Assessment of pericardial constraint: the relation between right ventricular filling pressure and pericardial pressure measured after pericardiocentesis

Experimental studies have shown that right ventricular filling pressure (that is, intracavitary diastolic pressure) approximates pericardial surface pressure but, in many patients after removal of pericardial effusion, right ventricular filling pressure has been found to markedly exceed pericardial pressure recorded by an open catheter. The aim of this study was to determine whether this apparent contradiction was related to the technique of pericardial pressure measurement. Nine patients with chronic pericardial effusion were studied and, although these pressures diverged to varying degrees in individual patients, the previous observation was confirmed in that, although initially similar, right ventricular filling pressure and pericardial pressure (measured by means of an open catheter) tended to diverge during removal of the effusate; when the evacuation was as complete as possible pericardial pressure was 2.1 +/- 1.0 (mean +/- SE), while right ventricular filling pressure was 8.7 +/- 1.7 mm Hg (p less than 0.01). In six open chest, anesthetized, volume-loaded dogs with pericardial effusion (50 ml), right ventricular filling pressure and pericardial pressures measured with both open catheter and flat balloon were all equal. With decreasing volume of pericardial fluid, right ventricular filling pressure and pericardial pressure (by catheter) diverged as had been observed in patients. However, pericardial pressure (balloon) continued to be equal to right ventricular filling pressure. (With 0 ml in the pericardium, right ventricular filling pressure = 12.9 +/- 0.9 mm Hg, pericardial pressure [catheter] = 1.4 +/- 1.9 mm Hg and pericardial pressure [balloon] = 12.4 +/- 1.5 mm Hg.) Thus, these observations support the use of right ventricular filling pressure as an estimate of pericardial constraint in patients.     

Optimal right ventricular filling pressures and the role of pericardial constraint in right ventricular infarction in dogs.

BACKGROUND. Previous studies have reported an important role for right ventricular function in the pathophysiology of the low cardiac output state that can accompany right ventricular infarction. Some studies have suggested that right ventricular distensibility impairs right ventricular filling and stroke output; others have demonstrated that the pericardium can mediate depressed left ventricular filling and stroke output. METHODS AND RESULTS. To determine the role of pericardial constraint and optimal volume loading in an experimental model of right ventricular wall infarction, six mongrel dogs were studied before and after right ventricular wall infarction and after volume loading. The pericardium was then opened in two phases. In the first phase, the pericardium was opened partially to allow the atria to distend freely, and in the second phase, the pericardium was opened completely. The animals were preinstrumented with two sets of piezoelectric crystals attached to the right ventricular free wall, one in the infarct and the other in the noninfarct territory. Left ventricular size was estimated by left ventricular crystals on the anterior wall of the left ventricle. Right ventricular and left ventricular Millar catheters were used to assess intracavitary pressure, and a flat balloon was used to assess intrapericardial pressure. Right ventricular infarction reduced cardiac output by 23% and stroke volume by 30%. End-diastolic segment length and transmural pressure of the left ventricle decreased. Volume loading restored cardiac output to baseline values and was mediated by a significant increase in end-diastolic length in the noninfarct territory. This was achieved by increasing right ventricular end-diastolic pressure from 9 +/- 2 to 16 +/- 3 mm Hg (p less than 0.01). Partial opening of the pericardium mediated significant increases in both end-diastolic segment lengths of the left ventricle and the noninfarct territory. Left ventricular end-diastolic pressure decreased slightly by 3 mm Hg (p = NS). Complete opening of the pericardium increased cardiac output and stroke volume and mediated a significant decrease in right and left ventricular end-diastolic pressures. Left ventricular transmural pressure and end-diastolic segment lengths of the left ventricle and the noninfarct territory increased. Left ventricular diastolic pressure-segment length relations were shifted upward by right ventricular infarction. A partial opening of the pericardium shifted this relation downward in all animals, and complete opening of the pericardium shifted the relation rightward and further downward. CONCLUSIONS. Cardiac output is restored to baseline values by volume loading sufficient to increase the right ventricular diastolic pressure to 16 +/- 3 mm Hg. Evidence of pericardial constraint was observed and appears to be mediated by an atrioventricular interaction in addition to the direct ventricular interaction.     

Nonuniformity of pericardial surface pressure in dogs

Previously, we have shown that pericardial constraint cannot be measured by true (hydrostatic) pressure except when an excess of pericardial fluid is present and that a device such as a balloon (which reflects radial contact stress as well as hydrostatic pressure) must be used. Since radial contact stress is the major component of the constraint exerted by the pericardium when little pericardial liquid is present, it follows that the pressure measured by the balloon might be different over different parts of the heart. In an attempt to test this hypothesis, in 11 anesthetized dogs we placed pericardial balloons over the right and left ventricular free walls, instrumented the animals to measure ventricular dimensions (sonomicrometry) and pressure, mounted pneumatic constrictors on the aortic and pulmonary artery, reapproximated the pericardium, and closed the chest under suction. We studied the transient effects of constrictions of the ascending aorta and pulmonary artery and of angiotensin infusion before and after intravenous saline infusion. Aortic constriction and, to a lesser degree, angiotensin increased pericardial pressure over the left ventricle more than over the right ventricle. Pulmonary artery occlusion increased pericardial pressure over the right ventricle but significantly decreased pericardial pressure over the left ventricle. We conclude that there are significant local differences in pericardial pressure (recorded by balloon) over the lateral ventricular surfaces during acute changes in afterload. These observations may be explained in part by decreased venous return to the contralateral ventricle, the tendency of the heart to resist lateral displacement, and the limited mobility of the pericardium.     

Intraoperative measurement of pericardial constraint: role in ventricular diastolic mechanics

The pressure of pericardial constraint was measured in 20 patients undergoing elective cardiac surgery (10 in Group I with normal cardiac size; 10 in Group II with cardiomegaly) using a catheter with a collapsible latex end balloon. Right atrial pressure and other hemodynamic variables including right ventricular stroke work index were also measured before and after the pericardium was widely opened. The pericardium was grossly normal in all patients and only small physiologic effusions were present. In Group I mean pericardial pressure was 8 +/- 2 mm Hg as was mean right atrial pressure. In Group II mean pericardial pressure was 6 +/- 2 mm Hg versus mean right atrial pressure of 10 +/- 5 mm Hg (p less than 0.05). Excluding 2 of the 20 patients with outlying data, pericardial pressure showed linear correlation with right atrial pressure (r = 0.689). In Group I right ventricular stroke work index rose from 5.0 +/- 2.0 to 6.4 +/- 2.1 g-m/m2 (p less than 0.01) after pericardiotomy with no significant increase in mean right atrial pressure; similar findings in Group II were consistent with removal of external constraint. Thus, even in the absence of an abnormal effusion the normal pericardium exerts a significant pressure on the heart, which is often similar in magnitude to right atrial pressure. In certain notable exceptions, however, right atrial pressure far exceeds pericardial pressure. Such pericardial constraint has important implications for ventricular diastolic mechanics.     

The importance of pericardial constraint in experimental pulmonary embolism and volume loading.

To clarify the magnitude of the contribution of pericardial constraint to the hemodynamic deterioration that is observed during acute pulmonary embolism, hemodynamics and chamber dimensions (sonomicrometry) were measured during pulmonary embolization and subsequent volume loading in six anesthetized and instrumented open-chest, open-pericardium dogs. Embolization markedly increased peak right ventricular systolic pressure (38 +/- 5 mm Hg before embolism to 64 +/- 12 mm Hg after repeated embolization, p less than 0.05). However, right ventricular stroke volume decreased by only an insignificant amount (17 +/- 7 ml to 15 +/- 6 ml, p = not significant). Indices of left ventricular end-diastolic volume (left ventricular area = anteroposterior x septum-to-left ventricle free wall diameters) and stroke work (stroke work = area of the left ventricular pressure-area loop) were also similar before and after repeated embolization. Volume loading after repeated embolization resulted in increased right ventricular stroke volume (15 +/- 6 ml to 20 +/- 4 ml, p = 0.06), left ventricular area (3320 +/- 600 mm2 to 3470 +/- 580 mm2, p less than 0.05) and stroke work (261 +/- 158 mm Hg to 425 +/- 170 mm Hg x mm2, p less than 0.05). These results are in marked contrast to those in a previously reported study in a closed-chest and closed-pericardium model in which there was a decrease in left ventricular preload and systolic function after similar embolization-induced right ventricular pressure loading. Moreover, there was a further decrease in these parameters as a result of volume loading after embolism in the closed pericardium experiments. In conclusion, pericardial constraint contributes to hemodynamic deterioration during both acute right ventricular pressure loading and subsequent volume loading. The hemodynamic response to both interventions in the intact animal is determined not only by the degree of right ventricular dysfunction but also by the degree of direct ventricular interaction.     

Identification of blood in the pericardial cavity in dogs by two-dimensional echocardiography

The echocardiographic characteristics of hemopericardium with and without thrombus formation were investigated in 10 dogs and compared with that of saline solution injected into the pericardial cavity. Injection of 80 to 120 ml of saline solution produced an echolucent space between both pericardial layers and was considered as the control image in each dog for comparison with hemopericardium. Injection of heparinized blood filled the pericardial cavity with irregular echoes of variable acoustical impedence. High-density echoes of irregular distribution were observed in 3 dogs, in 5 dogs the echoes were of low acoustical density and in 2 dogs blood echoes were present but scarcely visible. Injection of clotted blood in 9 dogs (adding 20 mg of protamin sulphate and 8 mg of aminocaproic acid) produced echoes of high acoustical density easily identified in the 2-dimensional echocardiographic images. In 4 dogs attenuation and damping controls were increased to the point where myocardial echoes disappeared, while intrapericardial echoes were still visible. Thus, hemopericardium with or without thrombus formation may be identified by 2-dimensional echocardiography and differentiated from other types of pericardial effusion of lower acoustical density. Echogenicity of fluid blood in the pericardial cavity may be related to blood stasis.     

Assessment of pericardial diseases and cardiac masses with cardiovascular magnetic resonance

Imaging plays an important diagnostic and prognostic role in the assessment of pericardial diseases and cardiac tumors and in differentiating these conditions from other cardiac and noncardiac diseases. A number of imaging modalities are available for this task; each has advantages and limitation. Cardiovascular magnetic resonance (CMR) is a highly versatile imaging modality that provides detailed anatomical information, tissue characterization, cardiac function assessment, and evaluation of the impact of these conditions on hemodynamics. In this review we focus on the current state-of-the-art application of cardiovascular magnetic resonance in assessing pericardial diseases and cardiac tumors.     

Adenoviral-mediated gene transfer induces sustained pericardial VEGF expression in dogs: effect on myocardial angiogenesis

OBJECTIVE: Angiogenic peptides like VEGF (vascular endothelial growth factor) and bFGF (basic fibroblast growth factor) have entered clinical trials for coronary artery disease. Attempts are being made to devise clinically relevant means of delivery and to effect site-specific delivery of these peptides to the cardiac tissue, in order to limit systemic side-effects. We characterized the response of the pericardium to delivery of a replication-deficient adenovirus carrying the cDNA for AdCMV.VEGF165, and assessed the effect of pericardial VEGF165 on myocardial collateral development in a canine model of progressive coronary occlusion. METHODS: Ameroid constrictors were placed on the proximal left circumflex coronary artery of mongrel dogs. Ten days later, 6 x 10(9) pfu AdCMV.VEGF165 (n = 9). AdRSV.beta-gal (n = 9), or saline (n = 7) were injected through an indwelling pericardial catheter. Transfection efficiency was assessed by X-gal staining. Pericardial and serum VEGF levels were measured serially by ELISA. Maximal myocardial collateral perfusion was quantified with radiolabeled or fluorescent microspheres 28 days after treatment. RESULTS: In AdRSV.beta-gal-treated dogs, there was extensive beta-gal staining in the pericardium and epicardium, with minimal beta-gal staining in the mid-myocardium and endocardium. Pericardial delivery of AdCMV.VEGF165 resulted in sustained (8-14 day) pericardial transgene expression, with VEGF levels peaking 3 days after infection (> 200 ng/ml) and decreasing thereafter. There was no detectable increase in serum VEGF levels. Maximal collateral perfusion, a principal correlate of collateral development and angiogenesis, was equivalent in all groups. CONCLUSION: Adenoviral-mediated gene transfer is capable of inducing sustained VEGF165 expression in the pericardium; however, locally targeted pericardial VEGF delivery failed to improve myocardial collateral perfusion in this model.     

Effects of pericardial effusates of various conductivities on body-surface potentials in dogs. Documentation of the eccentric spheres model

The purpose of this study was to discover the cause and magnitude of changes in the body-surface potentials occurring when: (1) fluids of various conductivity were added to the pericardial sac, or (2) the volume of the blood within chambers of the heart was either increased or decreased. Fluids added to the pericardium were physiological saline, whole-blood, and mineral oil. Magnitudes of body-surface potentials were compared to the predictions based on a mathematical eccentric spheres model of the heart and torso developed previously by Rudy and Plonsey. Data demonstrated conclusively that there is a nonlinear relationship between the body-surface potentials and the conductivity of the pericardial layer. This relationship is one in which the body-surface potentials of the anterior chest were found to decrease when conductivity of the pericardial layer was either increased or decreased. These changes in body-surface potentials were caused solely by alterations in the conductivity and volume of the fluid effusate. It was demonstrated that these changes were not caused by any "stretching" or "compression" of the cardiac tissue caused by the altered fluid volumes in and around the heart. Findings were accurately predicted by the eccentric spheres model, thereby confirming the model's usefulness as a predictive instrument. The model provides an explanation for the nonlinear relationship that was exhibited by the data.     

Closed pericardial drainage for relief of pericardial tamponade

The method of continuous catheter drainage for pericardial tamponade as used in 108 patients is described. The efficacy of this procedure in relieving tamponade resulting from a variety of diseases is demonstrated. Blood clot in the pericardium probably constitutes a contraindication to catheter drainage.     

Hemorrhagic pericardial effusion causing pericardial tamponade in hereditary hemorrhagic telangiectasia

Osler-Weber-Rendu disease, or Hereditary Hemorrhagic Telangiectasia (HHT), is a rare, inherited autosomal dominant disorder characterized by telangiectasia and arteriovenous malformations in various organs. We report a unique case of HHT-associated hemorrhagic pericardial effusion presenting with pericardial tamponade.     

Physiological features of pericardial constriction in the absence of pericardial disease.

To sustain a clinical diagnosis of constriction it is classically held that the fibrous pericardium must be thickened and adherent to the surface of the heart. A case is presented in which leukaemic infiltration of the fat overlying the myocardium resulted in the physiological features of constriction, although all layers of the pericardium itself were normal. Constriction is thus a physiological diagnosis; it may develop in the absence of the classical anatomical findings.     

Assessment of the efficacy of Ankaferd blood stopper on the prevention of postoperative pericardial adhesions

Postoperative pericardial adhesion formation occurs frequently after cardiac surgery and is an important cause of morbidity and mortality at the time of re-operation. As the number of patients undergoing cardiac surgery continues to increase, the number of potential candidates for re-operation is increasing exponentially. Despite ongoing improvements during cardiac re-operation surgery, the presence of pericardial adhesions not only adds to the surgery time but also increases the risk of life-threatening injuries to the heart, great vessels or previously placed coronary bypass conduits by obscuring the true anatomy.1Various methods and materials have been investigated to prevent or reduce the severity of postoperative adhesions in the retrosternal spaces and mediastinal structures. Fibrinolytic agents, histamine antagonists, anti-coagulants, anti-inflammatory drugs (corticosteroids, non-steroidal drugs), antibiotics, several natural physical barriers (heterologous pericardium, omentum, peritoneum, amnion, fibrin, gelatin, collagen and hyaluronic acid) and synthetic physical barriers (rubber, silicon-based materials, cellulose, polytetrafluoroethylene, polyvinyl alcohol and polyester derivatives) have been tried with variable success for such purposes.2-6 Unfortunately, despite continuous advances and research, to date there is no ideal method to prevent or reduce postoperative pericardial adhesion formation.Ankaferd blood stopper® (ABS) (Ankaferd Ilac Kozmetik AS, Istanbul, Turkey) is a folkloric medicinal plant extract. Ankaferd has been used as a blood-stopping agent against various types of bleeding. It has been approved by the Ministry of Health in Turkey for the management of bleeds due to external injury and dental surgery. It has also been used as a topical agent for the prevention of postoperative intra-abdominal fibrosis in experimental studies, and variable results have been obtained.7,8To the best of our knowledge, there is no report on the effect of Ankaferd in preventing postoperative pericardial adhesions to date. The present experimental study was designed to investigate the effect of intrapericardially administered Ankaferd on reducing postoperative pericardial adhesion formation in the rabbit model.     

心包腔容积—压力关系的临床研究

１６ 例中到大量心包积液患者在Ｘ线下使用Ｓｅｌｄｉｎｇｅｒ法,经剑突下穿刺心包放置７Ｆ导鞘,心包造影,定量抽液及压力测定。资料完整的１５ 例患者显示:心包腔内压力与心包积液量无相关性。有心包填塞症状者,当抽液量达到１５０ ｍ ｌ时,心包内压力下降曲线最为陡峭:幅度最大,而以后随积液量减少,压力下降徐缓。当抽液到２５０ ｍ ｌ时心包腔舒张压在０．４０ ｋＰａ～－ １．４６ ｋＰａ 之间,大多数低于文献报道的右房舒张压。在积液基本抽完时,１２ 例心包腔平均压在０～－ １．３３ ｋＰａ之间,最低可达－ ２．０ ｋＰａ,与胸膜腔压近似。１ 例有肺气肿的老年患者和２ 例有胸腔积液者压力在０．１３ ｋＰａ～０．５３ ｋＰａ之间     

心包穿刺置管引流术的临床应用体会

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Relationship between pericardial pressure and lymphatic pericardial fluid transport in sheep

We investigated the relationship between pericardial pressure and the volumetric lymphatic clearance rate of pericardial fluid in sheep. A single catheter perfusion system was established to deliver tracer to the pericardial cavity and control pericardial pressure. In addition, catheters were placed into the thoracic duct and into the jugular vein at the base of the neck. (125)I-human serum albumin (HSA) was administered into the pericardial perfusate to serve as the lymph flow marker and its concentration monitored in the effluent from the outflow end of the perfusion system. (131)I-HSA was injected intravenously to permit calculation of plasma tracer loss and tracer recirculation into lymphatics. From mass balance equations, estimates of total pericardial clearance into lymphatics increased significantly as pericardial pressures were elevated in 2. 5 cm H(2)O increments from 2.5 to 12.5 cm H(2)O (P = 0.018). Pericardial lymph transport ranged from 0.89 +/- 0.10 to 3.09 +/- 0. 66 ml/h at 2.5 and 12.5 cm H(2)O pericardial pressure, respectively. The majority of transport occurred through mediastinal vessels with a small proportion (10.3 to 23.9%) being cleared into lymphatics leading to the thoracic duct. We conclude that lymphatic pericardial fluid transport increases approximately 3.5-fold over a pericardial pressure range that encompasses the transition between the shallow and steep portions of the pericardial pressure-volume relationship.