Low-Pressure Cardiac Tamponade
ELLIOTT M. ANTMAN, M.D.; VICTORIA CARGILL, M.D.; and WILLIAM GROSSMAN, M.D.; Boston,
Massachusetts
An elderly man developed cardiac tamponade from a
tuberculous pericardial effusion but without such typical
manifestations as pulsus paradoxus and jugular-vein
distension. This case illustrates the difficulties in clinical
recognition of low-pressure cardiac tamponade, which can
develop in the presence of dehydration and hypovolemia.
The hemodynamic factors that account for this
phenomenon are discussed.
C A R D I A C COMPRESSION due to pericardial disease may
take the form of constrictive pericarditis, cardiac tampo-
nade, or an intermediate condition called effusive-con-
strictive pericarditis. Precise diagnosis often requires
careful right-heart catheterization with pericardiocentesis
where indicated. The hemodynamics of these entities
have been elegantly reviewed over the past several years
(1-4). Recognition of the presence of a pericardial effu-
sion has been greatly simplified by current echocardio-
graphic techniques. Effusions that develop slowly poten-
tially can become quite large before there is embarass-
ment of the cardiovascular system (4-6). When cardiac
tamponade does develop, tachycardia, hypotension, pul-
sus paradoxus, and jugular venous distention are usually
present and alert the clinician to the diagnosis (6). How-
ever, in the setting of hypovolemia, identification of those
effusions that are causing compromise of the cardiovascu-
lar system can be subtle and especially difficult. We re-
cently encountered a patient who illustrates this uncom-
mon problem and who exhibited the salient features of
"low-pressure cardiac tamponade."
Case History
The patient is a 76-year-old black man who presented with 1
week of anorexia, malaise, fatigue, and shortness of breath. He
denied a history of cough, hemoptysis, or excessive weight loss.
On physical examination, he appeared frail and chronically ill.
There was obvious dyspnea (respiratory rate, 32) but without
orthopnea. Rectal temperature was initially 37.2 °C but rose
shortly to 38.1 °C. Blood pressure was 110/90 mm Hg with 5
mm Hg of pulsus paradoxus. The pulse was 120 beats per min-
ute and regular. There was diminished skin turgor and no ap-
parent jugular venous distention. The chest was clear. Cardiac
examination showed an indistinct point of maximal impulse
with a possible summation gallop rhythm. Abdomen and ex-
tremities were unremarkable. Initial laboratory data included a
chest roentgenogram that showed clear lung fields and a
markedly enlarged cardiac silhouette in a "water bottle'* config-
uration; an electrocardiogram that showed borderline low-volt-
age, sinus tachycardia at 120 beats per minute and a frontal
plane QRS axis of 0 degrees (nonspecific ST-T wave abnormali-
ties were present); and an echocardiogram that showed large
pericardial effusion with diminished ventricular volumes (cardi-
ac oscillation without respiratory variation in cardiac-chamber
size or mitral-valve motion was noted). The blood urea nitrogen
level was 63 mg/dL, and serum creatinine was 3.1 mg/dL.
• From the Cardiovascular Division, Department of Medicine, Peter Bent Brig-
ham Hospital; Boston, Massachusetts.
Annals of Internal Medicine. 1 9 7 9 ; 9 1 : 4 0 3 - 4 0 6 .
Downloaded From: http://annals.org/pdfaccess.ashx?url=/data/journals/aim/19550/ by a University of California San Diego User on 01/13/2017
Because of concern about the possibility of cardiac tampo-
nade, a therapeutic pericardiocentesis was done using a subxi-
phoid approach. Simultaneously, a right-heart catheterization
was done to allow measurement of right atrial and intrapericar-
dial pressures during removal of fluid.
The hemodynamic findings before pericardiocentesis includ-
ed a cardiac output of 2.3 L/min, equal mean right atrial, intra-
pericardial, and pulmonary capillary-wedge pressure of 8 mm
Hg, pulmonary artery pressure of 32/16 (mean, 26) mm Hg,
right ventricular pressure of 32/8 mm Hg, and femoral artery
pressure of 110/90 (mean, 95) mm Hg. After removal of 200
mL of pericardial fluid the mean right atrial and intrapericardi-
al pressures fell together to 4 mm Hg, and femoral artery pres-
sure rose to 120/80 mm Hg. After a total of 600 mL of an
exudative sanguinous effusion was removed, the mean right
atrial and intrapericardial pressures had both fallen to 0 mm
Hg, and femoral artery pressure rose to 135/80 mm Hg. Perti-
nent pressure tracings are illustrated in Figure 1. There was
obvious improvement in the patient's clinical status as shown
by widening of the arterial pulse pressure and a decline in the
respiratory rate.
Microbiologic studies of the fluid were negative for acid-fast
bacilli. Shortly thereafter, the patient underwent an open peri-
cardial biopsy. Nofluidwas encountered at surgery. The histol-
ogy of the pericardium showed scattered granulomas with cen-
tral caseation and minimal fibrosis around the granulomas.
There was no evidence of widespread pericardial fibrosis.
Discussion
Total intrapericardial volume consists of pericardial
fluid and heart volume. Intrapericardial pressure is a
function of the compliance of the pericardial sac and to-
tal intrapericardial volume. A s pericardial fluid increases,
the intrapericardial pressure rises, the rate of rise being
highly dependent on the compliance characteristics of the
pericardium (4). Eventually, intrapericardial pressure
equilibrates with right atrial pressure and the pericardial
pressure-volume curve rises sharply (5, 7). In chronic
tamponade, intracardiac volume is maintained by virtue
of an expanded intravascular volume and elevated venous
pressure. When intrapericardial pressure increases to the
point that elevated venous pressure or increased intravas-
cular volume no longer can maintain stroke volume, car-
diac output falls precipitously (8). Similarly, when intra-
vascular fluid depletion occurs, the cardiac volume and
stroke volume decrease concordantly. If this situation
continued uninterrupted, eventually stroke volume would
fall to a level incompatible with life.
An intermediate situation exists that we have termed
low-pressure cardiac tamponade. This is characterized by
moderate-to-moderately severe intravascular fluid deple-
tion in the presence of a compressive pericardial effusion.
The right atrial pressure as reflected in bedside estimates
or measurements of the central venous pressure may be
normal. Such a situation has been well described in ex-
perimental preparations (9-11), but is mentioned only
© 1 9 7 9 American College of Physicians 403

briefly in clinical reviews of cardiac tamponade (1, 4).
The hemodynamics can be best understood by exami-
nation of the relation between pericardial effusion vol-
ume, intrapericardial pressure, and intracardiac volume.
In the presence of hypovolemia, intracardiac volume is
reduced and right atrial pressure is low.
Curve A in Figure 2 depicts the pericardial pressure-
volume relation in the hypovolemic patient described
above. Because of the markedly reduced circulating
blood volume, as the mean intrapericardial pressure rose
it rapidly equilibrated with the initially low mean right
atrial pressure (Curve A'). In this case, Curves A and A*
were superimposable over the entire range of pericardial
volumes, and therefore an element of tamponade was
present virtually continuously.
By contrast, the data from a normovolemic patient
studied in this laboratory because of cardiac tamponade
are presented in Curves B and B'. When no pericardial
fluid was present the resting mean right atrial pressure
was 8 mm Hg. A significant amount of fluid accumulated
in the compliant pericardial sac before intrapericardial
pressures equilibrated with right atrial pressure. Tampo-
nade occurred and Curves B and B' then became super-
imposable.
The pairs of Curves A, A' and B, B' both represent
4 0 4 September 1979 • Annals of Internal Medicine • Volume 91 • Number 3
Downloaded From: http://annals.org/pdfaccess.ashx?url=/data/journals/aim/19550/ by a University of California San Diego User on 01/13/2017
Figure 1 . Simultaneous pressure curves recorded f r o m the right
atrium (RA) and pericardium at the time of pericardiocentesis. Pha-
sic pressures are on the left and mean pressures are on the right of
each panel. Pressure scale in m m Hg is on the left of each panel
and vertical time lines are seen at 1-s intervals. A is the initial set of
recordings before fluid removal and B and C are those obtained
after removal of 2 0 0 and 6 0 0 mL of pericardial fluid respectively.
Note the prominent X descent in the RA tracing (arrow) prepericar-
diocentesis and lack of the appearance of a predominant Y descent
after removal of 6 0 0 mL of fluid. On all panels, the phasic decrease
in the RA pressure corresponds to inspiration. Mean RA pressure
was equal to pericardial pressure initially and fell in an identical
fashion to pericardial pressure as pericardiocentesis proceeded.
The right atrial pressure of zero after removal of the pericardial
effusion suggests the presence of significant hypovolemia. This last
finding in association with the lack of development of a predomi-
nant Y descent, continued respiratory phasic variations in RA pres-
sure, and absence of an early diastolic dip in the right ventricular
pressure tracing (not shown) make effusive-constrictive pericardi-
tis unlikely ( 4 , 14).
instances of cardiac compression by a pericardial effusion
but with different total intrapericardial volumes. The ab-
solute intrapericardial and right atrial pressures are
therefore different, but hemodynamic consequences are
the same. Hypovolemia lowers the slope of the pericardi-
al pressure volume curve, and, thus, potentially severe
cardiac tamponade can occur with only a modest eleva-
tion of central venous pressure (Curve A, Figure 2) (1).
Clinical signs of venous hypertension may not be appar-
ent until volume deficits have been corrected (Curve B,
Figure 2) (12).
Although pulsus paradoxus is a usual feature of classic
cardiac tamponade, it was not found in our case. As has
been summarized recently (4, 8, 13) pulsus paradoxus
may be absent in tamponade when left ventricular dias-
tolic pressure is intrinsically elevated and exceeds right
ventricular diastolic pressure throughout the respiratory
cycle, an atrial septal defect or significant aortic insuffi-
ciency is present, localized collections of blood compress
one side of the heart, or extreme tamponade with hypo-
tension is present. Futhermore, as stressed by Stein, Shu-
bin, and Weil (12) the absolute value of the pulsus para-
doxus is a function of the pulse pressure. Therefore, using
an absolute value of 10 mm Hg can be misleading espe-
cially when the pulse pressure has narrowed to 20 mm
 Hg. For this reason, some authors have suggested using
either the ratio of pulsus paradoxus to pulse pressure (2)
or expressing the pulsus paradoxus as a percent decrease
in systolic arterial pressure with inspiration (8).
The hemodynamic findings in our case are consistent
with tamponade (1) in that [1] there is a diminished
stroke volume; [2] the right atrial pressure curve predom-
inantly demonstrates an X descent; [3] the right atrial
mean, right ventricular end-diastolic, and pulmonary
capillary-wedge mean pressure are equal to the intraperi-
cardial pressure, which itself was abnormally elevated;
[4] there was a phasic decrease in mean right atrial pres-
sure with inspiration; [5] the right atrial mean pressure
fell and systolic-systemic arterial pressure and pulse pres-
sure rose concordantly with removal of pericardial fluid
and a decrease in the intrapericardial pressure; and [6]
the right ventricular pressure tracings at no time showed
an early diastolic "dip" toward the baseline.
Although this patient did not receive rapid volume ex-
pansion for diagnostic purposes after pericardiocentesis,
effusive-constrictive pericarditis seemed unlikely, because
the characteristic hemodynamic findings of Hancock (3)
and Mann (14) were absent (see Figure 1 legend).
Figure 2 . Mean intrapericardial and right atrial pressures in m m Hg
are plotted on the vertical axis versus pericardial effusion volume in
ml_ on the horizontal axis. Curves A and A' represent values f r o m
the hypovolemic patient. Because no fluid was encountered at sur-
gery, it was assumed that the 6 0 0 mL of pericardial fluid removed
at pericardiocentesis was the entire effusion volume. Curves B and
B' are data f r o m a normovolemic patient suffering f r o m cardiac
tamponade. See text f o r discussion. RA = right atrial. (Note: The
difference in slopes between the two pairs of curves may theoreti-
cally be due in part t o a difference in pericardial compliance be-
tween the two patients. That this plays a major role in view of the
widely disparate volume status of the two patients is unlikely.)
Downloaded From: http://annals.org/pdfaccess.ashx?url=/data/journals/aim/19550/ by a University of California San Diego User on 01/13/2017
This patient underscores the necessity for carefully
evaluating all hemodynamic variables when assessing the
severity of a pericardial effusion. In retrospect, the extent
of this patient's dehydration was underestimated on ini-
tial evaluation. As emphasized by Spodick (15), rapid in-
travenous expansion in cases of chronic "occult constric-
tive pericardial disease" may be dangerous. However, by
raising venous pressure and improving cardiac output in
cases of acute cardiac tamponade, it can be life-saving.
Low-pressure tamponade can occur in the acute form as
exemplified by penetrating wounds of the heart in a bat-
tlefield situation (16) or a chronic form as exemplified by
this case report. In either case, cautiously administering a
fluid challenge intravenously to any patient suspected of
suffering from this syndrome seems wise. In the acute
situation, it will stabilize the patient in preparation for a
thoracotomy; in the chronic situation, it will stabilize the
patient in preparation f r a pericardiocentesis and un-
mask the severity of the i.emodynamic derangement.
Finally, this case raises the issue of whether pericardio-
centesis or open pericardial biopsy is the preferable
course in such a clinical setting. The relative advantages
and disadvantages of the two approaches were recently
summarized by Hancock (4). Pericardiocentesis in our
patient was chosen because of the ready availability of a
skilled invasive cardiac catheterization team and the need
to promptly provide hemodynamic relief from possible
cardiac tamponade. It was recognized that the diagnostic
yield of pericardial aspirate culture for tuberculosis is
only about 50%, whereas pericardiectomy or pericardial
biopsy can establish the diagnosis of tuberculosis in about
80% of cases (17). For this reason pericardiocentesis was
followed shortly by open pericardial biopsy, which estab-
lished the diagnosis. In centers where a cardiologist
skilled in pericardiocentesis is not available, or when the
clinical circumstances allow it, the incremental diagnos-
tic yield of an open procedure may be preferable.
ACKNOWLEDGMENTS: The authors thank Ms. Annmarie Condon for
editorial assistance and Ms. Rachel Malakoff for help in preparation of this
manuscript.
Grant support: in part by National Heart, Lung, and Blood Institute
Training Grant HL 07049-03, National Institutes of Health. Dr. Grossman
is an Established Investigator of the American Heart Association.
• Requests for reprints should be addressed to William Grossman, M.D.;
Cardiovascular Division, Peter Bent Brigham Hospital; 721 Huntington Av-
enue; Boston, MA 02115.
Received 18 December 1978; revision accepted 9 April 1979.
References
1. SHABETAI R, FOWLER NO, GUNTHEROTH WG. The hemodynamics of
cardiac tamponade and constrictive pericarditis. Am J Cardiol.
1970;26:480-9.
2. SPODICK DH. Acute cardiac tamponade: pathologic physiology, diagno-
sis, and management. Prog Cardiovasc Dis. 1967;10:64-96.
3. HANCOCK EW. Subacute effusive-constrictive pericarditis. Circulation.
1971;43:183-92.
4. HANCOCK EW. Cardiac tamponade. Med Clin North Am. 1979;63:223-
37.
5. E V A N S JM, W A L T E R CW, HELLEMS HK. Alterations in the circulation
during cardiac tamponade due to pericardial effusion: an experimental
study employing cardiac catheterization. Am Heart J. 1950;39:181-7.
6. SCHEPERS GWH. Tuberculous pericarditis. Am J Cardiol. 1962;9:248-
76.
7. ISAACS JP, B E R G L U N D E, SARNOFF SJ. Ventricular function: III. The
pathologic physiology of acute cardiac tamponade studied by means of
ventricular function curves. Am Heart J. 1954;48:66-76.
8. R E D D Y PS, CURTISS EI, O'TOOLE JD, SHAVER JA. Cardiac tampo-
Antmanetal. • Cardiac Tamponade 405
 nade: hemodynamic observations in man. Circulation. 1978;58:265-72.
9. MORGAN BC, GUNTHEROTH WG, D I L L A R D DH. Relationship of peri-
cardial to pleural pressure during quiet respiration and cardiac tampo-
nade. CircRes. 1965;16:493-8.
10. DEGRISTOFARO D, LIU CK. The hemodynamics of cardiac tamponade
and blood volume overload in dogs. Cardiovasc Res. 1969;3:292-8.
11. FRIEDMAN HS, LAJAM F, Z A M A N Q, et al. Effect of autonomic block-
ade on the hemodynamic findings in acute cardiac tamponade. Am J
Physiol. 1977;232:H5-11.
12. STEIN L, SHUBIN H, W E I L MH. Recognition and management of peri-
cardial tamponade. JAMA. 1973;225:503-6.
406 Annals of Internal Medicine. 1979;91:406-409.
Downloaded From: http://annals.org/pdfaccess.ashx?url=/data/journals/aim/19550/ by a University of California San Diego User on 01/13/2017
13. SHABETAI R: The pericardium: an essay on some recent developments.
Am J Cardiol. 1978;42:1036-43.
14. M A N N T, BRODIE BR, GROSSMAN W, M C L A U R I N L. Effusive-constric-
tive hemodynamic pattern due to neoplastic involvement of the pericar-
dium. Am J Cardiol. 1978;41:781-6.
15. SPODICK DH. Pericardial constriction. Circulation. 1978;57:1235. Let-
ter.
16. TASSI AA, DAVIES AL. Pericardial tamponade due to penetrating frag-
ment wounds of the heart. Am J Surg. 1969;118:535-8.
17. ROONEY JJ, CROCCO JA, LYONS HA. Tuberculous pericarditis. Ann
Intern Med. 1970;72:73-8.
© 1 9 7 9 American College of Physicians