Original Article
Elevated Arterial Blood Pressure in Cardiac Tamponade
N Engl J Med 1992; 327:463-466August 13, 1992
- Abstract
- Abstract
Background.
In cardiac tamponade cardiac output falls, but peripheral vascular resistance increases, so that systemic blood pressure may be maintained at normal or near-normal levels. We recently observed a patient with cardiac tamponade whose blood pressure was markedly elevated.
Methods.
To determine the frequency of elevated blood pressure in patients with cardiac tamponade and their hemodynamic characteristics, we studied 18 consecutive patients with cardiac tamponade from a variety of causes using right heart catheterization.
Results.
Six of the 18 patients had systolic arterial blood pressures ranging from 150 to 210 mm Hg (mean [±SD], 176±26) and diastolic pressures ranging from 100 to 130 mm Hg (mean, 113±14). All six had previously been hypertensive. After pericardiocentesis there was a significant decrease in blood pressure (to 139±13 mm Hg systolic, P<0.05; and 83±6 mm Hg diastolic, P<0.01) and peripheral vascular resistance (from 2150±588 to 1207±345 dyn · sec · cm-5, P<0.01). Cardiac output increased in all six. The other 12 patients, 3 of whom had a history of hypertension, had significant increases in cardiac output and systolic blood pressure (from 119±13 to 127±7 mm Hg, P<0.05) after pericardiocentesis, whereas peripheral vascular resistance decreased. Both groups had similar degrees of cardiac tamponade, as indicated by measurements of cardiac output and intrapericardial, right atrial, and pulmonary-artery wedge pressures.
Conclusions.
Elevated blood pressure may occur in some patients with cardiac tamponade who have preexisting hypertension. Moreover, blood pressure may fall after pericardiocentesis in patients who have elevated blood pressure associated with tamponade. (N Engl J Med 1992;327:463–6.)
Article Activity
- Article
CARDIAC tamponade, a serious manifestation of pericardial effusion, has a broad range of clinical and hemodynamic features. The hemodynamic findings may vary from normal intracardiac pressures and cardiac output in mild cardiac tamponade to a state characterized by marked elevation in intrapericardial pressure, intracardiac pressure, and systemic vascular resistance, with a substantial decline in cardiac output.1 2 3 4 5 6 7 In cardiac tamponade due to medical conditions (such as uremia or infection), blood pressure is commonly maintained within or near the lower end of the normal range,2 , 6 , 8 unlike cardiac tamponade due to acute hemorrhage into the pericardial space from trauma or rupture of the myocardium or aorta, in which profound hypotension is present.7
We recently observed a patient with a long history of hypertension who presented with cardiac tamponade and marked elevation of systemic blood pressure in spite of severe cardiac compression and reduced cardiac output. We therefore undertook a prospective study to examine the frequency of this occurrence and to assess associated hemodynamic features.
Methods
Patients
We studied 18 consecutive patients with the clinical diagnosis of cardiac tamponade who were referred to the echocardiography laboratory at our institution. All the patients were suspected of having cardiac tamponade on clinical grounds (elevated jugular venous pressure; pulsus paradoxus, with an inspiratory decrease in aortic systolic pressure of more than 10 mm Hg; or an enlarged cardiac silhouette on chest film). The patients ranged in age from 29 to 68 years. Eight were women, and 10 were men. The causes of the pericardial effusions were determined in all the patients (Table 1Table 1
Characteristics of the 18 Study Patients.).Nine patients had a history of hypertension. In six of these nine patients, cardiac tamponade occurred during hospitalization. Their blood pressures had been documented to be in the normal range (<140 mm Hg systolic and <90 mm Hg diastolic) before cardiac tamponade was suspected. Four of the six had blood pressures in the hypertensive range at the time of diagnosis of cardiac tamponade. In the remaining three patients with a history of hypertension, cardiac tamponade began outside the hospital. They stated that they had been receiving antihypertensive therapy before admission. Two of these three patients had elevated blood pressure at the time of diagnosis of cardiac tamponade. None of the patients were receiving β-adrenergic—blocking drugs.
All the patients gave informed consent to participate in the study. The study protocol was approved by the institutional review board of Harlem Hospital Center.
Echocardiographic Studies
Echocardiography was performed by experienced technologists or one of the investigators in standard two-dimensional long-axis and short-axis views using a Hewlett-Packard 77020AC or Advanced Technology Laboratories UltraMark 9 ultrasound system. The degree of pericardial effusion was judged to be large in all the patients. A large pericardial effusion was defined as a circumferential effusion associated with separation of more than 1 cm of the epicardial and parietal pericardial echoes in systole and diastole in all imaging planes, with or without exaggerated motion of the heart. Echocardiographic criteria of tamponade included compression or flattening of the anterior wall of the right ventricle,9 early diastolic collapse or invagination of the right ventricle,10 11 12 13 14 and collapse or invagination of the right atrium during ventricular systole.15 16 17 18 All patients had one or more of these echocardiographic findings of cardiac tamponade.
Hemodynamic Measurements
Right heart catheterization was performed with a 7-French triple-lumen balloon-flotation catheter inserted percutaneously into the subclavian or internal jugular vein. Right atrial, pulmonary-artery, and pulmonary-artery wedge pressures were measured, and cardiac output was determined in triplicate by the thermodilution method. Cardiac tamponade was defined as elevation of the mean right atrial pressure and near-equalization with the intrapericardial pressure.2 , 4 , 19 Systemic arterial pressure was measured in an indwelling cannula inserted into the radial or brachial artery and was monitored continuously. Blood pressures were recorded immediately before and after pericardiocentesis and 15 and 30 minutes after pericardiocentesis. All values were averages of five consecutive cardiac cycles.
Systemic vascular resistance (expressed in dyn · sec · cm-5) was determined with the following formula:
Pericardiocentesis was then performed with a 7-French multihole pigtail catheter introduced percutaneously from the subxiphoid approach. Intrapericardial pressure was recorded just before the pericardial fluid was removed. Cardiac output, intracardiac pressures, and systemic arterial blood pressures were measured before and 15 minutes after the removal of as much pericardial fluid as possible. Antihypertensive drugs were withheld throughout the period of data collection.Statistical Analysis
Data are presented as means ±SD. Statistical analysis was performed with nonpaired and paired t-tests where appropriate.20 All P values of less than 0.05 were considered to indicate significance.
Results
The clinical characteristics of the study patients are summarized in Table 1. The causes of the pericardial effusions varied and included common as well as uncommon causes. Nine of the patients had a history of hypertension lasting more than one year.
The echocardiographic findings are summarized in Table 2Table 2
Echocardiographic Results in the 18 Study Patients.. All the patients had right ventricular collapse in early diastole. Invagination or collapse of the right atrium in systole was found in nearly all of them. A patient with mesothelioma and cardiac tamponade did not have this echocardiographic sign, probably because of the involvement of the right atrial wall with the tumor, which limited the ability of the wall to respond to elevated pressure within the pericardial space. The other two diagnostic signs of tamponade listed in Table 2 — a decrease in the dimension of the left ventricle on inspiration and narrowing of the right ventricular cavity — proved not to be sensitive signs of cardiac tamponade, in keeping with previous results in our laboratory.Six patients were found to have elevated blood pressure (defined as a systolic pressure of ≥140 mm Hg, a diastolic blood pressure of ≥90 mm Hg, or both) before pericardiocentesis (Table 3Table 3
Hemodynamic Data on the 18 Study Patients before and after Pericardiocentesis.*) and were designated as group 1 (patients with elevated blood pressure). In this group, systolic arterial blood pressure ranged from 150 to 210 mm Hg (mean, 176±26) and diastolic pressure ranged from 100 to 130 mm Hg (mean, 113±14).In 12 patients, designated as group 2 (patients without elevated blood pressure), systolic blood pressure ranged from 100 to 138 mm Hg (mean, 119±13) and diastolic pressure ranged from 60 to 85 mm Hg (mean, 75±9). Peripheral vascular resistance was significantly higher in the patients with elevated blood pressure (P<0.001) (Table 3). All the patients with elevated blood pressures before pericardiocentesis had preexisting hypertension.
Right heart catheterization confirmed the presence of cardiac tamponade in all 18 patients (Table 3). The cardiac output was low, and values were similar in both groups. Mean intrapericardial and right atrial pressures were elevated and nearly identical, and approximated the mean pulmonary-artery wedge pressure.
An average of 630 ml of pericardial fluid (range, 300 to 1050) was removed from the study patients. After pericardiocentesis, blood pressures in group 1 fell from an average of 176 mm Hg systolic and 113 mm Hg diastolic to 139 mm Hg and 83 mm Hg, respectively. Peripheral vascular resistance, which was 2150 dyn · sec · cm-5 before the removal of pericardial fluid, fell to 1207 dyn · sec · cm-5 after pericardiocentesis. In group 2, on the other hand, systolic blood pressure rose from 119 to 127 mm Hg (P<0.05), diastolic blood pressure was virtually unchanged, and peripheral vascular resistance fell from 1560±394 to 1215±117 dyn · sec · cm-5 (P<0.05) after the removal of pericardial fluid.
The magnitude of the increase in cardiac output and decline in intracardiac pressures after pericardiocentesis did not differ significantly between groups. Although cardiac output increased in all patients, there was a wide variation in systolic blood pressures in group 2 after pericardiocentesis (Fig. 1Figure 1
Plot of Systolic Blood Pressure and Cardiac Output before (Open Circles) and after (Solid Circles) Pericardiocentesis in Groups 1 and 2.).In all but one patient the mean right atrial pressure fell to less than 6 mm Hg, indicating that cardiac tamponade was the cause of the elevated intracardiac pressures. In the patient with mesothelioma, the mean right atrial pressure remained elevated at 8 mm Hg, suggesting effusive—constrictive disease of the pericardium.21 , 22
Discussion
Cardiac tamponade in patients with a gradual accumulation of pericardial effusion is a distinctly different clinical entity than the syndrome described by Beck,7 in which elevated venous pressure, low arterial blood pressure, and an imperceptible or quiet heart occurred as a result of the rapid accumulation of fluid in the pericardial space. Such rapid accumulation may occur after rupture of the heart or aorta or because of penetrating wounds to the heart. The impairment in diastolic filling of the heart is sudden and severe; hence, the normal compensatory mechanisms of an increase in heart rate, enhanced systolic emptying of the heart, and an increase in systemic venous and arterial resistance, which ordinarily serve to maintain cardiac output and arterial blood pressure in cardiac tamponade, fail. In patients with cardiac tamponade in which the rate of accumulation of fluid in the pericardial space is slow, circulatory adaptations usually maintain systemic arterial pressure at near-normal levels for longer periods.2 , 6 , 8 In experimental and clinical cardiac tamponade, peripheral vascular resistance is uniformly increased, helping to maintain arterial blood pressure, albeit at a reduced level, in the face of a declining cardiac output.13 , 23 24 25 Fowler et al.4 , 26 and Pegram et al.27 emphasized the role of the interplay of increased peripheral vascular resistance and enhanced adrenergic drive to the heart as compensatory factors in maintaining blood pressure and cardiac output in patients with cardiac tamponade. In dogs after long-term catheterization of the heart, maintenance of systemic blood pressure with cardiac tamponade was shown to depend primarily on α-adrenergic mechanisms until late in the course of tamponade, when mean arterial blood pressure fell.28
In the group of patients with pericardial effusion and cardiac tamponade of diverse medical causes described by Guberman et al.,6 nearly two thirds presented with systolic blood pressures of 100 mm Hg or higher. Twelve of 14 subjects with cardiac tamponade in a hemodynamic study by Reddy and colleagues had systolic blood pressures of 110 mm Hg or higher.2
Our finding of high arterial blood pressures in one third of our patients with tamponade, all of whom had a history of hypertension, is similar to the observations made by Geer and Brown29 in hypertensive subjects undergoing exercise testing. They reported high levels of arterial blood pressure in response to treadmill exercise in hypertensive patients. An association between acute pulmonary edema and a marked elevation in blood pressure in patients with established hypertension, and the subsequent decline of blood pressure to normal after the resolution of the pulmonary edema, has also been reported.30
The underlying cause of the hypertensive vascular response in some patients with tamponade is speculative. A number of mechanisms, among which are increased serum catecholamine levels, enhanced nonadrenergic reactivity of the vascular smooth muscle,31 , 33 and an increase in the binding of α1,-adrenergic receptors,34 , 35 may have been involved.
Whether renin and angiotensin contribute to elevated peripheral vascular resistance in patients with cardiac tamponade is unknown. In dogs, increases in plasma renin activity and angiotensin II levels occurred only when progressive tamponade had reduced mean arterial pressure to 70 percent of base line.28
In the patients with tamponade and hypertension at presentation, the normalization of blood pressure after pericardiocentesis supports the conclusion that the initial elevation in blood pressure was not a consequence of inadequate control of hypertension but was due to cardiac tamponade. In addition, the rapid return of the blood pressure to normal within 15 minutes of the pericardiocentesis strongly argues against the possibility that a residual effect of antihypertensive medications could account for this change. Indeed, blood pressure would be expected to return to normal if functional and compensatory factors were responsible for the initial high blood pressure. The fact that only six of nine hypertensive patients presented with elevated blood pressures indicates that this finding is not invariable in hypertensive subjects in whom cardiac tamponade develops.
In a recent echocardiographic study by Levine et al.8 of 50 patients with cardiac tamponade, a subgroup of 28 patients with preserved systolic blood pressure was identified. A mean (±SE) systolic blood pressure of 141±32 mm Hg in this group indicates that some systolic blood pressures were in the hypertensive range. The patients were not classified according to whether they had a history of hypertension or on the basis of level of systolic blood pressure. There was no significant change in the mean systolic blood pressure after pericardiocentesis in their patients. Because individual blood pressure data were not available in the report, the possibility that there was a decrease in systolic blood pressure in some patients cannot be excluded.
Our experience is not large enough to draw conclusions about the prevalence of elevated blood pressure in cardiac tamponade. However, on the basis of our study and the data from the studies of Reddy et al.2 and Levine et al.,8 it can be concluded that there is a distinct subgroup of patients with cardiac tamponade who present with elevated rather than low or normal arterial blood pressure. Patients with a history of hypertension appear to be more likely to have elevated blood pressure at presentation. Moreover, blood pressure decreases in this group of patients as a consequence of pericardiocentesis. Consequently, elevated blood pressure should not be used to exclude the diagnosis of cardiac tamponade.
We are indebted to Ms. Mariam Heath for assistance in the preparation of the manuscript and to Dr. Charlotte Ellis for assistance with statistical methods.
Source Information
From the Division of Cardiology, Department of Medicine, Harlem Hospital Center, College of Physicians and Surgeons, Columbia University, New York. Address reprint requests to Dr. Brown at the Division of Cardiology, Department of Medicine, Harlem Hospital Center, 506 Lenox Ave., New York, NY 10037.
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Daljeet Singh Gill, Mary Fedelaine P. Noarbe, Raymond K.K. Lee, Quek-Wei Yong, Kheng-Siang Ng. (2005) Cardiac tamponade associated with an elevated arterial blood pressure. European Journal of Internal Medicine 16:7, 515-517
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