Symposium on a Physiologic Approach to Critical Care
Cardiac Tamponade
Walter J. Pories, M.D.,* and Vincent A. Gaudiani, M.D.t
Three related parameters determine the natural history of cardiac tamponade: the structure of the pericardium, the rate of pericardial fluid accumulation, and the hemodynamic response to cardiac compression. The pericardium is a fibroserous sac which envelops the heart. 28 It is flexible, but inelastic, and distends only as a result of prolonged pressure. When fluid or gas collects in the pericardium, the initial 80 to 120 ml are easily accommodated in the anatomic pericardial recesses. 60 The response to further effusion depends on the rate of fluid accumulation. If rapid, an additional 50 ml may cause death; if slow, several liters may cause little impairment. The immediate hemodynamic response to elevated pressure within the pericardium is decreased cardiac output, but compensatory mechanisms mitigate this effect. When they are overwhelmed by further increases in intrapericardial pressure, cardiac tamponade occurs. Tamponade is a surgical emergency because death follows rapidly if the pressure is not relieved. The etiology of the effusion and its pH composition and flora determine future prognosis and therapy, but prompt correction of the immediate threat to life must be the surgeon's first task. To accomplish it, he must recognize the clinical situations in which tamponade might occur, and he must understand the pathophysiology and how to reverse it.
PATHOLOGIC PHYSIOLOGY The fatal potential of cardiac tamponade has been recognized for several hundred years, but its mechanism has remained controversial into the present century. Ambrose Pare 3 described a case of. traumatic hemopericardiuin in the sixteenth century. In the seventeenth century, 'Professor of Surgery, Case Western Reserve University School of Medicine; Director, Department of Surgery, Cleveland Metropolitan General Hospital, Cleveland, Ohio t Assistant Resident Surgeon, Case Western Reserve University School of Medicine at Cleveland Metropolitan General Hospital, Cleveland, Ohio
Surgical Clinics of North America- Vol. 55, No.3, June 1975
573
574
WALTER
J.
PORIES AND VINCENT
A; GAUDIANI
Lowers1 described the heart "compressed with water on every side so that ... it ... cannot dilate to receive the blood'; then truly the pulse diminishes until at length it is suppressed by even more water, when syncope, and death itself follows." Rose 53 introduced the term cardiac tamponade in 1884, and by 1900 Cohnheim8 and Starling63 had independently experimented with tamponade as a model of cardiac failure. Both demonstrated a fall in aortic pressure. Cohnheim erroneously attributed it to obstructed cardiac filling at the venoatrial junction. Starling reas&hed correctly that aortic pressure fell because "diastolic expansion of the ventricles began to be affected." The venoatrial theory was widely accepted until 1954 when Isaacs and his co-workers 30 clearly documented Starling's position by showing that no appreciable pressure gradient occurred at the venoatrial junction. The crucial hemodynamic sequence in cardiac tamponade is impaired ventricular filling causing decreased cardiac output. Isaacs applied Starling's later work on the control of cardiac output to explain how this occurs. The Frank-Starling mechanism, Starling's law,64 holds that stroke volume is directly proportional to ventricular filling. Filling, in turn, depends on the gradient between venous pressure and ventricular diastolic pressure. In tamponade, increased pericardial pressure is transmitted through the ventricular wall and elevates ventricular diastolic pressure. Therefore, the filling pressure gradient diminishes. A small decrease in this gradient causes a large decrease in flow because resistance in the venous circuit is low. Less blood fills the ventricle, the myocardium is stretched less, and the stroke volume and the force of contraction fall. 27 A simplified diagram of these events is presented in Figure 1. The decreased cardiac output produces a fall in arterial pressure, venous return, and tissue perfusion. Myocardial blood flow drops because of increased pressure on the coronary vessels and lowered perfusion pressure. 44 While tamponade has caused myocardial necrosis and enzyme changes in experimental animals,12 the final effect of tamponade on coronary flow is unsettled. 21 Compensatory Mechanisms Compensatory mechanisms can counteract the progressive hemodynamic changes of tamponade. Heart rate increases to maintain systemic output because stroke volume is limited. In the peripheral circulation, catecholamines support arterial pressure and venous return by vasoconstriction. If the onset of tamponade is sufficiently prolonged, decreased renal. blood flow will promote sodium retention and increased intravascular volume. The net effect is elevated venous pressure to maintain cardiac filling. . These compensatory mechanisms may themselves stress the heart. 60 Tachycardia decreases coronary blood flow by increasing the proportion of the cardiac cycle spent in systole, and elevated catecholamines increase myocardial oxygen consumption. If successful, however, compensatory mechanisms reestablish circulatory homeostasis and allow the pericardium to stretch or possibly absorb the effusion.
575
CARDIAC TAMPONADE
THE
PATHOPHYSIOLOGY OF CARDIAC
TAMPONADE
Fluid or Gas I ItlNTRAPERICARDIAL PRESSURE I Distending the Pericardium ~ ....____tpressure on Atria S. Ventricles
l l
tCoronary Blood Flow
tVentricular Diastolic Pressure
I. VENTRICULAR
tStroke
FILLING I
l
*
Volume
~l~
,Arterial Pressure
tVenous Return
Wide A-V O2 Difference
Figure 1. The crucial hemodynamic sequence in cardiac tamponade is impaired ventricular filling causing decreased stroke volume.
Further increases in pericardial effusion have increasingly severe effects. Morgan and his associates,41 studying the pressure-volume characteristics of the pericardium, demonstrated an exponential effect of volume on pressure. A considerable volume may be necessary to cause an initial increase in pericardial pressure, but subsequent small additions may sharply increase pressure and cause sudden catastrophic deterioration. This relationship is shown in Figure 2. They also demonstrated hysteresis in pericardial pressure-volume curves. This explains why removing a small amount of pericardial fluid decreases pressure sharply and causes dramatic clinical improvement. A diagrammatic summary of the major compensatory mechanisms in cardiac tamponade is shown in Figure 3. Compensatory mechanisms fail when tachycardia and vasoconstriction can no longer counterbalance a falling stroke volume. Cardiac output falls as do venous return and arterial pressure. With venous return decreasing, the ventricular filling pressure gradient becomes even smaller, and a deteriorating cycle is established between output and pressure gradient which leads to total circulatory collapse.
DIAGNOSIS In 1935 Beck5 summarized the major clinical findings in acute cardiac compression: a rising venous pressure, a falling arterial pressure, and small, quiet heart. Although Beck's triad is not always present, it remains a valuable reminder that central venous hypertension, decreased cardiac output, and the pericardial effusion are responsible for the majority of signs and symptoms of cardiac tamponade. Elevated venous pressure distends neck veins, and if persistent, causes hepatomegaly, ascites, hepatojugular reflux, and peripheral edema. Decreased
a
«
576
WALTER
J.
PORIES AND VINCENT
A.
GAUDIANI
10
0
N
I
8
E
.:: w
6
0::
::::> (f) (f)
w
4
0::
a..
...J
2
« 0
0::
«
*
0
u
-
0::
w -2
a..
-4
40 80 120 160 PERICARDIAL VOLUME
200
240
IN ML
Figure 2. Pressure drops more sharply on removing fluid from the pericardium (out), than it rises when fluid accumulates (in). This explains why the onset of tamponade is frequently insidious and rapid relief may be obtained by aspirating only small amounts. (Redrawn from Morgan, B. C., et al.: Relationship of pericardial to pleural pressure during quiet respiration and cardiac tamponade. Circ. Res., 16:493, 1965.)
+ Peri cord io I Pre ssu re tvenous
t~S~T.~R~O~~E.E~IIi~V'!:.L!:.U.~'M~E=.J1
- - - - i...U!
Return
'IAct""'~ In,,", p"""," Pressure Receptors +cotechoL mines
RENAL BLOOD FLOW
TACHYCARDIA
/
tNo Retention
j Return
-------I.... +cordioc
Output
Figure 3. Compensatory mechanisms can counteract the progressive hemodynamic changes of tamponade.
CARDIAC TAMPONADE
577
cardiac output leads to tachycardia, poor peripheral pulses, and vasoconstriction. Dyspnea, tachypnea, and oppressive precordial discomfort radiating to the arms and varying with position arise from the mechanical effect of the effusion as well as inadequate systemic output. Ankle swelling, increasing abdominal girth, and nonspecific abdominal complaints result from systemic venous engorgement. 60 Many signs have been related to the pericardial effusion. The precordium is quiet and heart sounds are diminished. Dressler's sign, retrosternal flatness to percussion, and Ewart's sign, dullness and bronchial breathing in the midscapular lines, may be elicited. If the pericardium is inflamed, a friction rub may be audible even with a large effusion, and in hydropneumopericardium, a metallic splashing sound can be heard.
Pulsus Paradoxus Perhaps the most specific sign of tamponade, although not pathognomonic, is pulsus paradoxus. Kussmaup5 first used this term in 1873 to define an exaggerated inspiratory decline in arterial pressure which reverted to its normal contour on expiration. He called it "paradoxic," not because it is a reversal of the usual physiologic state, which it is not, but because there is no evidence of cardiac irregularity while these changes occur. Over the past 50 years, the mechanism of Kussmaul's pulse has generated considerable controversy.23 Previous investigators postulated inspiratory traction on the pericardimp12 and left ventricular compression by the right ventricle during inspiration 13 as possible mechanisms. Shabetai and his coworkers 55 ,56 have established the current concepts. First, they showed that the usual pattern of augmented right heart filling during inspiration persists in tamponade. Second, they showed that in the absence of augmented right heart filling during inspiration, pulsus does not occur. Finally, they concluded that the inspiratory increase in right heart outp,ut becomes manifest in the systemic circulation two or three beats later as an expiratory increase in systemic flow and pressure. This pathologic decline in arterial pressure with inspiration, pulsus paradoxus, may occur in any state which augments variations in intrapleural pressure, and hence right heart filling. Most common is obstructive respiratory disease. 19 While there is some controversy concerning the incidence of pulsus in tamponade,54 it is generally held that this sign is uniformly present. 60 In severe cases the pulse will disappear on inspiration in a patient who is breathing at his physiologic rate and volume. In more subtle presentations it can be measured with a blood pressure cuff. Air is allowed to escape very slowly after inflating the cuff. Because systolic blood pressure will be higher in expiration, the first sounds heard should be those in expiration, and this can be confirmed by observing the patient. As cuff pressure falls further, Korotkoff sounds from the inspiratory phase will gradually become audible. Eventually, sounds from the heart beats in both parts of the respiratory cycle will become uniformly
578
WALTER
J.
PORIES AND VINCENT
A.
GAUDIANI
audible. The difference between this pressure and the pressure when sounds are first heard in expiration defines the magnitude of the pulsus paradoxus.
Diagnostic Approaches
Cardiac Tamponade
Walter J. Pories, M.D.,* and Vincent A. Gaudiani, M.D.t
Three related parameters determine the natural history of cardiac tamponade: the structure of the pericardium, the rate of pericardial fluid accumulation, and the hemodynamic response to cardiac compression. The pericardium is a fibroserous sac which envelops the heart. 28 It is flexible, but inelastic, and distends only as a result of prolonged pressure. When fluid or gas collects in the pericardium, the initial 80 to 120 ml are easily accommodated in the anatomic pericardial recesses. 60 The response to further effusion depends on the rate of fluid accumulation. If rapid, an additional 50 ml may cause death; if slow, several liters may cause little impairment. The immediate hemodynamic response to elevated pressure within the pericardium is decreased cardiac output, but compensatory mechanisms mitigate this effect. When they are overwhelmed by further increases in intrapericardial pressure, cardiac tamponade occurs. Tamponade is a surgical emergency because death follows rapidly if the pressure is not relieved. The etiology of the effusion and its pH composition and flora determine future prognosis and therapy, but prompt correction of the immediate threat to life must be the surgeon's first task. To accomplish it, he must recognize the clinical situations in which tamponade might occur, and he must understand the pathophysiology and how to reverse it.
PATHOLOGIC PHYSIOLOGY The fatal potential of cardiac tamponade has been recognized for several hundred years, but its mechanism has remained controversial into the present century. Ambrose Pare 3 described a case of. traumatic hemopericardiuin in the sixteenth century. In the seventeenth century, 'Professor of Surgery, Case Western Reserve University School of Medicine; Director, Department of Surgery, Cleveland Metropolitan General Hospital, Cleveland, Ohio t Assistant Resident Surgeon, Case Western Reserve University School of Medicine at Cleveland Metropolitan General Hospital, Cleveland, Ohio
Surgical Clinics of North America- Vol. 55, No.3, June 1975
573
574
WALTER
J.
PORIES AND VINCENT
A; GAUDIANI
Lowers1 described the heart "compressed with water on every side so that ... it ... cannot dilate to receive the blood'; then truly the pulse diminishes until at length it is suppressed by even more water, when syncope, and death itself follows." Rose 53 introduced the term cardiac tamponade in 1884, and by 1900 Cohnheim8 and Starling63 had independently experimented with tamponade as a model of cardiac failure. Both demonstrated a fall in aortic pressure. Cohnheim erroneously attributed it to obstructed cardiac filling at the venoatrial junction. Starling reas&hed correctly that aortic pressure fell because "diastolic expansion of the ventricles began to be affected." The venoatrial theory was widely accepted until 1954 when Isaacs and his co-workers 30 clearly documented Starling's position by showing that no appreciable pressure gradient occurred at the venoatrial junction. The crucial hemodynamic sequence in cardiac tamponade is impaired ventricular filling causing decreased cardiac output. Isaacs applied Starling's later work on the control of cardiac output to explain how this occurs. The Frank-Starling mechanism, Starling's law,64 holds that stroke volume is directly proportional to ventricular filling. Filling, in turn, depends on the gradient between venous pressure and ventricular diastolic pressure. In tamponade, increased pericardial pressure is transmitted through the ventricular wall and elevates ventricular diastolic pressure. Therefore, the filling pressure gradient diminishes. A small decrease in this gradient causes a large decrease in flow because resistance in the venous circuit is low. Less blood fills the ventricle, the myocardium is stretched less, and the stroke volume and the force of contraction fall. 27 A simplified diagram of these events is presented in Figure 1. The decreased cardiac output produces a fall in arterial pressure, venous return, and tissue perfusion. Myocardial blood flow drops because of increased pressure on the coronary vessels and lowered perfusion pressure. 44 While tamponade has caused myocardial necrosis and enzyme changes in experimental animals,12 the final effect of tamponade on coronary flow is unsettled. 21 Compensatory Mechanisms Compensatory mechanisms can counteract the progressive hemodynamic changes of tamponade. Heart rate increases to maintain systemic output because stroke volume is limited. In the peripheral circulation, catecholamines support arterial pressure and venous return by vasoconstriction. If the onset of tamponade is sufficiently prolonged, decreased renal. blood flow will promote sodium retention and increased intravascular volume. The net effect is elevated venous pressure to maintain cardiac filling. . These compensatory mechanisms may themselves stress the heart. 60 Tachycardia decreases coronary blood flow by increasing the proportion of the cardiac cycle spent in systole, and elevated catecholamines increase myocardial oxygen consumption. If successful, however, compensatory mechanisms reestablish circulatory homeostasis and allow the pericardium to stretch or possibly absorb the effusion.
575
CARDIAC TAMPONADE
THE
PATHOPHYSIOLOGY OF CARDIAC
TAMPONADE
Fluid or Gas I ItlNTRAPERICARDIAL PRESSURE I Distending the Pericardium ~ ....____tpressure on Atria S. Ventricles
l l
tCoronary Blood Flow
tVentricular Diastolic Pressure
I. VENTRICULAR
tStroke
FILLING I
l
*
Volume
~l~
,Arterial Pressure
tVenous Return
Wide A-V O2 Difference
Figure 1. The crucial hemodynamic sequence in cardiac tamponade is impaired ventricular filling causing decreased stroke volume.
Further increases in pericardial effusion have increasingly severe effects. Morgan and his associates,41 studying the pressure-volume characteristics of the pericardium, demonstrated an exponential effect of volume on pressure. A considerable volume may be necessary to cause an initial increase in pericardial pressure, but subsequent small additions may sharply increase pressure and cause sudden catastrophic deterioration. This relationship is shown in Figure 2. They also demonstrated hysteresis in pericardial pressure-volume curves. This explains why removing a small amount of pericardial fluid decreases pressure sharply and causes dramatic clinical improvement. A diagrammatic summary of the major compensatory mechanisms in cardiac tamponade is shown in Figure 3. Compensatory mechanisms fail when tachycardia and vasoconstriction can no longer counterbalance a falling stroke volume. Cardiac output falls as do venous return and arterial pressure. With venous return decreasing, the ventricular filling pressure gradient becomes even smaller, and a deteriorating cycle is established between output and pressure gradient which leads to total circulatory collapse.
DIAGNOSIS In 1935 Beck5 summarized the major clinical findings in acute cardiac compression: a rising venous pressure, a falling arterial pressure, and small, quiet heart. Although Beck's triad is not always present, it remains a valuable reminder that central venous hypertension, decreased cardiac output, and the pericardial effusion are responsible for the majority of signs and symptoms of cardiac tamponade. Elevated venous pressure distends neck veins, and if persistent, causes hepatomegaly, ascites, hepatojugular reflux, and peripheral edema. Decreased
a
«
576
WALTER
J.
PORIES AND VINCENT
A.
GAUDIANI
10
0
N
I
8
E
.:: w
6
0::
::::> (f) (f)
w
4
0::
a..
...J
2
« 0
0::
«
*
0
u
-
0::
w -2
a..
-4
40 80 120 160 PERICARDIAL VOLUME
200
240
IN ML
Figure 2. Pressure drops more sharply on removing fluid from the pericardium (out), than it rises when fluid accumulates (in). This explains why the onset of tamponade is frequently insidious and rapid relief may be obtained by aspirating only small amounts. (Redrawn from Morgan, B. C., et al.: Relationship of pericardial to pleural pressure during quiet respiration and cardiac tamponade. Circ. Res., 16:493, 1965.)
+ Peri cord io I Pre ssu re tvenous
t~S~T.~R~O~~E.E~IIi~V'!:.L!:.U.~'M~E=.J1
- - - - i...U!
Return
'IAct""'~ In,,", p"""," Pressure Receptors +cotechoL mines
RENAL BLOOD FLOW
TACHYCARDIA
/
tNo Retention
j Return
-------I.... +cordioc
Output
Figure 3. Compensatory mechanisms can counteract the progressive hemodynamic changes of tamponade.
CARDIAC TAMPONADE
577
cardiac output leads to tachycardia, poor peripheral pulses, and vasoconstriction. Dyspnea, tachypnea, and oppressive precordial discomfort radiating to the arms and varying with position arise from the mechanical effect of the effusion as well as inadequate systemic output. Ankle swelling, increasing abdominal girth, and nonspecific abdominal complaints result from systemic venous engorgement. 60 Many signs have been related to the pericardial effusion. The precordium is quiet and heart sounds are diminished. Dressler's sign, retrosternal flatness to percussion, and Ewart's sign, dullness and bronchial breathing in the midscapular lines, may be elicited. If the pericardium is inflamed, a friction rub may be audible even with a large effusion, and in hydropneumopericardium, a metallic splashing sound can be heard.
Pulsus Paradoxus Perhaps the most specific sign of tamponade, although not pathognomonic, is pulsus paradoxus. Kussmaup5 first used this term in 1873 to define an exaggerated inspiratory decline in arterial pressure which reverted to its normal contour on expiration. He called it "paradoxic," not because it is a reversal of the usual physiologic state, which it is not, but because there is no evidence of cardiac irregularity while these changes occur. Over the past 50 years, the mechanism of Kussmaul's pulse has generated considerable controversy.23 Previous investigators postulated inspiratory traction on the pericardimp12 and left ventricular compression by the right ventricle during inspiration 13 as possible mechanisms. Shabetai and his coworkers 55 ,56 have established the current concepts. First, they showed that the usual pattern of augmented right heart filling during inspiration persists in tamponade. Second, they showed that in the absence of augmented right heart filling during inspiration, pulsus does not occur. Finally, they concluded that the inspiratory increase in right heart outp,ut becomes manifest in the systemic circulation two or three beats later as an expiratory increase in systemic flow and pressure. This pathologic decline in arterial pressure with inspiration, pulsus paradoxus, may occur in any state which augments variations in intrapleural pressure, and hence right heart filling. Most common is obstructive respiratory disease. 19 While there is some controversy concerning the incidence of pulsus in tamponade,54 it is generally held that this sign is uniformly present. 60 In severe cases the pulse will disappear on inspiration in a patient who is breathing at his physiologic rate and volume. In more subtle presentations it can be measured with a blood pressure cuff. Air is allowed to escape very slowly after inflating the cuff. Because systolic blood pressure will be higher in expiration, the first sounds heard should be those in expiration, and this can be confirmed by observing the patient. As cuff pressure falls further, Korotkoff sounds from the inspiratory phase will gradually become audible. Eventually, sounds from the heart beats in both parts of the respiratory cycle will become uniformly
578
WALTER
J.
PORIES AND VINCENT
A.
GAUDIANI
audible. The difference between this pressure and the pressure when sounds are first heard in expiration defines the magnitude of the pulsus paradoxus.
Diagnostic Approaches
