Critical illness

Hypovolemic shock.

Common causes of hypovolemic shock include hemorrhage, dehydration, and massive capillary leak. Decreased cardiac filling pressures are the hallmark of these conditions.

Cardiogenic shock.

The most common cause of cardiogenic shock is acute myocardial infarction (MI) involving 40% or more of the left ventricular mass. Cardiomyopathies and valvular lesions are other etiologies. In contrast to hypovolemic shock, cardiac filling pressures are increased in cardiogenic shock.

Obstructive shock.

The most common causes of obstructive shock include pericardial tamponade, acute pulmonary embolism, and tension pneumothorax. Cardiac filling pressures are usually increased owing to outflow obstruction, impaired ventricular filling, or decreased ventricular compliance. Therefore the clinical manifestations of cardiogenic and obstructive shock may be similar.

Septic shock.

Sepsis is the most common etiology of hyperdynamic distributive shock. Direct mediators of the inflammatory response and tissue hypoperfusion result in cellular injury and organ dysfunction in septic patients.

Traumatic shock.

Severe trauma may result in traumatic shock through an inflammatory mechanism that is similar to the genesis of septic shock on a molecular, cellular, and phenotypic level. Shock in trauma patients is especially likely to be multifactorial, including a distributive immunologically mediated response to injury as well as shock resulting from hemorrhage.

General resuscitative measures.

The SSC guidelines recommend resuscitation of patients with sepsis and septic shock to begin immediately, at the time of diagnosis. For sepsis-induced hypoperfusion, at least 30 mL/kg of intravenous (IV) crystalloid is administered within the first 3 hours. Additional fluid administration is guided by serial reassessments, including physical examination; physiologic variables, including heart rate, blood pressure, arterial oxygen saturation, respiratory rate, temperature, and urine output; and noninvasive or invasive monitoring. The target mean arterial pressure (MAP) is 65 mm Hg. An additional end point is normalization of lactate in those patients who present with elevated lactate levels as markers of tissue hypoperfusion. Resuscitative end points must be individualized.

Diagnosis of septic source.

Hospitals and healthcare systems should establish performance improvement programs for sepsis, including screening algorithms. Blood cultures and other applicable cultures should be obtained prior to initiation of antibiotic therapy. If indicated, imaging studies should be performed to confirm potential sources of infection.

Empirical antibiotic therapy and infection source control.

Administration of empirical broad-spectrum antimicrobials should occur within 1 hour of recognition of sepsis or septic shock. When appropriate, the choice of antimicrobial drugs should be reassessed daily for the potential to deescalate from broad-spectrum antibiotics to more specifically tailored antibiotics. Infection source control should occur as soon as possible.

Fluid resuscitation.

Initial fluid resuscitation should be undertaken with crystalloid. Volume resuscitation should continue as long as the patient demonstrates volume responsiveness based on either dynamic or static variables. The addition of albumin to the resuscitation fluid can be considered in patients who continue to require substantial quantities of crystalloid to maintain an adequate MAP. Hydroxyethyl starches should be avoided.

Vasopressor and inotropic medications.

Once intravascular volume is deemed to be optimal, vasopressors may be necessary to achieve adequate perfusion pressures, typically targeted to the aforementioned MAP of 65 mm Hg. However, if the degree of shock is profound, volume resuscitation may occur simultaneously with the initiation of vasopressor support, particularly if diastolic hypotension is severe. Norepinephrine is the first-line vasopressor for management of septic shock. Epinephrine can be added when an additional drug is required to maintain an adequate MAP. Low-dose vasopressin can also be added at the nontitratable sepsis dose (0.03 U/min) but should not be used as the initial vasopressor. Dopamine is not recommended as an alternative to norepinephrine except in selected patients such as those with a low risk of tachydysrhythmias and absolute or relative bradycardia. Dobutamine can be added to vasopressor support in the presence of myocardial dysfunction or when hypoperfusion persists despite adequacy of intravascular volume and MAP.

Steroid management.

Empirical IV corticosteroids should be avoided if adequate volume resuscitation and vasopressor therapy restore hemodynamic stability. If this cannot be achieved, IV hydrocortisone 200 mg per day in four divided doses is recommended.

Hemoglobin target.

In the absence of myocardial ischemia, severe hypoxemia, or acute hemorrhage, the transfusion trigger is generally less than 7.0 g/dL.

Ventilator measures for sepsis-induced acute respiratory distress syndrome.

First and foremost, a low tidal volume and limitation of inspiratory plateau pressure are recommended for ventilator management of sepsis-induced acute respiratory distress syndrome (ARDS). The target tidal volume is 6 mL/kg, and the upper limit goal for plateau pressure is 30 cm H ₂ O. Application of at least a minimal amount of positive end-expiratory pressure (PEEP) is also advised; higher levels of PEEP are used for moderate or severe ARDS. Recruitment maneuvers can be used in patients with severe refractory hypoxemia. Prone positioning may be used in patients with a Pao ₂ /Fio ₂ ratio of 150 mm Hg or less in critical care units familiar with this mode of hypoxemic rescue. A short course of neuromuscular blockade (≤48 hours) for adjunctive management of ARDS and a Pao ₂ /Fio ₂ less than 150 mm Hg can be undertaken. The head of the bed should be elevated in all mechanically ventilated patients unless contraindicated. In patients with established ARDS who are adequately volume resuscitated, a conservative fluid strategy should be employed. Finally, protocols for spontaneous breathing trials, weaning, and minimizing of sedation should be used.

General critical care management.

Protocols for blood glucose management are recommended, targeting a blood glucose level of 180 mg/dL or less. Continuous venovenous hemofiltration (CVVH) and intermittent hemodialysis are considered equivalent in patients with sepsis and acute renal failure (ARF) because they achieve similar short-term survival rates. However, CVVH is much better tolerated in hemodynamically unstable patients with septic shock. Additional recommendations call for venous thromboembolism prophylaxis, stress ulcer prophylaxis, and early enteral feeding initiation. Finally, the goals of care, including treatment plans and end-of-life discussions if appropriate, should occur as soon as possible, but within 72 hours of ICU admission.

The systemic inflammatory response.

The similarity between the pathophysiologic response to sepsis and to traumatic injury is immunologically mediated and, by extrapolation, is a genomic and molecular phenomenon. Both sepsis and traumatic injury activate the innate immune system, which results in a systemic inflammatory response that ideally limits damage and restores homeostasis. Sepsis requires an identifiable source of infection. Conversely, it is widely accepted that systemic inflammation following trauma is sterile.

The two general components of the systemic inflammatory response include (1) an acute proinflammatory response mediated by an increase in the expression of innate immunity genes and (2) an antiinflammatory response that modulates the proinflammatory phase to affect the restoration of homeostasis. It is likely that both components of the response occur simultaneously rather than sequentially following severe traumatic injury. The degree of systemic inflammation following trauma is proportional to the severity of the injury and is an independent predictor of organ dysfunction and mortality.

Compensatory antiinflammatory response syndrome (CARS).

CARS is associated with the antiinflammatory component of systemic inflammation. It is a suppression of adaptive immunity mediated by suppression of associated genes. A major consequence of CARS is the enhanced susceptibility of critically ill patients to nosocomial infections. This has been demonstrated in animal “two-hit” models, manifested as an increased susceptibility to infection after a first insult.

Persistent inflammation, immunosuppression, and catabolism syndrome (PICS).

Chronic critical illness describes patients who survive their initial episode of critical illness but remain dependent on ICU care and never fully recover. PICS describes this form of chronic critical illness. Severely injured trauma patients with complicated outcomes are older and sicker and require more ventilator days compared to their “uncomplicated” counterparts. They have persistent leukocytosis and low lymphocyte and albumin levels. Genomic analysis of these complicated patients demonstrates persistent expression of changes consistent with defects in the adaptive immune response and increased inflammation. Clinically, this manifests as persistent inflammation, including a prolonged acute-phase response, immunosuppression, protein catabolism, malnutrition, and reduced functional and cognitive abilities. The unifying pathology is low-level inflammation inducing immune suppression and progressive protein catabolism. These patients typically have a long and complicated course culminating in transfer to a long-term acute care facility where they experience a further protracted decline and death.

Overview and general principles.

Damage control resuscitation or hemostatic resuscitation is a useful adjunct in the prevention and reversal of the aforementioned coagulopathy associated with massive hemorrhage and injury. General principles include early hemorrhage control, permissive hypotension until hemorrhage is controlled, avoidance of crystalloids, and early use of blood components facilitated by implementation of institutionally based massive transfusion protocols (MTPs). Correction of hypothermia, acidosis, and hypocalcemia are important adjuncts.

Clotting factors.

Fresh frozen plasma (FFP) contains all of the clotting factors. Individual recombinant clotting factors are also available for the management of a coagulopathy due to inadequate amounts of one or a few clotting factors. The most widely studied and utilized recombinant clotting factor since the turn of this century has been recombinant human coagulation factor VIIa (rFVIIa), approved in 1999 for the treatment of bleeding in patients with hemophilia and in patients who have inhibitors to factor VIII or factor IX. The clotting mechanism is initiated by activation of factors IX and X in the presence of tissue factor. Activated factor X, in conjunction with factor V, calcium, and phospholipids, converts prothrombin to thrombin, which converts fibrinogen to fibrin. Thrombin generation on the surface of activated platelets is also promoted. This process results in formation of a fibrin-platelet plug at the site of vascular injury.

Bleeding surgical and trauma patients are obviously different than those with hemophilia, since massive blood loss results in deficiency of all clotting factors, platelets, and RBCs. The use of rFVIIa was never approved for use in trauma patients, but its off-label use in this population was initially widespread. It was also used by the US military during the Iraq and Afghanistan conflicts. As rFVIIa was subjected to further investigation, it became apparent that this intervention failed to improve outcomes in trauma patients, and concern developed regarding the risk of thrombotic complications. At present, the consensus is that there are no proven clinically significant benefits of rFVIIa as a general hemostatic agent in patients who do not have hemophilia. Especially given its potential thrombotic risks, the use of rFVIIa as a general hemostatic agent in patients without hemophilia is not recommended. When damage control resuscitation using high-ratio blood component replacement is used, all of the clotting factors, platelets, and RBCs required for clot generation are administered, making use of individual recombinant factors unnecessary.

One special scenario in which low-volume rapid reversal of coagulopathy is essential is the management of elderly trauma patients who are anticoagulated with warfarin, particularly in the setting of traumatic brain injury. Rapid infusion of large volumes of FFP is often impossible owing to comorbidities predisposing to volume overload (e.g., congestive heart failure, renal failure). Prothrombin complex concentrates (PCCs) provide rapid and low-volume delivery of vitamin K–dependent clotting factors. These products contain factors II, IX, and X, with variable quantities of factor VII and the anticoagulant proteins C and S. The prothrombin complex concentrate that includes factor VII is four-factor PCC. In addition to use in traumatic brain injury, studies have demonstrated prothrombin complex concentrates can be effective in rapidly reversing coagulopathy to allow for surgery or to control postoperative bleeding in patients who have been taking warfarin. There are no data to support use of prothrombin complex concentrates in the absence of warfarin use, but these products are often used as salvage therapy for reversal of persistent coagulopathy that occurs despite appropriate use of blood component therapy.

Antifibrinolytic agents.

Under normal circumstances, plasmin initiates clot resolution by degradation of fibrin. Trauma-associated coagulopathy is characterized by poor clot formation and rapid lysis of clots. Tranexamic acid is an antifibrinolytic drug that binds with plasminogen to prevent its activation to plasmin, thereby interfering with the process of clot lysis and slowing bleeding. Experts in trauma resuscitation have developed evidence-based guidelines for the use of tranexamic acid in adult trauma patients. Administration should be limited to patients with severe hemorrhagic shock (systolic blood pressure <75 mm Hg) with known predictors for fibrinolysis or with documented fibrinolysis on thromboelastography. It should be administered only if the time since injury is less than 3 hours. The recommended dose is 1 g IV over 10 minutes followed by 1 g by infusion over 8 hours.

Platelet dysfunction and thrombocytopenia.

Inhibition of platelet activation is crucial for the management of patients who have ischemic cardiovascular disease and atherosclerosis. Platelet inhibitors and antiplatelet drugs increase the risk of bleeding.

Aspirin is an irreversible platelet cyclooxygenase and thromboxane A ₂ inhibitor and is also a relatively weak antiplatelet agent. More potent antiplatelet drugs include the glycoprotein IIb/IIIa receptor antagonists (abciximab, tirofiban, and eptifibatide). Additional potent antiplatelet drugs include clopidogrel, prasugrel, and ticagrelor, which selectively and irreversibly bind to the P2Y12 receptor to inhibit the adenosine diphosphate–dependent mechanism of glycoprotein IIb/IIIa receptor expression and platelet activation.

Clopidogrel is the major antiplatelet drug in current use. Dual antiplatelet therapy (i.e., aspirin and clopidogrel) is standard treatment following revascularization by percutaneous coronary intervention (PCI) with stent placement. Dual therapy is recommended for up to 4 weeks after placement of bare-metal stents and for 6 to 12 months after placement of drug-eluting stents. Methods for monitoring the effects of clopidogrel have not been established, and specific therapy in the event of associated bleeding is not available. In patients who have coronary artery stents and require surgery, the operation should be deferred for more than 6 weeks after bare-metal stent placement and more than 6 months after drug-eluting stent placement if possible. In patients who require surgery within 6 weeks of bare-metal stent placement or within 6 months of drug-eluting stent placement, antiplatelet therapy should be continued perioperatively. The actively bleeding patient with recent placement of coronary stents comprises a third category. In these patients, the risks and benefits of stopping clopidogrel must be weighed against the risk of stent thrombosis and against the need for surgical intervention.

Platelet dysfunction without thrombocytopenia may occur in many clinical circumstances, including inherited and acquired coagulopathies. Desmopressin (DDAVP) is a synthetic analogue of the natural hormone arginine vasopressin. DDAVP injection has been approved for and is indicated in patients with hemophilia A with factor VIII coagulant activity levels above 5% and for patients with mild to moderate classic von Willebrand disease (type I) with factor VIII levels above 5%. In these patients, the bleeding time is shortened or corrected by release of endogenous factor VIII from storage pools. DDAVP has also been demonstrated to shorten or correct the bleeding time in uremia, but the mechanism of this action is unknown. The use of DDAVP in the actively hemorrhaging patient with platelet dysfunction is not well established.

Thrombocytopenia is the most common coagulation disorder in the ICU and is defined as a platelet count below 150,000/mm ³ . The two most important etiologies of thrombocytopenia in this setting are sepsis and heparin-induced thrombocytopenia (HIT). However, other potential causes are many and are generally classified according to whether platelets are consumed, sequestered, or underproduced. HIT is a special circumstance, and platelet transfusion should be avoided in these patients because of the risk of exacerbation of the prothrombotic state. Likewise, platelets are not usually transfused if the thrombocytopenia is due to immune-mediated destruction, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, or uncomplicated cardiac bypass surgery.

The threshold for prophylactic transfusion of thrombocytopenic ICU patients is not clear. However, we do know that thrombocytopenia is associated with an increased risk of bleeding with surgery or invasive procedures only when the platelet count is below 50,000/mm ³ . Spontaneous bleeding, especially intracerebral bleeding, usually does not occur until the platelet count is below 10,000/mm ³ . Therefore, in the absence of active bleeding or the need for an invasive procedure, most patients with very low platelet counts and no associated risk factors for bleeding are transfused when the platelet count is below 10,000/mm ³ . If they have additional risk factors for bleeding, the trigger is typically less than 20,000/mm ³ . In the presence of an associated coagulopathy, active bleeding, or platelet dysfunction, a more liberal transfusion strategy is undertaken, but guidelines for platelet transfusion triggers are not well established.

In the massively hemorrhaging patient, platelet transfusions in conjunction with correction of plasma coagulation factor deficits are indicated when the platelet count is below 50,000/mm ³ or below 100,000/mm ³ in the presence of diffuse microvascular bleeding. If the patient meets criteria for activation of an MTP, a 1:1:1 ratio of units of plasma:platelets: PRBCs should be administered.

Cardiac etiologies.

Circulatory collapse attributable to cardiac dysfunction can involve the myocardium, the pericardium, the cardiac valves, and the outflow tract of the heart. Disease processes involving these components of the heart are reviewed in detail elsewhere in this textbook. However, principles pertaining to the acute deterioration typical of critically ill surgical patients are highlighted here.

Acute deterioration attributable to myocardial dysfunction is most often associated with an acute coronary syndrome (ACS), which includes a continuum of associated disorders such as ST-segment elevation myocardial infarction (STEMI), non–ST-segment elevation myocardial infarction (NSTEMI), and unstable angina pectoris (UA). The pathophysiology shared by these disorders is rupture of a previously quiescent atherosclerotic plaque, which triggers the release of vasoactive substances and activation of platelets and the coagulation cascade. All patients suspected of ACS should be treated with supplemental oxygen, sublingual nitroglycerine (unless systolic pressure is <90 mm Hg), and aspirin. Despite the common etiology of the subtypes of ACS, rapid recognition of the STEMI variant is crucial because these patients benefit from immediate reperfusion and should be treated with fibrinolytic therapy or urgent revascularization. Conversely, fibrinolytics have demonstrated no benefit and an increased risk of adverse events when used in patients with NSTEMI or unstable angina. Multiple clinical trials have demonstrated that the early administration of fibrinolytic agents in STEMI reduces infarct size, preserves left ventricular function, and reduces short- and long-term mortality. Tissue plasminogen activator (tPA) is the fibrinolytic drug most commonly used. However, systemic fibrinolysis poses a special problem in the trauma and surgical patient population because trauma or major surgery within 2 weeks of fibrinolysis that could be a source of rebleeding is an absolute contraindication to fibrinolytic therapy in STEMI. In the surgical patient, the risk of thrombolysis may be prohibitive, and emergency coronary angiography with a PCI may be preferable. However, PCI mandates use of antiplatelet drugs and immediate adjunctive therapeutic anticoagulation, which can also be problematic in the trauma or surgical patient. A risk-benefit analysis of reperfusion by each method is imperative for each patient. If a patient is deemed to be a candidate for reperfusion, the time to revascularization is crucial. A medical contact-to-needle time for initiation of fibrinolytic therapy of under 30 minutes or a medical contact-to-balloon time for PCI of under 90 minutes are the currently accepted goals. In patients with diffuse and complex coronary lesions, coronary artery bypass grafting (CABG) may be preferred. The invasive nature of CABG must be weighed against the likelihood of a requirement for repeated interventions after initial PCI. PCI may be a reasonable alternative in patients with complex coronary lesions and severe coexisting diseases that substantially increase the risk of coronary bypass surgery.

Cardiogenic shock, resulting from either left ventricular pump failure or mechanical complications, is the next leading cause of in-hospital death after MI. Systolic dysfunction results in decreased cardiac output and decreased stroke volume. Systemic perfusion is decreased, which results in compensatory vasoconstriction and fluid retention, which can contribute to further myocardial dysfunction. Hypotension causes a decrease in coronary perfusion pressure and worsens myocardial ischemia. Diastolic dysfunction can also cause an increase in left ventricular end-diastolic pressure, pulmonary congestion, and hypoxemia, which can also worsen myocardial ischemia. Interruption of this cycle of ischemia and myocardial dysfunction is the basis for treatment of cardiogenic shock. Adequate oxygenation and ventilation are maintained with endotracheal intubation and mechanical ventilation if necessary. Electrolyte abnormalities are corrected, narcotics are administered, and dysrhythmias and heart block are corrected with antidysrhythmic drugs, cardioversion, or pacing. Preload should be optimized and is especially important in patients who have right ventricular infarction. If hypotension persists despite adequate volume resuscitation, vasopressors may be needed to maintain coronary perfusion pressure. Norepinephrine is superior to dopamine for management of hypotension in cardiogenic shock. Phenylephrine may be added if tachydysrhythmias are problematic. If tissue perfusion is inadequate despite achieving an adequate blood pressure, inotropic support and/or intraaortic balloon pump (IABP) counterpulsation are initiated. Dobutamine, a selective β ₁ -adrenergic receptor agonist, is the initial drug of choice in patients with systolic pressures above 80 mm Hg. Phosphodiesterase inhibitors (e.g., milrinone) are less dysrhythmogenic than catecholamines but may cause hypotension. Intraaortic balloon counterpulsation reduces systolic afterload, augments diastolic perfusion pressure, increases cardiac output, and improves coronary blood flow, all without increasing oxygen demand. However, IABP counterpulsation does not improve blood flow distal to a critical coronary stenosis and has not been demonstrated to improve mortality when used without reperfusion therapy or revascularization. Rather, use of an IABP can serve as a bridge to help stabilize patients prior to definitive therapeutic measures. Ventricular assist devices may also be used in appropriate clinical settings. Randomized trials have demonstrated that cardiogenic shock in the setting of acute MI is a class I indication for emergency revascularization, either by PCI or CABG. Systemic fibrinolysis is not a preferred option in this circumstance.

Additional complications of acute MI include postinfarction angina, ventricular free wall rupture, ventricular septal rupture, acute mitral regurgitation, and right ventricular infarction. A high index of suspicion and familiarity with the presentation of these entities allows for their prompt diagnosis and treatment.

Postinfarction angina is a syndrome of chest pain that may occur at rest or with minimal activity that occurs 24 hours or later after an acute MI. It may result from ischemia around the fresh infarction or at a distance and is generally associated with a poor long-term prognosis. It can be diagnosed clinically and evaluated by coronary angiography and is an indication for revascularization. PCI is useful for anatomically appropriate lesions. CABG is considered in patients with left main coronary artery disease, three-vessel coronary artery disease, and for lesions unsuitable for percutaneous interventions. IABP counterpulsation is often required as a bridge to revascularization if the angina cannot be controlled medically or if the patient is hemodynamically unstable.

Ventricular free wall rupture may occur during the first week after infarction. The typical patient is elderly, female, and hypertensive. Left ventricular pseudoaneurysm formation with leakage may be a sentinel event, presenting as chest pain, nausea, and anxiety, but frank rupture is catastrophic and presents with shock and electromechanical dissociation. Echocardiography will demonstrate a pericardial effusion. Postinfarction pericardial effusions larger than 10 mm in width on echo images taken in diastole are frequently associated with cardiac rupture. Pericardiocentesis may be required to relieve acute tamponade but is best performed in the OR immediately prior to thoracotomy and ventricular repair.

Ventricular septal rupture presents with severe heart failure or cardiogenic shock. Auscultation demonstrates a pansystolic murmur and a parasternal thrill. The hallmark on echocardiography is a left-to-right intracardiac shunt. Rapid institution of IABP counterpulsation and supportive pharmacologic therapy must be undertaken. Operative repair should occur within 48 hours of the rupture.

Acute mitral regurgitation is usually associated with an inferior wall MI and ischemia or infarction of the posterior papillary muscle, but anterior papillary muscle rupture is also possible. Papillary muscle rupture occurs in a bimodal distribution: either within 24 hours or as late as 3 to 7 days after an acute MI. The presentation is catastrophic, with pulmonary edema, hypotension, and cardiogenic shock. The murmur may be limited to early systole, soft or even inaudible. Echocardiography is essential for diagnosis. Management may include afterload reduction, IABP counterpulsation, inotropic support, and vasopressor therapy as a bridge to surgical valve repair or replacement, which should occur as soon as possible.

Right ventricular infarction occurs in up to one-third of patients with inferior wall MI. The classic presentation is a clear chest x-ray and jugular venous distention in a patient with a known inferior wall MI. ST-segment elevation is present in the right precordial leads. Right atrial and right ventricular end-diastolic pressures are elevated, pulmonary artery occlusion pressure is normal to low, and cardiac output is low. Echocardiography demonstrates decreased right ventricular contractility. Right ventricular preload should be maintained with volume resuscitation. Some patients may require inotropic support or IABP counterpulsation. Reperfusion of the occluded coronary artery is also imperative.

Acute deterioration associated with pericardial pathology is usually caused by pericardial effusion and/or cardiac tamponade. A pericardial effusion may be characterized as a transudate, an exudate, a pyopericardium, or a hemopericardium. Large effusions are common with cancer. Loculated effusions tend to occur in the postsurgical patient, the trauma patient, and those with purulent pericarditis. Heart sounds are distant. Symptoms include orthopnea, cough, and dysphagia. Pericarditis is associated with typical chest pain, a pericardial friction rub, fever, and diffuse ST-segment elevation. Large effusions look like globular cardiomegaly on chest x-ray. (See Chapter 11 for details about pericardial diseases.) The size of an effusion can be graded by echocardiography, which can also detect signs of cardiac tamponade. One-third of patients with asymptomatic large pericardial effusions will go on to develop cardiac tamponade. Triggers for the development of tamponade include hypovolemia, tachydysrhythmias, and acute pericarditis. Pericardiocentesis is indicated for immediate management of tamponade. Patients with very large effusions, electrical alternans, or pulsus paradoxus should also undergo pericardiocentesis. Patients with penetrating cardiac wounds, postinfarction myocardial rupture, or dissecting aortic hematomas presenting as tamponade require emergency cardiac surgery.

Valvular heart disease can present in two ways in the critically ill patient: (1) acute valve dysfunction resulting in acute heart failure and (2) decompensation of chronic valve disease. Regurgitation is the most common type of acute valve dysfunction. Although stenosis is typically chronic and slowly progressive, acute decompensation may occur if there is a significant superimposed hemodynamic demand. For instance, previously asymptomatic mitral stenosis may present with pulmonary edema in the setting of systemic infection, and asymptomatic aortic stenosis may present with cardiogenic shock in the setting of acute gastrointestinal hemorrhage. Echocardiography is essential in the diagnosis of all these entities.

In addition to acute MI, common etiologies of acute mitral regurgitation include endocarditis and mitral valve prolapse. These patients can present with pulmonary edema, and the characteristic murmur may be soft or absent. Surgical repair should occur as soon as possible.

Causes of acute aortic regurgitation include endocarditis and aortic dissection. The diastolic murmur may be indistinct. Treatment is emergency surgery.

Rheumatic mitral stenosis usually occurs in young women and may present during pregnancy. Acute decompensation can often be treated conservatively. Percutaneous balloon mitral valvulotomy is the preferred intervention in this situation.

Aortic stenosis is common in the elderly patient population. Decompensation occurs with an increased hemodynamic demand. A systolic murmur is auscultated. Conservative management for decompensation is appropriate. Aortic valve replacement is performed for severe symptomatic disease.

Mechanical valves are subject to valve thrombosis, and management of this problem is controversial. Options include therapeutic anticoagulation, surgical intervention with valve replacement, and systemic thrombolytic therapy. Tissue valves degenerate within 10 to 15 years after implantation. Acute regurgitation associated with tissue valves is similar to native valve regurgitation and requires valve replacement.

Obstruction to cardiac outflow is most commonly encountered in patients with a pulmonary embolism, which is the most common preventable cause of hospital death. Acute pulmonary embolism can be divided into several overlapping syndromes: (1) transient dyspnea and tachypnea; (2) pulmonary infarction or congestive atelectasis manifested by pleuritic chest pain, cough, hemoptysis, pleural effusion, or pulmonary infiltrates; (3) right ventricular failure associated with severe dyspnea and tachypnea; (4) cardiovascular collapse with hypotension, syncope, and coma (massive pulmonary embolism); and (5) nonspecific symptoms, including confusion, coma, pyrexia, wheezing, recalcitrant heart failure, and dysrhythmias. Thrombolytic therapy is indicated for patients with cardiovascular collapse and for some who have clinical evidence of right ventricular failure or right ventricular hypokinesis on echocardiography. Thrombolytic therapy provides rapid lysis of a pulmonary embolism and rapid restoration of right ventricular function. However, many trauma and surgical patients are not candidates for systemic thrombolysis, but some may be candidates for catheter-directed thrombolytic therapy. Thoracotomy and surgical pulmonary embolectomy remains an option for life-threatening hemodynamic collapse due to a pulmonary embolism when thrombolysis and catheter-directed therapy are not feasible.