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[ Contemporary Reviews in Critical Care Medicine ] 56

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Tamponade 61
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8 Q1 Hemodynamic and Echocardiographic Diagnosis 63
9 64
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Q12 Mark J. Kearns, MD; and Keith R. Walley, MD
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12 67
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Cardiac tamponade is a medical emergency that can be readily reversed with timely recognition
14 69
and appropriate intervention. The clinical diagnosis of cardiac tamponade requires synthesis of
15 70
16 a constellation of otherwise nonspecific features based on an understanding of the underlying
71
17 pathophysiological characteristics. Although echocardiographic examination is a central 72
18 component of diagnosis, alone it is insufficient to establish the physiological diagnosis of 73
19 hemodynamically significant cardiac tamponade. The hemodynamic diagnosis of cardiac tam- 74
20 ponade requires clinical evidence of low cardiac output and stroke volume in the setting of 75
21 elevated cardiac filling pressures, with evidence of increased sympathetic tone (eg, tachy- 76
22 cardia, peripheral vasoconstriction), and exclusion of other causes of shock as the primary 77
23 problem (particularly cardiogenic shock). The hemodynamic features of tamponade are 78
24 79
revealed by considering the effects of pericardial constraint. Pulsus paradoxus and loss of the
25 80
normal “y” descent of a jugular venous pressure waveform may be appreciated on clinical
26 81
examination. When a pulmonary artery catheter is placed, equalization of diastolic pressures
27 82
across all chambers is observed. Echocardiographic examination confirms the size, location,
28 83
29 and other characteristics of the causal pericardial collection. Several echocardiographic features
84
30 support the hemodynamic diagnosis of tamponade, including early diastolic collapse of the right 85
31 ventricle, late diastolic collapse of the right atrium, respiratory variation in mitral valve inflow 86
32 (akin to pulsus paradoxus), and decreased early filling (E wave) of mitral valve inflow (related to 87
33 loss of the y descent). Echocardiographic examination then supports decisions about the early 88
34 treatment and drainage of the tamponading effusion. CHEST 2017; -(-):--- 89
35 90
KEY WORDS: cardiac tamponade; diastole; effusion; goal-directed echocardiography; pericardium Q4
36 91
37 92
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Cardiac tamponade occurs when distributed develop is critical, as the fibrous
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or localized intrapericardial collections (and pericardium is acutely noncompliant but
40 95
41
occasionally extrapericardial factors) raise chronically can adapt to accommodate very 96
42 intrapericardial pressure or locally constrain large volumes of fluid without 97
43 cardiac filling sufficiently to impact hemodynamic effect. The principal clinical 98
44 hemodynamics. Cardiac tamponade is manifestations of cardiac tamponade are 99
45 classically considered “obstructive shock,”1 reduced stroke volume, elevated filling 100
46 although physiologically it involves pressures, and attendant compensatory 101
47 restriction of cardiac chamber filling. The changes associated with increased 102
48 rate at which intrapericardial collections sympathetic tone (eg, tachycardia and 103
49 104
50 105
51 ABBREVIATIONS: CVP = central venous pressure; SHOCK = septic, CORRESPONDENCE TO: Keith R. Walley, MD, Centre for Heart Lung
106
52 hypovolemic, obstructive, cardiac Innovation, 1081 Burrard St, Vancouver, BC, Canada, V6Z 1Y6; 107
53 AFFILIATIONS: From the Division of Cardiovascular Surgery (Dr e-mail: keith.walley@hli.ubc.ca 108
54 Kearns), the Division of Critical Care Medicine (Dr Walley), and the Copyright Ó 2017 American College of Chest Physicians. Published by 109
Centre for Heart Lung Innovation (Drs Kearns and Walley), University Elsevier Inc. All rights reserved.
55 Q2 Q3 of British Columbia, Vancouver, BC, Canada. 110
DOI: https://doi.org/10.1016/j.chest.2017.11.003

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111 increased systemic vascular resistance). These TABLE 1 ] Causes of Pericardial Effusion or Increased 166
112 manifestations are not specific for cardiac tamponade2,3 Juxtacardiac Pressures, and Tamponade 167
113 168
and can be further complicated in ICU settings, in Increased pericardial pressures
114 169
which multiple cardiac and noncardiac causes may Hemopericardium
115 170
account for the observed physiological abnormalities, Aortic dissection (including traumatic)
116 171
and causes of shock can overlap. Furthermore, patients Ventricular rupture (most commonly post-MI)
117 172
118
in the ICU are frequently mechanically ventilated, Postthoracotomy/pericardiotomy 173
119 receiving vasoactive medications, and occasionally Postcoronary intervention, biopsy, pacemaker 174
120 supported by circulatory-assist devices. These factors placement 175
121 also contribute to difficulty in interpreting Post-transcatheter aortic valve replacement 176
122 echocardiographic findings associated with cardiac Post-myocardial infarction, post-cardiotomy syndrome 177
123 tamponade.4 Nevertheless, cardiac tamponade is (Dressler syndrome) 178
124 primarily a clinical diagnosis, and clinicians must be Malignant effusion 179
125 familiar with its hemodynamic and echocardiographic Postradiation 180
126 181
features. Prompt diagnosis and treatment are essential Renal failure
127 182
to improving patient outcomes.5 Inflammatory diseases (eg, systemic lupus
128 erythematosus, rheumatoid arthritis, mixed 183
129 This review focuses on the early clinical examination, connective tissue disease) 184
130 which raises the possibility of cardiac tamponade, and Infection (eg, viral pericarditis, TB, purulent) 185
131 then the hemodynamic and echocardiographic 186
Hypothyroidism
132 diagnostic features, based on an understanding of 187
Idiopathic pericardial effusion
133 188
the underlying pathophysiological characteristics. Pneumopericardium (tamponade almost exclusive to
134 189
The list of conditions that may lead to cardiac pediatric patients)
135 190
tamponade is long (Table 1) and is touched on Extrapericardial increase in pressure
136 191
137
only peripherally. Pleural effusion 192
138 Mechanical ventilation 193
139 Tension pneumothorax 194
140
Clinical Findings of Cardiac Tamponade 195
Increased intraabdominal pressure
141 Rapid Bedside Assessment/Clinical Suspicion 196
142 197
Timely recognition of obstructive shock due to cardiac
143 198
144
tamponade and exclusion of other causes of shock is Physical Examination Findings 199
145
Q5 facilitated by stepping through the “SHOCK” mnemonic 200
First, a relevant history pointing toward an underlying
146 at the bedside.6 Septic (S) or distributive shock is 201
cause (Table 1) can be invaluable. In view of the
147 distinguished from other forms of shock by evidence of 202
preceding rapid bedside assessment, a patient with
148 increased cardiac output—warm shock rather than cold. 203
hemodynamically significant cardiac tamponade will
149 Hypovolemic (H) shock is then separated from the 204
classically display physical examination findings
150 remaining forms of shock by evidence of low cardiac 205
151
consistent with low cardiac output and stroke volume 206
filling pressures (jugular venous pressure, central venous
152 with high right-sided (venous) filling pressures and 207
pressure [CVP], tissue turgor, history of volume loss)
153 compensatory increased sympathetic tone. Evidence of a 208
vs high cardiac filling pressures associated with
154 low cardiac output, and hence a low stroke volume, 209
obstructive (O) and cardiogenic (C) shock. Obstructive
155 include a low mean arterial pressure and a low pulse 210
shock is then distinguished from cardiogenic shock by
156 pressure, which also manifests as a “thready pulse” on 211
157
evidence that the lungs are clear on physical 212
palpation. Other features include central and peripheral
158 examination and chest radiography.7 Pulmonary 213
cyanosis, delayed capillary refill, and mottled and cool
159 embolism, pneumothorax, and cardiac tamponade are 214
skin. Evidence of an increase in sympathetic tone
160 the most common causes of obstructive shock, so the 215
includes tachycardia, anxiety, diaphoresis, and poor
161 physical examination next focuses on distinguishing 216
peripheral perfusion.
162 these causes. Using this approach, the possibility of 217
163 cardiac tamponade can be recognized quickly at the During inspiration, increased filling of the right-sided 218
164 bedside of the hypotensive or hemodynamically chambers can further reduce the limited space within 219
165 220
unstable patient. the pericardium so that the left-sided chambers are

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221 further compressed.8 This results in decreased stroke inflammation may produce tamponade with small 276
222 volume so that during spontaneous inspiration, pulse amounts of fluid. 277
223 278
pressure and mean arterial pressure both decrease with a
224 279
marked decreased in systolic arterial pressure. Clinically, Pathophysiology of Cardiac Tamponade
225 280
this is measured as pulsus paradoxus, which is a cardinal
226 The Cardiac Cycle 281
clinical feature of hemodynamically significant cardiac
227 282
228
tamponade. A decrease in systolic pressure > 10 mm Hg The cardiac cycle starts with isovolumic ventricular 283
229 during inspiration is considered clinically significant.9 contraction (Fig 1A). When ventricular pressure exceeds 284
230 Jugular venous pressure is elevated (> 3 cm above the pulmonary (right side of the heart) or aortic pressure 285
231 sternal angle) or greatly elevated (distending facial and (left side of the heart), ventricular ejection begins. 286
232 scalp veins) in hemodynamically significant cardiac Ventricular volume decreases due to ejection and ends 287
233 tamponade. Kussmaul’s sign—an increase in CVP with when the ventricle approaches the end-systolic pressure- 288
234 inspiration—can also be observed. volume relationship (Fig 1A). Ventricular pressure then 289
235 relaxes exponentially, with no change in volume until 290
236 Precordial palpation may reveal a lack of palpable 291
the atrioventricular valves open14 (Fig 1A). This is
237 cardiac impulses, and heart sounds may be indistinct. A 292
followed by diastolic filling along a diastolic pressure-
238 pericardial friction rub is common in inflammatory 293
volume relationship (Figs 1A, 1B), which is the primary
239 effusions10 but may be lacking when the pericardial 294
240
issue during cardiac tamponade. 295
effusion is large. In drawing a distinction between
241 cardiac tamponade and left ventricular heart failure, 296
Diastolic Filling Phase
242 clear breath sounds point toward tamponade, whereas 297
243 The ventricle fills during diastole along a compliant 298
dependent crackles suggest heart failure.7
244 pressure-volume relationship (Fig 1B). The diastolic 299
245 pressure-volume relationship is approximately 300
Electrocardiographic Findings
246 exponential in shape but starts at negative 301
247 If the cause of the pericardial effusion is acute intraventricular pressure (diastolic suction) so that at 302
248 pericarditis, elevation of ST segments may be observed low diastolic volumes, the ventricle fills easily (Fig 2, Q6 303
249 diffusely on electrocardiography, with reciprocal ST 304
top). As the ventricle fills, it becomes progressively less
250 depression in aVR. When ST segments are elevated, the 305
compliant (stiffer).15 At very high volumes, the ventricle
251 possibility of myocardial infarction must still be 306
is very noncompliant, primarily due to pericardial
252 considered. Low voltages (< 0.5 mV in limb leads) may 307
253
constraint15 (Fig 1B). As a result, most ventricular filling 308
be observed as the effusion size increases.11 In large normally occurs early in diastole (E wave of mitral valve
254 309
effusions, T-wave inversions may occur. Electrical inflow) (Fig 2, bottom) with a final component due to
255 310
alternans may be seen with large effusions due to cardiac atrial contraction (A wave of mitral valve inflow) (Fig 2,
256 311
257
motion in a fluid-filled pericardial sac and frequently is bottom). 312
258 associated with hemodynamically significant 313
tamponade.12 Ventilation impacts diastolic filling because pleural
259 314
260
pressure swings are within the range of diastolic filling 315
261 Chest Radiography pressures and therefore contribute substantially to 316
262 transmural atrial and ventricular pressures. During 317
With large pericardial effusions (typically > 200 mL) the
263 normal spontaneous breathing, right ventricular filling is 318
cardiopericardial silhouette is enlarged on chest
264 increased on inspiration by the reduction in 319
radiography. The pericardium does not extend very far
265 intrathoracic pressures relative to extrathoracic 320
past the cardiac chambers, so the cardiopericardial
266 pressures. In addition, descent of the diaphragm 321
267
silhouette tapers rapidly toward the great vessels. A 322
increases intraabdominal pressure, providing an added
268 pericardial fat stripe, left-sided pleural effusion, and an 323
pressure gradient driving right atrial and ventricular
269 increase in transverse cardiac diameter are specific but 324
filling.
270 not sensitive.13 Clear lung fields on chest radiography 325
271 point toward obstructive shock, whereas cardiogenic When pericardial pressure increases, the diastolic 326
272 pulmonary edema suggests left ventricular heart failure. pressure-volume relationship shifts upward so that 327
273 The chest radiographic findings are highly dependent on greater absolute right ventricular filling pressure is 328
274 the time course. Malignant effusions can be very large required to maintain the same transmural ventricular 329
275 330
with only a small hemodynamic effect, whereas acute filling pressure and, hence, maintain end-diastolic

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331 volume16,17 (Fig 1C). In health, the pericardium 386
A
332 contributes substantially to the shape and stiffness of the 387
333 150 388
ESPVR diastolic ventricle,16,17 particularly limiting maximal
334 389
ventricular volume (Fig 1B). However, pericardial fluid
335 390
LV Pressure

2 adds pressure throughout diastole (Fig 1C).

336 100 391
Consequently, the most highly impacted phase is early
337 392
338 Diastolic diastolic filling (Fig 2) due to loss of very low, and even 393
3 1
339 50
PVR negative, early diastolic intraventricular pressures. The 394
340 chest wall also contributes pressure throughout 395
341 4
diastole.17 Positive airway pressures are transmitted 396
342 0 across the lungs to add to pericardial pressures.18 Unlike 397
343 0 50 100 normal pericardial constraint (which limits late 398
344 ventricular filling), these contributions to pericardial 399
345 B 400
25 pressure preferentially impact early diastolic filling
346 401
(decreased E wave of mitral valve inflow) (Fig 2,
347 20 402
Total Diastolic bottom).
348 403
PVR
LV Pressure

349 15 During tamponade, the heart is operating on the steep 404

350 part of the diastolic filling curve so that there is a large 405
10 Ventricle
351 change in pressure for a change in volume. The actual 406
352 Diastolic "suction": 407
5 big E wave
change in transmural chamber pressures with
353 408
inspiration will be highly dependent on the pressure in
354 0 409
the upstream reservoir (ie, the abdomen). In a chronic
355 0 50 100 410
condition with prolonged elevation of central pressures,
356 –5 411
Pericardium that reservoir will be charged and provides a larger force
357 412
358 to drive volume back to the heart. High transpulmonary 413
C pressures, due to mechanical ventilation or high
359 25 414
360 Total Diastolic respiratory effort, may increase right ventricular 415
20 No early diastolic PVR
361 gradiant: afterload and, consequently, chamber volumes. This 416
362 (loss of E wave) further shifts the heart to the steeper part of its diastolic 417
LV Pressure

15
363 filling curve. 418
364 10 419
365 Ventricle:
After Cardiac Surgery/Intervention 420
366 (unchanged) 421
5 Pericardium:
Postprocedure pericardial bleeding may form a clot,
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367 (shifted up) 422

368 0 typically posterior due to gravity, which compresses the 423
0 50 100 atria or ventricles, which is often referred to as
369 424
370
–5 LV Volume “tamponade” because it shares the clinical features of 425
371 Figure 1 – Ventricular pressure-volume relationships. Pressure refers to obstructive shock. We highlight this condition because 426
372 transmural pressure. In tamponade, the external pressure is raised so many of the classic tamponade signs are not present and 427
that transmural pressure can decrease even though the absolute pressure
373 within the cardiac chamber is high as indicated, for example, by elevated the diagnosis is missed. For example, transthoracic 428
374 central venous pressure (CVP), which is measured with respect to echocardiograms may not adequately visualize the 429
375 atmospheric pressure. A, A cardiac cycle follows a pressure-volume loop 430
(1,2,3,4). During isovolumic systole (1), pressure rises with no change in posterior clot and the y descent may persist with
376 volume until ventricular pressure exceeds aortic pressure. The ventricle 431
localized clot. It is critical that clinicians remain aware of
377 then ejects volume (2) until the end of systole when the pressure-volume 432
loop touches the end-systolic pressure-volume relationship. Intraven- this challenge when diagnosing tamponade after cardiac
378 433
379
tricular pressure falls exponentially during isovolumic relaxation (3). surgery or an intervention. In the appropriate setting, 434
Diastolic filling then occurs (4), normally at low pressures along a dia-
380 Q13 stolic pressure-volume relationship (PVR). B, The total diastolic PVR is
such as a postoperative patient who is bleeding after 435
381 the sum of the ventricular PVR and the pericardial PVR. The latter cardiac surgery and has a rising CVP, rising heart rate, 436
contributes very little to the total diastolic PVR until pericardial volume
382 approaches its maximum value and then the pericardial PVR becomes 437
383 very steep. Therefore, in health, the pericardium does not limit early PVR early in systole eliminates the large pressure gradient so that early 438
384 diastolic filling (big E wave on mitral inflow velocity) but does provide a diastolic filling is greatly reduced (loss of E-wave height on Doppler 439
fixed upper volume limit to the diastolic ventricle. C, Pericardial fluid echocardiography). ESPVR ¼ end-systolic pressure-volume relationship;
385 440
applies pressure throughout diastole. The elevation in the total diastolic LV ¼ left ventricular; PVR ¼ pressure-volume relationship.

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441 due to descent of the diaphragm, adding to the pressure 496
20 20
442 driving venous return. If the volume of blood 497
PLV, PLA

443 498
mm Hg
transmitted from abdominal venous capacitance cannot
444 10 10 499
be accommodated by the diastolic right atrium, right
445 500
atrial pressure will increase. This increase may exceed
446 0 0 501
the inspiratory decrease in intrathoracic pressure, so the
447 Diastolic suction 502
448
Early diastolic filling
no y descent
net result is an increase in right atrial and jugular venous 503
449 10 10 pressure during inspiration. Particularly in cases in 504
mm Hg

a c which a degree of pericardial constriction is present,

CVP

450 y descent x
505
451 0 0 Kussmaul’s sign may be observed. This effect is 506
452 E analogous to the hepatojugular reflux or 507
MV inflow
velocity

453 abdominojugular reflux in which increased venous 508

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454 A E A
return cannot be accommodated by the heart (in this 509
455 case due to decreased diastolic compliance), so jugular 510
456 511
Normal Tamponade venous pressure rises.
457 512
Figure 2 – Left ventricular pressure, central venous pressure (CVP), and
458 Pulmonary Artery (Swan-Ganz) Catheter Pressure 513
mitral valve inflow waveforms. Normally (left hand panels), left ven-
459 tricular pressure (PLV) falls in early diastole to very low values (even Waveforms 514
460 negative values), which promotes rapid early diastolic filling from the left 515
atrium (left atrial pressure [PLA]) and results in the y descent of left Pulmonary artery catheters are used infrequently
461 516
atrial pressure and CVP. This early ventricular filling generates the compared with several decades ago. Nevertheless, in
462 prominent E wave when mitral valve inflow velocity is measured using 517
463 Doppler echocardiography. During tamponade (right hand panels), PLV some instances, such as postcardiac surgery, a 518
is high throughout diastole, so early diastolic filling is particularly pulmonary artery catheter may be in place, or
464 519
impaired, resulting in the loss of the y descent in atrial pressure and CVP
465 and a reduction in the mitral valve E wave. CVP ¼ central venous occasionally a pulmonary artery catheter will be placed 520
466 pressure; MV ¼ mitral valve; PLA ¼ left atrial pressure; PLV ¼ left to help diagnose hemodynamically significant cardiac 521
Q11 ventricular pressure.
467 tamponade. When a significant volume of pericardial 522
468 fluid is present, elevated pericardial pressure is applied 523
469 and falling blood pressure, the diagnosis is clear and equally to all cardiac chambers. During diastole, this 524
470 does not require a delay for diagnostic imaging before elevated pericardial pressure can be the dominant 525
471 immediate surgical intervention—again illustrating that 526
component so that all diastolic chambers have equal
472 527
cardiac tamponade is a clinical diagnosis. pressures to within several mm Hg. Pulmonary artery
473 528
diastolic pressure approximates pulmonary capillary
474 529
475
wedge pressure, which, in turn, approximates left and 530
Hemodynamic Features right atrial pressure.19 Therefore, there is equalization of
476 531
477 Central Venous Pressure all of the cardiac and pulmonary artery diastolic 532
478 pressures. Indeed, even the waveform configurations 533
Pericardial pressure is applied throughout diastole and
479 track each other during diastole. 534
systole. Therefore, early diastolic filling, which occurs at
480 535
481
the lowest atrial pressures, is disproportionately Many of the preceding features are also present with 536
482 diminished. Because early diastolic filling is impaired in hemodynamically significant pulmonary embolism. 537
483 cardiac tamponade, the y descent of the jugular venous Although evidence of venous stasis, marked arterial 538
484 or CVP waveform is diminished or lacking (Fig 2, hypoxemia, and an increased shunt fraction may help 539
485 middle) in contrast to constrictive physiology, in which point toward pulmonary embolism, the distinction is 540
486 ventricular filling is similarly limited, but the y descent is often challenging at the bedside. Therefore, urgent 541
487 prominent. Likewise, the rapid increase in early diastolic echocardiographic examination, leading to an accurate 542
488 pressure in atria and ventricles due to early diastolic diagnosis, can be lifesaving. 543
489 544
filling is reduced.
490 545
491 Kussmaul’s sign, which is an increase in CVP with Echocardiographic Features 546
492 inspiration, is more likely to be observed with The echocardiographic findings associated with cardiac 547
493 constrictive pericarditis but can be observed with cardiac tamponade provide diagnostic value in settings in which 548
494 tamponade. Although intrathoracic pressure decreases the likelihood of cardiac tamponade is high (eg, 549
495 550
during inspiration, intraabdominal pressure increases decreased cardiac output/stroke volume, venous

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551 congestion, tachycardia, and the presence of a Other key echocardiographic findings associated with 606
552 pericardial effusion).20 Echocardiographic findings can cardiac tamponade that can be identified with a goal- 607
553 608
be nondiagnostic for cardiac tamponade in certain directed bedside examination include diastolic collapse
554 609
settings such as postcardiac surgery because the of the right-sided heart chambers and vena caval
555 610
tamponading collection may be a clot behind the right engorgement.31 These findings are discussed in the
556 611
atrium that is poorly visualized yet hemodynamically following sections.
557 612
558
significant.21 Also, predictive echocardiographic features 613
559 of cardiac tamponade, such as diastolic atrial collapse, Features on a Comprehensive Echocardiographic 614
560 can sometimes be found in nontamponade settings such Examination 615
561 as hypovolemia in which diastolic atrial pressure drops When clinical examination raises the possibility of 616
562 to less than the surrounding pericardial pressure.22,23 cardiac tamponade and goal-directed bedside 617
563 Definitive diagnosis of cardiac tamponade can be echocardiography demonstrates a substantial pericardial 618
564 particularly challenging in critically ill patients receiving effusion, a comprehensive echocardiographic 619
565 advanced forms of life support, including extracorporeal 620
examination yields additional information that helps
566 621
membrane oxygenation.24 characterize the pericardial pathologic condition.32
567 622
568 Two-dimensional echocardiography: The diagnosis of 623
Readily Available Data From a Goal-directed
569
Bedside Examination pericardial effusion was one of the first indications for 624
570 echocardiography,33 which is currently the modality of 625
571 When clinical suspicion of cardiac tamponade is raised 626
choice for assessing pericardial effusions. Right-sided
572 by a rapid clinical bedside assessment (as described 627
heart findings are most predictive of cardiac tamponade,
573 earlier), a goal-directed bedside echocardiographic 628
largely because of the right side of the heart’s greater
574 Q7 examination (also termed a FOCUS examination) is 629
compliance relative to the left side of the heart. Right-
575 often readily available and is a fundamentally important 630
576
sided pressures are lower and right-sided heart 631
supplement to the physical examination findings.6,25 In
577 chambers become visibly impacted at earlier stages of 632
addition to pericardial effusion, relevant pathologic
578 hemodynamic significance.20 633
conditions to consider at a bedside examination include
579 634
pulmonary embolism, ventricular failure, acute valvular Early diastolic collapse of the right ventricle is a specific
580 635
dysfunction, aortic dissection, complications related to finding for cardiac tamponade34 (Fig 3). With
581 636
582
recent cardiac interventions, and hypovolemia.26,27 increasing intrapericardial pressure, compression may 637
583 progress from involving primarily the right ventricle 638
In the ICU, and particularly in supine patients receiving
584 outflow to its basal portion. Late diastolic collapse, or 639
positive pressure ventilation, presence of a pericardial
585 invagination, of the right atrium is a sensitive finding of 640
effusion is often best demonstrated using a subcostal
586 cardiac tamponade (Fig 4). The specificity and 641
view. Separation of pericardial layers can be appreciated
587 predictive value of late diastolic right atrial collapse can 642
588
with as little as 15 to 35 mL of accumulated fluid.28 643
be increased using the right atrial inversion time index,
589 Although the absolute volume of pericardial effusion 644
which quantitates the fraction of the cardiac cycle in
590 does not dictate its hemodynamic impact, effusion size 645
which diastolic collapse occurs.35,36 In general, if right
591 and volume can be correlated rapidly using its maximal 646
atrial collapse persists for one-third or more of the
592 dimension in diastole. Furthermore, documentation of 647
cardiac cycle, it is very specific for cardiac tamponade.26
593 size allows for serial comparisons. Effusions < 10 mm 648
594 are considered small and generally represent volumes of Other morphologic features suggestive of cardiac 649
595 300 mL or less. Effusions 10 to 20 mm in dimension are tamponade include inferior vena caval dilation,37 with 650
596 moderate in size and can range from 400 to 600 mL, and absence of normal inspiratory collapse and abnormal 651
597 652
effusions > 20 mm, particularly if circumferential, are septal motion. Inferior vena caval dilation is sensitive
598 653
large and are often associated with volumes > 700 mL but not specific for cardiac tamponade,37 and abnormal
599 654
and tamponade.26,29,30 As previously stated, rapid septal motion (right-to-left shift during diastole)
600 655
601
accumulation of even a small pericardial effusion, as in contributes to pulsus paradoxus. A swinging heart may 656
602 an acute ventricular rupture, can cause tamponade be seen in the presence of large effusions, which is the 657
603 physiology because the pericardium is not acutely very basis for the electrocardiographic finding of electrical 658
604 distensible. alternans. Isolated left atrial or left ventricular 659
605 660

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661 716
662 717
663 718
664 719
665 720
666 721
667 722
668 723
669 724
670 725
671 726
672 727
673 728
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674 729
675 730
676 731
677 732
Figure 3 – Early diastolic collapse of the right ventricle. A, An echocardiographic parasternal long-axis image of the heart at end systole within a very
678 large pericardial effusion. B, Early in diastole, pericardial pressure exceeds right ventricular pressure, so transmural pressure results in invagination of 733
679 the right ventricular free wall (white arrow). 734
680 735
681 736
compression may be seen with localized compression In healthy patients, there is little respiratory variation in
682 737
or in the presence of severe pulmonary mitral valve inflow. In spontaneously breathing patients
683 738
hypertension.38,39 with cardiac tamponade, early diastolic filling is
684 739
685
decreased.41 Inspiration results in prolonged isovolumic 740
686
Doppler echocardiography: This mode of relaxation time, delayed mitral valve opening, decreased 741
687 echocardiography requires more advanced skill but is mitral E-wave velocity, and reduced left ventricular 742
688 also generally more sensitive in identifying compressive filling.38,42 On expiration, the reverse occurs. Tricuspid 743
689 hemodynamics than two-dimensional valve inflow velocities also vary with respiration, 744
690 echocardiography.40 Doppler features of cardiac increasing with spontaneous inspiration and decreasing 745
691 tamponade depend on complex phasic heart-lung on expiration. In general, approximately 30% reduction 746
692 interactions as well as series and parallel in inspiratory mitral peak E-wave velocity is considered 747
693 interdependence of the ventricles in the setting of diagnostic of cardiac tamponade,42 whereas an 748
694 749
intrapericardial constraint.9 inspiratory increase in tricuspid valve peak E-wave
695 750
696 751
697 752
698 753
699 754
700 755
701 756
702 757
703 758
704 759
705 760
706 761
707 762
708 763
709 764
710 765
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711 766
712 767
713 768
714 769
Figure 4 – Late diastolic right atrial collapse. A, An echocardiographic apical four-chamber image of the heart early in diastole shows a full right atrium
715 770
(white arrow). B, For the final one-third of diastole, invagination of the right atrium occurs (white arrow).

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771 velocity > 40% to 50% is also consistent with cardiac Cardiogenic shock: In this condition, as in 826
772 tamponade.40,41,43 These features distinguish tamponade hypovolemia, decreased systolic contractility will Q8 827
773 828
physiology from constrictive physiology. accentuate the clinical features of cardiac tamponade
774 829
because impaired systolic ejection will inadequately
775 Doppler interrogation of the pulmonary veins may 830
empty cardiac chambers, leaving little space for diastolic
776 reveal inspiratory decreases and expiratory increases in 831
filling on the subsequent cardiac cycle.
777 diastolic forward flow. Furthermore, diastolic flow 832
778 reversal of the hepatic veins is also characteristic of Septic shock: This condition is associated with 833
779 cardiac tamponade.40 The superior vena cava is intravascular hypovolemia due, in part, to increased 834
780 835
intrathoracic and is less impacted by phasic respiratory vascular endothelial permeability. Septic shock is also
781 836
variation. frequently accompanied by decreased systolic
782 837
contractility.47 Both of these features increase the
783 The preceding Doppler findings have been 838
hemodynamic impact of pericardial constraint. Low
784 demonstrated in spontaneously breathing patients. In 839
785
systemic vascular resistance is typically accompanied by 840
patients receiving positive-pressure ventilation, the
786 increased cardiac output and stroke volume is 841
opposite findings may be seen or potentially rendered Q9
787 resuscitated septic shock. If this increase in stroke 842
inaccurate.
788 volume is limited by even a mild degree of pericardial 843
789 Three-dimensional echocardiography: In selected cases constraint, BP will fall further. Therefore, a relatively 844
790 in which patient stability permits detailed small pericardial effusion that would otherwise be 845
791 echocardiographic examination, three-dimensional unlikely to be hemodynamically significant can have a 846
792 echocardiography can provide greater anatomic major hemodynamic effect. 847
793 848
delineation of effusions in cardiac tamponade,26
794 Atrial fibrillation: In cardiac tamponade, early diastolic 849
including the nature of strands within the effusion and
795 filling is impaired, so substantial diastolic filling occurs 850
their relation to adjacent structures.44 Abnormal septal
796 during atrial contraction. Therefore, atrial fibrillation 851
motion, caval dilation, and phasic respiratory variation
797 and atrial flutter can greatly impair cardiac filling. New 852
in transvalvular flow velocities can also be noted using
798 onset of atrial fibrillation precipitated by pericardial 853
799 three-dimensional echocardiography.45 854
disease can have dramatic adverse consequences.
800 855
Transesophageal echocardiography: Frequently,
801 856
transthoracic echocardiography proves inadequate in
802 857
the ICU context because of mechanical ventilation, Treatment in the Emergency Setting
803 858
804
patient body habitus, presence of drains and surgical Cardiac tamponade is particularly important, because in 859
805 dressings, or lung pathologic conditions (eg, most patients many or all of the preceding clinical 860
806 emphysema). Furthermore, the ability to visualize features can be treated by prompt surgical intervention. 861
807 localized compressive thrombus after cardiac surgery Emergent drainage of the pericardial space can be 862
808 using transthoracic echocardiography is often impaired. accomplished by placing a catheter drain or by surgical 863
809 Transesophageal echocardiography is then indicated to decompression, which are important procedures that 864
810 aid in the diagnosis and treatment of cardiac exceed the scope of this review. While preparing for 865
811 tamponade.46 these procedures, a number of temporizing measures 866
812 867
can be considered. Cardiac tamponade is diastolic
813 Clinical Scenarios That Modify Tamponade and 868
dysfunction (Fig 2). External pressure on the heart at or
814 Interpretation of Echocardiographic Findings 869
greater than normally low diastolic pressures impairs
815 870
Hypovolemia: This condition, which is manifested as filling of cardiac chambers so that stroke volume and,
816 871
817
low peripheral venous pressure, will greatly accentuate hence, cardiac output is decreased. This yields three 872
818 the clinical features of cardiac tamponade. It the important insights. First, careful additional fluid 873
819 setting of cardiac tamponade, right atrial pressure is administration is an important temporizing measure in 874
820 increased through compression of the heart by some cases. Rapid fluid resuscitation reverses any 875
821 surrounding structures. Therefore, the pressure contribution of hypovolemia and maximizes diastolic 876
822 gradient driving blood flow back to the heart is filling. However, when no further diastolic ventricular 877
823 very low during hypovolemia so that decreased filling is possible due to pericardial constraint, further 878
824 venous return, which equals cardiac output, is increases in intravascular volume and pressure will 879
825 880
accentuated. disproportionately distend the right atrium and

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881 ventricle. The intraventricular septum shifts from right Acknowledgments 936
882 to left, resulting in decreased left ventricular Financial/nonfinancial disclosures: The authors have reported to 937
883 CHEST the following: K. R. W. is a shareholder and Director of Cyon 938
end-diastolic volume, so stroke volume decreases
884 Therapeutics. He is an inventor on a patent owned by the University of 939
further. The presence of Kussmaul’s sign may be an British Columbia and licensed to Cyon Therapeutics. None declared
885 (M. J. K.). 940
indicator that the limit of pericardial constraint has been
886 941
exceeded.
887 References Q10 942
888 Second, because the problem of cardiac tamponade is 1. Astiz ME. Pathophysiology and classification of shock states. In: 943
889 diastolic, inotropic agents are generally ineffective. Vincent JL, ed. Textbook of Critical Care. Philadelphia PA: Saunders; 944
2011:677-683.
890 945
However, if decreased systolic function is present 2. Fowler NO. Cardiac tamponade. A clinical or an echocardiographic
891 946
concurrently, there is a role for increasing inotropy. diagnosis? Circulation. 1993;87:1738-1741.
892 947
More important, when diastolic filling is limited by 3. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349:
893 684-690. 948
894
cardiac tamponade (or another pathologic condition), 4. Romero-Bermejo FJ, Ruiz-Bailen M, Guerrero-De-Mier M, et al. 949
895 cardiac output becomes highly heart rate-dependent Echocardiographic hemodynamic monitoring in the critically ill 950
patient. Curr Cardiol Rev. 2011;7:146-156.
896 (because maximum stroke volume is fixed). Thus, if the 951
5. Ristic AD, Imazio M, Adler Y, et al. Triage strategy for urgent
897 heart rate is unusually low, increasing heart rate and management of cardiac tamponade: a position statement of the 952
898 reversing decreased systolic contractility using a European Society of Cardiology Working Group on Myocardial and 953
Pericardial Diseases. Eur Heart J. 2014;35:2279-2284.
899 combined inotropic agent/vasopressor (to prevent 954
6. Walley PE, Walley KR, Goodgame B, et al. A practical approach to
900 unopposed arterial and venous vasodilation) may be 955
goal-directed echocardiography in the critical care setting. Crit Care.
901 part of the acute therapeutic plan. 2014;18:681. 956
902 7. Spodick DH. Low atrial natriuretic factor levels and absent 957
903 Third, it is essential to identify and rapidly reverse other pulmonary edema in pericardial compression of the heart. Am J 958
Cardiol. 1989;63:1271-1272.
904 contributing factors leading to elevated external pressure 959
8. Settle HP, Adolph RJ, Fowler NO, et al. Echocardiographic study of
905 compressing diastolic cardiac chambers. Although cardiac tamponade. Circulation. 1977;56:951-959. 960
906 pericardial fluid is generally the primary cause, it is also 9. Hamzaoui O, Monnet X, Teboul JL. Pulsus paradoxus. Eur Respir J. 961
907 important to consider the contribution from other 2013;42:1696-1705. 962
908 surrounding structures. Pleural air (pneumothorax) or 10. Spodick DH. Pericardial rub. Prospective, multiple observer 963
investigation of pericardial friction in 100 patients. Am J Cardiol.
909 964
very large fluid collections (pleural effusion or 1975;35:357-362.
910 965
hemothorax) are important contributors or primary 11. Bruch C, Schmermund A, Dagres N, et al. Changes in QRS voltage in
911 cardiac tamponade and pericardial effusion: reversibility after 966
causes. Elevated pulmonary pressures in mechanically pericardiocentesis and after anti-inflammatory drug treatment. J Am
912 967
ventilated patients contribute. Increased intraabdominal Coll Cardiol. 2001;38:219-226.
913 968
pressure resulting in an elevated diaphragm can 12. Goyal M, Woods KM, Atwood JE. Electrical alternans: a sign, not a
914 diagnosis. South Med J. 2013;106:485-489. 969
915 contribute. Altering ventilation strategies reduces mean 13. Eisenberg MJ, Dunn MM, Kanth N, et al. Diagnostic value of chest 970
916 airway pressure. Drainage of pleural air or fluid, or both, radiography for pericardial effusion. J Am Coll Cardiol. 1993;22: 971
588-593.
917 reduces the contribution of these features. Acutely 972
14. Raff GL, Glantz SA. Volume loading slows left ventricular
918 reducing the application of intraabdominal pressure to 973
isovolumic relaxation rate. Evidence of load-dependent relaxation in
919 the diaphragm and heart is sometimes as simple as the intact dog heart. Circ Res. 1981;48:813-824. 974
920 repositioning the patient. 15. Gilbert JC, Glantz SA. Determinants of left ventricular filling and of 975
921 the diastolic pressure-volume relation. Circ Res. 1989;64:827-852. 976
922 16. Kingma I, Smiseth OA, Frais MA, et al. Left ventricular external 977
constraint: relationship between pericardial, pleural and esophageal
923 Conclusions pressures during positive end-expiratory pressure and volume 978
924 loading in dogs. Ann Biomed Eng. 1987;15:331-346. 979
A structured rapid bedside assessment based on the
925 17. Tyberg JV, Misbach GA, Glantz SA, et al. A mechanism for shifts in 980
SHOCK mnemonic can identify obstructive shock. the diastolic, left ventricular, pressure-volume curve: the role of the
926 981
pericardium. Eur J Cardiol. 1978;7(suppl):163-175.
927
Hemodynamic features of cardiac tamponade are readily 982
18. Craven KD, Wood LD. Extrapericardial and esophageal pressures
928 explained by, and beautifully illustrate, the diastolic with positive end-expiratory pressure in dogs. J Appl Physiol Respir 983
929 filling phase of the cardiac cycle. Echocardiographic Environ Exerc Physiol. 1981;51:798-805. 984
930 examination, first at the bedside followed by a 19. Sharkey SW. Beyond the wedge: clinical physiology and the Swan- 985
Ganz catheter. Am J Med. 1987;83:111-122.
931 comprehensive examination, clarifies the diagnosis and 986
20. Guntheroth WG. Sensitivity and specificity of echocardiographic
932 features of the pericardial pathologic condition and, evidence of tamponade: implications for ventricular interdependence 987
933 importantly, guides treatment.46,48 However, it is and pulsus paradoxus. Pediatr Cardiol. 2007;28:358-362. 988
934 important to remember that cardiac tamponade (a 21. Pepi M, Muratori M, Barbier P, et al. Pericardial effusion after 989
cardiac surgery: incidence, site, size, and haemodynamic
935 990
hemodynamic state) is a clinical diagnosis. consequences. Br Heart J. 1994;72:327-331.

chestjournal.org 9

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991 22. Klopfenstein HS, Cogswell TL, Bernath GA, et al. Alterations in 37. Himelman RB, Kircher B, Rockey DC, et al. Inferior vena cava 1046
992 intravascular volume affect the relation between right ventricular plethora with blunted respiratory response: a sensitive 1047
diastolic collapse and the hemodynamic severity of cardiac echocardiographic sign of cardiac tamponade. J Am Coll Cardiol.
993 tamponade. J Am Coll Cardiol. 1985;6:1057-1063. 1988;12:1470-1477. 1048
994 23. Kennedy Hall M, Coffey EC, Herbst M, et al. The “5Es” of 38. Tsang TS, Oh JK, Seward JB, et al. Diagnostic value of 1049
995 emergency physician-performed focused cardiac ultrasound: a echocardiography in cardiac tamponade. Herz. 2000;25:734-740. 1050
protocol for rapid identification of effusion, ejection, equality, exit,
996 and entrance. Acad Emerg Med. 2015;22:583-593. 39. Tsang TS, Oh JK, Seward JB. Diagnosis and management of cardiac 1051
997 tamponade in the era of echocardiography. Clin Cardiol. 1999;22: 1052
24. Chung M, Shiloh AL, Carlese A. Monitoring of the adult patient on 446-452.
998 venoarterial extracorporeal membrane oxygenation. 1053
ScientificWorldJournal. 2014;2014:393258. 40. Burstow DJ, Oh JK, Bailey KR, et al. Cardiac tamponade:
999 characteristic Doppler observations. Mayo Clin Proc. 1989;64: 1054
1000 25. Beaulieu Y. Bedside echocardiography in the assessment of the 312-324. 1055
critically ill. Crit Care Med. 2007;35:S235-S249.
1001 41. Appleton CP, Hatle LK, Popp RL. Cardiac tamponade and 1056
26. Field LC, Guldan GJ 3rd, Finley AC. Echocardiography in the pericardial effusion: respiratory variation in transvalvular flow
1002 intensive care unit. Semin Cardiothorac Vasc Anesth. 2011;15:25-39. 1057
velocities studied by Doppler echocardiography. J Am Coll Cardiol.
1003 27. Ceriani E, Cogliati C. Update on bedside ultrasound diagnosis of 1988;11:1020-1030. 1058
1004 pericardial effusion. Intern Emerg Med. 2016;11:477-480. 1059
42. Klein AL, Cohen GI. Doppler echocardiographic assessment of
1005 28. McCanny P, Colreavy F. Echocardiographic approach to cardiac constrictive pericarditis, cardiac amyloidosis, and cardiac 1060
tamponade in critically ill patients. J Crit Care. 2017;39:271-277. tamponade. Cleve Clin J Med. 1992;59:278-290.
1006 1061
29. Imazio M, Adler Y. Management of pericardial effusion. Eur Heart J. 43. Klein AL, Abbara S, Agler DA, et al. American Society of
1007 2013;34:1186-1197. 1062
Echocardiography clinical recommendations for multimodality
1008 30. Maisch B, Seferovic PM, Ristic AD, et al. Guidelines on the diagnosis cardiovascular imaging of patients with pericardial disease: endorsed 1063
1009 and management of pericardial diseases executive summary; The by the Society for Cardiovascular Magnetic Resonance and Society of 1064
Task force on the diagnosis and management of pericardial diseases Cardiovascular Computed Tomography. J Am Soc Echocardiogr.
1010 2013;26:965-1012.e1015. 1065
of the European Society of Cardiology. Eur Heart J. 2004;25:587-610.
1011 1066
31. Reydel B, Spodick DH. Frequency and significance of chamber 44. D’Cruz IA, Minderman D, Dockery BK. Three-dimensional imaging
1012 collapses during cardiac tamponade. Am Heart J. 1990;119: of intrapericardial adhesions within a large pericardial effusion. Can 1067
1013 1160-1163. J Cardiol. 2009;25:366. 1068
1014 32. Adler Y, Charron P. The 2015 ESC guidelines on the diagnosis and 45. Hernandez CM, Singh P, Hage FG, et al. Live/real time three- 1069
management of pericardial diseases. Eur Heart J. 2015;36:2873-2874. dimensional transthoracic echocardiographic assessment of
1015 pericardial disease. Echocardiography. 2009;26:1250-1263. 1070
33. Feigenbaum H, Waldhausen JA, Hyde LP. Ultrasound diagnosis of
1016 pericardial effusion. JAMA. 1965;191:711-714. 1071
46. Porter TR, Shillcutt SK, Adams MS, et al. Guidelines for the use of
1017 34. Singh S, Wann LS, Schuchard GH, et al. Right ventricular and right echocardiography as a monitor for therapeutic intervention in 1072
1018 atrial collapse in patients with cardiac tamponade—a combined adults: a report from the American Society of Echocardiography. 1073
echocardiographic and hemodynamic study. Circulation. 1984;70: J Am Soc Echocardiogr. 2015;28:40-56.
1019 966-971. 1074
47. Parker MM, Shelhamer JH, Bacharach SL, et al. Profound but
1020 35. Gillam LD, Guyer DE, Gibson TC, et al. Hydrodynamic compression reversible myocardial depression in patients with septic shock. Ann 1075
1021 of the right atrium: a new echocardiographic sign of cardiac Intern Med. 1984;100:483-490. 1076
1022 tamponade. Circulation. 1983;68:294-301. 48. Tsang TS, Enriquez-Sarano M, Freeman WK, et al. Consecutive 1127 1077
1023 36. Kronzon I, Cohen ML, Winer HE. Diastolic atrial compression: a therapeutic echocardiographically guided pericardiocenteses: clinical 1078
sensitive echocardiographic sign of cardiac tamponade. J Am Coll profile, practice patterns, and outcomes spanning 21 years. Mayo
1024 Cardiol. 1983;2:770-775. Clin Proc. 2002;77:429-436. 1079
1025 1080
1026 1081
1027 1082
1028 1083
1029 1084
1030 1085
1031 1086
1032 1087
1033 1088
1034 1089
1035 1090
1036 1091
1037 1092
1038 1093
1039 1094
1040 1095
1041 1096
1042 1097
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