Journal List > Heart > v.90(3); Mar 2004

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Heart. 2004 March; 90(3):
255–256.

doi:
10.1136/hrt.2003.024810.

PMCID:
PMC1768129

Copyright
© Copyright 2004 by Heart

Pericardial effusion: haemodynamic spectrum

R Shabetai

Correspondence to:
Ralph
Shabetai
MD, VA Health Care System, Cardiology 111 A, La Jolla, CA
92161, USA; rshabetai/at/ucsd.edu

Keywords: pericardial effusion, haemodynamics

Other
Sections▼

CLASSIC
TAMPONADE

ATYPICAL
TAMPONADE

REFERENCES

Haemodynamic abnormalities, caused
by pericardial effusion, range from undetectable or mild, to life
threatening, depending on the determinants discussed below. These include
the rate at which the effusion accumulates and whether or not the
pericardium is scarred and thus adds an element of constrictive
pericarditis. Pericardial adhesions or organisation of the fluid can
result in localised, and thus atypical, tamponade. Pericardial effusion is
the cause of a number of distinct clinical and haemodynamic
syndromes.

Fundamental to understanding their
pathophysiology are the biomechanical properties of the pericardium. The
pressure–volume relation of normal pericardium, after an initial short
shallow portion that allows the pericardium to stretch slightly in
response to physiological events, such as changes in posture or volume
status, shows a minimal increase in pericardial pressure. Thereafter, the
pressure increase is extremely steep. This J shaped curve1 indicates that a sudden increase in the volume of
pericardial fluid can slightly stretch the pericardium, and thus an
increase of as little as 100 or 200 ml may elevate pericardial pressure
from its normal ambient, or slightly sub-ambient value, to 30 mm Hg or
more, defining severe cardiac tamponade.

At the other extreme, a pericardial
effusion developing over several weeks or months may reach a volume
measured in litres accompanied by a considerably more modest increase in
pericardial pressure.2 The explanation for this difference is that the
response of the pericardium to gradual stretch differs from its response
to acute stretch. A slower accumulation of pericardial fluid causes
pericardial compliance to increase; its pressure–volume curve is shifted
to the right and the slope of the steep portion is greatly reduced, such
that for a given increment in volume, the pressure rise is appreciably
less.3 This is the tamponade usually encountered in medical
clinics and wards, whereas acute tamponade is found in interventional
cardiac laboratories, as a consequence of puncture of a cardiac chamber or
a vessel, in trauma units to which victims of mediastinal injury are
admitted, and in intensive care units where acute tamponade is a sequel to
rupture of a myocardial infarction or aortic aneurysm. Because the
pressure–volume relation is curved, compliance decreases with increasing
volume. Even in “medical tamponade” pericardial pressure may rise to 30 mm
Hg as fluid continues to accumulate faster than it can be absorbed.
However, this elevation occurs at much greater volume of pericardial fluid
compared with acute tamponade. The volume of effusion at which this
development occurs depends on how quickly the effusion grows and may be
anywhere between a few hundred millilitres to several litres. The
therapeutic consequence of the different haemodynamics of acute versus
chronic tamponade is that, in the former, removal of 100 ml of fluid can
drop pericardial pressure dramatically and be life saving, whereas in the
latter, considerably more fluid must be removed to attain comparable
relief of tamponade. Between these extremes is a broad spectrum of
pericardial volume and pressure.

Other
Sections▼

CLASSIC
TAMPONADE

ATYPICAL
TAMPONADE

REFERENCES

CLASSIC TAMPONADE

Pericardial pressure, by definition,
is elevated. The circulation adapts by increasing central systemic and
pulmonary venous pressures to equal the pericardial pressure, thereby
preventing total collapse of the cardiac chambers. Left and right
ventricular diastolic, right atrial, and pulmonary wedge pressures all
rise to equal the pressure in the pericardium, making atrial and
ventricular diastolic transmural pressures essentially zero. This
equalisation of pressures is the hallmark of tamponade.4 Stroke volume is reduced, but cardiac output is
partially preserved by tachycardia, driven by increased adrenergic tone.
The increased ventricular diastolic pressure mandates commensurate
pulmonary hypertension to maintain pulmonary circulation. Pulmonary
arterial systolic pressure seldom significantly exceeds 40 mm Hg.

When the pericardium is tightly stretched, it
becomes virtually inextensible. As a result, total pericardial volume is
constant throughout the respiratory cycle. Any change in the volume of one
side of the heart then causes the opposite change in volume of the other
side, a phenomenon referred to as ventricular interaction or
interdependence. The manifestations of this greatly enhanced ventricular
interaction are pulsus paradoxus4,5 and increased respiratory variation in the velocity
of atrioventricular filling.6

Inspiration increases systemic venous
return by the same mechanism as in normal physiology. The resulting
increase in right heart volume can only occur by bulging the atrial and
ventricular septa into the left atrium and ventricle. This redistribution
of blood volume within the heart accompanying each respiratory cycle is
the cause of decreased left ventricular stroke input and output and
systemic arterial systolic pressure (pulsus paradoxus). Pulsus paradoxus
can be palpated in the peripheral pulses, or measured by sphygmomanometry,
or by cannulating a systemic artery. Respiratory changes in the pulmonary
circulation are nearly 180° out of phase with those in the systemic
circulation as a consequence of ventricular interaction.5

Severity spectrum

Incipient or preclinical
tamponade exists when pericardial pressure equals the normal right, but
remains lower than left atrial pressure. When pericardial pressure rises
to the level of normal right atrial pressure, cardiac tamponade is
trivial; when it equals normal left atrial pressure, tamponade is mild.
When pericardial pressure increases further, it reaches left atrial
pressure. When pericardial pressure exceeds 10–12 mm Hg, moderate
tamponade is present7 and detectable at the bedside by the abnormal jugular
pulse and echocardiography that shows compression of the right heart
chambers.8 The outer wall of the right atrium becomes concave
(right atrial compression)9 and the right ventricular free wall indents toward
the septum (right ventricular diastolic collapse) due to transient
reversal of the transmural ventricular diastolic pressure.10 At this stage, pulsus paradoxus is often absent and
the blood pressure and cardiac output are only slightly lowered. Increased
respiratory variation of ventricular filling velocities is more
pronounced. This phenomenon is detected by Doppler interrogation of
ventricular inflow. For ease of measurement, the change in peak velocity,
not velocity–time index or stroke volume, is traditionally used. When
tamponade is severe (pericardial pressure more than 25 mm Hg), pulsus
paradoxus is prominent, stroke volume and blood pressure are significantly
reduced, and sinus tachycardia is usual. With increasing severity of
tamponade, haemodynamics decline to the point of shock and, if not
promptly treated, death.

Other
Sections▼

CLASSIC
TAMPONADE

ATYPICAL
TAMPONADE

REFERENCES

ATYPICAL TAMPONADE

Cardiac co-morbidity

It is important to bear in mind that
pre-existing heart disease modifies the classic haemodynamics of
tamponade. Conditions that greatly increase left ventricular diastolic
pressure, atrial septal defect, and aortic regurgitation prevent pulsus
paradoxus, even in severe tamponade.4 Patients with chronic renal disease and pericardial
effusion therefore often fail to show pulsus paradoxus.7 Right heart failure or right ventricular hypertrophy
prevents compression of right heart chambers.

Loculated effusion may cause regional
tamponade.11 When the atria and great veins are spared, the
features of tamponade are less for a given elevation of pericardial
pressure.12 Regional tamponade found after cardiac surgery may
compress the left ventricle instead of the right.13

Low pressure tamponade

While central venous pressure
is typically elevated in proportion to tamponade, hypovolaemia may keep
the central venous pressure low in spite of significant tamponade.14 In tamponade secondary to trauma, the explanation
is exsanguination. In other cases the cause may be excessive diuretic
treatment, often given in the belief that heart failure was the cause of
raised central venous pressure. The most troublesome example is
haemodialysis. If these patients are under-treated, the effusion may
disappear after increased frequency of dialysis. On the other hand
dialysis may have induced hypovolaemia, in which case the patient requires
volume infusion.

Chronic effusive pericarditis

These massive effusions may
persist for years. Less commonly they are recurrent.15 They accumulate slowly, accounting for their huge
volume. The pericardium has stretched gradually, therefore pericardial
pressure is only mildly elevated. The cases meet the criteria for
preclinical or mild tamponade, which of itself does not require treatment.
A significant proportion of the cases unpredictably develop classic
tamponade, which is the reason for pericardiocentesis, and when that is
followed by recurrences, pericardiectomy is recommended.15

Effusive constrictive pericarditis

Here, cardiac tamponade develops in
the setting of a scarred pericardium causing constriction. Common causes
are prior radiation and neoplasm.2

Less commonly, this syndrome follows
acute pericarditis, in which the constriction may be transient.16 Pulsus paradoxus is less common than in classic
tamponade and the central venous pressure often shows a prominent y
descent, whereas this descent is absent in classic tamponade. When
haemodynamics are measured during pericardiocentesis, elevation of the
central and pulmonary venous pressures persists after pericardial pressure
has been reduced to normal.

Other
Sections▼

CLASSIC
TAMPONADE

ATYPICAL
TAMPONADE

REFERENCES

REFERENCES

1. Holt
JP, Rhode EA, Kines H. Pericardial and ventricular pressure.
Circ Res 1960;8:1171–81. [PubMed]

2. Sagrista-Sauleda J, Angel J,
Permanyer-Miralda G, et al. Long-term follow-up of idiopathic
chronic pericardial effusion. N Engl J Med
1999;341:2054–9. [PubMed]

3. LeWinter
MM, Pavelec R. Influence of the pericardium on left ventricular
end–diastolic pressure-segment relations during early and late stages of
experimental chronic volume overload in dogs. Circ
Res 1982;50:501–9. [PubMed]

4. Shabetai
R, Fowler NO, Guntheroth WG. The hemodynamics of cardiac
tamponade and constrictive pericarditis. Am J
Cardiol 1970;26:480–9. [PubMed]

5. Shabetai
R, Fowler NO, Fenton JC, et al. J Clin Invest 1965;44:1882–98. [PubMed]

6. Appleton
CP, Hatle LK, Popp RL. Cardiac tamponade and pericardial
effusion: respiratory variation in transvalvular flow velocities studied
by Doppler echocardiography. J Am Coll
Cardiol 1988;11:1020–30. [PubMed]

7. Reddy
PS, Curtiss EI, O’Toole JD, et al. Cardiac tamponade:
hemodynamic observations in man. Circulation 1978;58:265–72. [PubMed]

8. Klopfenstein HS, Cogswell TL, Bernath GA,
et al. Alterations in intravascular volume affect the relation
between right ventricular diastolic collapse and the hemodynamic severity
of cardiac tamponade. J Am Coll Cardiol
1985;6:1057–63. [PubMed]

9. Gillam
LD, Guyer DE, Gibson TC, et al. Hydrodynamic compression
of the right atrium: a new echocardiographic sign of cardiac tamponade.
Circulation 1983;68:294–301. [PubMed]

10. Leimgruber PP, Klopfenstein HS, Wann LS,
et al. The hemodynamic derangement associated with right
ventricular diastolic collapse in cardiac tamponade: an experimental
echocardiographic study. Circulation
1983;68:612–20. [PubMed]

11. Fowler
NO, Gabel M. Regional cardiac tamponade: a hemodynamic study.
J Am Coll Cardiol 1987;10:164–9. [PubMed]

12. Fowler
NO, Gabel M. The haemodynamic effects of cardiac tamponade:
mainly the result of atrial, not ventricular, compression. Circulation 1985;71:154–7. [PubMed]

13. Chuttani
K, Pandian NG, Mohanty PK, et al. Left ventricular
diastolic collapse. An echocardiographic sign of regional cardiac
tamponade. Circulation 1991;83:1999–2006. [PubMed]

14. Hayes
SN, Freeman WK, Gersh BJ. Low pressure cardiac tamponade:
diagnosis facilitated by Doppler echocardiography. Br Heart J 1990;63:136–40. [PubMed]

15. Hancock
EW. Subacute effusive-constrictive pericarditis. Circulation 1971;43:183–92. [PubMed]

16. Sagrista-Sauleda J, Permanyer-Miralda G,
Candell-Riera J, et al. Transient cardiac constriction: an
unrecognized pattern of evolution in effusive acute idiopathic
pericarditis. Am J Cardiol 1987;59:961–6. [PubMed]

Articles from Heart
are provided here courtesy of

BMJ Group

PubMed articles by these authors

Shabetai,
R.

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PubMed

Pericardial
and ventricular pressure.

Circ Res. 1960 Nov; 8():1171-81.
[Circ Res. 1960]

See
more articles cited in this paragraph

Long-term
follow-up of idiopathic chronic pericardial effusion.

N Engl J Med. 1999 Dec 30;
341(27):2054-9.
[N Engl J Med. 1999]

Influence
of the pericardium on left ventricular end-diastolic pressure-segment
relations during early and later stages of experimental chronic volume
overload in dogs.

Circ Res. 1982 Apr; 50(4):501-9.
[Circ Res. 1982]

See
more articles cited in this paragraph

The
hemodynamics of cardiac tamponade and constrictive pericarditis.

Am J Cardiol. 1970 Nov; 26(5):480-9.
[Am J Cardiol. 1970]

See
more articles cited in this paragraph

The
hemodynamics of cardiac tamponade and constrictive pericarditis.

Am J Cardiol. 1970 Nov; 26(5):480-9.
[Am J Cardiol. 1970]

Pulsus
paradoxus.

J Clin Invest. 1965 Nov;
44(11):1882-98.
[J Clin Invest. 1965]

ReviewCardiac tamponade and pericardial effusion:
respiratory variation in transvalvular flow velocities studied by Doppler
echocardiography.

J Am Coll Cardiol. 1988 May;
11(5):1020-30.
[J Am Coll Cardiol.
1988]

See
more articles cited in this paragraph

Pulsus
paradoxus.

J Clin Invest. 1965 Nov;
44(11):1882-98.
[J Clin Invest. 1965]

See
more articles cited in this paragraph

Cardiac
tamponade: hemodynamic observations in man.

Circulation. 1978 Aug; 58(2):265-72.
[Circulation. 1978]

Alterations
in intravascular volume affect the relation between right ventricular
diastolic collapse and the hemodynamic severity of cardiac tamponade.

J Am Coll Cardiol. 1985 Nov;
6(5):1057-63.
[J Am Coll Cardiol. 1985]

Hydrodynamic
compression of the right atrium: a new echocardiographic sign of cardiac
tamponade.

Circulation. 1983 Aug;
68(2):294-301.
[Circulation. 1983]

The
hemodynamic derangement associated with right ventricular diastolic collapse
in cardiac tamponade: an experimental echocardiographic study.

Circulation. 1983 Sep; 68(3):612-20.
[Circulation. 1983]

See
more articles cited in this paragraph

The
hemodynamics of cardiac tamponade and constrictive pericarditis.

Am J Cardiol. 1970 Nov; 26(5):480-9.
[Am J Cardiol. 1970]

Cardiac
tamponade: hemodynamic observations in man.

Circulation. 1978 Aug; 58(2):265-72.
[Circulation. 1978]

See
more articles cited in this paragraph

Regional
cardiac tamponade: a hemodynamic study.

J Am Coll Cardiol. 1987 Jul;
10(1):164-9.
[J Am Coll Cardiol. 1987]

The
hemodynamic effects of cardiac tamponade: mainly the result of atrial, not
ventricular, compression.

Circulation. 1985 Jan; 71(1):154-7.
[Circulation. 1985]

Left
ventricular diastolic collapse. An echocardiographic sign of regional cardiac
tamponade.

Circulation. 1991 Jun;
83(6):1999-2006.
[Circulation. 1991]

See
more articles cited in this paragraph

Low
pressure cardiac tamponade: diagnosis facilitated by Doppler
echocardiography.

Br Heart J. 1990 Feb; 63(2):136-40.
[Br Heart J. 1990]

See
more articles cited in this paragraph

Subacute
effusive-constrictive pericarditis.

Circulation. 1971 Feb; 43(2):183-92.
[Circulation. 1971]

See
more articles cited in this paragraph

Long-term
follow-up of idiopathic chronic pericardial effusion.

N Engl J Med. 1999 Dec 30;
341(27):2054-9.
[N Engl J Med. 1999]

See
more articles cited in this paragraph

Transient
cardiac constriction: an unrecognized pattern of evolution in effusive acute
idiopathic pericarditis.

Am J Cardiol. 1987 Apr 15;
59(9):961-6.
[Am J Cardiol. 1987]

See
more articles cited in this paragraph

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