Stem Case and Key Questions
A 50-year-old female with rheumatic heart disease initially presented for mitral valve replacement. The intraoperative course was uneventful, with postbypass echocardiographic interrogation revealing a well-seated bioprosthetic valve in the mitral position, no significant mitral regurgitation, and good biventricular function. Over the course of several hours after being transported to the intensive care unit, she required an escalating amount of norepinephrine to maintain adequate blood pressure and had declining urine output. The heart rate was 118 beats per minute with a blood pressure of 86/52. The patient was noted to have cool extremities, cardiac index had fallen from 3 to 1.7 L/min/m2, and a significant rise in pulmonary artery and central venous pressures was noted. Pulse oximetry revealed a poor waveform, but when a numeric value was seen, it was in the low 90s. Inspiratory oxygen percentage had been increased to 100% about an hour prior. An electrocardiogram (ECG) showed sinus tachycardia, without significant ST segment changes. The mediastinal drain had not produced output in over 2 hours. A point-of-care transthoracic echocardiogram (TTE) was obtained; it revealed a large pericardial hematoma compressing the left atrium. Other significant findings were an underfilled but adequately functioning left ventricle and a distended and poorly functioning right ventricle. Mitral and tricuspid flow velocities did not change significantly during the respiratory cycle. The patient was emergently taken back to the operating room for chest exploration, where fresh blood and a large thrombus were removed from the pericardial space, and a small tear in the left atrium was repaired (Figure 8.1). The hemodynamics of the patient improved quickly, and she went on to have an uneventful postoperative course.
What Is Cardiac Tamponade? What Is the Differential Diagnosis?
Cardiac tamponade is a clinical syndrome that occurs when accumulating fluid within the pericardial sac results in rising intrapericardial pressure with consequent decreased ventricular filling and cardiac output. It is a life-threatening emergency that requires prompt recognition and treatment to prevent cardiovascular collapse. In situations similar to this scenario, when a patient develops tachycardia and hypotension shortly after open-heart surgery, cardiac tamponade should always be high on the differential diagnosis. Cardiogenic shock due to myocardial ischemia should also be considered. The left circumflex coronary artery lies in close proximity to the posterior mitral annulus, and distortion or injury to this artery during mitral valve replacement is possible.1 Because the patient is receiving positive pressure mechanical ventilation, tension pneumothorax is also a consideration. Other possible causes of this presentation would include mitral valve dehiscence, aortic dissection, and pulmonary embolism.
What Is the Pathophysiology of Cardiac Tamponade?
Tamponade results from increasing pericardial pressure causing impaired filling and compression of some or all of the cardiac chambers. The elevated pericardial pressure decreases the filling pressure of the heart, also called the transmural pressure (intracardiac pressure minus pericardial pressure), which results in impaired diastolic filling.2 In an acute setting, the pericardial space is a relatively small volume (~20–50 mL). Once that space has been occupied, the limits of pericardial stretch are quickly reached, and further accumulation of fluid will dramatically increase intrapericardial pressure (Figure 8.2). In contrast, in chronic pericardial effusions, the pericardium can accommodate the slow accumulation of fluid by stretching over time, although eventually the pericardium will become noncompliant, and further increases in pericardial volume will result in tamponade physiology. In both scenarios, it is not the absolute volume of the pericardial effusion but rather the increasing pericardial pressure that causes cardiac tamponade.
What Findings Will Be Seen on Transesophageal Echocardiography in This Patient?
An important finding in cardiac tamponade is a large (>20 mm), echolucent (black) circumferential space around the heart that is present in multiple views (Figure 8.3). However, after cardiac surgery, as in this case, the collection may be confined to only a single cardiac chamber, causing localized tamponade (Figure 8.1). These effusions are often clotted blood or fibrinous material and are echodense (white or gray), making them difficult to differentiate from myocardial tissue. As a result, a single view may prove to be inadequate for a prompt diagnosis, and additional echocardiographic windows will be necessary. Whether the effusion is circumferential or regional, the most sensitive finding in cardiac tamponade is chamber collapse3 (Figure 8.4). This more commonly involves the right side of the heart because the intracavitary pressures are lower. Right ventricular free-wall collapse typically occurs early in diastole, while right atrial collapse occurs late in diastole and often persists into systole. Left atrial collapse is not a common finding but is very specific for tamponade.4 Left ventricular collapse is rare due to its muscular character. Other findings include a distended inferior vena cava (IVC), reflecting increased central venous pressure and, in spontaneously breathing patients, significant variation in chamber inflow and outflow velocities.
How Are the Echocardiographic Findings Different in Spontaneously Breathing Versus Mechanically Ventilated Patients with Cardiac Tamponade?
Exaggerated respiratory variations in transvalvular Doppler flow velocities are seen in spontaneously breathing patients, but not in those on mechanical ventilation. During spontaneous inspiration, there are marked increases in diastolic transtricuspid flow and decreases in transmitral flow as assessed by pulsed-wave Doppler.5 The opposite is true during expiration. Patients on positive pressure ventilation, on the other hand, show minimal changes in transvalvular flow, and Doppler assessment should not be relied on for the diagnosis of tamponade.6 There may also be a more pronounced septal shift toward the left ventricle during inspiration in spontaneously breathing patients as a result of differential ventricular filling.
What Are the Surgical Options?
The definitive treatment of cardiac tamponade is drainage of the compressing pericardial contents, and this should be undertaken as soon as possible. Options include percutaneous techniques (pericardiocentesis) and open surgery, with clinical circumstances, urgency, available resources, and practitioner expertise dictating the course of action. Pericardiocentesis is chosen for relative ease of execution and ability to be performed at the bedside (though image guidance is recommended) but carries a high risk of recurrence and can be ineffective in loculated effusions (common in postsurgical patients). Open techniques allow for evacuation of fluid and solid contents as well as for correction of bleeding. These approaches include sternotomy/resternotomy, subxiphoid drainage, and creation of a peritoneal- or pleural-pericardial window.
What Is the Anesthetic Management of Cardiac Tamponade?
The possibility of proceeding under local anesthesia with or without judicious use of intravenous sedation should always be considered, especially in unstable patients. If general anesthesia is required, blood pressure should be monitored continuously, and the surgical team should be ready to proceed if hemodynamics deteriorate. Agents that depress myocardial performance or cause vasodilation should be avoided; for that reason, ketamine and etomidate are popular choices as induction agents. Vasopressors and ionotropes (norepinephrine and epinephrine) should be immediately available. Mechanical ventilation has traditionally been avoided but may not be clinically detrimental if airway pressures are kept low.
Cardiac tamponade is a life-threatening clinical condition that occurs when accumulating pericardial fluid results in significantly decreased ventricular filling and hemodynamic instability. In the initial phases of tamponade, the signs and symptoms are often subtle; therefore, understanding the physiological changes that occur is essential for prompt recognition and treatment before cardiovascular collapse. The diagnosis should always be considered when the cause of hemodynamic instability is uncertain, especially in patients recently undergoing any type of cardiac procedure.
Any process that causes a pericardial effusion has the ability to deteriorate into cardiac tamponade. Some conditions affecting the pericardial space with the highest rate of progression toward tamponade include bacterial and fungal infections as well as malignancies. Chest trauma, interventional cardiology procedures, and type A aortic dissections are the most common, acute, life-threatening causes. The conditions most likely to produce significant hemodynamic compromise pertinent to the anesthesiologist can be found in Table 8.1.
Table 8.1 Causes of Cardiac Tamponade Relevant to the Anesthesiologista
More Common Causes
Less Common Causes
Interventional cardiology proceduresa
Central venous cathetersa
Extracorporeal membrane oxygenation cannulationa
Inflammatory and autoimmune
Other causes of tamponade-like physiology
Extrinsic compression (mediastinal mass or hematoma, large pleural effusion
a Reprinted from J Crit Care, Vol. 39, McCanny P, Colreavy F, Echocardiographic approach to cardiac tamponade in critically ill patients, 271–277, 2017, with permission from Elsevier.
b May cause regional tamponade from localized chamber compression or global pericardial effusion.
A pericardial effusion occurs when the intrapericardial fluid exceeds the amount normally present in the pericardial space (~20–50 mL). When an effusion becomes significant enough to cause cardiac chamber compression, the result is tamponade. It is not the absolute volume of the pericardial effusion, but rather the increasing pericardial pressure that determines the severity of this compression and, consequently, symptoms. The pericardium is able to stretch over time in response to chronic effusions; however, in acute tamponade the limits of pericardial stretch are reached with relatively small increases in pericardial fluid. Further accumulation of even small amounts of fluid can dramatically increase intrapericardial pressure (Figure 8.2). In contrast, the slow rate of accumulation in chronic pericardial effusions allows the pericardium to accommodate much larger volumes (at times ≥ 2 L) without hemodynamic consequences, although the pericardium will eventually become noncompliant, at which point small increases in pericardial volume will result in tamponade physiology. As pericardial pressure continues to increase, cardiac chambers are compressed, causing decreases in myocardial diastolic compliance.7 The result is a profound drop in venous return and cardiac output with eventual equalizing of mean diastolic pericardial and cardiac chamber pressures between 15 and 30 mm Hg.8
The filling pressure of the heart, or transmural pressure, is defined as the intracardiac pressure minus pericardial pressure.2 Ordinarily, the pericardial pressure follows the intrapleural pressure such that both fall during inspiration. However, in tamponade the elevated pericardial pressure decreases less than intrapleural pressure during inspiration, resulting in decreased transmural pressure. This fall in transmural pressure first results in impaired right-side filling, and, as pericardial pressure continues to rise, left-side chambers are ultimately affected. It is important to note that mechanical ventilation may hasten the cardiovascular compromise in tamponade. The increased intrapleural pressure from positive pressure ventilation is transmitted to the pericardial space, further decreasing transmural pressure.9 The actual clinical implications of this phenomenon are debatable, especially if airway pressures are low.4
Compensatory mechanisms aimed at maintaining cardiac output and arterial blood pressure include adrenergic-mediated increases in heart rate and vascular tone. Neurohormonal responses also attempt to preserve circulatory homeostasis by increasing blood volume, which can increase transmural pressure in the face of elevated pericardial pressure.
Patients with cardiac tamponade present in different ways depending on the clinical situation and the chronicity of the pericardial effusion. Acute tamponade, which can develop over minutes, usually appears as cardiogenic shock.7 Regional tamponade, usually acute, occurs when only a portion of the heart is compromised by a hematoma or loculated effusion. As a result of only selected cardiac chambers being compressed, the presentation and physical findings may be vague, and a high index of suspicion should be maintained, especially after pericardiotomy, myocardial infarction, or interventional cardiology procedures. Subacute tamponade is a much less impressive presentation, often with nonspecific symptoms (i.e., dyspnea, tachypnea, and chest pain) developing over days to weeks; however, once a critical intrapericardial pressure is reached, signs and symptoms of tamponade will appear (Figure 8.2). Last, low-pressure tamponade occurs in patients with preexisting pericardial effusions who are asymptomatic and otherwise display no hemodynamic derangements but who develop signs and symptoms after becoming severely hypovolemic.10,11 In these circumstances, relatively low pericardial pressure results in chamber compression because of even lower intracardiac pressures. Low-pressure tamponade may arise in the context of hemodialysis, major hemorrhage, or aggressive diuretic administration.
Depending on the severity and type of cardiac tamponade present, the physical findings may vary. The diagnosis may remain uncertain until critical tamponade is reached, as none of the characteristic signs are highly sensitive or specific.10 Sinus tachycardia is usually present to compensate for decreased stroke volume, although there are some exceptions (i.e., bradycardia with myxedema and uremia).12 The classically described Beck’s triad (hypotension, muffled heart sounds, and jugular venous distension) is pathognomonic for tamponade, although all three findings are rarely seen together.13,14 Relative or absolute hypotension is almost always present and may be accompanied by cool and cyanotic extremities owing to dramatic declines in cardiac output. Distant heart sounds may be appreciated on physical examination due to the isolating effects of the pericardial fluid. Jugular venous distension is almost universally seen and may even be evident in the scalp and forehead in the nonsupine position. Exceptions to this rule can be seen in low-pressure tamponade, where the intracardiac venous pressures are relatively normal (i.e., 6–12 mm Hg)10 and in regional tamponade when only the left-side chambers are affected.
A common finding in tamponade, pulsus paradoxus, which is conventionally defined as an exaggerated fall in systolic blood pressure (>10 mm Hg) during inspiration, may be seen in spontaneously breathing patients. Normally, there are subtle decreases in cardiac output and blood pressure (<10 mm Hg) during inspiration owing to increased venous return to the right heart with decreased filling to the left heart. However, in the setting of cardiac tamponade, this increased venous return to the right ventricle will be at the expense of left-side filling because of a fixed total heart volume. There is only a finite amount of space within the pericardium, and with a large pericardial effusion, the volume the heart can occupy becomes fixed. During inspiration, increased venous return causes the interventricular septum to bow to the left, which decreases left ventricular size and impairs its filling. With already reduced left-side volumes owing to the pericardial effusion, the result is a significant decrease in left-side stroke volume and an exaggerated decline in systolic blood pressure during inspiration. The pattern of changes observed in pulsus paradoxus is attenuated or even reversed in mechanically ventilated patients; namely, the systolic blood pressure will increase during inspiration and decrease during expiration.15 It should be noted that pulsus paradoxus is not specific for tamponade, as this physical finding is also present in other medical conditions (i.e., pulmonary embolism, obstructive lung disease, severe hemorrhage, obesity, obstructive sleep apnea).16 In addition, certain coexisting conditions, such as aortic regurgitation, heart failure, or atrial septal defects, may alter intracardiac pressures and result in the absence of pulsus paradoxus in superimposed cardiac tamponade.
If a patient is hemodynamically unstable and the history and physical examination suggest cardiac tamponade, emergent treatment can be lifesaving and should never be delayed for further testing. When time permits, however, additional workup can include a chest radiograph, ECG, and, most importantly, an echocardiogram. An anteroposterior chest radiograph will demonstrate an enlarged, flask-shaped cardiac silhouette along with clear lung fields in chronic effusions of at least 200 mL17,18 (Figure 8.5). Otherwise, in acute tamponade, when the pericardium is unable to stretch to accommodate increased pericardial fluid, the chest radiograph will show a normal heart size. Chest radiography is neither sensitive nor specific in the diagnosis of tamponade.
The ECG will usually show sinus tachycardia. Other ECG findings may include diffuse low voltage and electrical alternans18,19 (Figure 8.5). The insulating effects of the increased pericardial fluid and myocardial inflammation are thought to cause reduced voltage20,21; the finding is nonspecific (it can also be seen in conditions such as chronic obstructive pulmonary disease, pneumothorax, obesity, and cardiomyopathies). Electrical alternans is present when there are beat-to-beat variations in both axis and voltage, which are thought to result from swaying of the heart within the pericardial fluid. Electrical alternans is the most specific sign of cardiac tamponade, especially when there are both P and QRS alterations. This finding, however, is not sensitive and can be seen in large pericardial effusions alone.11
Echocardiography provides important information regarding location, size, and hemodynamic significance of a pericardial effusion and whether tamponade is present. Because the diagnosis can be mistaken for other conditions that present with similar signs and symptoms, echocardiography is an invaluable diagnostic tool in determining the etiology (Table 8.2).
Table 8.2 Conditions that Cause Tachycardia, Elevated Central Venous Pressure, and Pulsus Paradoxusa
Superior vena cava syndrome
Extreme obesity (e.g., pulmonary embolism)
Acute right heart failure
a Reprinted from J Crit Care, Vol. 39, McCanny P, Colreavy F, Echocardiographic approach to cardiac tamponade in critically ill patients, 271–277, 2017, with permission from Elsevier.
Echocardiography has become the imaging modality of choice in establishing the diagnosis of tamponade and should be obtained emergently.22,23,24 Computerized tomography and magnetic resonance imaging are often less readily available and are usually unnecessary unless echocardiography is unavailable. Tamponade classically manifests as a circumferential fluid layer, compressed cardiac chambers, high ventricular ejection fractions, and inflow and outflow velocities that vary with the respiratory cycle.11 Fluid accumulation greater than 50 mL will typically result in an anechoic pericardial space throughout the cardiac cycle, and effusions are characterized as small (9 mm or less), moderate (10–19 mm), and large (>20 mm) based on the size of this layer.23 Effusions can exist in a free-flowing fashion, which tend to accumulate in the dependent portion of the pericardial space, or can be loculated, in which case the adjacent portion of the heart is most affected. The size of the effusion may not correlate with symptoms, particularly in the latter case. Clotted and loculated effusions are more common after cardiac surgery due to pericardial adhesions and are better detected with TEE versus TTE.25,26 A posterior hematoma may be particularly difficult to identify via transthoracic windows; it is recommended, therefore, that if tamponade is suspected in a postsurgical patient and the TTE is negative, urgent TEE should be strongly considered.27
The most characteristic echocardiographic feature of tamponade is chamber collapse (Figure 8.4). This most commonly affects the right atrium, which, if observed during at least 30% of the cardiac cycle, is highly sensitive and specific for tamponade.3,28 The second most frequently affected chamber is the right ventricle, which will be observed to invaginate during early diastole, most commonly in the vicinity of the right ventricular outflow tract.26 The right atrium, on the other hand, is prone to collapse during late diastole and into systole. Left atrial compression occurs in a minority of cases but is a highly specific finding.4 Bulging of the intraventricular septum toward the left ventricle during inspiration (in a spontaneously breathing patient) explains the physical examination finding of pulsus paradoxus. M-mode echocardiography can be helpful in appreciating both chamber collapse and septal shift and is particularly useful in correlating the motion of structures with the cardiac cycle (Figure 8.4).24 Distension of the IVC (>21 mm) that maintains more than 50% of its diameter during inspiration (so-called IVC plethora) is another common finding but, while 90% sensitive and indicative of elevated central venous pressure, is not a specific finding.29 Absence of IVC plethora, however, in a spontaneously breathing patient essentially rules out tamponade.
Doppler studies can also contribute to the echocardiographic diagnosis and will typically include significant variation in transvalvular flows during the respiratory cycle. Elevated pericardial pressure and fixed intracardiac volume dictate that filling of the right and left sides of the heart occur in alternating fashion (“one side at the expense of the other”). The characteristics of this cycle are determined by intrathoracic pressure fluctuations that occur during the respiratory cycle; the flow through each chamber therefore varies significantly more in tamponade than under normal conditions.5 Velocities measured via pulse-wave Doppler provide a good surrogate of these flows. The pulse-wave cursor can be placed at the tricuspid valve for right ventricular inflow, in the right ventricular outflow tract for right ventricle outflow (best obtained from a transgastric position), at the mitral valve for left ventricular inflow, and at the left ventricular outflow tract for left ventricle outflow (deep transgastric). Respiratory variations exceeding 25% for right ventricle inflow, 15% for left ventricle inflow, and 10% for both right and left ventricle outflow suggest tamponade. According to the 2013 guidelines from the American Society of Echocardiography, a 30% variation in left ventricular or a 60% variation in right ventricular inflow velocities is diagnostic of tamponade.24 It is important to note that respiratory variation should only be expected to occur in spontaneously breathing patients. A study involving positive pressure ventilation in a canine model of cardiac tamponade revealed only slight variations in transmitral flow during the respiratory cycle. This suggests that the compressing pericardial substance is the predominant factor limiting ventricular filling, and that variations in pleural and airway pressures have little additional effect.6
Though medical management may be necessary when attempting to stabilize a deteriorating patient, definitive therapy via drainage should be undertaken as soon as possible. Temporizing measures include strategies for supporting cardiac output, such as augmenting filling with cautious administration of fluid or infusions of vasopressors and ionotropes.4 These measures are of temporary and limited benefit.
Fluid resuscitation is mentioned as being indicated in most cardiology textbooks.30 The physiological rationale resembles that in hypovolemic shock: As venous pressure approaches intracardiac pressure, initial fluid therapy is thought to be effective at augmenting cardiac filling.8 This logic is supported by experiments conducted in canine models of tamponade.31 The actual clinical benefits of fluid therapy, however, have more recently been called into question. Some argue that in normovolemic patients aggressive resuscitation could, at worst, exacerbate tamponade and precipitate pulmonary edema and, at best, have only modest clinical benefit.11 This perspective is based on concerns that expanding intravascular volume could lead to increased right ventricular volume and septal shift (thereby worsening left ventricular filling), as well as increased left ventricular end-diastolic pressure (with resultant risk of pulmonary edema). Interestingly, clinical data have shown fluid therapy to be most efficacious in hypotensive patients,30 and most of the benefits were observed only after the first 250–500 mL.32 The utility of more aggressive volume administration in hypovolemic patients, on the other hand, such as those with low-pressure tamponade or trauma victims with a penetrating injury is generally accepted. All in all, in the absence of well-established guidelines, fluid therapy should be undertaken with appropriate vigilance and expectations, taking into account the specific clinical scenario and available hemodynamic and echocardiographic data.
Vasoactive and ionotropic medications may also provide limited hemodynamic benefit. Because tamponade physiology typically involves fixed, small stroke volumes, maintenance of cardiac output relies primarily on heart rate, adequate filling, and contractility. Dobutamine has been employed for the theoretical advantages conferred by its chronotropic and ionotropic properties, and animal studies have suggested its potential to augment organ perfusion and delay the onset of lactic acidosis.33 Clinical research by Martins et al., however, found only marginal improvement in cardiac output with no improvement in blood pressure or organ perfusion after dopamine and isoproterenol administration. Blood pressure did improve, interestingly, after administration of norepinephrine, albeit modestly.34 Some argue that the actual clinical benefits of these infusions are likely limited because, during an episode of tamponade, endogenous catecholamine stimulation is probably maximized.11 That being said, when faced with an unstable patient and tenuous hemodynamics, few would forgo intervention with vasoactive medications despite the potential for futility, and norepinephrine and epinephrine are reasonable choices.
Pericardiocentesis and Surgical Management
The definitive therapy for cardiac tamponade is drainage of the extraneous pericardial contents, either immediately when faced with life-threatening hemodynamics or urgently if vital signs are more stable. This can be accomplished by either needle pericardiocentesis or various open surgical approaches. Because unstable patients cling to an extremely steep portion of the intracardiac pressure-volume curve, the removal of as little as 50 mL of fluid can lead to significant clinical improvement.4
If pericardiocentesis is planned, imaging guidance with either echocardiography or fluoroscopy can be helpful in decreasing potential complications such as coronary artery laceration, cardiac puncture, and pneumothorax.22 In the case of impending circulatory collapse, however, it is reasonable to proceed “blindly.”11 A large case series confirmed the relative safety of echocardiography guided pericardiocentesis, noting a success rate of 97%, total complication rate of 4.7%, and one procedural death, all of which compare favorably to morbidity and mortality associated with proceeding blindly (20% and 6%, respectively).22 A 16- or 18-guage angiocath needle is typically inserted between the xiphoid process and the left costal margin. A 15° angle is initially required to bypass the costal margin, after which the path is redirected toward the left shoulder and the needle advanced until fluid is aspirated. The needle core can then be withdrawn, a wire inserted, followed by a pigtail catheter using a Seldinger technique. The catheter is typically left in place until less than 50 mL per day is draining.11 Despite the relative safety of the procedure, however, pericardiocentesis has fallen out of relative favor due to the high incidence of effusion recurrence, which may approach 60%.35
Open surgical drainage is typically indicated if the effusion persists or recurs following pericardiocentesis, if there is a significant amount of pericardial clot, if the effusion is loculated and inaccessible to a needle, or if significant ongoing bleeding is suspected.26 If tamponade develops in the immediate postoperative period, the cardiothoracic surgery team will often elect to proceed with mediastinal exploration via resternotomy, which allows for both direct drainage and possible identification and correction of bleeding sources.27 Mediastinal exploration is also indicated in hemopericardium from aortic dissection, penetrating trauma, and ventricular rupture. Other surgical approaches include subxiphoid and subcostal pericardiotomy and creation of a peritoneal-pericardial or pleural-pericardial window. The latter can be accomplished thorascopically or through a small anterior thoracotomy.36 Open approaches allow for more effective removal of clot, other fibrinous debris, and loculated effusions, all of which are common in tamponade that develops after cardiac surgery.25 Subxiphoid approaches involve reduced postsurgical pain and mechanical ventilation requirements but may have increased rates of recurrence.35 Thoracotomy or thoracoscopy may be required to correct lateral or apical loculated effusions.26 Despite the relative merits of the aforementioned approaches, however, practitioner expertise and preference often dictate the choice of surgical strategy.
When anesthesia support is required for surgical intervention, there is unfortunately a paucity of evidence-based recommendations available to guide intraoperative care. Anesthesia providers, however, should keep several considerations in mind when caring for these critically ill patients.
First, the possibility of proceeding exclusively with judicious sedation and local anesthesia should be considered, especially in unstable patients. Numerous case reports exist in the literature describing drainage, usually via a subxiphoid approach, under local anesthesia and with small amounts of midazolam, fentanyl, or ketamine for sedation.37 If necessary, after an amount of fluid has been drained that allows for an improvement in hemodynamics, general anesthesia can be induced and a more extensive exploration undertaken.
General anesthesia will often be required prior to intervention, particularly in post–cardiac surgery patients in whom TEE is requested. Induction and maintenance of anesthesia are usually possible without worsening the clinical picture but demand thoughtfulness and diligence on the part of the provider. If time permits, placement of an arterial catheter for continuous blood pressure monitoring prior to proceeding is useful, as this monitor will allow for prompt recognition and treatment of hypotension, which can develop suddenly. Classic teaching calls for sterile preparation of the surgical site and for team members to be gowned and gloved before induction, but specifics of the case can dictate the necessity of these measures. Drugs that depress myocardial performance (via decreased contractility, heart rate, and sympatholysis) or cause significant vasodilation should be avoided, as a precipitous drop in cardiac output and cardiac arrest can immediately follow their administration. Ketamine and etomidate are often chosen for their relatively neutral hemodynamic profile. The former should be used with caution, as myocardial depression can occur in patients with depleted catecholamine stores. When considering etomidate, the potential for adrenal suppression and possible association with increased mortality in critically ill patients should be taken into account.38 Regardless of the induction agent chosen, vasoactive and ionotropic medications (epinephrine and norepinephrine, as previously discussed) should be immediately available as boluses and infusions.
Positive pressure ventilation has been traditionally avoided in tamponade. Increased intrathoracic pressures can decrease transmural pressure, increase right ventricular afterload (worsening septal shift), and further reduce venous return to the right atrium. These changes, when imposed suddenly, carry the potential to overwhelm compensatory mechanisms and cause a precipitous drop in cardiac output. Awake fiber-optically guided endotracheal intubation following airway topicalization has been described as a potentially beneficial technique that allows for the maintenance of spontaneous ventilation and can precede cautious administration of hypnotic agents.39 Securing the airway in this fashion, however, can be time consuming, and the risks and benefits of delaying definitive treatment need to be considered. That being said, it has also been suggested that the actual clinical effects of mechanical ventilation on tamponade physiology are small provided that airway pressure (i.e., tidal volume) is kept to a minimum.4 This viewpoint correlates with echocardiographic assessment of ventricular filling during tamponade, which shows little respiratory variation in mitral inflow during positive pressure ventilation.6
Cardiac tamponade is a life-threatening condition, and prompt recognition and appropriate treatment are vital to patient survival. All anesthesiologists should be able to identify signs and symptoms of tamponade, quickly develop a differential diagnosis, and employ further testing when appropriate. Because echocardiography is typically the first-line test, knowledge of common echocardiographic findings can be helpful and, when using TEE to guide surgical intervention, even essential. Proper medical management, while temporizing and of limited benefit, should still be initiated when appropriate. Removal of the compressing pericardial contents, the definitive therapy for tamponade, should be undertaken as soon as possible, and anesthesiologists should be familiar with the various percutaneous and surgical techniques that may be employed.
• Cardiac tamponade is a life-threatening condition that occurs when accumulating fluid within the pericardial space results in rising intrapericardial pressure with consequent decreased ventricular filling and cardiac output.
• It is not the absolute volume of the pericardial effusion, but rather the increasing pericardial pressure that determines the severity of cardiac tamponade.
• Beck’s triad (hypotension, muffled heart sounds, and jugular venous distension) is pathognomonic for tamponade, although all three findings are rarely seen together. None of the signs or symptoms of tamponade is highly sensitive or specific.
• Pulsus paradoxus is due to increased venous return to the right ventricle at the expense of left-side filling because of a fixed total heart volume. During inspiration, increased venous return causes the interventricular septum to bow to the left, which further decreases an already reduced left ventricular size and impairs cardiac output.
• Echocardiography is the test of choice in establishing the diagnosis of tamponade and should be obtained urgently.
• Echocardiographic findings include compressed cardiac chambers (most specific), a pericardial effusion (may be a circumferential fluid layer or more localized collection), transvalvular velocities that vary significantly with respiration (in spontaneously breathing patients), septal shift, and a dilated IVC (sensitive but not specific).
• Removal of the compressing pericardial contents is the only definitive therapy for tamponade.
• The benefits of pericardiocentesis include relative ease, well-established safety profile, and ability to be performed at the bedside in rapidly deteriorating patients. It may be ineffective, however, in some circumstances.
• Open surgical approaches are preferred in certain situations, including the evacuation of loculated effusions (common following cardiac surgery). Techniques include sternotomy and subxiphoid, subcostal, and thoracic incisions aimed at drainage or the creation of a pleural- or peritoneal-pericardial window.
• Medical management is of temporary and limited benefit and can include the administration of vasoactive drugs (epinephrine and norepinephrine) and fluids. The latter is thought to be most helpful in hypovolemic patients (trauma, “low-pressure” tamponade, etc.). In normovolemic patients, liberal fluid therapy should be undertaken with caution.
• There are few, if any, evidence-based recommendations for anesthetic management. Local anesthesia and light sedation should be considered. Agents that depress myocardial performance or cause vasodilation should probably be avoided. Positive pressure ventilation may negatively affect cardiac filling and output, but the clinical consequences may not be significant if airway pressures are low.
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