Pericardial Pressure Research Articles

Mycoplasma pneumoniae Pericarditis and Cardiac Tamponade in a 7-Year-Old Girl with Cystic Fibrosis

). The high pericardial pressure led to the collapse of the right atrium and ventricle, and the left atrium, and there was also an initial inversion of the left ventricle in late systole with paradoxical septal movements. The right ventricular out-flow wall was deflected posteriorly after the mitral valve opened, whereas there was no compression of the left ventricular outflow.

Low-Pressure Cardiac Tamponade

Low-pressure cardiac tamponade is a form of cardiac tamponade in which a comparatively low pericardial pressure results in cardiac compression because of low filling pressure. This syndrome is poorly characterized because only isolated cases have been reported. We conducted a study of its clinical and hemodynamic profiles. From 1986 through 2004, we evaluated all patients at our institution with combined pericardiocentesis and cardiac catheterization. We identified those patients who fulfilled catheterization-based criteria of low-pressure cardiac tamponade and compared their clinical and catheterization data with those of patients with classic tamponade. A total of 1429 patients with pericarditis were evaluated, 279 of whom underwent combined pericardiocentesis and catheterization. Criteria of low-pressure cardiac tamponade were met in 29, whereas 114 had criteria of classic cardiac tamponade. Patients with low-pressure tamponade less frequently had clinical signs of tamponade, but the rate of constitutional symptoms, use of diuretics, and echocardiographic findings of tamponade were similar in both groups. Patients with low-pressure tamponade showed a significant increase in cardiac output after pericardiocentesis, but they usually had less severe cardiac tamponade compared with patients with classic tamponade. Prognosis was related mainly to the underlying disease. Low-pressure cardiac tamponade was identified in 20% of patients with catheterization-based criteria of tamponade. Clinical recognition may be difficult because of the absence of typical physical findings of tamponade in most patients. Although some patients are critically ill, most show a stable clinical condition. However, these patients obtain a clear benefit from pericardiocentesis.

Assessment of right ventricular diastolic suction in dogs with the use of wave intensity analysis

Diastolic suction (DS) can be defined as that property of the ventricle by means of which it tends to refill itself during early diastole, independent of any force from the atrium. Although thought to be significant in the left ventricle (LV), DS in the right ventricle (RV) has received little attention, probably because of RV geometry. Our recent LV studies have shown that DS is related to both decreased elastance (i.e., tau, the relaxation time constant) and end-systolic volume (V(LVES)), thus reconciling the two mechanisms that have been used to explain the concept of DS. We hypothesized that RV DS would similarly depend on tau and V(RVES). In six anesthetized open-chest dogs, aortic, RV, right atrial (RA), pulmonary arterial (PA), and RV pericardial pressure, tricuspid velocity, and PA flow were measured. V(RVES) was calculated by measuring distances between eight ultrasonic crystals. An empirical index of relaxation, tau', and V(RVES) were manipulated by volume loading/caval constriction and isoproterenol/esmolol. We calculated the total energy (I(W-)) of the backward expansion wave generated during RV relaxation and that component causing DS [I(W-(DS))]; i.e., the energy remaining after tricuspid valve opening. I(W-) [I(W-(DS)) also] was found to be inversely related to tau' and to V(RVES) {i.e., I(W-) = -8.85.e((-0.0423tau')).e([-0.0665(%V(RVES))])}. Thus, as for the LV, the energy of the backward-going wave generated by the RV during relaxation depends on both the rate at which elastance decreases and the completeness of ejection. Despite the thin wall and nonspherical shape of the RV, DS appears to be an important mechanism.

A 2D FE model of the heart demonstrates the role of the pericardium in ventricular deformation

During pulmonary artery constriction (PAC), an experimental model of acute right ventricular (RV) pressure overload, the interventricular septum flattens and inverts. Finite element (FE) analysis has shown that the septum is subject to axial compression and bending when so deformed. This study examines the effects of acute PAC on the left ventricular (LV) free wall and the role the pericardium may play in these effects. In eight open-chest anesthetized dogs, LV, RV, aortic, and pericardial pressures were recorded under control conditions and with PAC. Model dimensions were derived from two-dimensional echocardiography minor-axis images of the heart. At control (pericardium closed), FE analysis showed that the septum was concave to the LV; stresses in the LV, RV, and septum were low; and the pericardium was subject to circumferential tension. With PAC, RV end-diastolic pressure exceeded LV pressure and the septum inverted. Compressive stresses developed circumferentially in the septum out to the RV insertion points, forming an arch-like pattern. Sharp bending occurred near the insertion points, accompanied by flattening of the LV free wall. With the pericardium open, the deformations and stresses were different. The RV became much larger, especially with PAC. With PAC, the arch-like circumferential stresses still developed in the septum, but their magnitudes were reduced, compared with the pericardium-closed case. There was no free wall inversion and flattening was less. From these FE results, the pericardium has a significant influence on the structural behavior of the septum and the LV and RV free walls. Furthermore, the deformation of the heart is dependent on whether the pericardium is open or closed.

Effect of pericardiotomy on exercise-induced pulmonary hypertension in the horse

AbstractThe role of cardiac function or dysfunction in the pathogenesis of exercise-induced pulmonary hypertension and haemorrhage in horses has been minimally investigated. We hypothesize that pericardiotomy would enhance diastolic function and attenuate pulmonary vascular pressures in maximally exercising horses. Our objective was to evaluate diastolic function and cardiopulmonary pressures before and after pericardiotomy, at rest and at maximal exercise. Study design was both self- and externally controlled. Five horses underwent pericardiotomy after a baseline exercise test. They subsequently performed the same exercise protocol at 1 week and 13 weeks post-operatively. An external, unoperated control group of five horses performed the same experimental protocol. Pulmonary arterial pressure (PAP), pulmonary artery wedge pressure (PWP), right ventricular pressure, heart rate (HR) and oesophageal pressure were measured continuously at rest and at maximal exercise; maximum rates of ventricular pressure decrease (−dP/dtmax), relaxation half-time (t1/2), time constant of isovolumic relaxation (τ) and pulmonary capillary pressures (PcapP) were derived. Statistical analysis was performed using two-tailed Wilcoxon's signed-rank and rank-sum tests, with significance set atP<0.05. No significant differences were found in any variable after pericardiotomy was performed or between the experimental and external control groups. We conclude that during a 13-week study period, pericardiotomy does not alter pulmonary or ventricular pressures or rate of ventricular relaxation in the resting or maximally exercising horse. Results indicate that, in past and future studies requiring an open pericardium in normal horses, the cardiopulmonary parameters measured here are not affected by reduced pericardial pressure.

Decrease in fluoroscopic cardiac silhouette excursion precedes hemodynamic compromise in intraprocedural tamponade

Acute pericardial tamponade is a life-threatening complication of invasive cardiovascular procedures. Survival depends on early recognition and treatment. A diagnostic test to detect pericardial fluid accumulation before a significant fall in blood pressure and without contamination of the sterile field would be valuable. We tested the hypothesis that fluoroscopic excursion of the cardiac silhouette decreases early in the course of acute pericardial tamponade and precedes hemodynamic compromise. The pericardial space of seven pigs was accessed by a sub-xiphoid puncture. Tamponade was produced by intrapericardial saline infusion at 20-25 mL/minute until the pericardial pressure equalized with right ventricular end diastolic pressure or the systolic blood pressure reached 40 mmHg. Supine fluoroscopic images were obtained every 2 minutes in the left anterior oblique view with simultaneous echocardiography. The fluoroscopic heart silhouette was digitized, and the maximum excursion during the cardiac cycle was quantified by custom software. The qualitative excursion of the fluoroscopic heart silhouette on randomly selected video images was also graded by two independent observers who were blinded to the time course of the experiment and the hemodynamics. During progressive pericardial fluid accumulation, the cardiac silhouette excursion quantified by the custom software (p < 0.001) and by video rating (p < 0.0001) was significantly reduced within 2 minutes. A statistically significant fall in blood pressure compared with baseline did not occur until 6 minutes (89 +/- 21 vs. 121 +/- 15 mmHg, p < 0.001). The interobserver agreement was very close, with a kappa statistic of 0.78. The reduction in cardiac silhouette excursion was apparent as soon as the effusion was detected by echocardiography. Cardiac silhouette excursion becomes reduced early in the course of acute pericardial fluid accumulation. This fluoroscopic observation can be used to detect impending pericardial tamponade before hemodynamic collapse.

Left Ventricular Cardiac Tamponade in the Setting of Cor Pulmonale and Circumferential Pericardial Effusion

Circumferential pericardial effusion typically results in biventricular tamponade and equalization of intracardiac and pericardial pressure during diastole. However, tamponade may involve the right or left ventricle. While isolated left ventricular cardiac tamponade (LVCT) can occur as a postoperative complication from localized posterior pericardial effusions, circumferential pericardial effusions leading to LVCT are rare. We report a case of a patient with severe pulmonary hypertension, a large nonloculated pericardial effusion, and LVCT, which was probably due to a chronic undifferentiated connective tissue disorder. This case illustrates that when evaluating patients with circumferential pericardial effusions and associated pulmonary hypertension, the typical findings of cardiac tamponade (pulsus paradoxus, right ventricular diastolic compression and hypotension) may be masked. The echocardiogram must be reviewed carefully as it may reveal left ventricular diastolic compression, the hallmark of LVCT, which may significantly compromise left ventricular filling and cardiac output.

Physiological changes in the Norway lobster Nephrops norvegicus (L.) escaping and discarded from commercial trawls on the West Coast of Scotland : 1. Body fluid volumes and haemolymph composition after capture and during recovery

The Norway Lobster Nephrops norvegicus (L.) was captured by trawling at depths of 120 to 150 m off the West Coast of Scotland using commercial fishing gears. Discarded animals (normally <25–35 mm carapace length) were sampled immediately after capture, and following emersion (exposure to air) on deck for 1 or 2 h. Their recovery from, and survival of, the stresses of being fished were examined in separate groups of animals transferred by SCUBA divers to underwater (u/w) cages on the seabed at a mean depth of 24 m. “Escaped” N. norvegicus were collected in a small-meshed (40 mm) “cover” around the cod-end and sampled without emersion. It was assumed that the physiological state of these animals would be similar to those passing through the cod-end meshes directly back into the surrounding sea during normal fishing operations. Groups of escaped animals were also transferred to u/w cages for recovery and survival studies. Control animals (creel-caught from the same fishing grounds) were sampled after recovery in u/w cages. Total body water content, haemolymph (blood) volume and composition were examined at various stages after capture and during recovery of control, discarded and escaped animals. Discarded animals showed significant reductions in total body water content compared to controls but recovered after 24 h. Controls that had been artificially damaged by puncturing also showed a reduction in water content. Escaped animals showed significantly higher mean water content compared to discards. Haemolymph volumes were also reduced in discarded animals suggesting that significant blood loss occurs during capture. There was also evidence of a shift of fluid from haemolymph to tissues in discarded animals. Pericardial (haemolymph) pressures were much reduced in discards compared to undisturbed control animals but showed significant recovery in surviving animals. Pressure reduction was less in escapes but was seen in control animals that had been exercised to exhaustion. Haemolymph osmotic concentrations, [Na +] and [K +] showed increases after discarding, notably after emersion, but haemocyanin [Hcy] and total haemolymph protein concentrations were less affected. The effect of these changes on longer term survival and recovery from the stress of capture are discussed.

Assessment of left ventricular diastolic suction in dogs using wave-intensity analysis

Two apparently different types of mechanisms have emerged to explain diastolic suction (DS), that property of the left ventricle (LV) that tends to cause it to refill itself during early diastole independent of any force from the left atrium (LA). By means of the first mechanism, DS depends on decreased elastance [e.g., the relaxation time constant (tau)] and, by the second, end-systolic volume (V(LVES)). We used wave-intensity analysis (WIA) to measure the total energy transported by the backward expansion wave (I(W-)) during LV relaxation in an attempt to reconcile these mechanisms. In six anesthetized, open-chest dogs, we measured aortic, LV (P(LV)), LA (P(LA)), and pericardial pressures and LV volume by orthogonal ultrasonic crystals. Mitral velocity was measured by Doppler echocardiography, and aortic velocity was measured by an ultrasonic flow probe. Heart rate was controlled by pacing, V(LVES) by volume loading, and tau by isoproterenol or esmolol administration. I(W-) was found to be inversely related to tau and V(LVES). Our measure of DS, the energy remaining after mitral valve opening, I(W-DS), was also found to be inversely related to tau and V(LVES) and was approximately 10% of the total "aspirating" energy generated by LV relaxation (i.e., I(W-)). The size of the Doppler (early filling) E wave depended on I(W-DS) in addition to I(W+), the energy associated with LA decompression. We conclude that the energy of the backward-going wave generated by the LV during relaxation depends on both the rate at which elastance decreases (i.e., tau) and V(LVES). WIA provides a new approach for assessing DS and reconciles those two previously proposed mechanisms. The E wave depends on DS in addition to LA decompression.

Pericardial and pericardioperitoneal canal relationships to cardiac function in the white sturgeon ( Acipenser transmontanus)

Sturgeons are primitive bony fishes and their hearts have structural features found in other primitive fishes. Sturgeons have a pericardioperitoneal canal (PPC), a one-way conduit into the peritoneum. A PPC also occurs in elasmobranchs (sharks and rays) and studies with that group demonstrate that pericardial pressure and pericardial fluid loss via the PPC affect stroke volume. A study of white sturgeon ( Acipenser transmontanus) heart function was conducted to test for a comparable PPC and pericardial effects. White sturgeon-elasmobranch heart-function similarities include biphasic ventricular filling, a comparable operational pericardial pressure (−0.03 kPa), and a strongly negative pressure (−0.2 to −0.6 kPa) with complete pericardial fluid withdrawal. Differences include the white sturgeon's relatively smaller atrium and ventricle but a larger conus arteriosus. Although white sturgeon heart size is also smaller, its pericardial volume is disproportionately less (2.4 to 2.7 vs. 3.5 to 5.4 ml kg −1 in elasmobranchs), meaning it has less scope for increasing stroke volume upon PPC fluid release. These differences may reflect the phylogenetic progression from the less complex operation of the elasmobranch heart, which lacks sympathetic innervation and has a mechanically mediated (PPC) stroke volume, to the condition in the more derived bony fishes which have sympathetic and parasympathetic regulation of both stroke volume and heart rate.

Atrioventricular nonuniformity of pericardial constraint.

Physiologists and clinicians commonly refer to "pressure" as a measure of the constraining effects of the pericardium; however, "pericardial pressure" is really a local measurement of epicardial radial stress. During diastole, from the bottom of the y descent to the beginning of the a wave, pericardial pressure over the right atrium (P(pRA)) is approximately equal to that over the right ventricle (P(pRV)). However, in systole, during the interval between the bottom of the x descent and the peak of the v wave, these two pericardial pressures appear to be completely decoupled in that P(pRV) decreases, whereas P(pRA) remains constant or increases. This decoupling indicates considerable mechanical independence between the RA and RV during systole. That is, RV systolic emptying lowers P(pRV), but P(pRA) continues to increase, suggesting that the relation of the pericardium to the RA must allow effective constraint, even though the pericardium over the RV is simultaneously slack. In conclusion, we measured the pericardial pressure responsible for the previously reported nonuniformity of pericardial strain. P(pRA) and P(pRV) are closely coupled during diastole, but during systole they become decoupled. Systolic nonuniformity of pericardial constraint may augment the atrioventricular valve-opening pressure gradient in early diastole and, so, affect ventricular filling.

A comparative echocardiographic assessment of ventricular function in five species of sharks

A comparative echocardiographic study was carried out on five shark species that differ in heart morphology and in aspects of their behavior and natural history. The study contrasted the ventricular function in the highly active mako shark (heart type IV) and four other sharks (heart type III) that differ in activity levels (i.e. the sedentary horn and swell sharks vs. the moderately active blue and smooth-hound sharks). All five species exhibited biphasic ventricular filling characterized by an early (conduit) and late (atrial systole) phase. In the mako shark, early filling was dominant as indicated by a higher early flow peak velocity, a greater early:late velocity ratio, and a greater early velocity time integral. In contrast, the late filling phase was the more important filling agent in the other species. Indices of systolic function such as ventricular ejection fraction and ventricular fractional shortening also reflect a more efficient cardiac pumping capacity in mako shark relative to the other four sharks. The comparative echocardiographic assessment of in vivo ventricular function integrates structural and functional features with shark activity level to arrive at a new perspective blending the occurrence of biphasic filling with functional concepts based on heart morphological typology and changing views regarding the role of factors such as central filling pressure and pericardial pressure on end-diastolic ventricular volume.

Echocardiographic tamponade in severe left ventricular dysfunction: the impact of small pericardial effusion and the absence of pulsus paradoxicus

Cardiac tamponade is a commonly encountered clinical entity. It is a clinical syndrome characterized by elevated filling pressures, pulsus paradoxicus, and eventually, hypotension. It occurs as intrapericardial pressure exceeds intracardiac pressures altering ventricular filling. Generally tamponade occurs with moderate or large accumulations of pericardial fluid that result in an increase in pericardial pressure. It is well known that rapid accumulation of relatively small volumes of fluid can cause tamponade pathophysiology. We report a less well-recognized phenomenon. In the setting of severe left ventricular dysfunction, small volumes of pericardial fluid can result in excessive intrapericardial pressure and echocardiographic tamponade in the absence of a significant pulsus paradoxicus.

Opening the pericardium during pulmonary artery constriction improves cardiac function.

During acute pulmonary hypertension, both the pericardium and the right ventricle (RV) constrain left ventricular (LV) filling; therefore, pericardiotomy should improve LV function. LV, RV, and pericardial pressures and RV and LV dimensions and LV stroke volume (SV) were measured in six anesthetized dogs. The pericardium was closed, the chest was left open, and the lungs were held away from the heart. Data were collected at baseline, during pulmonary artery constriction (PAC), and after pericardiotomy with PAC maintained. PAC decreased SV by one-half. RV diameter increased, and septum-to-LV free wall diameter and LV area (our index of LV end-diastolic volume) decreased. Compared with during PAC, pericardiotomy increased LV area and SV increased 35%. LV and RV compliance (pressure-dimension relations) and LV contractility (stroke work-LV area relations) were unchanged. Although series interaction accounts for much of the decreased cardiac output during acute pulmonary hypertension, pericardial constraint and leftward septal shift are also important. Pericardiotomy can improve LV function in the absence of other sources of external constraint to LV filling.

Preload changes by positive pressure ventilation can be used for assessment of left ventricular systolic function.

Assessment of preload independent left ventricular function with conductance volumetry is traditionally accomplished by inflating a balloon in the inferior caval vein. Our aim was to investigate if a similar change in preload could be achieved by positive pressure ventilation with large tidal volume. Conductance volumetry generating left ventricular pressure-volume loops was used in seven pentobarbital-anesthetized pigs. Changes in preload recruitable stroke work were studied, comparing the effects of inferior vena cava occlusion (IVCO) or large tidal volume (LTV). Cardiodepression was induced by halothane anesthesia and halothane + phenylephrine, and stimulation by epinephrine infusion. Although the decreasis in left ventricular end diastolic volume was slightly less with LTV (16.5 +/- 1.7 ml, mean +/- SEM) than with IVCO (22.4 +/- 1.7 ml) (P < 0.0001) the PRSW-slopes showed a high degree of correlation (r=0.80, P < 0.0001). Although peak tracheal pressures increased significantly to 27.8 +/- 0.9 mmHg during LTV, esophageal pressures (used as an indicator of pericardial pressure) were unchanged. Positive pressure ventilation with LTV is similar to IVCO in creating transient changes in preload, necessary for assessment of left ventricular systolic function. This observation was valid also during drug-induced cardiac depression and stimulation. The preload recruitable stroke work used for this validation was shown to be a reliable and stable method.

In vitro evaluation of the concept of pericardial pressure augmentation in isolated pig hearts

In vitro evaluation of the concept of pericardial pressure augmentation in isolated pig hearts

Effects of positive-pressure ventilation, pericardial effusion, and cardiac tamponade on respiratory variation in transmitral flow velocities

Objective: To determine the effects of positive-pressure ventilation and experimentally induced pericardial effusion and tamponade on transmitral flow velocities in dogs. Design: Descriptive. Setting: University laboratory. Participants: Eleven tracheally intubated and mechanically ventilated dogs. Interventions: Experimental pericardial effusion and cardiac tamponade were created by pericardial injection of warm saline. Measurements and Main Results: Hemodynamic parameters and pericardial pressures were monitored in the 11 dogs. Pulsed-wave Doppler tracings of mitral valve flow were obtained at the leaflet tips along with hemodynamic measurements at 4 stages: control, effusion (no decrease in mean arterial pressure), tamponade (≥40% decrease in mean arterial pressure), and tamponade relief (after evacuation of pericardial fluid). Maximal variation (36%) in transmitral flow velocity over the respiratory cycle during positive-pressure ventilation was seen in the control stage. In the effusion and tamponade stages, variation in transmitral flow velocity decreased progressively to 29% (p = 0.1804, not significant) and 16% (p < 0.0001), respectively. Conclusion: Intrathoracic pressure and lung volume changes caused by positive-pressure ventilation influence transmitral flow velocity patterns. Respiratory variation in transvalvular flow is pronounced during standard positive-pressure mechanical ventilation, decreases in the presence of pericardial effusion, and becomes almost nonexistent when cardiac tamponade is present. These findings show that the echocardiographic criteria used to diagnose cardiac tamponade based on mitral valve inflow patterns are different during positive-pressure ventilation from spontaneously breathing subjects. Copyright 2003, Elsevier Science (USA). All rights reserved.

Pericardium modulates left and right ventricular stroke volumes to compensate for sudden changes in atrial volume.

The pericardium may modulate acute compensatory changes in stroke volumes seen with sudden changes in cardiac volume, but such a mechanism has never been clearly demonstrated. In eight open-chest dogs, we measured left and right ventricular pressures, diameters, stroke volumes, and pericardial pressures during rapid (approximately 300 ms) systolic infusions or withdrawals of approximately 25 ml blood into and out of the left atrium and right atrium. Control beats, the infusion/withdrawal beat, and 4-10 subsequent beats were studied. With infusions, ipsilateral ventricular end-diastolic transmural pressure, diameter, and stroke volume increased. With the pericardium closed, there was a compensatory decrease in contralateral transmural pressure, diameter, and stroke volume, mediated by opposite changes in transmural end-diastolic pressures. The sum of the ipsilateral increase and contralateral decrease in stroke volume approximated the infused volume. Corresponding changes were seen with blood withdrawals. This direct ventricular interaction was diminished when pericardial pressure was <5 mmHg and absent when the pericardium was opened. Pericardial constraint appears essential for immediate biventricular compensatory responses to acute atrial volume changes.

Lymphatic Transport of Pericardial Effusate in Sheep

In this report, we quantified fluid loss from the pericardial cavity during simulated saline effusions and determined what proportion of this loss occurred through lymphatics. Fifty or 100 ml of Ringers lactate solution [containing 0.5% sheep albumin and 131I-human serum albumin (HSA)] was injected into the pericardial cavity of sheep. Pericardial pressures, systemic arterial pressures, and plasma/pericardial fluid concentrations of the radioactive tracer were measured. Lymph transport of pericardial fluid was estimated from the plasma recovery of tracer using a mass balance equation. Plasma recoveries were corrected for tracer loss using a coefficient of elimination calculated from the plasma disappearance curve of intravenously administered 125I-HSA. Over 4 h, 27.6 ± 4.9 (±SE) and 36.7 ± 4.2 ml were lost from the pericardial cavity in the 50- and 100-ml effusion series, respectively, of which 5.2 ± 0.8 (20.2 ± 3.8% of volume lost) and 7.7 ± 1.6 ml (21.5 ± 3.3% of volume lost) could be attributed to lymphatic transport. We conclude that lymphatic transport is one of the factors that contribute to pericardial “reserve” function by helping to restore pericardial fluid volume to resting levels.

Pathophysiologic mechanisms in pericardial disease.

The pericardium influences cardiac performance indirectly, but pathologic conditions may have profound effects on cardiac function. In recent years, several imaging modalities have been useful, both clinically and in understanding the pathophysiology of pericardial diseases. Rising pericardial pressures progressively reduce the average transmural pressure of the right and subsequently left cardiac chambers, compromising filling and output. This has become more relevant today, with the increased incidence of cardiac tamponade, attributed to the increased use of antiplatelet agents in combination with a more widespread use of invasive devices. On another front, although an uncommon diagnosis, constrictive pericarditis may be missed despite the excellence of a variety of noninvasive methods, and remains a difficult one to make.Introduction