The new england journal of medicine

review article

current concepts

Acute Cardiac Tamponade

David H. Spodick, M.D., D.Sc.

ardiac tamponade is life-threatening, slow or rapid compres-

From the Division of Cardiovascular Med-
icine, Department of Medicine, Saint Vin-
cent Hospital–Worcester Medical Center,
Worcester, Mass.

N Engl J Med 2003;349:684-90.

Copyright © 2003 Massachusetts Medical Society.
c sion of the heart due to the pericardial accumulation of fluid, pus, blood, clots,
or gas, as a result of effusion, trauma, or rupture of the heart.1,2 Because the
causes of pericardial disease1 and thus of tamponade are diverse, clinicians must choose
the most probable diagnosis, always anticipating surprises. Thus, traumatic tampon-
ade is most apt to follow cardiac surgery, and tuberculous tamponade is relatively com-
mon in Africa but rare in the United States.
Understanding the physiological changes produced by tamponade is essential to
diagnosis and treatment.3-12 The primary abnormality is rapid or slow compression of
all cardiac chambers as a result of increasing intrapericardial pressure. The pericardial
contents first reach the limit of the pericardial reserve volume6 — the volume that
would just distend the pericardium — and the rate of expansion then increases, soon
exceeding that of pericardial stretch. Although the pericardium stretches normally over
time, at any instant it is inextensible, making the heart compete with the increased peri-
cardial contents for the fixed intrapericardial volume.6,10 As the chambers become
progressively smaller and myocardial diastolic compliance is reduced, cardiac inflow
becomes limited, ultimately equalizing mean diastolic pericardial and chamber pres-
sures.1-3 Key elements are the rate of fluid accumulation relative to pericardial stretch
and the effectiveness of compensatory mechanisms. Thus, intrapericardial hemorrhage
from wounds or cardiac rupture occurs in the context of a relatively stiff, unyielding peri-
cardium and quickly overwhelms the pericardial capacity to stretch before most com-
pensatory mechanisms can be activated, whereas in the case of a slow increase in pericar-
dial volume as a result of inflammation, 2 liters or more may accumulate before critical,
life-threatening tamponade occurs.13
The stiffness of the pericardium determines fluid increments precipitating tam-
ponade, as illustrated by characteristic pericardial pressure–volume (strain–stress) curves
(Fig. 1): there is an initial slow ascent, followed by an almost vertical rise.2 This steep rise
makes tamponade a “last-drop” phenomenon: the final increment produces critical car-
diac compression, and the first decrement during drainage produces the largest relative
decompression.
The true filling pressure is the myocardial transmural pressure, which is intracardiac
minus pericardial pressure.14 Rising pericardial pressure reduces and ultimately offsets
this transmural pressure, first for the right heart and ultimately for all chambers. On av-
erage, during inspiration and expiration, the right heart increases its filling at the expense
of the left, so that its transmural pressure transiently improves and then reverts during
expiration.1,2,14 In florid tamponade such a mechanism cannot compensate for reduced
stroke volumes, since these volumes depend on the elements that protect cardiac output
and arterial pressures, principally beta-adrenergically increased heart rate, peripheral re-
sistance and ejection fractions, and given sufficient time, expansion of the blood vol-
ume. Additional compensation provided by neurohormonal stimulation is similar to
that occurring in heart failure,15 except that the levels of atrial natriuretic peptide do

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 current concepts

not increase because the compressed myocardium

cannot stretch.16
Acute tamponade thus reflects decompensation
as patients reach the steep portion of the pressure–
volume curve (Fig. 1). Moreover, intercurrent fac-
tors can cause the decompensation of any effusion
Critical Critical
— for example, the influx of blood, effusion-expand-

Pressure
tamponade tamponade
ing osmotic effects of fragmenting intrapericardial
clots, or inflammatory stiffening of the pericardi-
um.1,17,18 Finally, although coronary blood flow is
reduced in tamponade, there is no ischemic compo- Limit of pericardial stretch

nent because coronary flow remains proportional to

the reduced work and operational requirements of
Rapid effusion Slow effusion
the heart.8
Volume over Time

clinical findings
Figure 1. Cardiac Tamponade.
Critical tamponade is a form of cardiogenic shock, Pericardial pressure–volume (or strain–stress) curves are shown in which the
volume increases slowly or rapidly over time. In the left-hand panel, rapidly in-
and the differential diagnosis may initially be elu-
creasing pericardial fluid first reaches the limit of the pericardial reserve vol-
sive. Since most symptoms are nonspecific, tam- ume (the initial flat segment) and then quickly exceeds the limit of parietal
ponade must be suspected in many contexts — for pericardial stretch, causing a steep rise in pressure, which becomes even
example, in patients who have wounds of the chest steeper as smaller increments in fluid cause a disproportionate increase in
or upper abdomen and hypotension or in those who the pericardial pressure. In the right-hand panel, a slower rate of pericardial
filling takes longer to exceed the limit of pericardial stretch, because there is
have hypotension preceded by symptoms of an in-
more time for the pericardium to stretch and for compensatory mechanisms
citing pericardial disease, such as chest discomfort to become activated.
and pleuritic pain. Tachypnea and dyspnea on exer-
tion that progresses to air hunger at rest are the key
symptoms, but it may not be possible to obtain such
information from patients who are unconscious or cyanosis. Jugular venous distention is the rule, with
obtunded or who have convulsions at presentation. peripheral venous distention in the forehead, scalp,
Most patients are weak and faint at presentation and and ocular fundi unless the patient has hypovolemia.
can have vague symptoms such as anorexia, dyspha- Thus, rapid tamponade, especially acute hemoperi-
gia, and cough.1 The initial symptom may also be cardium, may produce exaggerated jugular pulsa-
one of the complications of tamponade, such as re- tions without distention, because there is insuffi-
nal failure.19 cient time for blood volume to increase. Venous
Most physical findings are equally nonspecif- waves usually lack the normal early diastolic y de-
ic.1,19 Tachycardia (a heart rate of more than 90 beats scent. In compressive pericardial disease (tampon-
per minute) is the rule. Exceptions include patients ade and constriction), venous waves are not out-
with bradycardia during uremia and patients with ward pulsations; rather, x and y collapse from a high
hypothyroidism. Contrary to common belief, a peri- standing pressure level.1
cardial rub is a frequent finding in patients with A key diagnostic finding, pulsus paradoxus21 —
inflammatory effusions.20 Heart sounds may be at- conventionally defined as an inspiratory systolic fall
tenuated owing to the insulating effects of the peri- in arterial pressure of 10 mm Hg or more during
cardial fluid and to reduced cardiac function. Al- normal breathing — is often palpable in muscular
though the precordium may seem quiet, an apical arteries. With very low cardiac output, however, a
beat is frequently palpable, and patients with preex- catheter is needed to identify pulsus paradoxus.
isting cardiomegaly or anterior and apical pericar- Other conditions causing pulsus paradoxus include
dial adhesions may have active pulsations. massive pulmonary embolism, profound hemor-
Clinically significant tamponade usually produc- rhagic shock, other forms of severe hypotension,
es absolute or relative hypotension; in rapid tam- and obstructive lung disease. Moreover, certain con-
ponade, patients are often in shock, with cool arms ditions can impede the identification of tamponade
and legs, nose, and ears and sometimes peripheral by making pulsus paradoxus undetectable (Table 1).

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 The new england journal of medicine

lines are uncommon but are highly specific for large

laboratory investigations
effusions.19
Cardiac catheterization will show equilibration of An electrocardiogram may show signs of peri-
average diastolic pressure and characteristic res- carditis, but the only quasispecific sign of tampon-
piratory reciprocation of cardiac pressures: an in- ade is electrical alternation,22 which may affect any
spiratory increase on the right and a concomitant or all23 electrocardiographic waves or only the QRS.
decrease on the left — the proximate cause of pul- If the QRS complex is affected, every other QRS com-
sus paradoxus. Except in low-pressure tamponade, plex is of smaller voltage, often with reversed po-
diastolic pressures throughout the heart are usually larity. Combined P and QRS alternation is virtually
15 to 30 mm Hg. These are similar to pressures specific for tamponade.1 In rare cases, very large ef-
present in heart failure, but for unknown reasons, fusions, even without tamponade, cause QRS alter-
tamponade does not cause alveolar pulmonary ede- nation. Echocardiography reveals its mechanism:
ma.16 Although any type of large cardiac silhouette swinging of the heart (Fig. 2).23,24 The volume of
in a patient with clear lung fields should suggest most nonhemorrhagic effusions that cause tam-
the presence of pericardial effusion, chest films may ponade is moderate to large (300 to 600 ml).
not be helpful initially, since at least 200 ml of fluid Doppler echocardiography is the principal tool
must accumulate before the cardiac silhouette is for diagnosing pericardial effusion and cardiac tam-
affected. In the lateral film, definite pericardial-fat ponade. Computed tomography (CT) and magnet-
ic resonance imaging are often less readily available
and are generally unneeded unless Doppler echo-
Table 1. Conditions Leading to the Absence of Diagnostic Pulsus Paradoxus cardiography is not feasible. In the absence of my-
in Cardiac Tamponade. ocardial disease or injury, echocardiography dem-
onstrates the usually circumferential fluid layer
Condition Consequence
and compressed chambers with high ventricular
Extreme hypotension, as in shock, May make respiration-induced ejection fractions.24 Doppler study discloses marked
and even severe tamponade pressure changes unmeasurable
respiratory variations in transvalvular flows. One
Acute left ventricular myocardial mechanism of pulsus paradoxus is visible: on inspi-
infarction with occasional —
effusion causing tamponade
ration, both the ventricular and atrial septa move
sharply leftward, reversing on expiration1; in other
Pericardial adhesions, especially over Volume changes impeded
the right heart words, each side of the heart fills at the expense of
the other, owing to the fixed intrapericardial volume.
Local (usually postsurgical) pericardial Local cardiac compression by
adhesions loculated fluid The inferior vena cava is dilated, with little or no
Pulmonary vein and left ventricular Reduced effects of respiration on
change on respiration.
diastolic pressures and left ven- right-heart filling Among echocardiographic signs, the most char-
tricular stiffness markedly exceed acteristic, although they are not entirely specific, are
those of the right ventricle*
chamber collapses, which are nearly always of the
Right ventricular hypertrophy without Causes right-sided resistance to the right atrium and ventricle. During early diastole, the
pulmonary hypertension effects of breathing
right ventricular free wall invaginates, and at end di-
Severe aortic regurgitation, with or Produces sufficient regurgitant flow astole, the right atrial wall invaginates.25 Right ven-
without severe left ventricular to damp down respiratory fluctua-
dysfunction tions tricular collapse is a less sensitive but more specific
finding for tamponade, whereas right atrial col-
Atrial septal defects Increased inspiratory venous return
balanced by shunting to the left lapse is more specific if inward movement lasts
atrium for at least 30 percent of the cardiac cycle. Right
Some cases of low-pressure Makes marked respiratory changes atrial collapse may be seen in patients with hypo-
tamponade in blood pressure diagnostically volemia who do not have tamponade. In about 25
insignificant
percent of patients, the left atrium also collapses,
and this finding is highly specific for tamponade.
* In patients with marked left ventricular hypertrophy or severe left-sided heart
failure, pericardial pressure effectively equilibrates only with right heart pres- Left ventricular collapse usually occurs under spe-
sures, a form of right ventricular tamponade, with the much less compliant cial conditions such as localized postsurgical tam-
left ventricle resisting phasically changing pericardial pressure. Under these ponade. These wall changes occur when respective
conditions, respiratory changes cannot alternately favor right- and left-sided
filling. chamber pressures temporarily fall below the peri-
cardial pressure.24,25

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 current concepts

A B
P
P

PE
PE

LV
LV

Figure 2. Swinging of the Heart with a Large Pericardial Effusion (PE), Causing Electrical Alternation and Consequent
Tamponade.
Apical four-chamber two-dimensional echocardiograms show the extremes of oscillation and the resultant effect on the
QRS complex. In Panel A, the heart swings to the right, and lead II shows a small QRS complex. In Panel B, the heart
swings to the left, and the QRS complex is larger. P denotes pericardium, and LV left ventricle.

pericardial adhesions, especially after cardiac sur-

variant forms
o f cardiac tamponade gery. Sometimes the typical hemodynamic abnor-
malities are found only in the compressed chambers
Low-pressure tamponade occurs at diastolic pres- or zones. However, loculation can also produce clas-
sures of 6 to 12 mm Hg and is virtually confined to sic tamponade, presumably by tightening the un-
patients with hypovolemia and severe systemic dis- involved pericardium; for example, loculated effu-
eases, hemorrhage, or cancer, or in patients with hy- sions after cardiac surgery may include hematomas
povolemia after diuresis.19 Patients are weak and over the right atrium and atrioventricular groove.28
generally normotensive, with dyspnea on exertion Localized right atrial tamponade may also cause
and no diagnostic pulsus paradoxus, but with char- right-to-left shunting through a patent foramen
acteristic respiratory fluctuations in transvalvular ovale or an atrial septal defect.29
diastolic Doppler flows. The low-pressure effusion After right ventricular infarction, loculated effu-
equilibrates only with right-sided diastolic pres- sion can cause selective right-heart tamponade in
sures and does so at first only during inspiration which right atrial pressure is higher than left atrial
(“inspiratory tracking”).1,3 A fluid challenge with pressure.28 The absence of pulsus paradoxus (Ta-
a liter of warm saline can evoke tamponade dy- ble 1) makes this form difficult to recognize. Effu-
namics.26 sive–constrictive pericarditis is characterized by
Hypertensive cardiac tamponade27 with all mixed clinical, imaging, and hemodynamic signs,
the classic features of tamponade, occurs at high because a constrictive epicarditis underlies the peri-
and very high arterial blood pressures (even over cardial effusion. In some patients with scarred, rig-
200 mm Hg)27 and is ascribed to excessive beta- id parietal and visceral pericardium, tamponade
adrenergic drive. Affected patients typically have can occur with relatively little accumulation of flu-
had antecedent hypertension. id. Effusive–constrictive pericarditis is revealed in
Regional cardiac tamponade19,24 occurs when these patients when drainage of pericardial fluid
any cardiac zone is compressed by loculated effu- does not cause intracardiac pressures to return to
sions, which are usually accompanied by localized normal.30,31

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 The new england journal of medicine

Recurrences, especially in patients with malig-

special problems
nant tamponade, may require balloon pericardi-
Postoperative tamponade,28 which is more frequent otomy through the use of special catheters that cre-
after valve surgery than after coronary-artery bypass ate “windows” between the pericardium and the
surgery and is more frequent with postoperative an- absorbing surface of the pleura or peritoneum.32
ticoagulant therapy, is due to trauma-induced peri- Death in patients with tamponade is usually her-
cardial effusion and bleeding. Since some degree of alded by pulseless electrical activity19: the electro-
pericarditis occurs after every cardiac operation,28 cardiogram continues to register complexes in the
and most patients have a small, seemingly benign absence of blood flow or pressure.
effusion postoperatively, it is not surprising that Medical treatment of acute cardiac tamponade,
tamponade eventually occurs in some. Postopera- including inotropic support with or without vaso-
tive myocardial stiffness, variable fluid–electrolyte dilators,17 is relatively controversial35 and is aimed
abnormalities, and hemorrhage tend to preclude at supporting compensatory mechanisms to reduce
the appearance of classic signs such as pulsus par- the elevated vascular resistance. Thus, dobutamine,
adoxus (Table 1); thus, when tamponade is suspect- administered to reverse the hypotension, is theo-
ed postoperatively, prompt imaging — particularly retically ideal.3,11,13 During tamponade, however,
Doppler echocardiography — is necessary. Late tam- endogenous inotropic stimulation of the heart is of-
ponade, occurring more than five days postopera- ten already maximal.
tively,32 must be suspected in any patient in whom The approach to medical therapy has been based
hypotension develops. Primary care physicians may on studies in animals. However, these results are
not be familiar with tamponade, and if it occurs the subject of controversy, since in short-term sur-
very late (two weeks or more) after surgery, they may gical experiments in anesthetized animals, the pres-
not suspect it. Some episodes of late hemorrhage ence of myocardial depression causes almost any
may be delayed because the rates of bleeding are rel- measure to improve function.7,12,35 Studies in in-
atively slow and intrapericardial clotting compli- tact, unanesthetized animals with indwelling in-
cates diagnosis and management. struments and euvolemia have yielded different
results that have cast doubt on the value of various
approaches, especially volume infusion.7,12,35 In-
management of acute
cardiac tamponade deed, increasing the volume may help only in pa-
tients with hypovolemia, since in patients with
The treatment of cardiac tamponade is drainage normovolemia and hypervolemia, volume infu-
of the pericardial contents, preferably by needle sion may increase intracardiac pressures as well
paracentesis19 (Fig. 3) with the use of echocardio- as heart size, which in turn increases pericardial
graphic or another type of imaging, such as fluoros- pressure, further reducing or eliminating the low
copy or CT. The needle tip is evident on imaging, transmural myocardial pressures supporting the
and imaging can thus safely be used to identify the circulation.7,12,19 Moreover, intravenous admin-
optimal point at which to penetrate the pericardi- istration of resuscitative fluid can precipitate tam-
um.33 Drainage may be performed in the catheter- ponade.36
ization laboratory when the diagnosis is uncertain An opioid mechanism contributes to the hypo-
or effusive constrictive pericarditis is possible. How- tension of cardiac tamponade; experiments in an-
ever, sudden circulatory collapse warrants the use imals show that naloxone counteracts the hypo-
of pericardiocentesis without imaging, since further tension,12 but this approach has not been used
decompensation may occur without warning. If the clinically.
heart cannot be reached by a needle or catheter, sur- Mechanical ventilation with positive airway pres-
gical drainage is required, usually through a subcos- sure should be avoided in patients with tampon-
tal incision. Surgical drainage is desirable in patients ade, because this further decreases cardiac output.19
with intrapericardial bleeding and in those with In patients with cardiac arrest and a large amount
clotted hemopericardium or thoracic conditions of pericardial fluid, external cardiac compression
that make needle drainage difficult or ineffective.34 has little or no value, because there is little room for
Subcritical uremic tamponade often responds to in- additional filling and because even if systolic pres-
tensified renal dialysis, but if this approach is un- sure rises, diastolic pressure falls and, in doing so,
successful, drainage is required. reduces coronary perfusion pressure.36

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 current concepts

pericardiocentesis
Needle drainage of pericardial fluid, whether or not
it is done on an emergency basis (e.g., in a patient
in rapidly worsening hemodynamic condition), re-
quires the clinician to select a point on the patient’s
chest or epigastrium to insert the needle. This is best
done with imaging, as already discussed, to deter-
mine which anterior landmarks, usually paraxiphoid
or apical, are closest to the fluid. The paraxiphoid
Hub of needle
approach is also most often used for pericardiocen- angled approximately
tesis that is performed without imaging.1 Common 15 degrees above skin Apical
points of access are illustrated in Figure 3. The nee- area
dle is usually inserted between the xiphoid process
and the left costal margin; in patients with tough Paraxiphoid
skin, a small nick may be made first with a scalpel. area
The needle is inserted at a 15-degree angle to bypass
the costal margin, and then its hub is depressed so
that the point is aimed toward the left shoulder. The
needle is then advanced slowly, until the pericar-
dium is pierced and fluid is aspirated. Electrocar- Figure 3. Most Common Sites of Blind and Image-Guided Insertion
diography should not be used to monitor the pa- of the Needle for Pericardiocentesis.
tient’s condition, since attaching an electrode to the In the paraxiphoid approach, the needle should be aimed toward the left
shoulder. In the apical approach, the needle is aimed internally.
needle may provide misleading results.1 The use of
a 16-gauge to 18-gauge polytetrafluoroethylene-
sheathed needle facilitates the process, since its
steel core can be withdrawn once the pericardium use of Doppler echocardiography to ensure that
has been breached, leaving only the sheath in the the pericardial space has been adequately drained
pericardial space. For prolonged drainage, a guide and to avert a recurrence. When the amount of
wire passed through the sheath will facilitate the fluid drained is less than 50 ml a day, the catheter
introduction of a pigtail angiographic catheter. may be withdrawn; the patient should continue to
Thereafter, patients should be followed with the be observed.

references
1. Spodick DH. Pericardial diseases. In: 7. Cogswell TL, Bernath GA, Keelan MH ber RE. Comparative effects of catechola-
Braunwald E, Zipes DP, Libby P, eds. Heart Jr, Wann LS, Klopfenstein HS. The shift in mines in cardiac tamponade: experimental
disease: a textbook of cardiovascular medi- the relationship between intrapericardial flu- and clinical studies. Am J Cardiol 1980;46:
cine. 6th ed. Vol. 2. Philadelphia: W.B. Saun- id pressure and volume induced by acute left 59-66.
ders, 2001:1823-76. ventricular pressure overload during cardiac 12. Klopfenstein HS, Mathias DW. Influence
2. Shabetai R. Diseases of the pericardium. tamponade. Circulation 1986;74:173-80. of naloxone on response to acute cardiac
In: Schlant RC, Alexander RW, eds. Hurst’s 8. Grose R, Greenberg MA, Yipintsoi T, tamponade in conscious dogs. Am J Physiol
the heart: arteries and veins. 6th ed. Vol. 1. Cohen MV. Cardiac tamponade in dogs with 1990;259:H512-H517.
New York: McGraw-Hill, 1994:1647-74. normal coronary arteries. I. Effect of chang- 13. Reddy PS, Curtiss EI, O’Toole JD, Shaver
3. Reddy PS, Curtiss EI, Uretsky BF. Spec- ing intravascular volume on hemodynamics JA. Cardiac tamponade: hemodynamic ob-
trum of hemodynamic changes in cardiac and myocardial blood flow. Basic Res Cardiol servations in man. Circulation 1978;58:265-
tamponade. Am J Cardiol 1990;66:1487-91. 1984;79:531-41. 72.
4. Beloucif S, Takata M, Shimada M, Ro- 9. Hurrell DG, Symanski JD, Chaliki HP, 14. Boltwood CM Jr. Ventricular perform-
botham JL. Influence of pericardial constraint Klarich KW, Pascoe RD, Nishimura RA. As- ance related to transmural filling pressure
on atrioventricular interactions. Am J Physi- sessment of right atrial pressure by hepatic in clinical cardiac tamponade. Circulation
ol 1992;263:H125-H134. vein Doppler echocardiography: a simulta- 1987;75:941-55.
5. Friedman HS, Lajam F, Zaman Q, et al. neous catheterization/Doppler echocardio- 15. Schrier RW, Abraham WT. Hormones
Effect of autonomic blockade on the hemo- graphic study. J Am Coll Cardiol 1996;27: and hemodynamics in heart failure. N Engl J
dynamic findings in acute cardiac tampon- Suppl A:212A. abstract. Med 1999;341:577-85.
ade. Am J Physiol 1977;232:H5-H11. 10. Santamore WP, Li KS, Nakamoto T, 16. Spodick DH. Low atrial natriuretic fac-
6. Spodick DH. Threshold of pericardial Johnston WE. Effects of increased pericar- tor levels and absent pulmonary edema in
constraint: the pericardial reserve volume and dial pressure on the coupling between the pericardial compression of the heart. Am
auxiliary pericardial functions. J Am Coll Car- ventricles. Cardiovasc Res 1990;24:768-76. J Cardiol 1989;63:1271-2.
diol 1985;6:296-7. 11. Martins JB, Manuel WJ, Marcus ML, Ker- 17. Gascho JA, Martins JB, Marcus ML, Ker-

n engl j med 349;7 www.nejm.org august 14, 2003 689

The New England Journal of Medicine

Downloaded from nejm.org at RICE UNIVERSITY on July 29, 2012. For personal use only. No other uses without permission.
Copyright © 2003 Massachusetts Medical Society. All rights reserved.
 current concepts

ber RE. Effects of volume expansion and in pericardial disease. Echocardiography 30. Spodick DH, Kumar R. Subacute con-
vasodilators in acute pericardial tamponade. 1997;14:207-14. strictive pericarditis with cardiac tamponade.
Am J Physiol 1981;240:H49-H53. 25. Reydel B, Spodick DH. Frequency and Dis Chest 1968;54:62-6.
18. Spodick DH. The normal and diseased significance of chamber collapses during 31. Hancock EW. Subacute effusive-constric-
pericardium: current concepts of pericardial cardiac tamponade. Am Heart J 1990;119: tive pericarditis. Circulation 1971;43:183-92.
physiology, diagnosis and treatment. J Am 1160-3. 32. Pepi M, Muratori M, Barbier P, et al. Peri-
Coll Cardiol 1983;1:240-51. 26. Angel J, Anivarro I, Domingo E, Soler- cardial effusion after cardiac surgery: inci-
19. Cooper JP, Oliver RM, Currie P, Walker Soler J. Cardiac tamponade: risk and benefit dence, site, size, and haemodynamic conse-
JM, Swanton RH. How do the clinical find- of fluid challenge performed while waiting quences. Br Heart J 1994;72:327-31.
ings in patients with pericardial effusions in- for pericardiocentesis. Circulation 1997;96: 33. Callahan JA, Seward JB. Pericardiocente-
fluence the success of aspiration? Br Heart Suppl I:I-30. abstract. sis guided by two-dimensional echocardiog-
J 1995;73:351-4. 27. Ramsaran EK, Benotti JR, Spodick DH. raphy. Echocardiography 1997;14:497-504.
20. Spodick DH. Pericardial rub: prospec- Exacerbated tamponade: deterioration of car- 34. Merce J, Sagrista-Sauleda J, Permany-
tive, multiple observer investigation of peri- diac function by lowering excessive arterial er-Miralda G, Soler-Soler J. Should pericar-
cardial friction in 100 patients. Am J Cardiol pressure in hypertensive cardiac tamponade. dial drainage be performed routinely in pa-
1975;35:357-62. Cardiology 1995;86:77-9. tients who have a large pericardial effusion
21. Shabetai R. Pericardial and cardiac pres- 28. Bommer WJ, Follette D, Pollock M, Are- without tamponade? Am J Med 1998;105:
sure. Circulation 1988;77:1-5. na F, Bognar M, Berkoff H. Tamponade in 106-9.
22. Spodick DH. Truly total electric alterna- patients undergoing cardiac surgery: a clini- 35. Spodick DH. Medical treatment of car-
tion of the heart. Clin Cardiol 1998;21:427-8. cal-echocardiographic diagnosis. Am Heart diac tamponade. In: Caturelli G, ed. Cura
23. Idem. Electric alternation of the heart: its J 1995;130:1216-23. intensiva cardiologica. Rome: TIPAR Poli-
relation to the kinetics and physiology of the 29. Thompson RC, Finck SJ, Leventhal JP, grafica, 1991:265-8.
heart during cardiac tamponade. Am J Car- Safford RE. Right-to-left shunt across a patent 36. Hashim R, Frankel H, Tandon M, Rab-
diol 1962;10:155-65. foramen ovale caused by cardiac tampon- inovici R. Fluid resuscitation-induced car-
24. D’Cruz I, Rehman AU, Hancock HI. ade: diagnosis by transesophageal echocar- diac tamponade. Trauma 2002;53:1183-4.
Quantitative echocardiographic assessment diography. Mayo Clin Proc 1991;66:391-4. Copyright © 2003 Massachusetts Medical Society.

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