Cardiac tamponade: A comparison of right versus left heart compression

It has been postulated that in cardiac tamponade, the hemodynamic effects of compression of the right heart chambers and great veins are more important than are the effects of left heart compression. In 10 anesthetized dogs with surgically compartmented pericardium, the hemodynamic effects of right atrial and right ventricular compression were compared with the hemodynamic effects of left atrial and left ventricular compression. The effects of right heart compression, left heart compression, and then effects of combined right and left heart compression, were compared at three levels of intrapericardial pressure: 10, 15 and 20 mm Hg.Aortic mean pressure decreased significantly at each level of intrapericardial pressure with right-sided tamponade but not with left-sided temponade. left atril mean pressures decreased significantly with right-sided tamponade and increased with left-sided and combined tamponade. Right atrial mean pressures increased significantly with right-sided and combined tamponade, but not with left-sided tamponade. Heart rate increased significantly with each of the three varieties of tamponade. Cardiac output and stroke volume, which decreased with each variety of tamponade, were significantly lower during right-sided than during left-sided tamponade. Combined tamponade lowered stroke volume more than did right-sided tamponade, and lowered cardiac output more at 15 and 20 mm Hg intrapericardial pressure.It is concluded that, in this preparation, right-sided cardiac compression has more important hemodynamic effects than does left-sided compression. However, left-sided tamponade still makes a significant contribution to the total hemodynamic picture of cardiac tamponade.     

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

Right ventricular diastolic collapse has been demonstrated to be a sensitive and specific sign of cardiac tamponade. Because the shape and position of the right ventricular wall are related to the relative pressures within the pericardial space and the right ventricular chamber, the usefulness of right ventricular diastolic collapse as a marker of cardiac tamponade may be influenced by intravascular volume and right heart filling pressures. This study was undertaken to determine the effects of volume loading and hemorrhage on the point within the hemodynamic progression of cardiac tamponade at which right ventricular diastolic collapse first appears. Five unanesthetized, chronically instrumented dogs were studied with two-dimensional echocardiography during 41 episodes of cardiac tamponade induced by the intrapericardial infusion of warm saline solution. Intravascular volume was adjusted before cardiac tamponade to a hypovolemic, euvolemic or hypervolemic state using saline solution and dextran infusion or hemorrhaging to achieve the prescribed mean right atrial blood pressure. The measurements recorded during each episode of cardiac tamponade were right atrial blood pressure, aortic blood pressure, cardiac output (by electromagnetic flow meter), heart rate and intrapericardial pressure. When compared with the euvolemic state, the onset of right ventricular diastolic collapse in volume contraction occurred at a lower intrapericardial pressure (with a lower aortic blood pressure and cardiac output), whereas in volume expansion it occurred at a higher intrapericardial pressure (with a higher aortic blood pressure and cardiac output). Volume expansion delayed the decrease in hemodynamic variables during cardiac tamponade in this canine model.     

Echocardiographic manifestations of tense pericardial effusion

Echocardiography has emerged as a sensitive study in the evaluation of pericardial effusion. The specificity of echocardiographic signs in cardiac tamponade remains undefined, however. Two such signs, early diastolic collapse of the right ventricular free wall and late diastolic collapse of the right atrial wall, were observed in two patients without clinical evidence of cardiac tamponade. Increased intrapericardial pressure was documented in each patient. Accumulation of pericardial fluid under high pressure results in a reversal of the instantaneous transmural pressure gradients in early and late diastole, causing collapse of the right ventricular and the right atrial wall, respectively; however, such a tense pericardial effusion may not cause hemodynamic embarrassment severe enough to yield clinical signs of cardiac tamponade.     

The physiological role of the pericardium: studies based on right heart inflow dynamics in cases of left-sided pericardial defect

Using pulsed Doppler echocardiography, the effects of postural change on the blood flow pattern in the superior vena cava and in the right ventricular inflow tract were investigated to evaluate the physiological role of the pericardium. Eight cases of left-sided pericardial defect and eight healthy subjects were examined. 1. Suppressed inflow into the right atrium during systole in left-sided pericardial defect was manifested as a reduction of the systolic wave (S) in the superior caval vein and impairment of the systolic shift of the tricuspid annulus. This suppression suggested unsatisfactory volume expansion in the right atrium due to the absence of negative intrapericardial pressure. 2. In left-sided pericardial defect, the right ventricular inflow pattern differed from the normal, most distinctly in the right lateral recumbent position, though the cardiac motion was nearly identical with that of the normal in this position. In this position, the ratio of the peak velocity of presystolic filling to that of rapid filling was increased, and the deceleration half time of rapid filling was prolonged. These findings indicated that the right ventricular rapid filling was retarded, and was compensated by the filling due to atrial contraction. It is assumed that right ventricular filling is influenced by hydrostatic pressure due to changes in posture in the absence of restriction by the pericardium. 3. It is concluded that the pericardium maintains negative intrapericardial pressure, so that each cardiac chamber is uniformly expanded for its filling, and that this function minimizes the influence of posture on cardiac hemodynamics.     

Effusive-constrictive hemodynamic pattern due to neoplastic involvement of the pericardium

Eight patients with metastatic malignancy of the pericardium who demonstrated the hemodynamics of subacute effusive-constrictive pericarditis were studied. All patients had clinical evidence of cardiac tamponade due to malignant pericardial effusion and were referred for therapeutic pericardiocentesis. In six in whom pericardiocentesis was successfully performed, right atrial pressure remained elevated after pericardiocentesis and return of the intrapericardial pressure to zero; in these patients, hemodynamic data were initially compatible with tamponade but suggested constriction after removal of the pericardial fluid. In the remaining two patients, echocardiography revealed pericardial fluid, but attempted pericardiocentesis was unsuccessful. In these two patients, the hemodynamic data suggested pericardial constriction; subsequent pathologic examination revealed neoplastic involvement of the visceral pericardium. Thus, subacute effusive-constrictive pericarditis, previously recognized as a complication of tuberculosis or mediastinal radiation, may also be due to metastatic malignancy. The syndrome can readily be demonstrated when right heart catheterization is performed in conjunction with pericardiocentesis.     

Effects of intravascular volume state on the value of pulsus paradoxus and right ventricular diastolic collapse in predicting cardiac tamponade

Both pulsus paradoxus and right ventricular diastolic collapse detected by two-dimensional echocardiography are noninvasive markers of impaired cardiac function in cardiac tamponade, yet the reliability of each may vary with the patient's state of hydration. To examine the relative value of these noninvasive markers at various states of hydration, we studied five chronically prepared, conscious mongrel dogs during 37 episodes of cardiac tamponade at three different intravascular volumes. We continuously measured cardiac output (electromagnetic flowmeter), aortic blood pressure, right atrial blood pressure, intrapericardial pressure, and respirations. Intravascular volume was varied by adjusting the mean right atrial blood pressure to hypovolemic (-2 to -6 mm Hg), euvolemic (0 to 4 mm Hg), or hypervolemic (6 to 10 mm Hg) levels. The sensitivity and specificity of right ventricular diastolic collapse in predicting increases in intrapericardial pressure remained high at all levels of hydration. Pulsus paradoxus showed good sensitivity and specificity at low intravascular volumes, but both sensitivity and specificity declined at higher intravascular volumes. Thus right ventricular diastolic collapse was more sensitive and more specific than pulsus paradoxus in detecting increases in intrapericardial pressure during euvolemia and hypervolemia whereas the two tests were equally valuable in hypovolemic states.     

The shift in the relationship between intrapericardial fluid pressure and volume induced by acute left ventricular pressure overload during cardiac tamponade

We hypothesized that a process leading to an acute increase in cardiac size would change the relationship between intrapericardial pressure and fluid volume during cardiac tamponade, resulting in a change in the time of onset of right ventricular diastolic collapse (RVDC) as seen on the two-dimensional echocardiogram. Five spontaneously breathing dogs were instrumented to measure ascending aortic and right atrial blood pressures and intrapericardial pressure (IPP). A hydraulic occluder was placed around the proximal descending thoracic aorta. Each animal underwent six consecutive episodes of cardiac tamponade, three in the presence alternating with three in the absence of aortic constriction. The onset of RVDC was recorded and the volume infused into the pericardial space was measured. In the presence of aortic constriction, the relationship between pericardial pressure and incremental pericardial fluid volume was shifted so that IPP was an average of 3.4 mm Hg higher at any given intrapericardial fluid volume (p less than .001). At the onset of RVDC, the mean IPP was higher and the intrapericardial fluid volume was lower during aortic constriction than under control conditions (p less than .001 for both comparisons). Thus, a rapid increase in left ventricular volume in the presence of an otherwise unimportant pericardial effusion may increase intrapericardial fluid pressure sufficiently to cause RVDC.     

限制型心肌病的临床表现

本文报告限制型心肌病１０例，其中５例诊断为心内膜心肌纤维化（右室型４例，左室型１例）。其临床特点为慢性右心压塞征象；心室流入道收缩变形，心尖部闭塞，流出道增宽，巨大右房或左房扩大，房室瓣反流，左室收缩功能大致正常，舒张功能受限。其他５例诊断为特发性限制型心肌病，其特点为肺和体循环淤血，不同程度房室瓣反流，房性心律失常，心房明显扩大，左室不扩大，双室舒张末压升高，无明显心肌缺血或心包疾患。３例患者心脏病症状出现后半年至７年，死于顽固性心力衰竭。１例右室型，１例左室型心内膜心肌纤维化患者行心室内膜剥脱和房室瓣替换手术。     

Diastolic heart failure: restrictive cardiomyopathy,constrictive pericarditis,and cardiac tamponade: clinical and echocardiographic evaluation

An understanding of the basic principles of diastolic function is important in order to recognize diseases that may result in diastolic dysfunction and diastolic heart failure. Although uncommon, restrictive cardiomyopathy, constrictive pericarditis, and cardiac tamponade are among the disorders that may affect primarily diastolic function with preservation of systolic function. Diastolic heart failure may manifest with chronic nonspecific symptoms or may present with acute hemodynamic compromise. Echocardiography plays a vital role in the diagnosis of diastolic dysfunction and differentiation of these disease processes. It also provides a basis for clinical decisions regarding management and surgical referral. This review summarizes the clinical features, pathophysiology, and hemodynamic and echocardiographic signs of restrictive cardiomyopathy, constrictive pericarditis, and cardiac tamponade.     

Regional cardiac tamponade: a hemodynamic study

In 10 dogs, atrial tamponade, ventricular tamponade and then combined atrioventricular (AV) tamponade were produced at 10, 15 and 20 mm Hg intrapericardial pressure. Cardiac output decreased significantly at 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, 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.     

Pericardiocentesis: usefulness in the routine determination of intrapericardial pressure

The usefulness of routine intrapericardial pressure determination and hemodynamic monitoring during therapeutic (n = 22) or diagnostic (n = 2) pericardiocentesis was analyzed. Hemodynamic data confirmed the presence of cardiac tamponade in all cases, including the 2 patients without clinical suspicion. Prior to fluid evacuation, abnormally elevated levels of intrapericardial (13 +/- 5 mmHg), right atrial (14 +/- 4 mmHg) and pulmonary capillary (16 +/- 3 mmHg) pressures were observed. A significant correlation was found between intrapericardial and right atrial pressures (r = 0.97, p less than 0.05) and also between intrapericardial and pulmonary capillary pressures (r = 0.69, p less than 0.05). The basal cardiac output was low (3 +/- 1 l/min) and increased after the pericardiocentesis in all but one patient. According to the results of pericardiocentesis, patients were classified into three groups. Group I: intrapericardial and right atrial pressures decreased to normal levels. The increment of cardiac output was high (72%) and the procedure was considered successful. Group II: right atrial and intrapericardial pressures remained elevated (7.7 +/- 4 and 7 +/- 2 mmHg, respectively) and the cardiac output increment was less marked (52%), thus indicating incomplete drainage. Group III: intrapericardial pressure decreased to normal levels but right atrial pressure remained elevated. All these patients were found to have associated cardiac disease, most frequently constriction. We conclude that routine determination of intrapericardial pressure: 1) reveals the presence of tamponade in cases without clinical suspicion; 2) indicates the efficacy of drainage; and 3) together with right atrial pressure recording, provides early diagnosis of associated cardiac disease, especially effusive-constrictive pericarditis.     

The hemodynamics of cardiac tamponade

The changes produced by acute pericardial tamponade were examined. Tamponade produced the expected hemodynamic alteration; namely, depression on cardiac output, left ventricular pressure and LV dp/dt and elevation of right atrial and intrapericardial pressures. The mechanism of the hemodynamic disturbances was that the elevation of the intrapericardial pressure produced a negative atrial transmural pressure and disturbed atrial and ventricle filling producing the vicious cycle: diminished venoatrial gradient leads to decreased cardiac output leads to attenuated effect of ventricular systole on atrial filling, and so forth. The myocardial contractility was not impaired in cardiac tamponade.     

Pathophysiologic mechanisms of cardiac tamponade and pulsus alternans shown by echocardiography

A pericardial effusion is easily recognized by echocardiography, but the diagnosis of cardiac tamponade by echocardiography is controversial. Recently, several reports have indicated that right ventricular (RV) or right atrial (RA) diastolic collapse represent highly specific and sensitive signs of a hemodynamically significant pericardial effusion. This report evaluates the pathophysiologic significance of these findings in 3 patients. One patient had classic clinical and hemodynamic features of tamponade without typical echocardiographic features; 1 had typical echocardiographic features of tamponade without the characteristic clinical or hemodynamic features; and 1 had all the findings characteristic of tamponade, including mechanical and electrical alternans. The first patient had increased right-sided cardiac pressures and RV hypertrophy, which prevented RV or RA collapse. The second patient had low right-sided intracardiac pressures, which allowed RV and RA diastolic compression to occur during early and mid-diastole. In the third patient, severe holodiastolic impairment of right-sided filling, and presumed decreased pulmonary venous and pericardial compliance, in the setting of tamponade produced a beat-to-beat alternation of RV and left ventricular filling with associated electrical and mechanical alternans. RV or RA collapse during diastole occurs when intrapericardial pressure equals or exceeds intracardiac pressure. Increases in wall stiffness of chamber pressures may prevent diastolic collapse in the setting of tamponade. Conversely, extremely low intracardiac pressures may allow diastolic collapse to occur in the absence of overt cardiac tamponade. The extent and timing of the RA or RV collapse, rather than its mere occurrence, are important in the diagnosis of cardiac tamponade by echocardiography.     

Regional distribution of blood flow at the onset of right ventricular diastolic collapse during cardiac tamponade

The onset of right ventricular diastolic collapse has been shown to be a very sensitive and specific sign of cardiac tamponade in both clinical and consclous canine studies, and is associated with a decline in cardiac output of about 20%. To determine if blood flow to critical regions was affected at the time of onset of right ventricular diastolic collapse, seven unanesthetized, chronically instrumented dogs were studied during cardiac tamponade induced by the intrapericardial infusion of warm saline solution. Aortic blood pressure, heart rate, and cardiac output (electromagnetic flowprobe) were recorded at baseline (drained pericardial space) and at the onset of right ventricular diastolic collapse as seen on two-dimensional echocardiography. Regional blood flow was measured with radionuclide-labeled microspheres. Despite the expected decline in cardiac output, there was no significant change in cardiac, ronal, or cerebral cortical blood flow at the onset of right ventricular diastolic coliapse. Therefore, this noninvaslve marker of early cardiac tamponade begins before vital organ perfusion is compromised, thus strengthening its clinical value.     

Restrictive cardiomyopathy versus constrictive pericarditis: role of endomyocardial biopsy in avoiding unnecessary thoracotomy

Despite careful clinical, noninvasive, and hemodynamic assessment of patients with constrictive/restrictive physiology, the differentiation of restrictive cardiomyopathy from constrictive pericarditis remains difficult. We examined the role of right ventricular endomyocardial biopsy in defining the underlying process in 54 patients with evidence of constrictive/restrictive physiology, including 38 patients with profound symptoms of heart failure in whom diagnostic/therapeutic thoracotomy was contemplated (group I) and 16 patients with milder symptoms (group II). All patients in group I had NYHA class III or IV heart failure with depressed cardiac index (mean 2.5 liters/min/m2), right atrial hypertension (mean 15 mm Hg), and normal left ventricular ejection fraction (mean 59%). Endomyocardial biopsy identified a specific source of restrictive cardiomyopathy in 15 of 38 patients (39%) (11 amyloid, four myocarditis). Of the 23 remaining patients with either normal biopsy findings or nonspecific abnormalities on biopsy, 18 had intraoperative or autopsy evaluation of their pericardium, and constriction was found in 14 (77%). A specific form of restrictive cardiomyopathy was also identified in four of the 16 patients with milder symptoms (group II). We conclude that endomyocardial biopsy is useful in patients with severe constrictive/restrictive physiology. It identifies a large subset of patients with specific forms of restrictive cardiomyopathy in whom thoracotomy should be avoided. It supports the need for thoracotomy and the likelihood of finding pericardial constriction in patients without specific pathologic findings.     

Influences on the distribution of blood flow during cardiac tamponade in the conscious dog

Cardiac tamponade is a spectrum ranging from pericardial effusions with minimal hemodynamic impairment to effusions causing circulatory collapse. In this study, we examined the roles played by the sympathetic nervous system and the renin-angiotensin system in controlling the distribution of blood flow in chronically instrumented conscious dogs during progressive cardiac tamponade. Fifty-one episodes of acute cardiac tamponade were induced to decompensation (decline in mean aortic blood pressure to 70% of the level present when the pericardium was free of fluid) in 6 dogs by intrapericardial infusion of warmed saline solution. Cardiac output (electromagnetic flow probe), intrapericardial pressure, aortic and right atrial blood pressures, and renal, coronary, and mesenteric artery blood flows (Doppler flow probes) were recorded during tamponade in the absence of blockade (control), during alpha-adrenergic blockade (phenoxybenzamine), beta-adrenergic blockade (propranolol), or angiotensin-converting enzyme blockade (captopril). Aortic and mesenteric artery blood flow decreased progressively during cardiac tamponade regardless of the presence or absence of blockade. Coronary artery blood flow did not significantly change during alpha-adrenergic blockade, suggesting that the continuous decline observed during cardiac tamponade in the absence of blockade was at least in part mediated by alpha-adrenergic mechanisms. Renal artery blood flow, in contrast, was well maintained in all situations, confirming the importance of autoregulation in this vascular bed during cardiac tamponade.     

Cardiac tamponade. Pathophysiology, diagnosis, and management.

Cardiac tamponade is a clinical syndrome that results from an increased intrapericardial pressure and leads to impaired cardiocirculatory function. The spectrum of cardiac tamponade is relatively wide, ranging from an asymptomatic elevation of intrapericardial pressure recognized during objective evaluation, to extreme hemodynamic compromise in the form of severe hypotension or electromechanical dissociation, and many variations between these extremes. This article discusses the causes, pathophysiology, clinical manifestations, diagnosis, and management of cardiac tamponade.     

Usefulness of right ventricular diastolic collapse in diagnosing cardiac tamponade and comparison to pulsus paradoxus

To compare the sensitivity, specificity and predictive value of right ventricular (RV) diastolic collapse and pulsus paradoxus as signs of cardiac tamponade, 21 consecutive patients with pericardial effusion and suspected cardiac tamponade underwent prospective hemodynamic and echocardiographic evaluation. Simultaneous hemodynamic and echocardiographic data were obtained in all patients before and after pericardiocentesis. Cardiac tamponade was considered present when there was diastolic equilibration of the intrapericardial, right atrial and pulmonary capillary wedge pressures and elevation of these pressures to more than 10 mm Hg. RV diastolic collapse was 93% sensitive and 100% specific in diagnosing cardiac tamponade, whereas pulsus paradoxus was only 79% sensitive and 40% specific. The positive and negative predictive values of RV diastolic collapse (100% and 83%) were considerably better than pulsus paradoxus (81% and 40%) and demonstrate that RV diastolic collapse is more sensitive, specific and predictive of cardiac tamponade than is pulsus paradoxus. Serial simultaneous hemodynamic and echocardiographic observations at multiple points during pericardiocentesis in a smaller subgroup (5 patients) also suggest that the hemodynamic effects of RV diastolic collapse in cardiac tamponade are mediated by an increase in intrapericardial pressure.     

The normal and diseased pericardium: Current concepts of pericardial physiology,diagnosis and treatment

The past quarter century has seen remarkable contributions to understanding the role of the pericardium in health and disease and to diagnostic methods in the context of significant changes in the clinical spectrum of acute pericarditis, pericardial effusion and their sequelae. Anatomic studieshave demonstrated pericardial ultrastructure and its relation to function and delineated the pericardial lymphatics and their participation in inflammation and tamponade. Physiologic investigationshave revealed the pericardium's mechanical, membranous and ligamentous functions and its role in ventricular interaction, pericardial modification of cardiac responses during acute cardiocirculatory loading and effects on diastolic function (and, at high filling pressures, systolic function), including reduction by pericardial fluid of true filling pressure—the myocardial transmural pressure. The diastolic mean pressure plateau and phasic venoatrial pressure and flow during cardiac tamponade have been further characterized and the mechanisms producing pulsus paradoxus have been elucidated, including the importance of inspiratory increase in right ventricular filling. A far reaching compensatory response to tamponade has been revealed, particularly adrenergic stimulation, and, over time, blood volume expansion. Right heart tamponade and low pressure tamponade have been identified and the importance of the pericardium in the restrictive dynamics of right ventricular myocardial infarction has been demonstrated. Constrictive pericarditis,And the currently more common effusive-constrictive pericarditis,have been studied, in depth, clinically and hemodynamically.Cardiography in pericardial diseasenow includes M-mode and two-dimensional echographic studies, enabling rapid diagnosis and further physiologic study in cardiac tamponade and constriction. The four stages of typical electrocardiographic evolutionin acute pericarditis and atypical variants have been codified and characteristic PR segment deviations identified. The non-etiologic role of acute pericarditis in arrhythmiashas been clarified in prospective clinical and postmortem investigations. Electric alternation has been elucidated and its relation to cardiac "swinging" has been at least partly explained. Special roles now exist for contrast roentgenography, computed tomography(especially for cysts) and radionuclide imaging. Clinical advancesin pericardial disease include changes in the prevalence of established etiologies and identification of new etiologies, for example, immunopathic processes to explain recurrent pericarditis and the post-injury (including postoperative) pericardial syndromes. New forms of constriction—uremic, postoperative, radiation—have appeared in increasing numbers. The pericardial rubhas been characterized and codified, confirming a typical three-component structure (with frequent exceptions).