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Regional cardiac tamponade: A hemodynamic study
164
JACC VoL 10, No. I July 1987: 164--9
Regional Cardiac Tamponade: A Hemodynamic Study NOBLE O. FOWLER, MD, FACC, MARJORIE GABEL Cincinnati. Ohio
In 10 dogs, atrial tamponade, ventricular tamponade and then combinedatrioventricular (AV) tamponade were produced at 10, 15 and 20 mm Hg intrapericardial pressure. Cardiac output decreased significantlyat each level of cardiac tamponade; the changes in cardiac output and mean aortic pressure were comparable with atrial and ventricular tamponade. Combined atrial and ventricular tamponade produced significantly greater increases of right and left atrial pressure and significantly greater decreases of cardiac output than did either atrial or ventricular tamponade. During atrial tamponade only,
Cardiac tamponade usually results from a general increase in intrapericardial pressure that is applied to the surfaces of the atria, the ventricles and the intrapericardial surfaces of the venae cavae and pulmonary veins, as well as the aorta and the pulmonary arteries. However, especially in postoperative patients, either because of clot formation or loculation of blood or other fluid, cardiac tamponade may result from localized or regional compression of the right atrium (I) or the left side of the heart (2). For this reason, the hemodynamic effects of regional cardiac compression are of practical interest. In addition, there is a theoretical interest in the hemodynamic effects of tamponade, because there is a postulate as well as experimental evidence that compression of the great veins, the atria or the right cardiac chambers may be of major significance in bringing about the fall in cardiac output and arterial blood pressure that is ordinarily associated with cardiac tamponade (3). In a previous study (4), we reported hemodynamic studies of regional cardiac tamponade that suggested that atrial compression was of major importance in producing the hemodynamic effects of tamponade . However, in that study , we were able to evaluate the effects of compression of only the right or the left ventricle separately. Because the effect of compression of both ventricles might well be different From the Division of Cardiology , Department of Medicine, University of Cincinnati College of Medicine , Cincinnati, Ohio. Manuscript received November 18, 1985; revised manuscript received November 19, 1986, accepted December IS, 1986. Addn:ss for reprints: Noble O. Fowler, MD, University of Cincinnati College of Medicine, Division of Cardiology, M.L.542, 231 Bethesda Avenue, Cincinnati, Ohio 45267. © 1987 by the American College of Cardiolo gy
a significant pressure gradient developed between the venae cavae and the right atrium. Compression of both ventricles by tamponade has a much greater hemodynamic effect than does compression of either ventricle alone. Compression of the entire heart has a greater hemodynamic effect than does compression of the atria alone or the ventricles alone. Compression of the great veins has a potential effect in tamponade, demonstrable when the ventricles could fill normally. (J Am Coil Cardiel 1987;10:164-9)
from that of compression of a single ventricle, we developed a method to study the comparative effects of compression of the two atria and great veins together, the two ventricles together and then of simultaneous compression of all four cardiac chambers in the same animal. We also studied pressure gradients between the venae cavae and the right atrium to look for evidence of caval compression as a contributing factor in the hemodynamic effect s of cardiac tamponade.
Methods Production of Regional Cardiac Tamponade This preparation was carried out in three stages requiring three separate thoracotomies . Ten mongrel dogs of either sex weighing between 17 and 30 kg were anesthetized with pentobarbital sodium, 25 mg/kg body weight, to obtain a surgical plane of anesthesia. First stage. Through a left lateral thoracotomy at the fourth intercostal space the pericardial sac was incised at the atrial level. The pericardium was sutured together and to the superficial myocardium with interrupted sutures using 3-0 silk with atraumatic needles previously soaked in phenol to ensure complete adhesions at the suture lines between pericardium and myocardium. Suturing was done so as to isolate the left and right ventricles from the atria avoiding compromise of the left circumflex and left anterior descending coronary arteries. On the left , the suture line was just inferior to the circumflex branch of the left coronary artery and great coronary vein, and just superior to the conus branch of the right coronary artery (Fig. I). With a cotton0735-1097/87/$3 .50
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FOWLER AND GABEL REGIONAL CARDIAC TAMPONADE
JACC Vol. 10. No. I July 1987:164-9
l. aur i c l e
,,
,
l. pu lmonary a.
_-, l. pu lmon ar y vv . ~
Aort i c ar ch - - - -
Figure 1. Stage I. Left thoracotomy. The placement of sutures for separation of atrial and ventricular pericardium is illustrated. (Modified with permission from Fig. 4-4 from Miller ME. Anatomy of the Dog. Philadelphia, London: WB Saunders, 1964.) a. = artery; br. = branch; L. = left; R. = right; v. = vein; vv. = veins.
- - - - Gr e a t c o r o na r y v ,
l. coronary a .
-
_
- - Sut ur e lin e -- - C i r c um fl e x b r an c h
R. aur icle __
Ventral Int e r v en t ri c ul ar br. - -Great coronary v . -- -- --
--- l. vent r icle
R. ventr icle
tipped swab a light coat of phenol was applied to the area of the suture line. The thoracotomy was repaired in four layers and the pneumothorax was reduced. During the operation, soluble Berocca-C (6 cc) and cephapirin sodium (Cefadyl) (20 g) were given intravenously followed by daily intramuscular injections of 2 ml Azimycin. All dogs were allowed to recover for at least 10 days to ensure complete adhesions at the suture line and myocardium. This stage provided separation of the anterior atrial pericardial space from the anterior ventricular pericardial space.
Second stage. Preparation was as previously described, except that a right thoracotomy was performed. Again the pericardium was incised and sutures were placed outlining the atrial and ventricular dividing line. Suturing followed a line just to the right of the right coronary artery and then just beneath the dorsal interventricular branch of the left coronary artery (Fig. 2). The suture area was painted with phenol. Postoperative care was the same as before, allowing 10 days for recovery. This stage provided separation of the
R. pulmonary vv. Po s t c a v a ,",
R. pulmonary a .
,,
/
D ors . in te r ven tric ula r br . 0 1 lelt co ro na ry a. ... .
Figure 2. Stage 2. Right thoracotomy. The placement of sutures for separation of atrial and ventricular pericardium is illustrated. (Modified with permissionfrom Fig. 4-5 from MillerME. Anatomyof the Dog. Philadelphia, London: WB Saunders, 1964.) Dors. = dorsal; other abbreviations as in Figure I.
I
, R. auricle
,,/
. .. . .
,. ---- A or t a
R. v ent r ic le -
- - Sut ur e line - -- Conus arter iosus
-- - -- -
R. coron ary a.
, Le l t v ent r ic l e I
I
I
V ent r al i nt er v en t ri cula r br . 01 le l t c o r o na r y a .
, I I
, I
R. atr ium
166
FOWLER AND GABEL REGIONAL CARDIAC TAMPONADE
posterior atrial pericardial space from the posterior ventricular pericardial space. In combination with the first stage, there was now complete separation between atrial and ventricular pericardial spaces. Third stage. Preparation was as previously described. A small right thoracotomy was performed at the third intercostal space. Tygon catheters (IOF) with multiple distal side holes were placed in the atrial and ventricular pericardial spaces and filled with heparinized saline solution and the proximal ends were closed. Catheters were tunneled to a right subcutaneous pocket. Postoperative care was as before, allowing 5 to 6 days for recovery. This stage provided for measurement of atrial and ventricular pericardial pressures separately during cardiac tamponade without the need to perform a thoracotomy during the tamponade experiments.
Experimental Procedure The dogs were reanesthetized with intravenous pentobarbital sodium, 25 mg/kg, and were breathing spontaneously. Under fluoroscopy, 7F Cournand catheters were placed in the right atrium, pulmonary artery and aorta of each for pressure measurements; a thermistor tipped catheter was placed through the jugular vein in the pulmonary artery for thermodilution cardiac output determinations. For the measurement of superior and inferior venae cavae pressures, 7F Cournand catheters were advanced to the extrapericardial positions of those vessels. For measurement of left atrial pressures, a Shirey catheter was passed from the carotid artery to the left atrium under fluoroscopy. Statham 23dB pressure transducers were used to measure right atrial, left atrial, intrapericardial and systemic arterial pressures. These pressures and an electrocardiogram (ECG) were recorded with an eight channel Grass 70 polygraph recorder. Electronically derived mean pressures were measured with the animal lying on its right side; the center of the thorax was used for zero reference. Aortic mean pressures were determined by planimetric integration. Pressure transducers were calibrated with mercury manometers before each experiment. Control cardiac pressures and cardiac outputs were measured. Cardiac tamponade was then induced by stepwise increases of intrapericardial pressure by injection of a 0.9% sodium chloride 37°C solution into the pericardial sac. Intrapericardial pressure was raised to 10 mm Hg and after 2 minutes of stabilization, hemodynamic measurements were made. Cardiac output and pressure measurements were then repeated. A similar procedure was carried out at intrapericardial pressures of 15 and then at 20 mm Hg. Each animal was evaluated with atrial tamponade, ventricular tamponade and combined atrial and ventricular tamponade. Ventricular tamponade was performed first in six dogs, atrial tamponade first in one and combined tamponade first in three. The
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absence of leaks across the suture line was demonstrated during the experiment by failure of the periventricular pericardial space pressure to rise during atrial tamponade. Mean intrapericardial pressure in the ventricular portion was - 3.4 mm Hg in the control period and was - 3.5 mm Hg when intrapericardial pressure was increased to 20 mm Hg in the atrial portion. When ventricular tamponade was produced with a pressure of 20 mm Hg, the intrapericardial pressure rose slightly in the atrial segment from a mean of zero to a mean of 2.2 mm Hg, probably owing to a rise in atrial pressure. At the termination of experiments. each dog was killed with an intravenous overdose of pentobarbital. Autopsy was performed and the absence of leaks between atrial and ventricular pericardial spaces was demonstrated by injection of physiologic saline solution colored with blue dye. The pericardial spaces themselves were demonstrated to be free of adhesions. Statistics. All values are expressed as mean values ± SEM. Values <0.05 were considered significant (Student's t test).
Results (Tables 1 and 2) Atrial tamponade. Tamponade of the two atria produced a significant decrease in cardiac output and stroke volume as compared with the control value at each level of intrapericardial pressure (10, 15 and 20 mm Hg). Heart rate increased significantly at the 15 and 20 mm Hg levels, but not at 10 mm Hg. Aortic mean blood pressure was not significantly lower than control at 10, 15 or 20 mm Hg intrapericardial pressure. Right atrial mean pressure was significantly above the control value at each level of intrapericardial pressure, but left atrial pressure did not change significantly. Ventricular tamponade. Tamponade of the two ventricles decreased cardiac output and stroke volume significantly below the control value at each level of intrapericardial pressure. Heart rate increased significantly at the 15 and 20 mm Hg levels, but not at the 10 mm Hg level. Aortic mean pressure was not significantly decreased at any of the three levels of intrapericardial pressure. Right and left atrial pressures were each significantly higher than control values at each of the three levels of intrapericardial pressure. Left, but not right, atrial pressure was significantly higher than that during atrial tamponade at each level of intrapericardial pressure. Cardiac output was lower at 20 mm Hg intrapericardial pressure with atrial than with ventricular tamponade; this was of borderline statistical significance but stroke volume was significantly lower with atrial tamponade. Aortic mean pressure changes were not significantly different between atrial and ventricular tamponade. Combined atrial and ventricular tamponade. With combined atrial and ventricular tamponade, the hemody-
E.>
'
~<
:-:J2. 0'_
t?
Table 1. Hemodynamic Effects of Regional Cardiac Tamponade in 10 Dogs Atrial Tamponade AnI' Control
RAP
LAP
'D
CO
SV
HR
RAP
LAP
CO
HR
SV
3.7 :': 0.6
8.8 :': 1.1
95 :': 6.6
176 :': 7.2
\2.7 :': 0.7
\52 :': 6.1
44 :': 0.8
8.2 :': 0.9
88 :': 5.7
170 :': 8.9
124
59
116 :': 1.0"11 12.7 ± 1 5 tll 14 ± 13 t!1
77
182 :': 81 192
98
± O.5t
195 :': 5 5*
7.9
8.8 :': 0.6 fll** 10.9 :': 1.2t§ 15.9 :': 1.3"11**
11.5
:±: 6.4*
143 :': 4.9t 138 .r: 4.4* 134 ± 7.0*
58 :': 3.5 tll** 46 :': 3 1"11** 33 :': 2.?tIl*'
188 :': 7.9' 205 ± 7. 7t~ 217
75 :': 07t~~ 54 :': 0·6t1l** 38 :': 0.5 tll**
144 :': 3.9
3.7 :': 07
8.1 :': 1.0
95 :': 5.2
173 :': 8.0
13.0 :': 0.7
146 :': 5.8 138.6 :': 6. J IJ96 ± 6.7
5.5 :': 0.7 t 68 :': 08t 79 :': 08"
80 :': 1 I 78 :': 1.2 8.6 :': 1.2
7J ± 4.7"
183 ± 6.0 194
94
145 :': 5.6 141 :': 63 141.1 :': 6.8
RAP
AoP
LAP
CO
SV
AoP 150.2 :': 6.9
Z
a
Atrial and Ventricular Tamponade
Ventricular Tamponade
HR
:':1.1
Pericardia! pressure
10 mm Hg 15 mm Hg 20 mm Hg
65 ± 4.lt
58 ± 4.6"
:!:
5.4*
203 ± 5.6"
± 0.5 f
7.9 :': 05t 6.7 :': 06"~
± 0.6i
6.8 :': 0.8t 8.3 :': 0.9"
:': 5.77 71 :': 5.4t 66 :': 40 f t
± 0.5t
8.6
± OAH
-t I. 1711
12.5 :': 1·6t1l 15.9 ± 13 tll
± 6, gt**
Values are expressed as mean values ± SE (Student's paired 1 test). *p < 0.02 versus control: tp < 0.01 versus control: :j:p = 0.053 versus atrial tamponade: §p < 0.05 versus atrial tamponade: lip <.01 versus atrial tamponade: ~Ip < 0.05 versus ventricular tamponade: **p < 0.01 versus ventricular tamponade. AoP= mean aortic blood pressure (rnm Hg): = cardiac output (nil/kg per min): HR = heart rate (heats/min): LAP = mean left atrial pressure (mm Hg): RAP = mean right atrial
eo
pressure (rnm Hg): SV
=
cardiac stroke volume (ml).
Table 2. Venae Caval and Right Atrial Pressures During Regional Cardiac Tamponade in Seven Dogs Atrial Tamponade
Control Pericardial pressure 10 mm Hg 15 mm Hg 20 mm Hg
RAP
sve
rvc
36 ± 0.7
46 ± 0611
4.7 ± 0.611
Atrial and Ventricular Tamponade
Ventricular Tamponade
eo 92A ± 7.0
RAP
sve
rvc
eo
RAP
sve
ivc
3.6 ± 1.7
42 ± 0611
4.3 ± 0711
90A ± 8.9
4.3 ± 0.9
4.9 ± 0.911
4.8 ± 0.9[[
eo 90.5 ± 5.7
;;c trt
C
o z
6.1 ± 0.8
8.3 ± 0.7*
7.9 ± 0.8*
63.0 ± IO.Rt
6.0 ± 0.8
6.7 ± 0.511
6.8 ± 0.811
74.6 ± 7.8::':
8.9 ± 0.8
10.2 ± 1.311
9. I ± 1.211
62.3 ± 2.8::':
7.6 ± 1.0
10.6 ± OAt
10.1 ± 0.6*
61.8 ± 5.6::':
7.1 ± 1.0
8.1 ± 0.711
8.\ ± 0911
68.8 ± 61::':
10.8 ± 1.7
12.9 :': 1.211
13.1 ± 1.311
479 ± 2.3+§
9.0 ± 1.2
12.9 ± 0.6t
11.8 :': 0.8"
54A :': 6.3:j:
8.6 ± 1.3
9.1 ± 0.911
96 ± 1211
63.3 ± 5 .\:j:
J5.2 ± 1.3
» r
n
»..,.,
;;co 16.6 ± 1.611
17.1 ± 1411
356 ± Vl:j:§
S2~
»t"" m
n...,;;c »» z 3:: ",0
::,:eo
Values are expressed as mean values ± SE (Students paired 1 test). *Signincantly greater than RAP, p < 0.02; tsignificantly greater than RAP, p < 0.01; signficantly less than control (p < O.Ol): § SIgnificantly less than during atrial or ventricular tamponade (p < 0.05): Iinot significantly different from RAP. p > 0.05. IvC = inferior caval mean pressure (mm Hg): SVC = superior caval mean pressure (rnrn Hgj: other abbreviations as in Table I.
eo
Oc
z» »c:>
Om
mr-
0\ --.I
168
FOWLER AND GABEL REGIONAL CARDIAC TAMPONADE
namic changes were more pronounced than with either atrial or ventricular tamponade alone regardless of the order in which tamponade was produced (Table I). Cardiac output and stroke volume were significantly lower and right atrial pressure was higher with combined atrial and ventricular tamponade than with either alone at each level of intrapericardial pressure. Heart rate increased significantly at each level of intrapericardial pressure and was significantly greater with combined than with ventricular tamponade, but not with atrial tamponade, at 15 and 20 mrn Hg intrapericardial pressure. Left atrial pressures were higher during combined tamponade than during atrial tamponade but not higher than during ventricular tamponade. The decrease in aortic pressure during combined tamponade was significant, but not significantly different from that during atrial or ventricular tamponade alone. Atrial waveforms. With atrial tamponade, waveforms were recorded in nine dogs. In the right atrium of five dogs large C-V waves or larger V waves developed; one dog showed a larger A wave and one a deeper X wave; two dogs showed no change. In the left atrium of four dogs, C-V waves or larger V waves developed; one dog showed a deeper X wave and four dogs had no change. With ventricular tamponade, five of seven dogs showed no change in right atrial waveforms and six of eight showed no change in left atrial waveforms. Two showed larger A waves in the right atrium and left atrium, one showed a large C-V wave and one a larger A wave. With combined tamponade, only one of six dogs showed a larger C-V wave in the right atrium and five showed no change. Only one of eight dogs developed a large C-V wave in the left atrium; three dogs showed smaller X waves, one a shallower Y wave and three showed no change. Thus, only with atrial tamponade did the majority develop V waves or large C-V waves suggesting tricuspid or mitral regurgitation; however, these changes might have been due to changes in atrial compliance. Larger A waves in a few dogs during ventricular tamponade might reflect decreased ventricular compliance. With combined tamponade, a few dogs showed shallower X waves. Only one showed a smaller Y wave as has been described in cardiac tamponade; none showed larger X waves. Superior and inferior venae cavae pressures. In seven animals, inferior and superior venae cavae pressures were measured during the control period and during cardiac tamponade at 10, 15 and 20 mm Hg intrapericardial pressure (Table 2). Control inferior and superior venae cavae pressures were not significantly different from right atrial mean pressures. However, the inferior vena cava pressure (7.9 ± 0.8 mm Hg) and superior vena cava pressure (8.3 ± 0.7 mm Hg) were significantly higher than right atrial mean pressure (6.1 ± 0.8 mm Hg) at 10 mm Hg intrapericardial pressure. At 15 mm Hg intrapericardial pressure, inferior vena cava mean pressure (10.1 ± 0.6 mm Hg) and superior
JACC Vol. 10. No. I July 1987:164-9
vena cava pressure (10.6 ± 0.4 mm Hg) were significantly higher than mean right atrial pressure (7.6 ± 1.0 mm Hg). This was also true at 20 mm Hg intrapericardial pressure: inferior vena cava pressure (11.8 ± 0.8 mm Hg) and superior vena cava pressure (12.9 ± 0.6 mm Hg) were both significantly greater than right atrial mean pressure (9.0 ± 1.2 mm Hg). With ventricular tamponade. inferior and superior venae cavae pressures were not significantly different from right atrial pressure at any time, either in the control period or during tamponade with intrapericardial pressures of 10, 15 and 20 mm Hg (Table I). This was also true with combined atrial and ventricular tamponade; the inferior and superior venae cavae pressures were not significantly different from right atrial pressure at the several degrees of cardiac tamponade.
Discussion Previous investigations. In a previous study of regional tamponade in dogs (4), we evaluated the hemodynamic effects of compression of both atria and one ventricle as compared with the effects of compression of either the right or the left ventricle alone. In that study, tamponade of either ventricle alone had little hemodynamic effect, whereas compression of one ventricle and the two atria had essentially the same effect on blood pressure and cardiac output as did generalized tamponade of the entire heart, including the intrapericardial great arteries and veins. That study thus suggested that the compression of the atria, venae cavae and pulmonary veins played the major role in the hemodynamic effects of tamponade of the heart. Hemodynamic effects of atrial or ventricular tamponade alone. The present investigation modified these conclusions in an important way. Although tamponade of one ventricle had little hemodynamic effect in the previous study, in the present study tamponade of both ventricles had a hemodynamic effect that was very similar to that of atrial tamponade, whereas neither atrial nor ventricular tamponade had effects on blood pressure or cardiac output that were as great as the effects of combined atrial and ventricular tamponade in the same animals. It is of interest to consider why the effects of tamponade of both ventricles are so much greater than the effects of tamponade of either ventricle alone. It appears probable that, when pressure is exerted on the surface of one ventricle alone, the ventricular septum may shift in the direction of the other ventricle, where pericardial pressure remains subatmospheric, thus permitting diastolic filling to occur with minimal hindrance. However, when both ventricles are subject to tamponade, diastolic filling must compete for space in the same pressurized chamber, thus leading to impairment of filling of both ventricles. The present study implies, therefore, that the maximal effects of cardiac tamponade require
JACC Vo!. 10. No. I
July 19R7:IM-9
pressure on the entire heart, and not just the atria or ventricles alone. This study does not deal with the suggestion of Ditchey et al. (3) that compression of the right heart is of much greater importance than compression of the left heart in the sequence of events that takes place in tamponade of the heart. Evidence for vena caval compression during cardiac tamponade. Another interesting feature of the present study concerns the relation of vena caval pressures to right atrial pressure during atrial tamponade. Caval pressures rose in the expected fashion in cardiac tamponade in all three settings: atrial tamponade, ventricular tamponade and combined atrial and ventricular tamponade. However, right atrial pressure rose as expected only with ventricular tamponade and combined tamponade, but not with atrial tamponade. Further, a signifi cant pressure difference developed between caval pressures and right atrial pressure during atrial tamponade only, suggesting that there is significant caval compression during tamponade. Cohnheim (5) had originally implied that increased intrapericardial pressure caused an obstacle to entrance of blood from systemic veins into the heart. The cavae, having thinner walls, may be expected to be more compliant than the right atrium. Cardiac tamponade, when the entire heart is involved. produces a rise in atrial and ventricular diastolic pressures. which at first usually are equal to the pressure level in the intrapericardial space. However, as the pressure in the pericardial space increases further, the rise in atrial and ventricular diastolic pressures is less than the rise in intrapericardial pressure. Thus the transmural atrial and ventricular diastolic pressures become negative (6). This effect is presumably owing to ventricular diastolic suction. We showed (6) that in experimental tamponade , negative transmural right atrial pressure developed when intrapericardial pressure was 10.8 mm Hg or greater. In that study, negative transmural right ventricular diastolic pressure of as much as 8 rnrn Hg was produced. In still another study (7). obstruction to venous inflow to the right heart was associated with negative transmural right ventricular diastolic pressure. In the present investigation, right atrial pressure did not rise significantly during atrial tamponade. Thus a negative transmural right atrial pressure was present as pericardial pressure exceeded right atrial pressure. The mechanism involved may well be similar to those cited before. The right ventricle, when its filling is limited by partial obstruction to inflow by the compression of the right atrium and venae cavae, is capable of exerting a diastolic suction effect. thus lowering atrial pressure below pericardial pressure and producing a negative transmural right atrial pressure. In the present study, when ventricular filling was impaired by ventricular tamponade or during combined tamponade, the potential ventricular diastolic suction effect was no longer demonstrated as evidenced by the absence of a signifi cant pressure difference between the venae cavae and
FOWLER AND GABEL REGIONAL CA RDIAC TA MPONADE
169
the right atrium. This finding agrees with the studies made by Isaacs et al. (8) in 1956, which showed no significant gradient of pressure between the venae cavae and right atrium when experimental animals were subjected to tamponade of the entire heart. Clinical implications. Regional cardiac tamponade may be of considerable clinical significance. especially after cardiac operations or trauma ( I,2). Yacoub et al. (9) described left atrial compression as a cause of cardiac tamponade in postoperative patients. Kidner et al. (10) described cardiac arrest in a patient with left atrial tamponade after cardiac perforation in the course of diagnostic cardiac catheterization. Kronzon et al. (II) reported three cases of loculated hematoma after cardiac operation causing compression of both atria in one patient and compression of the right atrium alone in two. All three patients had severe cardiac tamponade with shock and systemic venous pressure elevation. The investigators pointed out that regional tamponade, compressing the atria alone, may be missed by M-mode echocardiography, because there is no evidence of pericardial effusion surrounding the ventricles. Regional tamponade is especially likely to occur in postoperative patients. in whom adhesions and bleeding may cause loculated pericardial effusion. Isolated left atrial tamponade may produce shock without systemic venous pressure elevation in the postopcrative patient (9).
References I. Fyke fE III. Tancredi RG. Shub C. Julsrud PRo Sheedy PF II. Detection of intrapericardial hematoma after open heart surgery: the roles of echocardiography and computed tomography. J Am Coil Cardiel 19X5:5: 1496-9 . 2. D'Cr uz IA . Kensey K. Campbell C. Replogle R. Jain M. Two-dimensional echocardiogruphy in cardiac tamponade occurring after cardiac surgery. J Am Coli Cardie l 19X5 ;5: I25ll-2.
.I. Ditehey R. Engler R. LeWinter M. et al. The role of the right heart in acute cardiac tamponade in dogs. Circ Res 19X I;48:7ll1- 10. 4. Fowler NO. Gabel M. The hemodynamic effects of cardiac tamponade: mainly the result of atrial. not ventricular. compression. Circulation 19X5:71: 154-7 . 5. Cohnheim J. Lectures on General Pathology. vul I. The Circulation. London: New Sydenham Society. IXX9: 19- .1.1 (translated from the second German edition by Alexander B. McKee ). 6. Fowler NO. Shahetai R. Braunstein JR. Transmural ventricular pressures in experimental cardiac tamponade. Circ Res 1959:7:733- 9. 7. f owler NO. Couves C. Bewick J. Effect of inflow obstruction and rapid bleeding on ventricular diastolic pressure. J Thorac Surg 195X:35: 5.12- 7. X. Isaacs JP . Berglund E. Sarnoff SJ. Ventricular function: the pathologic physiology of acute cardiac tamponade studied by means of ventricular function curves. Am Heart J I954;4X:66-76. 9. Yacoub MH. Cleland WI'. Deal CWo Left atrial tamponade. Thorax 1966:2 Ull5-9 . Ill. Kidner PH. Kakkar VV. Cullum PA. Armstrong P. Left atrial tamponade. Report of a case after right heart catheterization . Br Heart J 1973:35:464-5 II. Kronzon I. Cohen ML. Winer HE. Cardiac tamponade by loculated pericardia! hematoma: limitations of M-mode echocardiography. J Am Coli Cardie l 1983;1:913-5 .
JACC VoL 10, No. I July 1987: 164--9
Regional Cardiac Tamponade: A Hemodynamic Study NOBLE O. FOWLER, MD, FACC, MARJORIE GABEL Cincinnati. Ohio
In 10 dogs, atrial tamponade, ventricular tamponade and then combinedatrioventricular (AV) tamponade were produced at 10, 15 and 20 mm Hg intrapericardial pressure. Cardiac output decreased significantlyat each level of cardiac tamponade; the changes in cardiac output and mean aortic pressure were comparable with atrial and ventricular tamponade. Combined atrial and ventricular tamponade produced significantly greater increases of right and left atrial pressure and significantly greater decreases of cardiac output than did either atrial or ventricular tamponade. During atrial tamponade only,
Cardiac tamponade usually results from a general increase in intrapericardial pressure that is applied to the surfaces of the atria, the ventricles and the intrapericardial surfaces of the venae cavae and pulmonary veins, as well as the aorta and the pulmonary arteries. However, especially in postoperative patients, either because of clot formation or loculation of blood or other fluid, cardiac tamponade may result from localized or regional compression of the right atrium (I) or the left side of the heart (2). For this reason, the hemodynamic effects of regional cardiac compression are of practical interest. In addition, there is a theoretical interest in the hemodynamic effects of tamponade, because there is a postulate as well as experimental evidence that compression of the great veins, the atria or the right cardiac chambers may be of major significance in bringing about the fall in cardiac output and arterial blood pressure that is ordinarily associated with cardiac tamponade (3). In a previous study (4), we reported hemodynamic studies of regional cardiac tamponade that suggested that atrial compression was of major importance in producing the hemodynamic effects of tamponade . However, in that study , we were able to evaluate the effects of compression of only the right or the left ventricle separately. Because the effect of compression of both ventricles might well be different From the Division of Cardiology , Department of Medicine, University of Cincinnati College of Medicine , Cincinnati, Ohio. Manuscript received November 18, 1985; revised manuscript received November 19, 1986, accepted December IS, 1986. Addn:ss for reprints: Noble O. Fowler, MD, University of Cincinnati College of Medicine, Division of Cardiology, M.L.542, 231 Bethesda Avenue, Cincinnati, Ohio 45267. © 1987 by the American College of Cardiolo gy
a significant pressure gradient developed between the venae cavae and the right atrium. Compression of both ventricles by tamponade has a much greater hemodynamic effect than does compression of either ventricle alone. Compression of the entire heart has a greater hemodynamic effect than does compression of the atria alone or the ventricles alone. Compression of the great veins has a potential effect in tamponade, demonstrable when the ventricles could fill normally. (J Am Coil Cardiel 1987;10:164-9)
from that of compression of a single ventricle, we developed a method to study the comparative effects of compression of the two atria and great veins together, the two ventricles together and then of simultaneous compression of all four cardiac chambers in the same animal. We also studied pressure gradients between the venae cavae and the right atrium to look for evidence of caval compression as a contributing factor in the hemodynamic effect s of cardiac tamponade.
Methods Production of Regional Cardiac Tamponade This preparation was carried out in three stages requiring three separate thoracotomies . Ten mongrel dogs of either sex weighing between 17 and 30 kg were anesthetized with pentobarbital sodium, 25 mg/kg body weight, to obtain a surgical plane of anesthesia. First stage. Through a left lateral thoracotomy at the fourth intercostal space the pericardial sac was incised at the atrial level. The pericardium was sutured together and to the superficial myocardium with interrupted sutures using 3-0 silk with atraumatic needles previously soaked in phenol to ensure complete adhesions at the suture lines between pericardium and myocardium. Suturing was done so as to isolate the left and right ventricles from the atria avoiding compromise of the left circumflex and left anterior descending coronary arteries. On the left , the suture line was just inferior to the circumflex branch of the left coronary artery and great coronary vein, and just superior to the conus branch of the right coronary artery (Fig. I). With a cotton0735-1097/87/$3 .50
165
FOWLER AND GABEL REGIONAL CARDIAC TAMPONADE
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l. aur i c l e
,,
,
l. pu lmonary a.
_-, l. pu lmon ar y vv . ~
Aort i c ar ch - - - -
Figure 1. Stage I. Left thoracotomy. The placement of sutures for separation of atrial and ventricular pericardium is illustrated. (Modified with permission from Fig. 4-4 from Miller ME. Anatomy of the Dog. Philadelphia, London: WB Saunders, 1964.) a. = artery; br. = branch; L. = left; R. = right; v. = vein; vv. = veins.
- - - - Gr e a t c o r o na r y v ,
l. coronary a .
-
_
- - Sut ur e lin e -- - C i r c um fl e x b r an c h
R. aur icle __
Ventral Int e r v en t ri c ul ar br. - -Great coronary v . -- -- --
--- l. vent r icle
R. ventr icle
tipped swab a light coat of phenol was applied to the area of the suture line. The thoracotomy was repaired in four layers and the pneumothorax was reduced. During the operation, soluble Berocca-C (6 cc) and cephapirin sodium (Cefadyl) (20 g) were given intravenously followed by daily intramuscular injections of 2 ml Azimycin. All dogs were allowed to recover for at least 10 days to ensure complete adhesions at the suture line and myocardium. This stage provided separation of the anterior atrial pericardial space from the anterior ventricular pericardial space.
Second stage. Preparation was as previously described, except that a right thoracotomy was performed. Again the pericardium was incised and sutures were placed outlining the atrial and ventricular dividing line. Suturing followed a line just to the right of the right coronary artery and then just beneath the dorsal interventricular branch of the left coronary artery (Fig. 2). The suture area was painted with phenol. Postoperative care was the same as before, allowing 10 days for recovery. This stage provided separation of the
R. pulmonary vv. Po s t c a v a ,",
R. pulmonary a .
,,
/
D ors . in te r ven tric ula r br . 0 1 lelt co ro na ry a. ... .
Figure 2. Stage 2. Right thoracotomy. The placement of sutures for separation of atrial and ventricular pericardium is illustrated. (Modified with permissionfrom Fig. 4-5 from MillerME. Anatomyof the Dog. Philadelphia, London: WB Saunders, 1964.) Dors. = dorsal; other abbreviations as in Figure I.
I
, R. auricle
,,/
. .. . .
,. ---- A or t a
R. v ent r ic le -
- - Sut ur e line - -- Conus arter iosus
-- - -- -
R. coron ary a.
, Le l t v ent r ic l e I
I
I
V ent r al i nt er v en t ri cula r br . 01 le l t c o r o na r y a .
, I I
, I
R. atr ium
166
FOWLER AND GABEL REGIONAL CARDIAC TAMPONADE
posterior atrial pericardial space from the posterior ventricular pericardial space. In combination with the first stage, there was now complete separation between atrial and ventricular pericardial spaces. Third stage. Preparation was as previously described. A small right thoracotomy was performed at the third intercostal space. Tygon catheters (IOF) with multiple distal side holes were placed in the atrial and ventricular pericardial spaces and filled with heparinized saline solution and the proximal ends were closed. Catheters were tunneled to a right subcutaneous pocket. Postoperative care was as before, allowing 5 to 6 days for recovery. This stage provided for measurement of atrial and ventricular pericardial pressures separately during cardiac tamponade without the need to perform a thoracotomy during the tamponade experiments.
Experimental Procedure The dogs were reanesthetized with intravenous pentobarbital sodium, 25 mg/kg, and were breathing spontaneously. Under fluoroscopy, 7F Cournand catheters were placed in the right atrium, pulmonary artery and aorta of each for pressure measurements; a thermistor tipped catheter was placed through the jugular vein in the pulmonary artery for thermodilution cardiac output determinations. For the measurement of superior and inferior venae cavae pressures, 7F Cournand catheters were advanced to the extrapericardial positions of those vessels. For measurement of left atrial pressures, a Shirey catheter was passed from the carotid artery to the left atrium under fluoroscopy. Statham 23dB pressure transducers were used to measure right atrial, left atrial, intrapericardial and systemic arterial pressures. These pressures and an electrocardiogram (ECG) were recorded with an eight channel Grass 70 polygraph recorder. Electronically derived mean pressures were measured with the animal lying on its right side; the center of the thorax was used for zero reference. Aortic mean pressures were determined by planimetric integration. Pressure transducers were calibrated with mercury manometers before each experiment. Control cardiac pressures and cardiac outputs were measured. Cardiac tamponade was then induced by stepwise increases of intrapericardial pressure by injection of a 0.9% sodium chloride 37°C solution into the pericardial sac. Intrapericardial pressure was raised to 10 mm Hg and after 2 minutes of stabilization, hemodynamic measurements were made. Cardiac output and pressure measurements were then repeated. A similar procedure was carried out at intrapericardial pressures of 15 and then at 20 mm Hg. Each animal was evaluated with atrial tamponade, ventricular tamponade and combined atrial and ventricular tamponade. Ventricular tamponade was performed first in six dogs, atrial tamponade first in one and combined tamponade first in three. The
JACC Vol. 10. No. I July 1987:164-9
absence of leaks across the suture line was demonstrated during the experiment by failure of the periventricular pericardial space pressure to rise during atrial tamponade. Mean intrapericardial pressure in the ventricular portion was - 3.4 mm Hg in the control period and was - 3.5 mm Hg when intrapericardial pressure was increased to 20 mm Hg in the atrial portion. When ventricular tamponade was produced with a pressure of 20 mm Hg, the intrapericardial pressure rose slightly in the atrial segment from a mean of zero to a mean of 2.2 mm Hg, probably owing to a rise in atrial pressure. At the termination of experiments. each dog was killed with an intravenous overdose of pentobarbital. Autopsy was performed and the absence of leaks between atrial and ventricular pericardial spaces was demonstrated by injection of physiologic saline solution colored with blue dye. The pericardial spaces themselves were demonstrated to be free of adhesions. Statistics. All values are expressed as mean values ± SEM. Values <0.05 were considered significant (Student's t test).
Results (Tables 1 and 2) Atrial tamponade. Tamponade of the two atria produced a significant decrease in cardiac output and stroke volume as compared with the control value at each level of intrapericardial pressure (10, 15 and 20 mm Hg). Heart rate increased significantly at the 15 and 20 mm Hg levels, but not at 10 mm Hg. Aortic mean blood pressure was not significantly lower than control at 10, 15 or 20 mm Hg intrapericardial pressure. Right atrial mean pressure was significantly above the control value at each level of intrapericardial pressure, but left atrial pressure did not change significantly. Ventricular tamponade. Tamponade of the two ventricles decreased cardiac output and stroke volume significantly below the control value at each level of intrapericardial pressure. Heart rate increased significantly at the 15 and 20 mm Hg levels, but not at the 10 mm Hg level. Aortic mean pressure was not significantly decreased at any of the three levels of intrapericardial pressure. Right and left atrial pressures were each significantly higher than control values at each of the three levels of intrapericardial pressure. Left, but not right, atrial pressure was significantly higher than that during atrial tamponade at each level of intrapericardial pressure. Cardiac output was lower at 20 mm Hg intrapericardial pressure with atrial than with ventricular tamponade; this was of borderline statistical significance but stroke volume was significantly lower with atrial tamponade. Aortic mean pressure changes were not significantly different between atrial and ventricular tamponade. Combined atrial and ventricular tamponade. With combined atrial and ventricular tamponade, the hemody-
E.>
'
~<
:-:J2. 0'_
t?
Table 1. Hemodynamic Effects of Regional Cardiac Tamponade in 10 Dogs Atrial Tamponade AnI' Control
RAP
LAP
'D
CO
SV
HR
RAP
LAP
CO
HR
SV
3.7 :': 0.6
8.8 :': 1.1
95 :': 6.6
176 :': 7.2
\2.7 :': 0.7
\52 :': 6.1
44 :': 0.8
8.2 :': 0.9
88 :': 5.7
170 :': 8.9
124
59
116 :': 1.0"11 12.7 ± 1 5 tll 14 ± 13 t!1
77
182 :': 81 192
98
± O.5t
195 :': 5 5*
7.9
8.8 :': 0.6 fll** 10.9 :': 1.2t§ 15.9 :': 1.3"11**
11.5
:±: 6.4*
143 :': 4.9t 138 .r: 4.4* 134 ± 7.0*
58 :': 3.5 tll** 46 :': 3 1"11** 33 :': 2.?tIl*'
188 :': 7.9' 205 ± 7. 7t~ 217
75 :': 07t~~ 54 :': 0·6t1l** 38 :': 0.5 tll**
144 :': 3.9
3.7 :': 07
8.1 :': 1.0
95 :': 5.2
173 :': 8.0
13.0 :': 0.7
146 :': 5.8 138.6 :': 6. J IJ96 ± 6.7
5.5 :': 0.7 t 68 :': 08t 79 :': 08"
80 :': 1 I 78 :': 1.2 8.6 :': 1.2
7J ± 4.7"
183 ± 6.0 194
94
145 :': 5.6 141 :': 63 141.1 :': 6.8
RAP
AoP
LAP
CO
SV
AoP 150.2 :': 6.9
Z
a
Atrial and Ventricular Tamponade
Ventricular Tamponade
HR
:':1.1
Pericardia! pressure
10 mm Hg 15 mm Hg 20 mm Hg
65 ± 4.lt
58 ± 4.6"
:!:
5.4*
203 ± 5.6"
± 0.5 f
7.9 :': 05t 6.7 :': 06"~
± 0.6i
6.8 :': 0.8t 8.3 :': 0.9"
:': 5.77 71 :': 5.4t 66 :': 40 f t
± 0.5t
8.6
± OAH
-t I. 1711
12.5 :': 1·6t1l 15.9 ± 13 tll
± 6, gt**
Values are expressed as mean values ± SE (Student's paired 1 test). *p < 0.02 versus control: tp < 0.01 versus control: :j:p = 0.053 versus atrial tamponade: §p < 0.05 versus atrial tamponade: lip <.01 versus atrial tamponade: ~Ip < 0.05 versus ventricular tamponade: **p < 0.01 versus ventricular tamponade. AoP= mean aortic blood pressure (rnm Hg): = cardiac output (nil/kg per min): HR = heart rate (heats/min): LAP = mean left atrial pressure (mm Hg): RAP = mean right atrial
eo
pressure (rnm Hg): SV
=
cardiac stroke volume (ml).
Table 2. Venae Caval and Right Atrial Pressures During Regional Cardiac Tamponade in Seven Dogs Atrial Tamponade
Control Pericardial pressure 10 mm Hg 15 mm Hg 20 mm Hg
RAP
sve
rvc
36 ± 0.7
46 ± 0611
4.7 ± 0.611
Atrial and Ventricular Tamponade
Ventricular Tamponade
eo 92A ± 7.0
RAP
sve
rvc
eo
RAP
sve
ivc
3.6 ± 1.7
42 ± 0611
4.3 ± 0711
90A ± 8.9
4.3 ± 0.9
4.9 ± 0.911
4.8 ± 0.9[[
eo 90.5 ± 5.7
;;c trt
C
o z
6.1 ± 0.8
8.3 ± 0.7*
7.9 ± 0.8*
63.0 ± IO.Rt
6.0 ± 0.8
6.7 ± 0.511
6.8 ± 0.811
74.6 ± 7.8::':
8.9 ± 0.8
10.2 ± 1.311
9. I ± 1.211
62.3 ± 2.8::':
7.6 ± 1.0
10.6 ± OAt
10.1 ± 0.6*
61.8 ± 5.6::':
7.1 ± 1.0
8.1 ± 0.711
8.\ ± 0911
68.8 ± 61::':
10.8 ± 1.7
12.9 :': 1.211
13.1 ± 1.311
479 ± 2.3+§
9.0 ± 1.2
12.9 ± 0.6t
11.8 :': 0.8"
54A :': 6.3:j:
8.6 ± 1.3
9.1 ± 0.911
96 ± 1211
63.3 ± 5 .\:j:
J5.2 ± 1.3
» r
n
»..,.,
;;co 16.6 ± 1.611
17.1 ± 1411
356 ± Vl:j:§
S2~
»t"" m
n...,;;c »» z 3:: ",0
::,:eo
Values are expressed as mean values ± SE (Students paired 1 test). *Signincantly greater than RAP, p < 0.02; tsignificantly greater than RAP, p < 0.01; signficantly less than control (p < O.Ol): § SIgnificantly less than during atrial or ventricular tamponade (p < 0.05): Iinot significantly different from RAP. p > 0.05. IvC = inferior caval mean pressure (mm Hg): SVC = superior caval mean pressure (rnrn Hgj: other abbreviations as in Table I.
eo
Oc
z» »c:>
Om
mr-
0\ --.I
168
FOWLER AND GABEL REGIONAL CARDIAC TAMPONADE
namic changes were more pronounced than with either atrial or ventricular tamponade alone regardless of the order in which tamponade was produced (Table I). Cardiac output and stroke volume were significantly lower and right atrial pressure was higher with combined atrial and ventricular tamponade than with either alone at each level of intrapericardial pressure. Heart rate increased significantly at each level of intrapericardial pressure and was significantly greater with combined than with ventricular tamponade, but not with atrial tamponade, at 15 and 20 mrn Hg intrapericardial pressure. Left atrial pressures were higher during combined tamponade than during atrial tamponade but not higher than during ventricular tamponade. The decrease in aortic pressure during combined tamponade was significant, but not significantly different from that during atrial or ventricular tamponade alone. Atrial waveforms. With atrial tamponade, waveforms were recorded in nine dogs. In the right atrium of five dogs large C-V waves or larger V waves developed; one dog showed a larger A wave and one a deeper X wave; two dogs showed no change. In the left atrium of four dogs, C-V waves or larger V waves developed; one dog showed a deeper X wave and four dogs had no change. With ventricular tamponade, five of seven dogs showed no change in right atrial waveforms and six of eight showed no change in left atrial waveforms. Two showed larger A waves in the right atrium and left atrium, one showed a large C-V wave and one a larger A wave. With combined tamponade, only one of six dogs showed a larger C-V wave in the right atrium and five showed no change. Only one of eight dogs developed a large C-V wave in the left atrium; three dogs showed smaller X waves, one a shallower Y wave and three showed no change. Thus, only with atrial tamponade did the majority develop V waves or large C-V waves suggesting tricuspid or mitral regurgitation; however, these changes might have been due to changes in atrial compliance. Larger A waves in a few dogs during ventricular tamponade might reflect decreased ventricular compliance. With combined tamponade, a few dogs showed shallower X waves. Only one showed a smaller Y wave as has been described in cardiac tamponade; none showed larger X waves. Superior and inferior venae cavae pressures. In seven animals, inferior and superior venae cavae pressures were measured during the control period and during cardiac tamponade at 10, 15 and 20 mm Hg intrapericardial pressure (Table 2). Control inferior and superior venae cavae pressures were not significantly different from right atrial mean pressures. However, the inferior vena cava pressure (7.9 ± 0.8 mm Hg) and superior vena cava pressure (8.3 ± 0.7 mm Hg) were significantly higher than right atrial mean pressure (6.1 ± 0.8 mm Hg) at 10 mm Hg intrapericardial pressure. At 15 mm Hg intrapericardial pressure, inferior vena cava mean pressure (10.1 ± 0.6 mm Hg) and superior
JACC Vol. 10. No. I July 1987:164-9
vena cava pressure (10.6 ± 0.4 mm Hg) were significantly higher than mean right atrial pressure (7.6 ± 1.0 mm Hg). This was also true at 20 mm Hg intrapericardial pressure: inferior vena cava pressure (11.8 ± 0.8 mm Hg) and superior vena cava pressure (12.9 ± 0.6 mm Hg) were both significantly greater than right atrial mean pressure (9.0 ± 1.2 mm Hg). With ventricular tamponade. inferior and superior venae cavae pressures were not significantly different from right atrial pressure at any time, either in the control period or during tamponade with intrapericardial pressures of 10, 15 and 20 mm Hg (Table I). This was also true with combined atrial and ventricular tamponade; the inferior and superior venae cavae pressures were not significantly different from right atrial pressure at the several degrees of cardiac tamponade.
Discussion Previous investigations. In a previous study of regional tamponade in dogs (4), we evaluated the hemodynamic effects of compression of both atria and one ventricle as compared with the effects of compression of either the right or the left ventricle alone. In that study, tamponade of either ventricle alone had little hemodynamic effect, whereas compression of one ventricle and the two atria had essentially the same effect on blood pressure and cardiac output as did generalized tamponade of the entire heart, including the intrapericardial great arteries and veins. That study thus suggested that the compression of the atria, venae cavae and pulmonary veins played the major role in the hemodynamic effects of tamponade of the heart. Hemodynamic effects of atrial or ventricular tamponade alone. The present investigation modified these conclusions in an important way. Although tamponade of one ventricle had little hemodynamic effect in the previous study, in the present study tamponade of both ventricles had a hemodynamic effect that was very similar to that of atrial tamponade, whereas neither atrial nor ventricular tamponade had effects on blood pressure or cardiac output that were as great as the effects of combined atrial and ventricular tamponade in the same animals. It is of interest to consider why the effects of tamponade of both ventricles are so much greater than the effects of tamponade of either ventricle alone. It appears probable that, when pressure is exerted on the surface of one ventricle alone, the ventricular septum may shift in the direction of the other ventricle, where pericardial pressure remains subatmospheric, thus permitting diastolic filling to occur with minimal hindrance. However, when both ventricles are subject to tamponade, diastolic filling must compete for space in the same pressurized chamber, thus leading to impairment of filling of both ventricles. The present study implies, therefore, that the maximal effects of cardiac tamponade require
JACC Vo!. 10. No. I
July 19R7:IM-9
pressure on the entire heart, and not just the atria or ventricles alone. This study does not deal with the suggestion of Ditchey et al. (3) that compression of the right heart is of much greater importance than compression of the left heart in the sequence of events that takes place in tamponade of the heart. Evidence for vena caval compression during cardiac tamponade. Another interesting feature of the present study concerns the relation of vena caval pressures to right atrial pressure during atrial tamponade. Caval pressures rose in the expected fashion in cardiac tamponade in all three settings: atrial tamponade, ventricular tamponade and combined atrial and ventricular tamponade. However, right atrial pressure rose as expected only with ventricular tamponade and combined tamponade, but not with atrial tamponade. Further, a signifi cant pressure difference developed between caval pressures and right atrial pressure during atrial tamponade only, suggesting that there is significant caval compression during tamponade. Cohnheim (5) had originally implied that increased intrapericardial pressure caused an obstacle to entrance of blood from systemic veins into the heart. The cavae, having thinner walls, may be expected to be more compliant than the right atrium. Cardiac tamponade, when the entire heart is involved. produces a rise in atrial and ventricular diastolic pressures. which at first usually are equal to the pressure level in the intrapericardial space. However, as the pressure in the pericardial space increases further, the rise in atrial and ventricular diastolic pressures is less than the rise in intrapericardial pressure. Thus the transmural atrial and ventricular diastolic pressures become negative (6). This effect is presumably owing to ventricular diastolic suction. We showed (6) that in experimental tamponade , negative transmural right atrial pressure developed when intrapericardial pressure was 10.8 mm Hg or greater. In that study, negative transmural right ventricular diastolic pressure of as much as 8 rnrn Hg was produced. In still another study (7). obstruction to venous inflow to the right heart was associated with negative transmural right ventricular diastolic pressure. In the present investigation, right atrial pressure did not rise significantly during atrial tamponade. Thus a negative transmural right atrial pressure was present as pericardial pressure exceeded right atrial pressure. The mechanism involved may well be similar to those cited before. The right ventricle, when its filling is limited by partial obstruction to inflow by the compression of the right atrium and venae cavae, is capable of exerting a diastolic suction effect. thus lowering atrial pressure below pericardial pressure and producing a negative transmural right atrial pressure. In the present study, when ventricular filling was impaired by ventricular tamponade or during combined tamponade, the potential ventricular diastolic suction effect was no longer demonstrated as evidenced by the absence of a signifi cant pressure difference between the venae cavae and
FOWLER AND GABEL REGIONAL CA RDIAC TA MPONADE
169
the right atrium. This finding agrees with the studies made by Isaacs et al. (8) in 1956, which showed no significant gradient of pressure between the venae cavae and right atrium when experimental animals were subjected to tamponade of the entire heart. Clinical implications. Regional cardiac tamponade may be of considerable clinical significance. especially after cardiac operations or trauma ( I,2). Yacoub et al. (9) described left atrial compression as a cause of cardiac tamponade in postoperative patients. Kidner et al. (10) described cardiac arrest in a patient with left atrial tamponade after cardiac perforation in the course of diagnostic cardiac catheterization. Kronzon et al. (II) reported three cases of loculated hematoma after cardiac operation causing compression of both atria in one patient and compression of the right atrium alone in two. All three patients had severe cardiac tamponade with shock and systemic venous pressure elevation. The investigators pointed out that regional tamponade, compressing the atria alone, may be missed by M-mode echocardiography, because there is no evidence of pericardial effusion surrounding the ventricles. Regional tamponade is especially likely to occur in postoperative patients. in whom adhesions and bleeding may cause loculated pericardial effusion. Isolated left atrial tamponade may produce shock without systemic venous pressure elevation in the postopcrative patient (9).
References I. Fyke fE III. Tancredi RG. Shub C. Julsrud PRo Sheedy PF II. Detection of intrapericardial hematoma after open heart surgery: the roles of echocardiography and computed tomography. J Am Coil Cardiel 19X5:5: 1496-9 . 2. D'Cr uz IA . Kensey K. Campbell C. Replogle R. Jain M. Two-dimensional echocardiogruphy in cardiac tamponade occurring after cardiac surgery. J Am Coli Cardie l 19X5 ;5: I25ll-2.
.I. Ditehey R. Engler R. LeWinter M. et al. The role of the right heart in acute cardiac tamponade in dogs. Circ Res 19X I;48:7ll1- 10. 4. Fowler NO. Gabel M. The hemodynamic effects of cardiac tamponade: mainly the result of atrial. not ventricular. compression. Circulation 19X5:71: 154-7 . 5. Cohnheim J. Lectures on General Pathology. vul I. The Circulation. London: New Sydenham Society. IXX9: 19- .1.1 (translated from the second German edition by Alexander B. McKee ). 6. Fowler NO. Shahetai R. Braunstein JR. Transmural ventricular pressures in experimental cardiac tamponade. Circ Res 1959:7:733- 9. 7. f owler NO. Couves C. Bewick J. Effect of inflow obstruction and rapid bleeding on ventricular diastolic pressure. J Thorac Surg 195X:35: 5.12- 7. X. Isaacs JP . Berglund E. Sarnoff SJ. Ventricular function: the pathologic physiology of acute cardiac tamponade studied by means of ventricular function curves. Am Heart J I954;4X:66-76. 9. Yacoub MH. Cleland WI'. Deal CWo Left atrial tamponade. Thorax 1966:2 Ull5-9 . Ill. Kidner PH. Kakkar VV. Cullum PA. Armstrong P. Left atrial tamponade. Report of a case after right heart catheterization . Br Heart J 1973:35:464-5 II. Kronzon I. Cohen ML. Winer HE. Cardiac tamponade by loculated pericardia! hematoma: limitations of M-mode echocardiography. J Am Coli Cardie l 1983;1:913-5 .