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Management of Cardiac Tamponade After Cardiac Surgery
REVIEW ARTICLE
Management of Cardiac Tamponade After Cardiac Surgery Paula Carmona, MD, Eva Mateo, MD, Irene Casanovas, MD, Juan J. Peña, MD, Jose Llagunes, MD, Federico Aguar, MD, Jose De Andrés, MD, and Carlos Errando, MD
A
CUTE POSTOPERATIVE CARDIAC TAMPONADE (defined as up to 7 days post-surgery)1 is an uncommon entity that requires prompt diagnosis and diligent management to avoid circulatory collapse and cardiorespiratory arrest. Anesthetic management for surgical pericardial drainage of an effusion causing cardiac tamponade in the postoperative period after cardiac surgery is a challenge for the anesthesiologist, considering the unstable hemodynamic situation resulting from abnormal ventricular filling and the subsequent reductions in systolic volume, cardiac output, and systemic blood pressure. Such a procedure requires extensive pathophysiologic knowledge and careful hemodynamic control. After cardiac surgery, two different variants of cardiac tamponade may occur, low-pressure tamponade and regional cardiac tamponade, when any cardiac zone is compressed by loculated effusions. When these entities is suspected, the diagnosis must be prompt. The European Society of Cardiology published its Guidelines on the Diagnosis and Management of Pericardial Diseases in 2004.2 However, the recent literature shows a lack of publications reviewing hemodynamic and anesthetic management of patients with cardiac tamponade after cardiac surgery. This article provides an updated synopsis of the pathophysiology, diagnosis (including key clinical and echocardiographic criteria), and perioperative anesthetic management of cardiac tamponade after cardiac surgery. EPIDEMIOLOGY/ETIOLOGY
In cardiac surgery, the incidence of cardiac tamponade may vary based on the type of surgery, ranging from 0.2% among patients undergoing coronary artery bypass graft surgery to 8.4% in heart transplant patients.1,3,4 Precipitating factors include the administration of anticoagulants, coagulation disorders, excessive mediastinal bleeding, the removal of epicardial pacing wires after cardiac surgery,5,6 autoimmune reactions, and the development of postpericardiotomy syndrome. Late tamponade (⬎7 days after surgery) is con-
From the Anaesthesia, Critical Care and Pain Medicine Department, Consorcio Hospital General of Valencia, Valencia, Spain. Address reprint requests to Paula Carmona, MD, Anaesthesia, Critical Care and Pain Medicine Department, Consorcio Hospital General of Valencia, Valencia, Spain. E-mail: [email protected] © 2012 Elsevier Inc. All rights reserved. 1053-0770/2602-0023$36.00/0 doi:10.1053/j.jvca.2011.06.007 Key words: cardiac tamponade, cardiac surgery, anesthesia, literature review 302
sidered to be a significant postoperative complication of cardiac surgery, with a higher mortality rate than early tamponade.7-9 Among postoperative patients with severe delayed pericardial effusions, the 30-day mortality rate was 3%. PATHOPHYSIOLOGY
In all variants of cardiac tamponade, including tamponade after cardiac surgery, the pericardial sac gradually can stretch to accommodate increasing volume. At any point in time, the total intrapericardial volume is relatively fixed throughout the cardiac cycle. When the ability of the pericardium to stretch is exceeded by rapid or massive accumulation of fluid, any additional fluid causes the pressure within the pericardial sac to increase. When the increasing intrapericardial pressure exceeds the intracardiac pressure, the positive transmural pressure gradient compresses the adjacent cardiac chamber or chambers. Because of the fact that intracardiac pressures vary throughout the cardiac cycle, the pericardial pressure will exceed the intracardiac pressure within different chambers at different points in the cardiac cycle. The right chambers, which have the lowest instantaneous pressures, are affected first.10 Ventricular filling in cardiac tamponade is seriously compromised and occurs in a complex fashion that is poorly understood. High diastolic ventricular pressures cause a reduction in ventricular filling, systolic volume, and systolic ventricular pressure depending on the contractile state of the ventricle and the level of the intrapericardial pressure. High end-diastolic ventricular pressure and high mean atrial pressure are accompanied by pulmonary and systemic venous hypertension. Although these venous pressures are maintained at a sufficient level with high atrial pressures, the inflow of blood into the ventricles can be maintained. In this situation, cardiac output is maintained primarily by tachycardia. In more advanced stages of tamponade, filling becomes possible only during atrial systole, especially when the heart rate increases. These phenomena lead to the disappearance of the “y” wave, which represents right ventricular filling during diastole on the right atrial pressure records. The “x” wave, which represents atrial filling, is maintained because during ventricular systole there is movement of the entire valve plane toward the apex of the ventricle, leading to a reduction of atrial pressure coinciding with ventricular ejection (Fig 1). The hemodynamic changes caused by the pericardial effusion can be categorized into several phases (Table 1). Especially after cardiac surgery, regional cardiac tamponade can occur when any cardiac zone is compressed by loculated effusions,4,11 which usually are accompanied by
Journal of Cardiothoracic and Vascular Anesthesia, Vol 26, No 2 (April), 2012: pp 302-311
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rate (beta effect), (2) an increase of diastolic relaxation (beta effect), (3) an increase of peripheral resistances to maintain adequate arterial pressure and coronary flow (alpha effect), and (4) an increase in inotropism to achieve an increase in ejection fraction. The Effects of Spontaneous Breathing and Mechanical Ventilation on Cardiac Tamponade
Fig 1. CVP waveform in cardiac tamponade. (A) Normal CVP waveform. “a” wave, atrial contraction; “c” wave: elevation of the valve plane at systole start; “x” descent, atrial relaxation and drop of valve plane during systole; “v” wave, rapid filling of atrium before opening of the tricuspid valve; “y” descent, opening of the tricuspid valve. (B) CVP waveform in cardiac tamponade. The “y” descent is lost or decreased because of limited ventricular filling and there is prominent “x” descent during ventricular systole.
localized pericardial adhesions. Loculation can produce classic tamponade (eg, loculated effusions over the right atrium and atrioventricular groove), but more often the typical hemodynamic abnormalities are found only in the compressed chambers or zones. The phenomena described previously occur earlier and at lower pressures in patients with hypovolemia, a situation that is quite frequent in the postoperative period. These patients can develop cardiac tamponade with diastolic pressures as low as 3 to 6 mmHg. Such situations are known as “low-pressure cardiac tamponade” and are extremely difficult to diagnose.11 Therefore, therapeutically-induced hypovolemia or filling pressure reduction (forced diuresis, vasodilators) may lead to severe impairment in cardiac output and blood pressure, which can be life threatening. Compensating mechanisms in this situation of cardiac tamponade are secondary to adrenergic (alpha and beta) stimulation. The activity exerted by these mechanisms can be summarized into 4 major effects: (1) an increase of heart
Respiration also affects intracardiac pressures, particularly those on the right side of the heart. During inspiration, in spontaneously breathing patients without cardiac tamponade, intrathoracic and intrapericardial pressures decrease. This results in augmented flow into the right atrium and right ventricle, with decreased flow out of the pulmonary veins into the left atrium and left ventricle. Reciprocal changes occur during expiration. In the presence of normal intrapericardial pressure, the normal respiratory variation in filling of the left and right heart causes a small (less than 10 mmHg) inspiratory decrease in systemic arterial systolic blood pressure. When the patient is suffering from a cardiac tamponade and is breathing spontaneously, there is an exaggeration of the phenomena described earlier, leading to pulsus paradoxus as a sign of the interventricular interdependence.12,13 Pulsus paradoxus is defined as a decrease of more than 10 mmHg in peripheral arterial pressure during inspiration.11,14 During positive-pressure mechanical ventilation, the reverse of the conventional pulsus paradoxus has been reported. The inspiratory increase in arterial blood pressure followed by a decrease on expiration has been called “reversed pulsus paradoxus.” In patients under mechanical ventilation suffering from cardiac tamponade, this phenomenon is more exaggerated.15 Mechanical ventilation increases pleural pressure and transpulmonary pressure (the difference between alveolar and pleural pressures). During inspiration, left ventricular stroke volume increases because left ventricular preload increases, whereas left ventricular afterload decreases. This leads to an increase in arterial blood pressure at the end of inspiration. In contrast, right ventricular stroke volume decreases during inspiration because venous return and right ventricular preload decrease, while right ventricular afterload increases. Because of the pulmonary transit time of blood (approximately 2 seconds), the inspiratory decrease in
Table 1. Hemodynamic Changes Caused by Pericardial Effusion
Phase I Phase II Phase III
Pericardial Pressure
RV Filling Pressure
LV Filling Pressure
Pulsus Paradoxus
Cardiac Output
1 1 (⫽ RV Pr) 1
1 1 1
1 11 1 (⫽ RV Pr)
⫺ ⫹ ⫹⫹
⫺ 2 22
NOTE. Phase I: pericardial and left and right ventricular pressures are elevated but not equilibrated, and cardiac output is not compromised. Phase II: elevated pericardial and right ventricular filling pressures are equilibrated with each other but not with left ventricular filling pressure, which is higher. Cardiac output is compromised, and pulsus paradoxus is present in most but not all patients. Phase III: elevated pericardial right ventricular and left ventricular filling pressures are equilibrated, cardiac output is severely compromised, and pulsus paradoxus is present in all patients spontaneously breathing and without other conditions that may suppress the pulsus paradoxus. Abbreviations: Pr, pressure; RV, right ventricle; LV, left ventricle. Modified with permission.82
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Fig 2. The effects of mechanical ventilation on hemodynamics in patients with cardiac tamponade. Mechanical ventilation increases pleural pressure and transpulmonary pressure. During inspiration, left ventricular stroke volume increases because of the increase in left ventricular preload, whereas left ventricular afterload decreases. This leads to an increase in arterial blood pressure at the end of inspiration. In contrast, right ventricular stroke volume decreases during inspiration because of the decrease in right ventricular preload, whereas right ventricular afterload increases. Because of the pulmonary transit time of blood, the inspiratory decrease in right ventricular output causes decreases in left ventricular filling and output only a few heartbeats later, usually during the expiratory period. This, in turn, leads to a decrease in arterial blood pressure at the end of expiration. (Adapted from Michard and Teboul,15 courtesy of BioMed Central.)
right ventricular output causes decreases in left ventricular filling and output only a few heartbeats later, usually during the expiratory period. This corresponds with a decrease in arterial blood pressure at the end of the expiration (Fig 2). Therefore, if positive-pressure ventilation is used with high tidal volumes and high levels of positive end-expiratory pressure, the right ventricular afterload may be increased and the ventricular septum can shift leftward, thereby reducing the distensibility of the left ventricle and, consequently, its preload.16 In conclusion, in patients with cardiac tamponade, the institution of mechanical ventilation and positive end-expiratory pressure (PEEP) may worsen hemodynamic status with reversed pulsus paradoxus.17-19 DIAGNOSIS
Clinical Presentation The clinical presentation of postoperative cardiac tamponade includes a wide range of nonspecific signs and symptoms such as dyspnea,20 orthopnea, attenuated cardiac sounds, chest pain,21 tachycardia and hypotension, and even cardiogenic shock.22 The nonspecific clinical scenario after cardiac surgery also may be influenced by the presence of low-pressure cardiac tamponade23 or loculated tamponade, which are relatively frequent in the post– cardiac surgery period.4,24 One of the most common clinical signs in these patients is hemodynamic impairment, characterized by the presence of tachycardia and hypotension, findings that may be associated with multiple diagnoses in a postoperative cardiac patient. The following factors can determine the presence of cardiac tamponade: the fluid accumulation rate, the previous ventricular function status, the patient’s blood volume, and the presence or absence of pre-existing hypertension.25 The development of pulsus paradoxus is a key clinical sign pointing to a diagnosis of cardiac tamponade in patients breathing
spontaneously.1 However, pulsus paradoxus may not always be present in postoperative patients under mechanical ventilation or may develop in patients with other comorbid conditions in the absence of cardiac tamponade (Table 2). As an indirect sign, respiratory variability in the pulse oximetry waveform should raise the suspicion of hemodynamic compromise in patients at risk for pericardial tamponade who are breathing spontaneously.26 The elevation of central venous pressure (CVP) has a low predictive value in the immediate postoperative setting because of the high rate of low-pressure tamponade, situations of concomitant hypovolemia, or in loculated tamponade. In addition, the elevation of CVP can occur in situations of right ventricular dysfunction, in the presence of tricuspid regurgitation, or ventilatory abnormalities requiring high PEEP. Furthermore, postoperative pericardial effusions of moderate volume may be found in the posterior space and partially compress one or more cardiac chambers. These cases may manifest as isolated increases in pulmonary artery occlusion pressure. Occasionally, the increases in CVP and jugular distention can occur together with the Kussmaul venous sign.2 The Kussmaul sign is a
Table 2. Conditions in Which Pulsus Paradoxus Is Suppressed in Cardiac Tamponade Left Ventricular Dysfunction Regional tamponade Positive-pressure ventilation Chronic obstructive pulmonary disease with cor pulmonale Pulmonary artery obstruction Severe aortic insufficiency Intracardiac shunt Modified with permission.25 Copyright 1993 by American Heart Association, Inc.
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Table 3. Echocardiographic Criteria for Cardiac Tamponade 2-Dimensional Mode
Doppler
Echo-free space around the heart Variation of heart dimensions with ventilation Right atrium compression Right ventricular diastolic collapse Dilated vena cava in the absence of inspiratory collapse Loculated effusion compressing the left atrium Left ventricular diastolic compression Abnormal opening of the mitral valve “Swinging heart”
Respiratory variation of transmitral and transtricuspid flows Respiratory variation of venous flows Increased reverse wave with atrial contraction in pulmonary vein flows.
Modified with permission.25 Copyright 1993 by American Heart Association, Inc.
distention of jugular veins in the neck during inspiration. In low-pressure tamponade, this is an uncommon sign; however, exaggerated jugular pulse wave without distention can sometimes be seen. The tracing of venous pulse waves shows a marked “x” wave and a reduction or absence of the “y” wave (Fig 1). On a chest x-ray, a normal heart size is seen until the effusion is moderate in volume (at least ⬎200 mL); thereafter, the cardiac silhouette is enlarged, taking the appearance of a flask or water-bottle. These findings might not be seen with loculated pericardial effusions. The only electrocardiographic (ECG) sign that is almost specific in cardiac tamponade is electrical alternans, which is a beat-to-beat variation of the contour and/or shape of the P wave, the QRS complex, the ST segment, and/or the T wave. This phenomenon can be explained by the presence of pericardial fluid, which drives the myocardium back and forth from the thoracic wall. Other potential, less specific findings are reductions of the QRS voltage and the T wave, depressed PR segment, changes in the ST-T, and bundlebranch blocks. Postoperative tamponade after cardiac surgery may have varied clinical and hemodynamic presentations because of selective chamber compression by loculated fluid27 or hypovolemia. The atypical clinical presentation of these events may simulate other disorders like severe hypovolemia, left ventricular dysfunction, major ischemic events, or systemic inflammatory response syndrome, and, therefore, the diagnosis of tamponade should be considered whenever hemodynamic deterioration or signs of low-output failure occur in the postcardiotomy patient.28
size of pericardial effusions, to quantify the hemodynamic consequences of any effusions, and even to drive treatment decisions (Table 3).31 The echocardiographic characteristics of cardiac tamponade on 2-dimensional transthoracic echocardiography or transesophageal echocardiography include the following: 1. Evidence of a moderate-to-severe circumferential pericardial effusion appearing as an echo-free space around the heart (Fig 3).10 Moderate pericardial effusion is considered to be present when the sum of diastolic echo-free anterior and posterior spaces is 10 to 20 mm; the effusion is considered to be large when greater than 20 mm.32 2. Compression of the right atrium during the early diastolic phase, which is defined as diastolic inversion of the right atrial free wall.13,33 3. Compression of the right ventricle during the late diastolic phase13,34 (Fig 4), which is defined as the occurrence of inward motion of the right ventricular wall. The collapse of both chambers is exaggerated during expiration when the right heart filling is reduced. 4. Abnormal opening of the mitral valve, delay of mitral valve opening during inspiration, suggesting compromise of left ventricular filling.35 5. Dilated inferior vena cava in the absence of inspiratory collapse.36 In the presence of tricuspid regurgitation or severe right ventricular dysfunction, this may have a low predictive value. 6. “Swinging heart” in the pericardial fluid collection.25,37 Collapse of the right atrium is more sensitive for diagnosing
Echocardiographic Diagnosis Although the diagnosis of cardiac tamponade is predominantly clinical, symptoms are usually nonspecific in postoperative cardiac patients and may complicate the decision-making process.1,29 If there is clinical suspicion of cardiac tamponade, an echocardiographic examination by transthoracic or transesophageal echocardiography must be performed without delay.2,28,30 Echocardiography is used to show the presence and
Fig 3. The transgastric 0° view: short axis of the right and leflt ventricles and a posterior pericardial effusion with right ventricle collapse appearing as an echo-free space around the right ventricle and inward motion of the RV posterior wall. LV, left ventricle; RV, right ventricle.
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Fig 5. A midesophageal 4-chamber view: hypoecogenic area corresponding to a loculated pericardial effusion around the LA with inversion of the LA free wall. LA, left atrium.
Fig 4. A midesophageal 4-chamber view: hypoecogenic area corresponding to a pericardial effusion, which is compressing the RV and the LA. Both show inward motion of the free wall. LA, left atrium; LV, left ventricle; RA, right atrium, RV, right ventricle.
tamponade; however, collapse of the right ventricle, which lasts more than a third of diastole, is more specific.38 In acute, hemorrhagic tamponade, thrombi can be identified as hyperechoic masses. The absence of atrial collapse (Table 4) generally excludes global but not regional tamponade, except in the context of acute or chronic elevations in right-sided pressures and in the presence of decreases of atrial or ventricular compliance caused by hypertrophy of these chambers.39-41 Doppler examination findings indicating the presence of tamponade include the following: 1. Respiratory variation of transmitral and transtricuspid flow velocities, which reflect increased ventricular interdependence, clinically appearing as pulsus paradoxus.13,42 Left ventricular filling decreases during inspiration, which manifests as prolonged isovolumic relaxation time and reduced E-wave velocity. During the expiratory phase, changes are reversed. Respiratory variation of transtricuspid flows is opposite to that of transmitral flows.43 2. Venous flow analysis: In cardiac tamponade, the characteristic venous flow pattern in the superior vena cava and/or suprahepatic vein consists of a marked predomTable 4. Conditions in Which There Is Absence of Right Atrial Collapse in Cardiac Tamponade Regional posterior tamponade Right ventricular dysfunction Severe pulmonary hypertension Chronic obstructive pulmonary disease with cor pulmonale
inance of systolic over diastolic component, a reduced increase of flow during inspiration, and suppression or inversion of the diastolic component in the 1st expiratory cardiac cycle. This abnormal pattern has high sensitivity and specificity and correlates well with clinical features of tamponade. The conditions most commonly precluding the analysis of venous flows are atrial fibrillation, tricuspid regurgitation, pacemaker rhythm, and technical difficulties to obtain an appropriate signal.44 Respiratory variation in tricuspid and venous flow is more dramatic than mitral and aortic flow, but there is progressive impairment in all intracardiac flow as the degree of tamponade worsens. The patterns described previously are characteristic of patients in spontaneous ventilation. However, in patients under mechanical positive-pressure ventilation, the echocardiographic criteria used to diagnose cardiac tamponade based on respiratory variation of tricuspid or mitral valve inflow patterns may be decreased or nonexistent in the context of pericardial effusion and cardiac tamponade.45 Doppler criteria for tamponade may be sensitive but can be nonspecific. An abnormal transmitral and transtricuspid flow pattern also can be observed in chronic obstructive pulmonary disease, pulmonary embolism, constrictive pericarditis, and right ventricular infarction.42 Hemodynamically significant pericardial collections occurring early after cardiac surgery may not show the classic echocardiographic features of tamponade.46 On occasion, postoperative effusions are small and loculated, with selective chamber compression.28,47 The most consistent sign observed after cardiac surgery is increased pericardial separation.48 Loculated effusions compressing the left atrium and left ventricle in the absence of right-heart abnormalities are not infrequent and can lead to severe hemodynamic compromise49 (Fig 5). TREATMENT
The decision to drain and how to proceed will be based on the patient’s clinical situation. In the early postoperative period after cardiac surgery, surgical decompression was indicated for
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patients with hemorrhagic cardiac tamponade and evidence of clots, which is the majority of cases.35 Emergency drainage is indicated if there is clinical evidence of tamponade either by pericardiocentesis or surgical pericardiotomy.50 In the largest series reported in the literature of postoperative cardiac patients with early and late cardiac tamponade1 for whom emergent surgical decompression was excluded, video-assisted51,52 and ultrasound-guided pericardiocentesis53 was the treatment of choice and proved effective in 97% of cases. Sternotomy was only required in the remaining 3%. In the late postoperative period, surgical decompression is also reserved54 for patients ineligible for echocardiographic examination, cases of percutaneous drainage failure, and the presence of intrapericardial hematoma. Drainage is also recommended when pericardial effusion is associated with left ventricular dysfunction in patients with PPV and in the presence of loculated effusions at the level of the left-sided chambers. Removal of as little as 50 mL of pericardial fluid commonly can produce significant hemodynamic improvement because of the steep pericardial pressurevolume relationship.55 In addition, some authors, including Hoit and Fowler41 and Little and Freeman,38 advocated drainage if the effusion is measured on ultrasound to be more than 20 mm and if there is collapse of the right chambers or if the duration has been less than 1 month, given the high risk for the development of tamponade.38,56 These criteria may be applicable to postoperative cardiac patients. ANESTHETIC MANAGEMENT
Objectives before and after induction include the following (Fig 6): 1. Optimization of preload: Increasing intravascular volume to optimal levels to maintain hemodynamic stability. This is particularly important in patients with volume depletion because in the setting of diastolic failure the effective increase of cardiac filling will oppose the significant increase in intrapericardial pressure. Filling pressures of up to 25 to 30 mmHg may be necessary.57 Blood products should be available in cases of hemorrhagic tamponade. However, in patients with normal or increased blood volume (which is very rare in the postoperative setting), the infusion of volume can result in an increase of intrapericardial pressures sufficient to cause right ventricular diastolic collapse.58 2. Optimization of inotropism: The use of inotropic drugs enhances the action of endogenous catecholamines. Dobutamine is considered the drug of choice by some clinicians because of its inotropic properties and the reduction of systemic resistances.59-61 Isoproterenol and dopamine showed beneficial hemodynamic effects in cardiac tamponade in animal models, but this has not been proven in the clinical setting.59 These drugs initially produce an increase in systolic volume by increasing ejection fraction and heart rate and an improvement in cardiac perfusion; however, there is no increase in perfusion of other organs, such as the brain or the kidneys. Additionally, isoproterenol improves flow perfusion in the epicardial tissue as opposed to the
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endocardial tissue and is a powerful vasodilator. Human studies have concluded that the positive effect of inotropic drugs in cardiac tamponade is limited.59 Metabolic acidosis needs to be corrected to avoid myocardial depressant effects and increase the response to catecholamines.62 3. Maintenance of afterload: Hypotension is relatively frequent in the postoperative cardiac surgery period, and the use of vasopressors, such as phenylephrine or norepinephrine, often may be necessary to increase coronary perfusion and improve ventricular function57 until resolution of the tamponade and recovery of the heart function. However, the use of vasopressors should be avoided as much as possible if blood pressure stays within the normal range because these agents might result in decreased cardiac output. Furthermore, the use of vasodilators in postoperative cardiac tamponade is controversial in the literature24 and might be indicated only if postoperative cardiac tamponade is associated with elevated systemic vascular resistance and elevated systemic arterial pressure 4. Maintenance of sinus rhythm: In both the early and late stages of a tamponade, it is not uncommon to see vagal depressor reflexes, which require the use of atropine, because bradycardia results in reduced cardiac output63 or pacing the heart if epicardial pacing wires are available. Ventricular filling depends primarily on atrial contraction, and, therefore, the development of atrial fibrillation or flutter has a negative impact on blood pressure and cardiac output. In this regard, antiarrhythmic drugs and a defibrillator must be available. 5. Ventilatory modes: Mechanical ventilation has great influence on cardiac tamponade patients.64,65 The maintenance of spontaneous ventilation throughout the procedure may be better tolerated in patients with tamponade than other modes of ventilation.66,67 There are isolated literature reports of intubation in patients who are kept awake and maintain spontaneous ventilation.68,69 Under mechanical ventilation, it is advisable to avoid high pressures and use low tidal volumes until the tamponade is released,70 in addition to using high respiratory rates and avoiding PEEP. Monitoring during surgical procedures for pericardial diseases is essential; however, it depends on the degree of emergency in each case. Monitoring should include ECG, arterial pressure, pulse oximetry, capnography, and urinary output. If possible, invasive monitoring is recommended including invasive monitoring of arterial pressure, cardiac output, and central venous saturation of oxygen using a pulmonary thermodilution catheter or continuous pulse contour analysis systems. In patients with cardiac tamponade, it is not unusual to find high left and right atrial pressure with “real” low preload. For this reason, monitoring with devices to assess stroke volume variation as a method of evaluating preload is recommended. Wherever possible, devices should be inserted under local anesthesia.57
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Anesthetic Management The induction of general anesthesia and mechanical ventilation have been associated with severe tachycardia and hypotension in patients with pericardial effusions.71 It should be kept in mind that many anesthetic drugs are myocardial depressants and vasodilators, which must therefore be used with caution. Ideally, the anesthetic agents should minimize bradycardia, myocardial depression, and the sudden reduction of preload and afterload. In any case, induction must be undertaken when the surgical field and the surgeons are ready to immediately proceed to drain. In acute and chronic tamponade, some authors72 recommend, as long as the patient’s situation allows, to drain the effusion through a subxiphoid incision under local anesthe-
sia to avoid the deleterious effect of the anesthesia and mechanical ventilation and, subsequently, induce general anesthesia after the pericardial fluid has been released. The recommended agents for induction are etomidate, ketamine, or diazepam, whereas inhalation agents are recommended for maintenance.70 In the authors’ experience, ketamine as an induction agent is the first choice. However, there are few reports on its use in the literature. Several authors69,73,74 have reported cases of anesthetic induction with ketamine and local anesthesia for reopening of sternotomy or performance of a pericardial window. In unstable patients, ketamine has a clearly beneficial effect for maintaining arterial pressure because it increases systemic resistances and maintains the heart
Suspected tamponade Clinical diagnosis
Echocardiographic conirmation
Hemodynamic maintenance
Optimization of preload Blood products available Correct acidosis
Afterload maintenance: If hypotension: norepinephrine, phenylephrine Avoid vasopressors if adequate MAP.
Anesthetic induction
Optimization of inotropism Dobutamine
Preserve sinus rhythm: cardioversion. Prevention of relex bradycardia: Atropine
Surgical team ready
Optimize ventilation: Spontaneous In pressure control: Reduced tidal volumes, elevated respiratory rate, avoid PEEP.
Drainage of pericardial effusion
Recommended agents: Ketamine, etomidate, opioids, inhaled agents
Treat post-drainage hypertension: Nitroglycerin, hydralazine, urapidil, nitroprusside
Fig 6. The perioperative management of postoperative cardiac tamponade. The perioperative management focusing on hemodynamic maintenance, anesthetic induction for surgery, and treatment after drainage.
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rate. Nevertheless, ketamine also can have deleterious effects, by increasing the afterload of the right ventricle, and some myocardial depressant effects.75 Maintenance with inhalation agents and low-dose opioids has minimal effects on hemodynamic stability. In the setting of cardiac arrest, it should be remembered that external cardiac compressions have little or no value because the tamponade leaves very little room for additional filling of the chambers. In addition, even though systolic pressure increases, diastolic pressure remains unchanged, and, therefore, perfusion pressure does not improve.76 In this situation, the best option is to reopen the chest immediately. After drainage, cardiac pressure and output may rise sharply because of the rapid increase in filling pressures, and it may become necessary to use vasodilators if arterial hypertension ensues. Nitroglycerin, nitroprusside, or urapidil are good options. Pericardiocentesis may be associated with a variety of complications, including laceration of the right ventricle or a coronary artery, arrhythmias, pneumothorax, and acute respiratory distress syndrome. Postpericardiocentesis acute left ven-
tricular failure, pulmonary edema, and cardiogenic shock have been reported.77-81 CONCLUSION
In conclusion, anesthesiologists who manage surgical pericardial drainage of a cardiac tamponade face an unstable hemodynamic situation resulting from abnormal ventricular filling and the consequent reduction in systolic volume. Diagnosis must be made early and based on clinical observation and echocardiographic examination. Anesthetic induction should be based on optimization of the preload, maintenance of inotropism and sinus rhythm, maintenance of the afterload according to hemodynamic status, and the use of induction drugs with little effect on inotropism (ketamine, benzodiazepines) and should be undertaken only when the surgical team is ready to operate. For ventilation, spontaneous breathing should be maintained until mechanical ventilation is established, with reduced tidal volumes and high respiratory rates, avoiding the use of PEEP.
REFERENCES 1. Tsang TS, Barnes ME, Hayes SN, et al: Clinical and echocardiographic characteristics of significant pericardial effusions following cardiothoracic surgery and outcomes of echo-guided pericardiocentesis for management: Mayo Clinic experience, 1979-1998. Chest 116:322331, 1999 2. Maisch B, Seferovic PM, Ristic AD, et al: Guidelines on the diagnosis and management of pericardial diseases executive summary: The Task Force on the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology. Eur Heart J 25:587610, 2004 3. Al-Dadah AS, Guthrie TJ, Pasque MK, et al: Clinical course and predictors of pericardial effusion following cardiac transplantation. Transplant Proc 39:1589-1592, 2007 4. Russo AM, O’Connor WH, Waxman HL: Atypical presentations and echocardiographic findings in patients with cardiac tamponade occurring early and late after cardiac surgery. Chest 104:71-78, 1993 5. Reade MC: Temporary epicardial pacing after cardiac surgery: A practical review. Part 2: Selection of epicardial pacing modes and troubleshooting. Anaesthesia 62:364-373, 2007 6. Saidi B, Roshanali F, Yousefnia MA, et al: Pericardial tamponade and right-to-left shunt through patent foramen ovale after epicardial pacing-wire removal. Tex Heart Inst J 37:574-575, 2010 7. Stevenson LW, Child JS, Laks H, et al: Incidence and significance of early pericardial effusions after cardiac surgery. Am J Cardiol 54:848-851, 1984 8. Alkhulaifi AM, Speechly-Dick ME, Swanton RH, et al: The incidence of significant pericardial effusion and tamponade following major aortic root surgery. J Cardiovasc Surg (Torino) 37:385-389, 1996 9. Harskamp RE, Meuzelaar JJ: Recurrent late cardiac tamponade following cardiac surgery: A deceiving and potentially lethal complication. Acta Cardiol 65:581-584, 2010 10. Wann S, Passen E: Echocardiography in pericardial disease. J Am Soc Echocardiogr 21:7-13, 2008 11. Spodick DH: Acute cardiac tamponade. N Engl J Med 349:684690, 2003 12. Ramachandran D, Luo C, Ma TS, et al: Using a human cardiovascular-respiratory model to characterize cardiac tamponade and pulsus paradoxus. Theor Biol Med Model 6:15, 2009
13. Guntheroth WG: Sensitivity and specificity of echocardiographic evidence of tamponade: Implications for ventricular interdependence and pulsus paradoxus. Pediatr Cardiol 28:358-362, 2007 14. Hoit BD, Shaw D: The paradoxical pulse in tamponade: Mechanisms and echocardiographic correlates. Echocardiography 11:477487, 1994 15. Michard F, Teboul JL: Using heart-lung interactions to assess fluid responsiveness during mechanical ventilation. Crit Care 4:282289, 2000 16. Aguar F, Febre E, Peña J, et al: Ventilación mecánica en cirugía cardiaca de adultosVentilación mecánica en anestesia y cuidados intensivos. Madrid, Spain, Aran Ediciones, S. L., 2009 17. Konchigeri HN, Levitsky S: Anesthetic considerations for pericardiectomy in uremic pericardial effusion. Anesth Analg 55:378-382, 1976 18. Mattila I, Takkunen O, Mattila P, et al: Cardiac tamponade and different modes of artificial ventilation. Acta Anaesthesiol Scand 28: 236-240, 1984 19. Luecke T, Pelosi P: Clinical review: Positive end-expiratory pressure and cardiac output. Crit Care 9:607-621, 2005 20. Wills CP, Young M, White DW: Pitfalls in the evaluation of shortness of breath. Emerg Med Clin North Am 28:163-181, 2010 21. Woo KM, Schneider JI: High-risk chief complaints. I: Chest pain—The big three. Emerg Med Clin North Am 27:685-712, 2009 22. Roy CL, Minor MA, Brookhart MA, et al: Does this patient with a pericardial effusion have cardiac tamponade? JAMA 297:1810-1818, 2007 23. Hayes SN, Freeman WK, Gersh BJ: Low pressure cardiac tamponade: Diagnosis facilitated by Doppler echocardiography. Br Heart J 63:136-140, 1990 24. Spodick DH: Acute cardiac tamponade. Am Heart J 122:1794, 1991 25. Fowler NO: Cardiac tamponade. A clinical or an echocardiographic diagnosis? Circulation 87:1738-1741, 1993 26. Stone MK, Bauch TD, Rubal BJ: Respiratory changes in the pulse-oximetry waveform associated with pericardial tamponade. Clin Cardiol 29:411-414, 2006 27. Saito Y, Donohue A, Attai S, et al: The syndrome of cardiac tamponade with “small” pericardial effusion. Echocardiography 25: 321-327, 2008
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28. Pepi M, Muratori M: Echocardiography in the diagnosis and management of pericardial disease. J Cardiovasc Med (Hagerstown) 7:533-544, 2006 29. Fagan SM, Chan KL: Pericardiocentesis: Blind no more! Chest 116:275-276, 1999 30. Yared K, Baggish AL, Picard MH, et al: Multimodality imaging of pericardial diseases. JACC Cardiovasc Imaging 3:650-660, 2010 31. Hosokawa K, Nakajima Y: An evaluation of acute cardiac tamponade by transesophageal echocardiography. Anesth Analg 106: 61-62, 2008 32. Weitzman LB, Tinker WP, Kronzon I, et al: The incidence and natural history of pericardial effusion after cardiac surgery—An echocardiographic study. Circulation 69:506-511, 1984 33. Kronzon I, Cohen ML, Winer HE: Diastolic atrial compression: A sensitive echocardiographic sign of cardiac tamponade. J Am Coll Cardiol 2:770-775, 1983 34. Armstrong WF, Schilt BF, Helper DJ, et al: Diastolic collapse of the right ventricle with cardiac tamponade: An echocardiographic study. Circulation 65:1491-1496, 1982 35. Tsang TS, Oh JK, Seward JB: Diagnosis and management of cardiac tamponade in the era of echocardiography. Clin Cardiol 22: 446-452, 1999 36. Himelman RB, Kircher B, Rockey DC, et al: Inferior vena cava plethora with blunted respiratory response: A sensitive echocardiographic sign of cardiac tamponade. J Am Coll Cardiol 12:1470-1477, 1988 37. Kronzon I, Cohen ML, Winer HE: Contribution of echocardiography to the understanding of the pathophysiology of cardiac tamponade. J Am Coll Cardiol 1:1180-1182, 1983 38. Little WC, Freeman GL: Pericardial disease. Circulation 113: 1622-1632, 2006 39. Frey MJ, Berko B, Palevsky H, et al: Recognition of cardiac tamponade in the presence of severe pulmonary hypertension. Ann Intern Med 111:615-617, 1989 40. Cunningham MJ, Safian RD, Come PC, et al: Absence of pulsus paradoxus in a patient with cardiac tamponade and coexisting pulmonary artery obstruction. Am J Med 83:973-976, 1987 41. Hoit BD, Fowler NO: Influence of acute right ventricular dysfunction on cardiac tamponade. J Am Coll Cardiol 18:1787-1793, 1991 42. Appleton CP, Hatle LK, Popp RL: Cardiac tamponade and pericardial effusion: respiratory variation in transvalvular flow velocities studied by Doppler echocardiography. J Am Coll Cardiol 11:10201030, 1988 43. Shaver JA, Reddy PS, Curtiss EI, et al: Noninvasive/invasive correlates of exaggerated ventricular interdependence in cardiac tamponade. J Cardiol 37:71-76, 2001 (suppl 1) 44. Merce J, Sagrista-Sauleda J, Permanyer-Miralda G, et al: Correlation between clinical and Doppler echocardiographic findings in patients with moderate and large pericardial effusion: Implications for the diagnosis of cardiac tamponade. Am Heart J 138:759-764, 1999 45. Faehnrich JA, Noone RB Jr, White WD, et al: Effects of positive-pressure ventilation, pericardial effusion, and cardiac tamponade on respiratory variation in transmitral flow velocities. J Cardiothorac Vasc Anesth 17:45-50, 2003 46. Price S, Prout J, Jaggar SI, et al: ’Tamponade’ following cardiac surgery: Terminology and echocardiography may both mislead. Eur J Cardiothorac Surg 26:1156-1160, 2004 47. Ionescu A, Wilde P, Karsch KR: Localized pericardial tamponade: Difficult echocardiographic diagnosis of a rare complication after cardiac surgery. J Am Soc Echocardiogr 14:1220-1223, 2001 48. Bommer WJ, Follette D, Pollock M, et al: Tamponade in patients undergoing cardiac surgery: A clinical-echocardiographic diagnosis. Am Heart J 130:1216-1223, 1995
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49. Chuttani K, Pandian NG, Mohanty PK, et al: Left ventricular diastolic collapse. An echocardiographic sign of regional cardiac tamponade. Circulation 83:1999-2006, 1991 50. Seferovic PM, Ristic AD, Imazio M, et al: Management strategies in pericardial emergencies. Herz 31:891-900, 2006 51. Uramoto H, Hanagiri T: Video-assisted thoracoscopic pericardiectomy for malignant pericardial effusion. Anticancer Res 30:46914694, 2010 52. Fibla JJ, Molins L, Mier JM, et al: [Pericardial window by videothoracoscope in the treatment of pericardial effusion and tamponade]. Cir Esp 83:145-148, 2008 53. Georghiou GP, Porat E, Fuks A, et al: Video-assisted pericardial fenestration for effusions after cardiac surgery. Asian Cardiovasc Thorac Ann 17:480-482, 2009 54. Ranucci M, Bozzetti G, Ditta A, et al: Surgical reexploration after cardiac operations: Why a worse outcome? Ann Thorac Surg 86:1557-1562, 2008 55. O’Connor CJ, Tuman KJ: The intraoperative management of patients with pericardial tamponade. Anesthesiol Clin 28:87-96, 2010 56. Hoit BD: Management of effusive and constrictive pericardial heart disease. Circulation 105:2939-2942, 2002 57. Lake CL: Anesthesia and pericardial disease. Anesth Analg 62:431-443, 1983 58. Cogswell TL, Bernath GA, Keelan MH Jr, et al: The shift in the relationship between intrapericardial fluid pressure and volume induced by acute left ventricular pressure overload during cardiac tamponade. Circulation 74:173-180, 1986 59. Martins JB, Manuel WJ, Marcus ML, et al: Comparative effects of catecholamines in cardiac tamponade: Experimental and clinical studies. Am J Cardiol 46:59-66, 1980 60. Reddy PS, Curtiss EI, O’Toole JD, et al: Cardiac tamponade: Hemodynamic observations in man. Circulation 58:265-272, 1978 61. Reddy PS, Curtiss EI, Uretsky BF: Spectrum of hemodynamic changes in cardiac tamponade. Am J Cardiol 66:1487-1491, 1990 62. Darby TD, Aldinger EE, Gadsden RH, et al: Effects of metabolic acidosis on ventricular isometric systolic tension and the response to epinephrine and levarterenol. Circ Res 8:1242-1253, 1960 63. Friedman HS, Lajam F, Gomes JA, et al: Demonstration of a depressor reflex in acute cardiac tamponade. J Thorac Cardiovasc Surg 73:278-286, 1977 64. Ho AM, Graham CA, Ng CS, et al: Timing of tracheal intubation in traumatic cardiac tamponade: A word of caution. Resuscitation 80:272-274, 2009 65. Barthelemy R, Bounes V, Minville V, et al: Prehospital mechanical ventilation of a critical cardiac tamponade. Am J Emerg Med 27:1020e1-1020e3, 2009 66. Moller CT, Schoonbee CG, Rosendorff C: Haemodynamics of cardiac tamponade during various modes of ventilation. Br J Anaesth 51:409-415, 1979 67. Rosamel P, Gostoli B, Lehot JJ, et al: [Anaesthetic management with spontaneous breathing for cardiac tamponade]. Ann Fr Anesth Reanim 26:383-384, 2007 68. Breen PH, MacVay MA: Pericardial tamponade: A case for awake endotracheal intubation. Anesth Analg 83:658, 1996 69. Webster JA, Self DD: Anesthesia for pericardial window in a pregnant patient with cardiac tamponade and mediastinal mass. Can J Anaesth 50:815-818, 2003 70. Muralidhar K: Anaesthetic management of cardiac tamponade after open heart surgery. Ind J Thorac Cardiovasc Surg 4:19-22, 1985 71. Moon GJ: Pericardial effusion and severe tachycardia. Anesth Analg 61:384-386, 1982 72. Stanley TH, Weidauer HE: Anesthesia for the patient with cardiac tamponade. Anesth Analg 52:110-114, 1973
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73. Kaplan JA, Bland JW Jr, Dunbar RW: The perioperative management of pericardial tamponade. South Med J 69:417-419, 1976 74. Aye T, Milne B: Ketamine anesthesia for pericardial window in a patient with pericardial tamponade and severe COPD. Can J Anaesth 49:283-286, 2002 75. Spotoft H, Korshin JD, Sorensen MB, et al: The cardiovascular effects of ketamine used for induction of anaesthesia in patients with valvular heart disease. Can Anaesth Soc J 26:463-467, 1979 76. Hashim R, Frankel H, Tandon M, et al: Fluid resuscitationinduced cardiac tamponade. J Trauma 53:1183-1184, 2002 77. Ligero C, Leta R, Bayes-Genis A: Transient biventricular dysfunction following pericardiocentesis. Eur J Heart Fail 8:102-104, 2006
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78. Bernal JM, Pradhan J, Li T, et al: Acute pulmonary edema following pericardiocentesis for cardiac tamponade. Can J Cardiol 23:1155-1156, 2007 79. Chamoun A, Cenz R, Mager A, et al: Acute left ventricular failure after large volume pericardiocentesis. Clin Cardiol 26:588-590, 2003 80. Karamichalis JM, Gursky A, Valaulikar G, et al: Acute pulmonary edema after pericardial drainage for cardiac tamponade. Ann Thorac Surg 88:675-677, 2009 81. Versaci F, Donati R, Mezzanotte R, et al: An unusual complication following pericardiocentesis: Reversible left ventricular dysfunction. J Cardiovasc Med (Hagerstown) 2010 Jul 9 [Epub ahead of print] 82. Reddy PS, EI C: Cardiac tamponade. Cardiol Clin 8:627-637, 1990
Management of Cardiac Tamponade After Cardiac Surgery Paula Carmona, MD, Eva Mateo, MD, Irene Casanovas, MD, Juan J. Peña, MD, Jose Llagunes, MD, Federico Aguar, MD, Jose De Andrés, MD, and Carlos Errando, MD
A
CUTE POSTOPERATIVE CARDIAC TAMPONADE (defined as up to 7 days post-surgery)1 is an uncommon entity that requires prompt diagnosis and diligent management to avoid circulatory collapse and cardiorespiratory arrest. Anesthetic management for surgical pericardial drainage of an effusion causing cardiac tamponade in the postoperative period after cardiac surgery is a challenge for the anesthesiologist, considering the unstable hemodynamic situation resulting from abnormal ventricular filling and the subsequent reductions in systolic volume, cardiac output, and systemic blood pressure. Such a procedure requires extensive pathophysiologic knowledge and careful hemodynamic control. After cardiac surgery, two different variants of cardiac tamponade may occur, low-pressure tamponade and regional cardiac tamponade, when any cardiac zone is compressed by loculated effusions. When these entities is suspected, the diagnosis must be prompt. The European Society of Cardiology published its Guidelines on the Diagnosis and Management of Pericardial Diseases in 2004.2 However, the recent literature shows a lack of publications reviewing hemodynamic and anesthetic management of patients with cardiac tamponade after cardiac surgery. This article provides an updated synopsis of the pathophysiology, diagnosis (including key clinical and echocardiographic criteria), and perioperative anesthetic management of cardiac tamponade after cardiac surgery. EPIDEMIOLOGY/ETIOLOGY
In cardiac surgery, the incidence of cardiac tamponade may vary based on the type of surgery, ranging from 0.2% among patients undergoing coronary artery bypass graft surgery to 8.4% in heart transplant patients.1,3,4 Precipitating factors include the administration of anticoagulants, coagulation disorders, excessive mediastinal bleeding, the removal of epicardial pacing wires after cardiac surgery,5,6 autoimmune reactions, and the development of postpericardiotomy syndrome. Late tamponade (⬎7 days after surgery) is con-
From the Anaesthesia, Critical Care and Pain Medicine Department, Consorcio Hospital General of Valencia, Valencia, Spain. Address reprint requests to Paula Carmona, MD, Anaesthesia, Critical Care and Pain Medicine Department, Consorcio Hospital General of Valencia, Valencia, Spain. E-mail: [email protected] © 2012 Elsevier Inc. All rights reserved. 1053-0770/2602-0023$36.00/0 doi:10.1053/j.jvca.2011.06.007 Key words: cardiac tamponade, cardiac surgery, anesthesia, literature review 302
sidered to be a significant postoperative complication of cardiac surgery, with a higher mortality rate than early tamponade.7-9 Among postoperative patients with severe delayed pericardial effusions, the 30-day mortality rate was 3%. PATHOPHYSIOLOGY
In all variants of cardiac tamponade, including tamponade after cardiac surgery, the pericardial sac gradually can stretch to accommodate increasing volume. At any point in time, the total intrapericardial volume is relatively fixed throughout the cardiac cycle. When the ability of the pericardium to stretch is exceeded by rapid or massive accumulation of fluid, any additional fluid causes the pressure within the pericardial sac to increase. When the increasing intrapericardial pressure exceeds the intracardiac pressure, the positive transmural pressure gradient compresses the adjacent cardiac chamber or chambers. Because of the fact that intracardiac pressures vary throughout the cardiac cycle, the pericardial pressure will exceed the intracardiac pressure within different chambers at different points in the cardiac cycle. The right chambers, which have the lowest instantaneous pressures, are affected first.10 Ventricular filling in cardiac tamponade is seriously compromised and occurs in a complex fashion that is poorly understood. High diastolic ventricular pressures cause a reduction in ventricular filling, systolic volume, and systolic ventricular pressure depending on the contractile state of the ventricle and the level of the intrapericardial pressure. High end-diastolic ventricular pressure and high mean atrial pressure are accompanied by pulmonary and systemic venous hypertension. Although these venous pressures are maintained at a sufficient level with high atrial pressures, the inflow of blood into the ventricles can be maintained. In this situation, cardiac output is maintained primarily by tachycardia. In more advanced stages of tamponade, filling becomes possible only during atrial systole, especially when the heart rate increases. These phenomena lead to the disappearance of the “y” wave, which represents right ventricular filling during diastole on the right atrial pressure records. The “x” wave, which represents atrial filling, is maintained because during ventricular systole there is movement of the entire valve plane toward the apex of the ventricle, leading to a reduction of atrial pressure coinciding with ventricular ejection (Fig 1). The hemodynamic changes caused by the pericardial effusion can be categorized into several phases (Table 1). Especially after cardiac surgery, regional cardiac tamponade can occur when any cardiac zone is compressed by loculated effusions,4,11 which usually are accompanied by
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rate (beta effect), (2) an increase of diastolic relaxation (beta effect), (3) an increase of peripheral resistances to maintain adequate arterial pressure and coronary flow (alpha effect), and (4) an increase in inotropism to achieve an increase in ejection fraction. The Effects of Spontaneous Breathing and Mechanical Ventilation on Cardiac Tamponade
Fig 1. CVP waveform in cardiac tamponade. (A) Normal CVP waveform. “a” wave, atrial contraction; “c” wave: elevation of the valve plane at systole start; “x” descent, atrial relaxation and drop of valve plane during systole; “v” wave, rapid filling of atrium before opening of the tricuspid valve; “y” descent, opening of the tricuspid valve. (B) CVP waveform in cardiac tamponade. The “y” descent is lost or decreased because of limited ventricular filling and there is prominent “x” descent during ventricular systole.
localized pericardial adhesions. Loculation can produce classic tamponade (eg, loculated effusions over the right atrium and atrioventricular groove), but more often the typical hemodynamic abnormalities are found only in the compressed chambers or zones. The phenomena described previously occur earlier and at lower pressures in patients with hypovolemia, a situation that is quite frequent in the postoperative period. These patients can develop cardiac tamponade with diastolic pressures as low as 3 to 6 mmHg. Such situations are known as “low-pressure cardiac tamponade” and are extremely difficult to diagnose.11 Therefore, therapeutically-induced hypovolemia or filling pressure reduction (forced diuresis, vasodilators) may lead to severe impairment in cardiac output and blood pressure, which can be life threatening. Compensating mechanisms in this situation of cardiac tamponade are secondary to adrenergic (alpha and beta) stimulation. The activity exerted by these mechanisms can be summarized into 4 major effects: (1) an increase of heart
Respiration also affects intracardiac pressures, particularly those on the right side of the heart. During inspiration, in spontaneously breathing patients without cardiac tamponade, intrathoracic and intrapericardial pressures decrease. This results in augmented flow into the right atrium and right ventricle, with decreased flow out of the pulmonary veins into the left atrium and left ventricle. Reciprocal changes occur during expiration. In the presence of normal intrapericardial pressure, the normal respiratory variation in filling of the left and right heart causes a small (less than 10 mmHg) inspiratory decrease in systemic arterial systolic blood pressure. When the patient is suffering from a cardiac tamponade and is breathing spontaneously, there is an exaggeration of the phenomena described earlier, leading to pulsus paradoxus as a sign of the interventricular interdependence.12,13 Pulsus paradoxus is defined as a decrease of more than 10 mmHg in peripheral arterial pressure during inspiration.11,14 During positive-pressure mechanical ventilation, the reverse of the conventional pulsus paradoxus has been reported. The inspiratory increase in arterial blood pressure followed by a decrease on expiration has been called “reversed pulsus paradoxus.” In patients under mechanical ventilation suffering from cardiac tamponade, this phenomenon is more exaggerated.15 Mechanical ventilation increases pleural pressure and transpulmonary pressure (the difference between alveolar and pleural pressures). During inspiration, left ventricular stroke volume increases because left ventricular preload increases, whereas left ventricular afterload decreases. This leads to an increase in arterial blood pressure at the end of inspiration. In contrast, right ventricular stroke volume decreases during inspiration because venous return and right ventricular preload decrease, while right ventricular afterload increases. Because of the pulmonary transit time of blood (approximately 2 seconds), the inspiratory decrease in
Table 1. Hemodynamic Changes Caused by Pericardial Effusion
Phase I Phase II Phase III
Pericardial Pressure
RV Filling Pressure
LV Filling Pressure
Pulsus Paradoxus
Cardiac Output
1 1 (⫽ RV Pr) 1
1 1 1
1 11 1 (⫽ RV Pr)
⫺ ⫹ ⫹⫹
⫺ 2 22
NOTE. Phase I: pericardial and left and right ventricular pressures are elevated but not equilibrated, and cardiac output is not compromised. Phase II: elevated pericardial and right ventricular filling pressures are equilibrated with each other but not with left ventricular filling pressure, which is higher. Cardiac output is compromised, and pulsus paradoxus is present in most but not all patients. Phase III: elevated pericardial right ventricular and left ventricular filling pressures are equilibrated, cardiac output is severely compromised, and pulsus paradoxus is present in all patients spontaneously breathing and without other conditions that may suppress the pulsus paradoxus. Abbreviations: Pr, pressure; RV, right ventricle; LV, left ventricle. Modified with permission.82
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Fig 2. The effects of mechanical ventilation on hemodynamics in patients with cardiac tamponade. Mechanical ventilation increases pleural pressure and transpulmonary pressure. During inspiration, left ventricular stroke volume increases because of the increase in left ventricular preload, whereas left ventricular afterload decreases. This leads to an increase in arterial blood pressure at the end of inspiration. In contrast, right ventricular stroke volume decreases during inspiration because of the decrease in right ventricular preload, whereas right ventricular afterload increases. Because of the pulmonary transit time of blood, the inspiratory decrease in right ventricular output causes decreases in left ventricular filling and output only a few heartbeats later, usually during the expiratory period. This, in turn, leads to a decrease in arterial blood pressure at the end of expiration. (Adapted from Michard and Teboul,15 courtesy of BioMed Central.)
right ventricular output causes decreases in left ventricular filling and output only a few heartbeats later, usually during the expiratory period. This corresponds with a decrease in arterial blood pressure at the end of the expiration (Fig 2). Therefore, if positive-pressure ventilation is used with high tidal volumes and high levels of positive end-expiratory pressure, the right ventricular afterload may be increased and the ventricular septum can shift leftward, thereby reducing the distensibility of the left ventricle and, consequently, its preload.16 In conclusion, in patients with cardiac tamponade, the institution of mechanical ventilation and positive end-expiratory pressure (PEEP) may worsen hemodynamic status with reversed pulsus paradoxus.17-19 DIAGNOSIS
Clinical Presentation The clinical presentation of postoperative cardiac tamponade includes a wide range of nonspecific signs and symptoms such as dyspnea,20 orthopnea, attenuated cardiac sounds, chest pain,21 tachycardia and hypotension, and even cardiogenic shock.22 The nonspecific clinical scenario after cardiac surgery also may be influenced by the presence of low-pressure cardiac tamponade23 or loculated tamponade, which are relatively frequent in the post– cardiac surgery period.4,24 One of the most common clinical signs in these patients is hemodynamic impairment, characterized by the presence of tachycardia and hypotension, findings that may be associated with multiple diagnoses in a postoperative cardiac patient. The following factors can determine the presence of cardiac tamponade: the fluid accumulation rate, the previous ventricular function status, the patient’s blood volume, and the presence or absence of pre-existing hypertension.25 The development of pulsus paradoxus is a key clinical sign pointing to a diagnosis of cardiac tamponade in patients breathing
spontaneously.1 However, pulsus paradoxus may not always be present in postoperative patients under mechanical ventilation or may develop in patients with other comorbid conditions in the absence of cardiac tamponade (Table 2). As an indirect sign, respiratory variability in the pulse oximetry waveform should raise the suspicion of hemodynamic compromise in patients at risk for pericardial tamponade who are breathing spontaneously.26 The elevation of central venous pressure (CVP) has a low predictive value in the immediate postoperative setting because of the high rate of low-pressure tamponade, situations of concomitant hypovolemia, or in loculated tamponade. In addition, the elevation of CVP can occur in situations of right ventricular dysfunction, in the presence of tricuspid regurgitation, or ventilatory abnormalities requiring high PEEP. Furthermore, postoperative pericardial effusions of moderate volume may be found in the posterior space and partially compress one or more cardiac chambers. These cases may manifest as isolated increases in pulmonary artery occlusion pressure. Occasionally, the increases in CVP and jugular distention can occur together with the Kussmaul venous sign.2 The Kussmaul sign is a
Table 2. Conditions in Which Pulsus Paradoxus Is Suppressed in Cardiac Tamponade Left Ventricular Dysfunction Regional tamponade Positive-pressure ventilation Chronic obstructive pulmonary disease with cor pulmonale Pulmonary artery obstruction Severe aortic insufficiency Intracardiac shunt Modified with permission.25 Copyright 1993 by American Heart Association, Inc.
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Table 3. Echocardiographic Criteria for Cardiac Tamponade 2-Dimensional Mode
Doppler
Echo-free space around the heart Variation of heart dimensions with ventilation Right atrium compression Right ventricular diastolic collapse Dilated vena cava in the absence of inspiratory collapse Loculated effusion compressing the left atrium Left ventricular diastolic compression Abnormal opening of the mitral valve “Swinging heart”
Respiratory variation of transmitral and transtricuspid flows Respiratory variation of venous flows Increased reverse wave with atrial contraction in pulmonary vein flows.
Modified with permission.25 Copyright 1993 by American Heart Association, Inc.
distention of jugular veins in the neck during inspiration. In low-pressure tamponade, this is an uncommon sign; however, exaggerated jugular pulse wave without distention can sometimes be seen. The tracing of venous pulse waves shows a marked “x” wave and a reduction or absence of the “y” wave (Fig 1). On a chest x-ray, a normal heart size is seen until the effusion is moderate in volume (at least ⬎200 mL); thereafter, the cardiac silhouette is enlarged, taking the appearance of a flask or water-bottle. These findings might not be seen with loculated pericardial effusions. The only electrocardiographic (ECG) sign that is almost specific in cardiac tamponade is electrical alternans, which is a beat-to-beat variation of the contour and/or shape of the P wave, the QRS complex, the ST segment, and/or the T wave. This phenomenon can be explained by the presence of pericardial fluid, which drives the myocardium back and forth from the thoracic wall. Other potential, less specific findings are reductions of the QRS voltage and the T wave, depressed PR segment, changes in the ST-T, and bundlebranch blocks. Postoperative tamponade after cardiac surgery may have varied clinical and hemodynamic presentations because of selective chamber compression by loculated fluid27 or hypovolemia. The atypical clinical presentation of these events may simulate other disorders like severe hypovolemia, left ventricular dysfunction, major ischemic events, or systemic inflammatory response syndrome, and, therefore, the diagnosis of tamponade should be considered whenever hemodynamic deterioration or signs of low-output failure occur in the postcardiotomy patient.28
size of pericardial effusions, to quantify the hemodynamic consequences of any effusions, and even to drive treatment decisions (Table 3).31 The echocardiographic characteristics of cardiac tamponade on 2-dimensional transthoracic echocardiography or transesophageal echocardiography include the following: 1. Evidence of a moderate-to-severe circumferential pericardial effusion appearing as an echo-free space around the heart (Fig 3).10 Moderate pericardial effusion is considered to be present when the sum of diastolic echo-free anterior and posterior spaces is 10 to 20 mm; the effusion is considered to be large when greater than 20 mm.32 2. Compression of the right atrium during the early diastolic phase, which is defined as diastolic inversion of the right atrial free wall.13,33 3. Compression of the right ventricle during the late diastolic phase13,34 (Fig 4), which is defined as the occurrence of inward motion of the right ventricular wall. The collapse of both chambers is exaggerated during expiration when the right heart filling is reduced. 4. Abnormal opening of the mitral valve, delay of mitral valve opening during inspiration, suggesting compromise of left ventricular filling.35 5. Dilated inferior vena cava in the absence of inspiratory collapse.36 In the presence of tricuspid regurgitation or severe right ventricular dysfunction, this may have a low predictive value. 6. “Swinging heart” in the pericardial fluid collection.25,37 Collapse of the right atrium is more sensitive for diagnosing
Echocardiographic Diagnosis Although the diagnosis of cardiac tamponade is predominantly clinical, symptoms are usually nonspecific in postoperative cardiac patients and may complicate the decision-making process.1,29 If there is clinical suspicion of cardiac tamponade, an echocardiographic examination by transthoracic or transesophageal echocardiography must be performed without delay.2,28,30 Echocardiography is used to show the presence and
Fig 3. The transgastric 0° view: short axis of the right and leflt ventricles and a posterior pericardial effusion with right ventricle collapse appearing as an echo-free space around the right ventricle and inward motion of the RV posterior wall. LV, left ventricle; RV, right ventricle.
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Fig 5. A midesophageal 4-chamber view: hypoecogenic area corresponding to a loculated pericardial effusion around the LA with inversion of the LA free wall. LA, left atrium.
Fig 4. A midesophageal 4-chamber view: hypoecogenic area corresponding to a pericardial effusion, which is compressing the RV and the LA. Both show inward motion of the free wall. LA, left atrium; LV, left ventricle; RA, right atrium, RV, right ventricle.
tamponade; however, collapse of the right ventricle, which lasts more than a third of diastole, is more specific.38 In acute, hemorrhagic tamponade, thrombi can be identified as hyperechoic masses. The absence of atrial collapse (Table 4) generally excludes global but not regional tamponade, except in the context of acute or chronic elevations in right-sided pressures and in the presence of decreases of atrial or ventricular compliance caused by hypertrophy of these chambers.39-41 Doppler examination findings indicating the presence of tamponade include the following: 1. Respiratory variation of transmitral and transtricuspid flow velocities, which reflect increased ventricular interdependence, clinically appearing as pulsus paradoxus.13,42 Left ventricular filling decreases during inspiration, which manifests as prolonged isovolumic relaxation time and reduced E-wave velocity. During the expiratory phase, changes are reversed. Respiratory variation of transtricuspid flows is opposite to that of transmitral flows.43 2. Venous flow analysis: In cardiac tamponade, the characteristic venous flow pattern in the superior vena cava and/or suprahepatic vein consists of a marked predomTable 4. Conditions in Which There Is Absence of Right Atrial Collapse in Cardiac Tamponade Regional posterior tamponade Right ventricular dysfunction Severe pulmonary hypertension Chronic obstructive pulmonary disease with cor pulmonale
inance of systolic over diastolic component, a reduced increase of flow during inspiration, and suppression or inversion of the diastolic component in the 1st expiratory cardiac cycle. This abnormal pattern has high sensitivity and specificity and correlates well with clinical features of tamponade. The conditions most commonly precluding the analysis of venous flows are atrial fibrillation, tricuspid regurgitation, pacemaker rhythm, and technical difficulties to obtain an appropriate signal.44 Respiratory variation in tricuspid and venous flow is more dramatic than mitral and aortic flow, but there is progressive impairment in all intracardiac flow as the degree of tamponade worsens. The patterns described previously are characteristic of patients in spontaneous ventilation. However, in patients under mechanical positive-pressure ventilation, the echocardiographic criteria used to diagnose cardiac tamponade based on respiratory variation of tricuspid or mitral valve inflow patterns may be decreased or nonexistent in the context of pericardial effusion and cardiac tamponade.45 Doppler criteria for tamponade may be sensitive but can be nonspecific. An abnormal transmitral and transtricuspid flow pattern also can be observed in chronic obstructive pulmonary disease, pulmonary embolism, constrictive pericarditis, and right ventricular infarction.42 Hemodynamically significant pericardial collections occurring early after cardiac surgery may not show the classic echocardiographic features of tamponade.46 On occasion, postoperative effusions are small and loculated, with selective chamber compression.28,47 The most consistent sign observed after cardiac surgery is increased pericardial separation.48 Loculated effusions compressing the left atrium and left ventricle in the absence of right-heart abnormalities are not infrequent and can lead to severe hemodynamic compromise49 (Fig 5). TREATMENT
The decision to drain and how to proceed will be based on the patient’s clinical situation. In the early postoperative period after cardiac surgery, surgical decompression was indicated for
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patients with hemorrhagic cardiac tamponade and evidence of clots, which is the majority of cases.35 Emergency drainage is indicated if there is clinical evidence of tamponade either by pericardiocentesis or surgical pericardiotomy.50 In the largest series reported in the literature of postoperative cardiac patients with early and late cardiac tamponade1 for whom emergent surgical decompression was excluded, video-assisted51,52 and ultrasound-guided pericardiocentesis53 was the treatment of choice and proved effective in 97% of cases. Sternotomy was only required in the remaining 3%. In the late postoperative period, surgical decompression is also reserved54 for patients ineligible for echocardiographic examination, cases of percutaneous drainage failure, and the presence of intrapericardial hematoma. Drainage is also recommended when pericardial effusion is associated with left ventricular dysfunction in patients with PPV and in the presence of loculated effusions at the level of the left-sided chambers. Removal of as little as 50 mL of pericardial fluid commonly can produce significant hemodynamic improvement because of the steep pericardial pressurevolume relationship.55 In addition, some authors, including Hoit and Fowler41 and Little and Freeman,38 advocated drainage if the effusion is measured on ultrasound to be more than 20 mm and if there is collapse of the right chambers or if the duration has been less than 1 month, given the high risk for the development of tamponade.38,56 These criteria may be applicable to postoperative cardiac patients. ANESTHETIC MANAGEMENT
Objectives before and after induction include the following (Fig 6): 1. Optimization of preload: Increasing intravascular volume to optimal levels to maintain hemodynamic stability. This is particularly important in patients with volume depletion because in the setting of diastolic failure the effective increase of cardiac filling will oppose the significant increase in intrapericardial pressure. Filling pressures of up to 25 to 30 mmHg may be necessary.57 Blood products should be available in cases of hemorrhagic tamponade. However, in patients with normal or increased blood volume (which is very rare in the postoperative setting), the infusion of volume can result in an increase of intrapericardial pressures sufficient to cause right ventricular diastolic collapse.58 2. Optimization of inotropism: The use of inotropic drugs enhances the action of endogenous catecholamines. Dobutamine is considered the drug of choice by some clinicians because of its inotropic properties and the reduction of systemic resistances.59-61 Isoproterenol and dopamine showed beneficial hemodynamic effects in cardiac tamponade in animal models, but this has not been proven in the clinical setting.59 These drugs initially produce an increase in systolic volume by increasing ejection fraction and heart rate and an improvement in cardiac perfusion; however, there is no increase in perfusion of other organs, such as the brain or the kidneys. Additionally, isoproterenol improves flow perfusion in the epicardial tissue as opposed to the
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endocardial tissue and is a powerful vasodilator. Human studies have concluded that the positive effect of inotropic drugs in cardiac tamponade is limited.59 Metabolic acidosis needs to be corrected to avoid myocardial depressant effects and increase the response to catecholamines.62 3. Maintenance of afterload: Hypotension is relatively frequent in the postoperative cardiac surgery period, and the use of vasopressors, such as phenylephrine or norepinephrine, often may be necessary to increase coronary perfusion and improve ventricular function57 until resolution of the tamponade and recovery of the heart function. However, the use of vasopressors should be avoided as much as possible if blood pressure stays within the normal range because these agents might result in decreased cardiac output. Furthermore, the use of vasodilators in postoperative cardiac tamponade is controversial in the literature24 and might be indicated only if postoperative cardiac tamponade is associated with elevated systemic vascular resistance and elevated systemic arterial pressure 4. Maintenance of sinus rhythm: In both the early and late stages of a tamponade, it is not uncommon to see vagal depressor reflexes, which require the use of atropine, because bradycardia results in reduced cardiac output63 or pacing the heart if epicardial pacing wires are available. Ventricular filling depends primarily on atrial contraction, and, therefore, the development of atrial fibrillation or flutter has a negative impact on blood pressure and cardiac output. In this regard, antiarrhythmic drugs and a defibrillator must be available. 5. Ventilatory modes: Mechanical ventilation has great influence on cardiac tamponade patients.64,65 The maintenance of spontaneous ventilation throughout the procedure may be better tolerated in patients with tamponade than other modes of ventilation.66,67 There are isolated literature reports of intubation in patients who are kept awake and maintain spontaneous ventilation.68,69 Under mechanical ventilation, it is advisable to avoid high pressures and use low tidal volumes until the tamponade is released,70 in addition to using high respiratory rates and avoiding PEEP. Monitoring during surgical procedures for pericardial diseases is essential; however, it depends on the degree of emergency in each case. Monitoring should include ECG, arterial pressure, pulse oximetry, capnography, and urinary output. If possible, invasive monitoring is recommended including invasive monitoring of arterial pressure, cardiac output, and central venous saturation of oxygen using a pulmonary thermodilution catheter or continuous pulse contour analysis systems. In patients with cardiac tamponade, it is not unusual to find high left and right atrial pressure with “real” low preload. For this reason, monitoring with devices to assess stroke volume variation as a method of evaluating preload is recommended. Wherever possible, devices should be inserted under local anesthesia.57
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Anesthetic Management The induction of general anesthesia and mechanical ventilation have been associated with severe tachycardia and hypotension in patients with pericardial effusions.71 It should be kept in mind that many anesthetic drugs are myocardial depressants and vasodilators, which must therefore be used with caution. Ideally, the anesthetic agents should minimize bradycardia, myocardial depression, and the sudden reduction of preload and afterload. In any case, induction must be undertaken when the surgical field and the surgeons are ready to immediately proceed to drain. In acute and chronic tamponade, some authors72 recommend, as long as the patient’s situation allows, to drain the effusion through a subxiphoid incision under local anesthe-
sia to avoid the deleterious effect of the anesthesia and mechanical ventilation and, subsequently, induce general anesthesia after the pericardial fluid has been released. The recommended agents for induction are etomidate, ketamine, or diazepam, whereas inhalation agents are recommended for maintenance.70 In the authors’ experience, ketamine as an induction agent is the first choice. However, there are few reports on its use in the literature. Several authors69,73,74 have reported cases of anesthetic induction with ketamine and local anesthesia for reopening of sternotomy or performance of a pericardial window. In unstable patients, ketamine has a clearly beneficial effect for maintaining arterial pressure because it increases systemic resistances and maintains the heart
Suspected tamponade Clinical diagnosis
Echocardiographic conirmation
Hemodynamic maintenance
Optimization of preload Blood products available Correct acidosis
Afterload maintenance: If hypotension: norepinephrine, phenylephrine Avoid vasopressors if adequate MAP.
Anesthetic induction
Optimization of inotropism Dobutamine
Preserve sinus rhythm: cardioversion. Prevention of relex bradycardia: Atropine
Surgical team ready
Optimize ventilation: Spontaneous In pressure control: Reduced tidal volumes, elevated respiratory rate, avoid PEEP.
Drainage of pericardial effusion
Recommended agents: Ketamine, etomidate, opioids, inhaled agents
Treat post-drainage hypertension: Nitroglycerin, hydralazine, urapidil, nitroprusside
Fig 6. The perioperative management of postoperative cardiac tamponade. The perioperative management focusing on hemodynamic maintenance, anesthetic induction for surgery, and treatment after drainage.
CARDIAC TAMPONADE
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rate. Nevertheless, ketamine also can have deleterious effects, by increasing the afterload of the right ventricle, and some myocardial depressant effects.75 Maintenance with inhalation agents and low-dose opioids has minimal effects on hemodynamic stability. In the setting of cardiac arrest, it should be remembered that external cardiac compressions have little or no value because the tamponade leaves very little room for additional filling of the chambers. In addition, even though systolic pressure increases, diastolic pressure remains unchanged, and, therefore, perfusion pressure does not improve.76 In this situation, the best option is to reopen the chest immediately. After drainage, cardiac pressure and output may rise sharply because of the rapid increase in filling pressures, and it may become necessary to use vasodilators if arterial hypertension ensues. Nitroglycerin, nitroprusside, or urapidil are good options. Pericardiocentesis may be associated with a variety of complications, including laceration of the right ventricle or a coronary artery, arrhythmias, pneumothorax, and acute respiratory distress syndrome. Postpericardiocentesis acute left ven-
tricular failure, pulmonary edema, and cardiogenic shock have been reported.77-81 CONCLUSION
In conclusion, anesthesiologists who manage surgical pericardial drainage of a cardiac tamponade face an unstable hemodynamic situation resulting from abnormal ventricular filling and the consequent reduction in systolic volume. Diagnosis must be made early and based on clinical observation and echocardiographic examination. Anesthetic induction should be based on optimization of the preload, maintenance of inotropism and sinus rhythm, maintenance of the afterload according to hemodynamic status, and the use of induction drugs with little effect on inotropism (ketamine, benzodiazepines) and should be undertaken only when the surgical team is ready to operate. For ventilation, spontaneous breathing should be maintained until mechanical ventilation is established, with reduced tidal volumes and high respiratory rates, avoiding the use of PEEP.
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