usually) to hypotension, so that O₂ delivery or uptake is inadequate for aerobic metabolism, resulting in a shift to anaerobic respiration with increased production and accumulation of lactic acid. When shock persists, impaired organ function is followed by irreversible cell damage and death. The degree of systemic hypotension necessary to cause shock varies and often is related to preexisting vascular disease. Thus, a modest degree of hypotension that is tolerated well by a young, relatively healthy person might result in severe cerebral, cardiac, or renal dysfunction in a patient who has significant arteriosclerosis.

Hypovolemic shock: Hypovolemic shock is associated with inadequate intravascular volume (absolute or relative), which produces diminished ventricular filling and reduced stroke volume. Unless compensated for by increased heart rate, it results in decreased cardiac output.

A common cause is acute hemorrhage (eg, from trauma, peptic ulcer, esophageal varices, or aortic aneurysm). Hemorrhage may be apparent (eg, hematemesis or melena) or concealed (eg, ruptured ectopic pregnancy).

Hypovolemic shock may also follow increased losses of body fluids other than blood. Hypovolemia usually takes several hours to develop and may be associated with a rising Hb or Hct (due to hemoconcentration).

Hypovolemic shock may be due to inadequate fluid intake, resulting in dehydration, often with increases in fluid loss. Frequently, because of neurologic or physical disability, patients cannot respond to thirst by increasing fluid intake. 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 given.

Vasodilatory shock: Vasodilatory shock results from a relative inadequacy of intravascular volume caused by vasodilation. Circulating blood volume is normal but insufficient for adequate cardiac filling. Various conditions may cause widespread venous or arteriolar dilation; eg, severe cerebral trauma or hemorrhage (neurogenic shock), liver failure, or ingestion of certain drugs or poisons. Shock associated with bacterial infection ( may be partly due to the vasodilatory effects of endotoxin or other chemical mediators on resistance vessels, thereby decreasing vascular resistance. In addition, some patients with acute MI and shock appear to have inadequate compensatory vasoconstriction in response to decreased cardiac output. If cardiac output does not increase commensurate with the reduction in vascular resistance, arterial hypotension develops. Below a critical systemic BP, vital organs will be inadequately perfused. Myocardial dysfunction secondary to inadequate coronary perfusion or other mechanisms (eg, release of myocardial depressant factor or other toxic substances) may complicate shock due to vasodilation.

Cardiogenic shock: A relative or absolute reduction in cardiac output due to factors other than inadequate intravascular volume may result in shock.

Symptoms and Signs

Symptoms and signs may be due to shock itself or to the underlying disease process. Mentation may be preserved, but lethargy, confusion, and somnolence are common. The hands and feet are cold, moist, and often cyanotic and pale. Capillary filling time is prolonged, and, in extreme cases, a bluish reticular pattern may appear over large areas. The pulse is weak and rapid unless heart block or terminal bradycardia is present; sometimes, only femoral or carotid pulses can be felt. Tachypnea and hyperventilation are present, but apnea may be a terminal event when the respiratory center fails due to inadequate cerebral perfusion. BP taken by cuff tends to be low (< 90 mm Hg systolic) or unobtainable, but direct measurement by intra-arterial cannula often gives significantly higher values.

In septic shock, a type of vasodilatory shock , fever, usually preceded by chills, is generally present. Elevated cardiac output is associated with diminished total peripheral resistance, possibly accompanied by hyperventilation and respiratory alkalosis. Thus, early symptoms may include a shaking chill, a rapid rise in temperature, warm flushed skin, a bounding pulse, and falling and rising BP (hyperdynamic syndrome). Urinary flow is decreased despite the high cardiac output. Mental status is usually impaired, and mental confusion may be a premonitory sign preceding hypotension by >= 24 h. However, these findings vary and may not be apparent even in patients whose markedly increased cardiac output and reduced vascular resistance are confirmed by direct hemodynamic measurement. In later stages, hypothermia may occur. Other causes of vasodilatory shock (eg, anaphylaxis) may present with findings that are similar to septic shock.

Complications

Pulmonary complications that often coexist or develop in patients with shock must not be overlooked. Pulmonary edema after hypovolemia usually is caused by excessive fluid infusion during resuscitation, although it may be confused with pneumonia due to unrecognized sepsis or aspiration of gastric contents due to transient CNS depression. Pulmonary edema in septic shock usually results from increased permeability of the pulmonary capillary and alveolar epithelium resulting in increased fluid exudation into the lungs. This complication (adult respiratory distress syndrome) is very serious. Hydrostatic pulmonary edema often complicates cardiogenic shock because of the marked increase in pulmonary capillary wedge pressure (PCWP).

Diagnosis

Diagnosis requires evidence of insufficient tissue perfusion due to reduced cardiac output or inadequate peripheral vasomotor tone. Most consider shock to be present in any patient with predisposing factors who develops a significant fall in BP, a urine flow of < 30 mL/h, and a progressive increase in the arterial lactic acid concentration or an increased anion gap associated with reduced HCO₃ levels. The diagnosis is supported by signs of hypoperfusion of specific organs (obtundation, oliguria, peripheral cyanosis) or signs relating to compensatory mechanisms (tachycardia, tachypnea, diaphoresis). In the earliest stages of shock, many of these signs may be absent or undetected if not specifically sought. Thus, treatment might not be initiated until the shock is advanced. None of these findings alone is specific for shock; each must be evaluated in the overall clinical context.

In any type of shock, manifestations of the underlying disease process may provide important diagnostic clues. Acute blood or fluid loss from a ruptured aorta, spleen, or tubal pregnancy or from peritonitis can be suspected from the physical findings. Signs of generalized dehydration are helpful in recognizing hypovolemia in patients with neurologic, GI, renal, or metabolic disorders. In septic shock, signs of preexisting pulmonary, GI, or UTI may be present, as may signs of an underlying malignancy or debilitating disease resulting in altered immunity against infection. In women of childbearing age, toxic shock syndrome due to tampon use may occur ; septic abortion, especially when performed illegally, can also cause septic shock. A systolic murmur may indicate ventricular septal rupture or mitral insufficiency, either of which may result in shock after acute MI. Pericardial tamponade is suggested by jugular venous distention, muffled heart sounds, a pericardial rub, and a paradoxical pulse. Massive pulmonary embolism is suspected in patients with a parasternal lift; a loud fourth heart sound at the left sternal border increased on inspiration; an accentuated, widely split pulmonary closure sound; and distended jugular neck veins.

Hypovolemic shock: Normal or reduced ventricular filling pressure with a low cardiac output in a patient with shock is diagnostic. A right ventricular filling pressure or central venous pressure (CVP) < 7 cm H₂O (< 5 mm Hg) suggests hypovolemia; CVP may be greater than this when hypovolemic shock occurs in patients with preexisting pulmonary hypertension. In some patients who have chronic lung diseases or cardiac dysfunction, measurement of the pulmonary end-diastolic pressure or PCWP, both of which are usually closely related to the left ventricular pressure during diastole, is a better test. Pulmonary end-diastolic pressure or PCWP < 8 mm Hg (or < 18 mm Hg in a patient with acute MI or preexisting left ventricular disease) suggests hypovolemia.

When hypovolemia is suspected, a therapeutic trial of volume loading--rapid infusion (500 mL/15 min) with 0.9% NaCl or colloid --may help confirm the diagnosis. Hypovolemia can be assumed when volume loading improves BP and urine flow and reduces the clinical manifestations of shock, with small increments in CVP or PCWP. However, low CVP and PCWP also occur in septic shock, so improvement after volume loading does not rule out sepsis as the cause.

Hypovolemic shock due to hemorrhage is usually associated with falling Hb and Hct. However, because shock may develop within minutes of acute blood loss, a normal Hb and Hct (before homeostatic hemodilution) does not rule out hemorrhage. A rising Hct and Hb in hypovolemic shock suggests hemoconcentration due to loss of other body fluids.

Vasodilatory shock: Vasodilatory shock should be suspected in patients with cerebral trauma, sepsis, drug intoxication, or heat exposure with vasoregulatory failure and dehydration. Hypovolemia is also frequently present.

Cardiogenic shock: Cardiogenic shock is suggested by engorged neck veins, signs of pulmonary congestion, and a gallop rhythm; however, in many patients with cardiogenic shock, these signs are absent. Diagnosis usually requires demonstration of reduced cardiac output with increased ventricular filling pressure. Pericardial tamponade, tension pneumothorax, or massive pulmonary embolism can usually be confirmed by echocardiography, chest radiography, or lung scan perfusion, respectively. When myocardial damage from an acute MI is sufficient to result in shock, the ECG is usually diagnostic ; however, prior infarction, left bundle branch block, or atrioventricular block with idioventricular or pacemaker rhythm may preclude an ECG diagnosis. In this case, the characteristic elevation of creatinine phosphokinase and the myocardial bands in the circulating plasma are helpful. The ECG helps also to identify arrhythmias that may, in themselves, cause or contribute to shock. Because hypovolemia may coexist with acute MI or preexisting heart disease, the shock cannot be assumed to be due entirely to myocardial damage, especially inferior or posterior infarcts, which may involve the right ventricle or atrium.

Prognosis and Treatment

Untreated shock is usually fatal. Even when treated, mortality from cardiogenic shock after massive MI and from septic shock is high. Prognosis depends on the cause, preexisting or complicating illness, time between onset and diagnosis, and adequacy of therapy.

First aid involves keeping the patient warm, with the legs raised slightly to improve venous return. Hemorrhage should be stopped, airway and ventilation checked, and respiratory assistance given if necessary. Nothing should be given by mouth, and the patient's head should be turned to avoid aspiration if emesis occurs. Because tissue hypoperfusion makes absorption unreliable, all drugs should be given IV if possible. Narcotics generally should be avoided, but severe pain may be treated with morphine 3 to 5 mg IV given over 2 min and repeated after 15 to 20 min if necessary. Although cerebral hypoperfusion may cause anxiety, sedatives or tranquilizers should not be given.

Supportive therapy stabilizes vital functions before diagnostic procedures can be carried out. Norepinephrine or dopamine may be needed . Supplemental O₂ by face mask should be provided immediately. If severe shock is present or ventilatory support is inadequate, endotracheal intubation is necessary to begin assisted ventilation with positive pressure and high O₂ concentrations.

Outside the hospital or in the emergency department, a temporary increase in BP may be achieved with military (or medical) antishock trousers (MAST). However, experience with MAST is required to avoid complications.

A large (16- to 18-gauge) catheter (particularly if hemorrhage is suspected) should be inserted into a peripheral vein (femoral, internal jugular, or antecubital) to infuse blood or other fluids and to administer drugs . Direct infusion of fluid into bone marrow provides an alternative emergency access to the circulation when veins are collapsed; in children, this route may be particularly useful, although infusion by the femoral vein is preferable if severe hypovolemic shock is present .

Giving IV sodium bicarbonate 50 to 100 mL of an 8.4% (1 mEq/mL) solution may help treat metabolic acidosis, but treatment of the underlying cause of shock (hypovolemia, sepsis, or low cardiac output) is more important.

Patients in whom shock is not immediately reversed should be considered critically ill, and definitive treatment should be continued in a special care area (eg, an ICU, a coronary care unit). Careful monitoring should include ECG; systemic arterial BP--preferably by direct intra-arterial cannula; respiratory rate and depth; urine flow (usually by indwelling bladder catheter); arterial blood pH, Pa_O2, and Pa_CO2; body temperature; and clinical status, including sensorium, pulse volume, skin temperature, and color. Measurement of CVP, PCWP, and thermodilution cardiac output using a balloon-tipped pulmonary arterial catheter is also helpful in patients with shock of uncertain or mixed etiology or with severe shock, especially when accompanied by severe oliguria or pulmonary edema. A well-designed flow sheet is extremely valuable. Serial measurements of arterial blood gases, Hct, serum creatinine, and plasma lactate may also be helpful.

Hypovolemic shock: Definitive treatment necessitates restoring intravascular volume and eliminating the underlying cause. Overly rapid infusion of fluids may precipitate pulmonary edema; therefore, monitoring CVP or PCWP is sometimes helpful. BP and urine flow should also be monitored. Generally, CVP or PCWP should not be raised > 12 to 15 mm Hg by fluid replacement. CVP monitoring alone may be misleading in patients with significant preexisting cardiac or pulmonary vascular disease. Care must be taken when interpreting filling pressures in patients during ventilatory assistance, particularly when end-expiratory pressure levels > 10 cm H₂O are being used, or in tachypneic patients with large negative pleural pressures. Measurements should be made at the end of expiration, and the transducer should be placed at the atrial level (midchest) and carefully calibrated. The precise mode and type of fluids to be given are determined by the clinical circumstances and are guided by frequent determination of Hct, serum electrolytes, urine flow, and arterial pH (ie, a search for evidence of resolving metabolic acidosis). 0.9% NaCl is as good as other solutions. After about 40 to 50% of the calculated blood volume deficit is replaced, whole blood or a colloid solution should be given. Whole blood should be cross-matched, but in an urgent situation, giving 1 to 2 U of O, Rh-negative blood is a good alternative Colloid solutions--6% hetastarch in 0.9% NaCl, plasma (fresh frozen plasma carries the risk of transmitting infection), or reconstituted 5% human serum albumin--lack RBCs and will dilute the Hct. Six percent hetastarch in 0.9% NaCl is an osmotic expander that is usually well tolerated but can prolong bleeding time. The usual maximum dosage is 20 mL/kg/24 h, although larger amounts have been used. Allergic reactions have been occasionally reported.

Shock unresponsive to volume replacement may be due to insufficient volume administration in the presence of ongoing blood loss or may be due to complicating factors (eg, coexisting cardiogenic shock due to myocardial damage or septic shock). When hypovolemia is not the probable cause or when systemic BP does not respond promptly to volume administration, a vasopressor drug should be considered.

Vasodilatory shock  Fluid resuscitation with 0.9% NaCl is almost always needed to treat the coexisting intravascular volume depletion that occurs from increased systemic vascular permeability, especially in sepsis. Vasopressor drugs (eg, dopamine, norepinephrine) are often necessary, particularly in profound hypotension. Dopamine is an inotropic drug that in low dosage (2 to 5 µg/kg/min) is less vasoconstrictive than norepinephrine but selectively improves mesenteric and renal blood flow; it may have advantages over other vasopressors in selected patients. Dobutamine, a more selective -agonist, increases cardiac output without vasoconstriction and thus may not be as useful in such patients. Norepinephrine or dopamine given by controlled IV infusion  may be used to raise the systolic pressure to between 90 and 100 mm Hg. Once BP is stabilized, efforts should be made to correct associated abnormalities (eg, hypoxemia, acidosis, hypovolemia, sepsis) so that administration of the vasopressor drug can be reduced or discontinued; prolonged vasoconstriction due to -receptor stimulation can further impair visceral microcirculation and increase myocardial work and O₂ demand. In the presence of heart failure or sepsis, the inotropic and chronotropic effects of norepinephrine or dopamine may improve cardiac output and systemic perfusion. In the absence of adrenal insufficiency, corticosteroid therapy is of no benefit. Little can be done when shock follows massive irreversible cerebral damage.

Cardiogenic shock Cardiogenic shock is treated by improving cardiac performance. Shock after acute MI should be treated with O₂ inhalation, stabilization of heart rate and rhythm, and volume expansion if associated with a normal PCWP. Shock after right ventricular MI occasionally responds favorably to rapid volume expansion, which should be considered after inferior wall MI when right-sided ventricular filling pressure (CVP) is significantly elevated in the absence of markedly elevated left-sided ventricular filling pressure (pulmonary end-diastolic pressure or PCWP). However, fluid administration alone will rarely correct the hemodynamic abnormality, and additional treatment with vasopressors may be required. Morphine 3 to 5 mg IV given over 2 min may relieve severe chest pain, help reduce elevated catecholamine levels, and reduce preload and afterload on the failing heart; the response must be closely monitored because morphine causes respiratory depression, is a venodilator, and may cause BP to fall. The initial dose can be repeated after 10 min if there is no evidence of respiratory depression or adverse BP response. Atropine 1 mg IV is occasionally effective in treating severe bradycardia (heart rate, < 50 beats/min) and hypotension that frequently occur very early after the onset of symptoms, particularly in inferior-posterior MI. Norepinephrine or dopamine is used to maintain arterial systolic pressure at > 90 mm Hg (but not > 110 mm Hg). Because it markedly increases O₂ demand, isoproterenol is contraindicated in patients with shock after acute MI unless it is needed temporarily for complete heart block.

When shock is complicated by bradycardia or advanced atrioventricular block, restoring BP with norepinephrine or dopamine (see above) and correcting acidosis usually result in an adequate ventricular rate. Temporary transvenous pacing may be necessary in patients with evidence of persistent high-grade atrioventricular block or severe sinus node dysfunction. Short-term administration of isoproterenol (2 mg/500 mL 5% D/W at 1 to 4 µg/min [0.25 to 1 mL/min]) may occasionally be needed before pacing in patients having prolonged asystolic periods or recurrent ventricular tachycardia or fibrillation associated with severe bradycardia. Digoxin is not routinely used in shock but may be of value in patients with supraventricular tachycardia. In the absence of severe systemic hypotension, dobutamine infusion or amrinone (0.75 mg/kg IV over 2 to 3 min followed by infusions of 5 to 10 µg/kg/min) may be used to improve cardiac output and reduce left ventricular filling pressure. Tachycardia and arrhythmias may occasionally occur during dobutamine administration, particularly at higher doses. Because amrinone is an inotrope and a vasodilator, arrhythmias and hypotension may occur during its administration. Amrinone may also cause thrombocytopenia, and platelet count should be monitored. Vasodilators (eg, nitroprusside, nitroglycerin), which increase venous capacitance or lower systemic vascular resistance, reduce the workload on the damaged myocardium and may be of value in patients without severe arterial 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.

Early use of intra-aortic balloon counterpulsation appears to be valuable for temporarily reversing shock in patients with acute MI and should be considered in patients who require vasopressor support (norepinephrine or dopamine) for > 30 min and in those with acute MI complicated by ventricular septal rupture or severe acute mitral regurgitation. Development of percutaneous techniques for bedside insertion makes balloon counterpulsation available to community hospitals.

Emergency surgical correction of mechanical defects (eg, ruptured intraventricular septum, pseudoaneurysm, severe mitral regurgitation, large dyskinetic segment) may also be necessary.

Emergency percutaneous transluminal coronary angioplasty (PTCA) to open an occluded coronary artery, if performed within a few hours after onset of acute MI, can reverse cardiogenic shock. Use of IV thrombolytic drugs before emergency PTCA is controversial. However, if emergency PTCA or cardiac surgery is not instituted, thrombolytic therapy should be considered as soon as possible, unless contraindicated.

Other considerations: Pericardial tamponade requires pericardiocentesis, and, in life-threatening situations, pericardial fluid may have to be removed at the bedside. Under less urgent circumstances, surgical creation of a pericardial window or pericardiectomy may be advisable to avoid recurrence. Massive pulmonary embolism resulting in shock is treated by supportive measures, including supplemental O₂, endotracheal intubation with assisted ventilation, vasopressor support (norepinephrine, dopamine), and IV heparin to prevent recurrent thrombosis. In patients who cannot be stabilized with these measures, emergency pulmonary angiography should be considered. The use of urokinase or streptokinase to lyse clots appears to be of value and is preferable to attempted embolectomy unless contraindicated (eg, because of recent major surgery, especially neurosurgical).

When pulmonary edema complicates shock, rapid resolution often results from treatment of coexisting heart failure with diuretics while administering O₂ as well as positive pressure ventilation. Pulmonary edema that develops from septic shock should similarly be treated with O₂ and positive pressure ventilation with positive end-expiratory pressure

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