Manual of Cardiovascular Diagnosis and Therapy

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CHAPTER 6. Shock


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  1. Introduction. Shock is a medical emergency that demands rapid action and constant attention on the part of physicians and nurses to prevent irreversible cell damage and death. Although the most frequent cause of shock in cardiac patients is massive myocardial infarction (MI), shock can be caused by a wide variety of disturbances, either cardiac or noncardiac in origin.

    1. Definition. Early definitions of shock emphasized a precipitous drop in systemic arterial blood pressure. It is now recognized that blood pressure varies considerably in shock, depending on the underlying etiology, duration, and adequacy of compensatory mechanisms. The essential concept to understand is that the major hemodynamic problem in shock is not inadequate pressure (although hypotension is often present) but inadequate tissue perfusion. The modern definition of shock is a circulatory state in which inadequate tissue perfusion occurs, thereby leading to progressive organ dysfunction that, unless rapidly reversed, results in irreversible organ damage and death. The early stage of organ hypoperfusion has been termed preshock. The cardinal signs of preshock and shock are manifestations of progressive dysfunction of vital organs—brain, heart, and kidneys. These signs are listed in Table 6-1.

      Despite advances in antibiotic therapy, blood-product separation, parenteral therapy, circulatory assistance devices, and hemodynamic monitoring, the mortality from shock remains distressingly high. Mortality from bacteremic shock may range as high as 40% to 80%, depending on the patient's age and a variety of comorbid predictors. Cardiogenic shock after MI is associated with a fatality rate that ranges from 45% to 90%. With these grim statistics in mind, considerable emphasis has been placed on early recognition and treatment of decreased perfusion (preshock or low-flow state) rather than waiting for the occurrence of true shock. In preshock or early shock, subtle signs of activated compensatory mechanisms substitute for the cardinal signs of shock as clues to the diagnosis (Table 6-1).

    2. Etiology. A wide variety of disease states can produce shock. Table 6-2 lists the major causes of shock. Although the list is lengthy and the clinical presentation varies depending on the underlying etiology, arterial hypotension, signs of organ hypoperfusion, and metabolic acidosis are common to most etiologies of shock.

      In the vast majority of patients with shock, the underlying etiology lies within one of the following three categories: cardiovascular shock, hypovolemic shock, or septic shock. The clinical recognition and treatment of these three entities are emphasized in this chapter. Although separated for discussion, in practice the categories often overlap.

    3. Pathophysiology. The clinical syndrome of shock is not a single entity but a dynamic state with many gradations. Patients who develop shock may be viewed as passing through the following three stages:

      1. Stage I. In the initial phase, the patient may be asymptomatic. Blood pressure may be either normal or slightly depressed. Compensatory mechanisms include sympathetic discharge that causes mild peripheral vasoconstriction (cool skin) and tachycardia. This stage may be viewed as equivalent to preshock. A previously healthy individual can compensate for approximately a 10% reduction in blood volume (about 1 U of blood) by means of these mechanisms.

      2. Stage II. Despite intense activity of compensatory mechanisms, in stage II blood pressure declines and organ hypoperfusion begins. Clinically, the patient often demonstrates declining blood pressure, tachycardia, and restlessness.

        If coronary artery disease is present, angina may occur. These signs develop after a 20% to 25% reduction in effective circulating blood volume.

      3. Stage III. As the patient progresses into stage III, organ dysfunction becomes evident. Cardiac output declines, urine production falls or ceases, and mental status proceeds from restlessness to agitation, followed by somnolence and coma. Unless circulating blood volume is restored rapidly, compensatory mechanisms contribute to the deteriorating clinical picture in a vicious circle (e.g., intense vasoconstriction increases afterload, thereby causing a further decline in cardiac output).

        Shock can have deleterious effects on a variety of vital organs. Arterial mean pressures below 70 to 80 mm Hg are inadequate to maintain adequate coronary arterial blood flow, myocardial oxygen, and nutrient supply. Pressures below 60 mm Hg are insufficient to maintain adequate cerebral blood flow. Even brief periods of severe hypotension are thought to contribute to the pulmonary vascular injury that is characteristic of adult respiratory distress syndrome. Hypovolemic damage to the liver can compromise its role in detoxification and thereby exacerbate the shock state as metabolic wastes accumulate in the blood. Renal function deteriorates, and the patient progresses from oliguria to anuria. If hypovolemia persists for several hours, irreversible tubular necrosis may occur.

  2. Diagnosis. Patients often arrive in the emergency department in shock. In this event, it is imperative to initiate therapy promptly, using general measures to support respiration and circulation (see Section ). Once the clinical situation has stabilized, the important issues are (i) determining the etiology of the shock state and (ii) instituting specific measures to correct the underlying problem

    1. History. Evidence of underlying disease should be sought. Of particular importance is a history of cardiac disease and/or hypertension.

      Episodes of chest pain, shortness of breath, exercise intolerance, or palpitations should be explored. Recent trauma or burns should be considered. The possibility of recent infection or reasons for hypovolemia must be taken into account (hemorrhage, gastrointestinal fluid or blood loss, renal disease). In the elderly or very young, insensible losses without adequate replacement have to be considered. History of neurologic disease (spinal cord injury, previous problems with orthostatic hypotension) should also be considered. A history of drug ingestion is important (both prescribed and nonprescribed drugs) because of the myocardial-depressant effects of some drugs (particularly antiarrhythmics) and the volume-depleting effect of others (diuretics). In addition, anaphylactic shock can arise from drug ingestion. Historical items of diagnostic relevance in shock are shown in Table 6-3.

    2. Physical examination. Physical findings in shock vary considerably, depending on the clinical stage and the underlying etiology of the shock state. Many of the physical findings relate either to compensatory mechanisms that have been activated or to the extent of organ hypoperfusion. The patient's general appearance can vary from normal to moribund. Skin is often cool, and peripheral cyanosis may be present; however, the skin may be warm in terminal stages of shock because blood vessels are unable to constrict. The skin also may be warm in septic shock because of the local effects of bacterial endotoxins that cause inappropriate dilatation of peripheral vessels. Beads of perspiration reflect heightened sympathetic tone. The level of the arterial blood pressure often indicates the degree of shock (numerous exceptions, however, preclude complete reliance on this sign). Heart rate usually reflects the adequacy of compensatory mechanisms, with tachycardia the rule.

      Respiratory rate and temperature reflect underlying hypoxia, acid-base imbalance, or possible infection. Chest examination can provide secondary evidence of high left ventricular filling pressures (rales). The cardiac examination should focus on findings compatible with complications of MI (ventricular septal rupture, aneurysm, papillary muscle dysfunction; see Chapter 15). It is important to remember that a murmur will be soft or absent in up to 50% of patients with papillary muscle rupture, leading to torrential mitral regurgitation and shock. Abdominal examination may reveal evidence of trauma or bowel obstruction. A rectal examination is essential to rule out gastrointestinal bleeding. Serial examination of adequacy of peripheral pulses provides one way of monitoring therapeutic progress. A neurologic examination is also important. Physical findings that may be present in shock are found in Table 6-4.

    3. Laboratory tests. Various laboratory tests are helpful in defining the underlying cause of shock and in monitoring therapy. Many of them will be needed daily or more frequently. Suggested tests are listed in Table 6-5. Evidence of disseminated intravascular coagulation is a frequent and ominous sign in shock of any cause. Insertion of a pulmonary arterial and peripheral arterial catheter often is necessary in cases of shock and facilitates necessary blood sampling without undue patient discomfort. A guide for the use of laboratory tests in shock is given in Table 6-5.

    4. Chest x-ray examination. Chest x-ray films should be obtained on a daily basis during the acute phase of shock. They are particularly important in demonstrating subtle signs of left ventricular failure, thereby aiding in monitoring fluid therapy. The chest x-ray film may reveal widening of the mediastinum in cases of aortic dissection. The chest x-ray examination may also reveal pulmonary edema or the picture of adult respiratory distress syndrome, improper placement of central venous pressure (CVP) and pulmonary arterial catheters, or incorrect placement of an endotracheal tube. Calcium should be sought in the aortic or mitral valves as well as in the coronary arteries.

    5. Echocardiography. Echocardiography may be useful in the initial diagnosis of shock if a cardiovascular etiology is suspected. Cardiovascular causes of shock include MI and its complications, dissection of the aorta, critical aortic stenosis, cardiac tamponade, and massive pulmonary embolism. Other cardiovascular causes of shock are listed in Table 6-2.

    6. Catheterization and angiography. Knowledge of cardiac filling pressures and cardiac output is often helpful in preshock patients and is essential in individuals with severe or progressive shock. Although it is possible to perform retrograde catheterization of the left ventricle to measure these parameters, this exposes the patient to the risks of cardiac catheterization. If catheterization is elected, use of a balloon-tipped catheter for measuring pulmonary artery pressures and cardiac output is preferred. If a thermodilution catheter is used, serial cardiac outputs can be measured.

    7. Protocol for the diagnosis of shock

      1. Confirmatory tests needed to make the diagnosis. The diagnosis of shock or preshock rests on the demonstration of organ hypoperfusion or signs of early compensatory mechanisms outlined in Table 6-1. It is important to distinguish among the various underlying etiologies that can lead to shock, so that therapy can be aimed at the specific disease process.

      2. Differential diagnosis of shock. A differential diagnostic list of conditions that cause shock is provided in Table 6-2. The most common underlying etiologies are cardiac disease, hypovolemia, and sepsis.

        1. Cardiogenic shock. A severe complication of acute MI, cardiogenic shock, is discussed in Chapter 13. Several items should be emphasized: (i) shock occurs in approximately 5% to 10% of patients hospitalized with the diagnosis of acute MI; (ii) shock usually occurs in patients in whom more than 40% of the left ventricle has been damaged; and (iii) mortality is high in these patients, ranging from 50% to 90% or more.

          Cardiogenic shock usually can be distinguished from septic and hypovolemic shock by history. Cardiogenic shock may involve an element of hypovolemia. The measurement of pulmonary capillary wedge pressure (PCWP) may be important to make this distinction in selected patients. Because the mortality from cardiogenic shock is high, it is also important to make the diagnosis as early as possible, for example, during the preshock period, so that appropriate therapy can be instituted. Urine output should be monitored carefully. Patients with large MIs who have trouble urinating, or whose urine output falls below 20 ml per hour, should have a Foley catheter placed in the bladder. Although direct damage to the left ventricular myocardium is by far the most common cause of cardiogenic shock, a variety of other cardiovascular conditions can also lead to the shock state. Used in the broadest sense, cardiogenic shock implies a pathophysiologic state in which the pumping function of the heart is so impaired that it is unable to provide for adequate tissue perfusion.

          A number of mechanical problems may accompany MI and lead to shock (see Chapter 15). Acute ventricular septal results from myocardial necrosis of the septum and usually occurs 1 to 7 days after MI. It is an equally common complication of inferior and anterior MI. Acute mitral regurgitation may result from papillary muscle dysfunction caused by ischemia, change in geometry or dilatation of the left ventricle, ruptured chordae tendineae, or ruptured papillary muscle. It is particularly important to recognize rupture of the papillary muscle because 75% of individuals with this lesion will expire within 24 hours unless surgical intervention is undertaken on an emergency basis.

          Acute valvular disruption may occur in settings other than MI and result in cardiogenic shock. Aortic dissection may lead to acute aortic insufficiency or may extend into the pericardium, thereby producing cardiac tamponade. Acute aortic insufficiency also may result from infectious endocarditis or disruption of the suture ring in a prosthetic aortic valve. Shock in a patient with a prosthetic valve should be considered prosthetic valve disruption until proven otherwise. Patients with long-standing mitral valve disease (on the basis of either rheumatic valvulitis or myxomatous degeneration) may suffer acute decompensation that leads to cardiogenic shock. Patients in both of these groups are susceptible to ruptured chordae tendineae and acute mitral regurgitation. Infectious endocarditis may also result in acute mitral regurgitation.

          Obstructive valvular lesions can also produce cardiogenic shock. Critical aortic stenosis or severe mitral stenosis can significantly impair cardiac output. Left atrial myxoma can severely compromise left ventricular filling, thereby markedly decreasing cardiac output. All these lesions should be considered when one assesses a patient with unexplained shock.

          Nonvalvular outflow obstruction from supravalvular or subvalvular aortic stenosis or hypertrophic obstructive cardiomyopathy also may result in cardiogenic shock. Rhythm disturbances such as the onset of atrial fibrillation can lead to acute decompensation in these patients. Cardiogenic shock caused by left ventricular outflow obstruction is an important entity to recognize because conventional therapy such as vasopressors or afterload reduction may lead to further deterioration. Cardiac lesions that restrict ventricular filling, such as constrictive pericarditis or tamponade, may result in cardiogenic shock. These lesions are also important to recognize, because specific therapies are available and may be lifesaving.

          Right ventricular infarction can also be a cause of cardiogenic shock. Some degree of right ventricular damage occurs in more than 40% of acute inferior MIs. Elevated CVPs, clear lung fields, and hypotension in the setting of an acute inferior MI should suggest right ventricular infarction. Right ventricular infarction usually responds to volume repletion, although occasionally atrioventricular sequential pacing is required to stabilize the patient.

          Finally, some degree of myocardial depression may be present in shock states that are not based on underlying cardiac pathologic conditions. The pathophysiology of this decrease in myocardial function may involve myocardial depressant substances such as tumor necrosis factor, nitric oxide, and altered acid-base status.

        2. Hypovolemic shock. Hypovolemia is present in many forms of shock. It is the main cause of shock in burns, hemorrhage, and trauma; however, enough volume depletion to result in shock may occur in patients with severe volume losses secondary to diabetic ketoacidosis, vomiting, diarrhea, and intestinal obstruction. Generally, intravascular volume loss in excess of 1 L is necessary before compensatory mechanisms fail and shock ensues.

          The diagnosis of hypovolemic shock is suggested by history. Insertion of a CVP catheter may provide information on the patient's volume status (patients with hypovolemia often have very low CVP readings). It is important to recognize, however, that compensatory mechanisms may allow CVP to remain relatively normal in the presence of significant hypovolemia. The most important evidence in the diagnosis of hypovolemic shock is whether the patient's condition improves after a volume challenge (for details, see Section III.).

        3. Septic shock. Septic shock is a state of organ hypoperfusion that may accompany severe infection. It is caused either by the circulatory spread of bacteria or by their metabolic products. Although a wide variety of pathogens may induce septic shock, it is most commonly seen with gram-negative bacterial infections. The mechanism of shock in this setting is the release of endotoxin (a component of the bacterial wall) into the bloodstream.

          Endotoxin interacts with vasoactive substances in the bloodstream and may cause syndromes that range from increased vascular permeability to disseminated intravascular coagulation. The diagnosis is suggested by a history of infection plus physical examination and laboratory studies consistent with an infective focus. Metabolic (lactic) acidosis is common in this form of shock. A progressively increasing anion gap carries grave implications and should prompt a reassessment of the therapeutic regimen.

  3. Therapy

    1. Medical treatment

      1. Monitoring the patient with shock. Probably no other entity demands more constant and skillful monitoring than shock. The potential for rapid deterioration demands that the physician expand clinical impressions with monitoring equipment that can provide accurate hemodynamic data. Four types of monitoring are commonly used in patients with shock: (i) CVP, (ii) pulmonary arterial pressure, (iii) systemic arterial pressure, and (iv) urine output (bladder catheterization). The combination of monitoring used is dictated by the clinical situation and the type of data needed. Pulmonary arterial hemodynamic monitoring is said by some authorities to be essential in these sick patients. However, data to support this contention are lacking, and many clinicians manage these patients without the use of invasive hemodynamic monitoring.

        1. CVP. A large-bore (no. 14 or no. 16) needle is used to introduce a cannula into a large vein that empties into the right side of the heart. Mean right ventricular filling (right atrial) pressures are measured (normal is 0 to 7 mm Hg). In the setting of significant pulmonary disease or left ventricular disease, CVP does not accurately reflect left-heart filling pressures, and a pulmonary arterial catheter must be used. In addition to monitoring pressure, the central venous line can be used to assess the response to initial fluid challenge (see Section III.A.1.b.2.a.). Right ventricular filling pressures as high as 15 mm Hg may be necessary to provide adequate cardiac output in the acute phase of shock.

        2. Pulmonary arterial pressure. The preferred instrument for monitoring left ventricular filling pressures is a balloon-tipped pulmonary arterial catheter (Swan-Ganz catheter) that may be introduced percutaneously and allowed to "float" out into the pulmonary artery. With the balloon deflated, the catheter is advanced to a small branch of the pulmonary arterial tree.

          When the balloon is reinflated, the small pulmonary artery is occluded and an approximation of PCWP is obtained. Utilization of the pulmonary arterial catheter is important when (i) the patient's blood pressure does not respond to an initial fluid challenge, or (ii) MI is suspected or known to underlie shock, and accurate left ventricular filling pressures may be useful in selecting and monitoring therapy. Normal PCWPs range from 2 to 12 mm Hg. In patients with cardiogenic shock, however, the heart is operating on a depressed Starling curve, and wedge pressures of 15 to 18 mm Hg usually are required to provide maximum cardiac output. As noted earlier, many physicians prefer to manage their patients in shock without invasive hemodynamic monitoring because no data exist that confirm the usefulness of pulmonary arterial hemodynamic monitoring in these patients.

          Thermodilution pulmonary arterial catheters can be used to monitor serial cardiac output. When pharmacologic agents such as inotropic drugs or vasodilators are used, a pulmonary arterial catheter provides useful hemodynamic data on the efficacy of treatment.

        3. Systemic arterial pressure. An arterial cannula is advisable in patients with overt shock. There are three major reasons: (i) in shock, the auscultatory blood pressure may not accurately reflect the true systemic arterial pressure, particularly in the patient who is peripherally vasoconstricted and has thready pulses. Because adequate blood pressure is essential to survival, accurate blood pressure determination by means of an arterial catheter is desirable. (ii) The vasoactive agents used to treat shock (both vasodilators and sympathomimetic agents) require continuous monitoring that is best achieved by an arterial catheter. (iii) Numerous blood samples (both arterial blood gases and blood chemistry samples) are necessary to monitor the therapy of shock. Patient comfort is maximized if blood is drawn through an indwelling arterial cannula.

        4. Urine output. Patients in shock or preshock should have a Foley catheter placed in the bladder to assist in monitoring hourly urine output.

      2. General measures. Shock is an acute situation that can rapidly deteriorate. Certain general measures should be instituted immediately for any patient in shock.

        1. Intravenous access. At least one and preferably two large-bore (no. 14 or no. 16) intravenous cannulas ensure adequate vascular access. Unless the patient has signs of fluid overload (rales, elevated neck veins), an initial fluid challenge of 500 ml over 30 minutes should be given. The choice of fluid remains controversial (normal saline, albumin, and dextran are all acceptable). The goal of fluid replacement is to establish a systolic pressure of 90 to 100 mm Hg, not the previous level of systemic blood pressure.

        2. Oxygen. An arterial Po2 of 70 mm Hg should be established by increasing inspiratory oxygen with nasal cannulas or a face mask, except in patients with obstructive pulmonary disease. Many patients with chronic obstructive pulmonary disease have an arterial Po2 in the 55 to 60 mm Hg range. Adequate respiratory function in these individuals is based on central nervous system hypoxic drive, and increasing arterial Po2 above 70 mm Hg can lead to respiratory arrest.

        3. Position. Patients with shock should be supine or in reverse Trendelenburg position.

        4. Pain relief. Careful administration of an analgesic (morphine, 2 to 4 mg intravenously, may be administered to relieve pain) is frequently necessary.

        5. Flow charts. Flow charts should be established to follow volume replacement, drugs administered, acid-base status, arterial Po2, pulmonary wedge pressure, systemic blood pressure, and urine output.

      3. Drugs. A wide variety of agents are available to treat shock. Two large classes of drugs commonly used are vasopressors and vasodilators. The use of any specific drug or class of drug is dictated by the clinical setting and suspected underlying etiology.

        1. Vasopressors. Often vasopressors are used incorrectly in the therapy of shock. Remember that shock indicates inadequate tissue perfusion rather than any absolute level of blood pressure. With this caveat in mind, vasopressors can serve as a valuable component of an overall plan to support adequate tissue perfusion. In general, vasopressors should not be used until an adequate fluid challenge has been attempted. If appropriate fluid has been given, and signs of inadequate organ perfusion persist, a trial of vasopressors is indicated.

          Which vasopressor should be used? The decision is based on two parameters: (i) the underlying pathophysiology of the shock state and (ii) a knowledge of the pharmacology of each vasopressor.

          Assessment of the pathophysiology of the compromised circulation is accomplished in the fashion outlined in Section III. This is combined with hemodynamic information derived from appropriate monitoring. Several classifications for vasopressors exist. The most rational classification is based on the type of sympathetic receptor affected by a given vasopressor. There are two types of sympathetic receptors: alpha and beta. Alpha-receptor stimulation causes arteriolar vasoconstriction, whereas beta stimulation augments cardiac performance and causes arteriolar vasodilatation. An example of a pure alpha-receptor stimulator is methoxamine; isoproterenol is a pure beta-receptor stimulator. Most vasopressors have both alpha and beta effects. In addition to alpha and beta effects, dopamine in low doses (2 to 10 g/kg per minute) has a dilative effect on the renal vascular bed, independent of beta effects. The choice of agent is dictated by the combination of myocardial stimulation and vasoconstriction/ vasodilatation required for a particular patient's hemodynamic status. In general, the larger the dose of vasopressor required to support the circulation, the less likely are the patient's chances of recovery.

          A list of the various vasopressors available and their modes of action, dosages, and side effects is found in Table 6-6. Practical guidelines for mixing solutions of vasopressors are shown in Table 6-7. Some of the more frequently used vasopressors are discussed briefly here.

          1. Levarterenol (Levophed, norepinephrine). Levarterenol stimulates both alpha- and beta-receptors. It has some stimulatory effect on the myocardium, although its principal action is through arteriolar vasoconstriction. It is most effective if used to raise blood pressure to 90 to 100 mm Hg (above this number, reflex bradycardia occurs with concomitant decreases in cardiac output).

          2. Dopamine (Intropin). Dopamine has primarily beta effects, with some alpha effects. In addition, low-dose dopamine has a direct vasodilative effect on the renal and mesenteric vascular beds.

          3. Dobutamine (Dobutrex). Dobutamine, a synthetic congener of isoproterenol, is effective in the treatment of severe left ventricular failure and cardiogenic shock. It possesses primarily beta1 (cardiac stimulation) activity. It does possess some beta2 (peripheral vasodilatation) activity, but much less than that of isoproterenol, and some alpha-adrenergic activity, although less than that of dopamine and much less than that of levarterenol. It does not possess the independent renal dilatation properties of dopamine. It is probably most useful when PCWP is markedly elevated and hypotension is not severe. If hypotension is the major problem, dopamine or levarterenol probably represent better choices. Dobutamine has the advantage over isoproterenol of causing less peripheral vasodilation and thus is less likely to provoke a compensatory tachycardia.

          4. Isoproterenol (Isuprel). Isoproterenol activates beta-receptors, which stimulate the myocardium; peripheral arteriolar vasodilatation and tachycardia also occurs.

        2. Vasodilators. Vasodilators have been used in patients with cardiogenic shock, elevated left ventricular filling pressures, systemic arterial pressures around 100 mm Hg, and low cardiac output. Vasodilator therapy has even been of benefit in occasional patients with systemic arterial pressures of 80 to 90 mm Hg. Pulmonary arterial and systemic arterial catheters should be inserted before vasodilator therapy is initiated. The patient must be monitored in an intensive care unit to prevent hypotension. Specific drugs and dosages of vasodilators are outlined in Chapter 4.

      4. Myocardial reperfusion. Improved cardiac function and outcome occur after myocardial reperfusion, whether brought about by pharmacologic thrombolysis, percutaneous transluminal coronary angioplasty, or emergency coronary artery bypass grafting. Recent multicenter trial data support early mechanical reperfusion by angioplasty or coronary bypass surgery as the best approach for the critically ill patient with cardiogenic shock after MI.

    2. Surgery

      1. General measures. Surgical intervention is indicated to remedy a number of the underlying disorders that cause shock (see Table 6-2). In some instances, such as hemorrhage, intestinal obstruction, and hemothorax, emergency surgery can be lifesaving and must be undertaken without delay. In other settings, as with burns, initial management is primarily medical, with subsequent surgical intervention. Shock can be compounded by surgery and general anesthesia. Fluid balance, oxygenation, electrolyte levels, and acid-base balance must be adjusted before an acutely ill patient is sent to surgery.

      2. Intraaortic balloon pump (IABP). In recent years, a number of mechanical methods have been used to support the circulation. The most commonly used mechanical device is the IABP. It is used for a variety of conditions, including intractable left ventricular failure after cardiopulmonary bypass, cardiogenic shock after MI, and refractory angina pectoris. The IABP is effective, at least temporarily, in reversing the shock state in patients with cardiogenic shock secondary to MI or its complications. Because IABP is not definitive therapy by itself, this intervention should be combined with angioplasty or cardiac surgery if mortality is to be avoided. Improvements of 15% to 20% in cardiac output can predictably be expected in such patients, and hemodynamic stability often will be achieved with the IABP in place. In the absence of any reversible lesion, however, such patients are almost impossible to wean from the IABP.

        In contrast, patients who experience the mechanical complications that accompany MI (e.g., acute mitral regurgitation, acute ventricular septic defect) may often be salvaged after IABP insertion, which allows them to be stabilized for cardiac catheterization and definitive surgical intervention. Patients with unstable angina refractory to maximal pharmacologic therapy may also benefit from IABP insertion, which allows them to undergo cardiac catheterization and surgical or catheter revascularization.

        The IABP is a helium-filled, sausage-shaped balloon, which is introduced into the thoracic aorta from the femoral artery. Balloon filling is electronically synchronized with the patient's ECG so that the balloon inflates during diastole and deflates during systole. The balloon influences the physiology of the heart in two ways: (i) it augments coronary blood flow through increased aortic diastolic pressure, and (ii) it decreases left ventricular afterload by deflation early in systole. Most centers report hemodynamic improvement in 80% to 90% of patients with shock following treatment with IABP.

Selected Readings

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Chou TM, Amidon TM, Ports TA, et al. Cardiogenic shock: thrombolysis or angioplasty? J Intensive Care Med 1995;11:37–48.

An up-to-date discussion of the benefits and limitations of these reperfusion techniques in cardiogenic shock.

Fink MP. Shock: An overview. In: Rippe JM, Irwin RS, Fink MP, et al., eds. Intensive care medicine. oston: Little, Brown and Company, 1995.

A comprehensive and up-to-date chapter by one of the leading investigators in the field.

Flesch M, Kilter H, Cremers B, et al. Effects of endotoxin on human myocardial contractility: involvement of nitric oxide and peroxynitrite. J Am Coll Cardiol 1999;33: 1062–1070.

Endotoxin exposure to the human myocardium leads to release of nitric oxide and subsequent myocardial depression.

Goldberg RJ, Samad NA, Yarzebski J, et al. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med 1999;340:1162–1168.

Short-term survival rates have improved in recent years for patients with cardiogenic shock after MI. This would appear to be the result of more aggressive reperfusion therapy in these patients.

Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. N Engl J Med 1999;341:625–634.

Early revascularization improves the outlook for patients who develop cardiogenic shock after MI.

Hochman JS, Sleeper LA, White HD, et al. One-year survival following early revascularization for cardiogenic shock. JAMA 2001;285:190–192.

Early revascularization results in improved 1-year survival for patients with acute MI and cardiogenic shock.

Price S, Anning PB, Mitchell JA, et al. Myocardial dysfunction in sepsis: mechanisms and therapeutic implications. Eur Heart J 1999;20:715–724.

An excellent review of the underlying mechanisms operating in septic shock.

White HD. Cardiogenic shock: a more aggressive approach is now warranted. Eur Heart J 2000;21:1897–1901.

Early reperfusion therapy is clearly warranted in patients with cardiogenic shock after MI.