Intrapericardial Pressure Research Articles

Pericardiocentesis and principles of echocardiographic imaging in the patient with cardiac neoplasia

Ultrasonography is a safe, noninvasive, sensitive, and specific tool for evaluation of the heart and pericardium in patients with cardiac neoplasia. In small animals, the incidence of cardiac neoplasia is low. In dogs, hemangiosarcoma and chemocdectoma are the two most common types of cardiac neoplasia. In cats, lymphosarcoma is the most common form of cardiac neoplasia. Pericardial effusion is a common and potentially life-threatening consequence of cardiac neoplasia. Pericardial effusion leads to a rise in the intrapericardial pressure, resulting in varying degrees of hemodynamic compromise. Cardiac tamponade occurs when the intrapericardial pressure equals or exceeds right ventricular diastolic filling pressures, leading to a decreased cardiac output. Pericardiocentesis is used to stabilize animals with life-threatening cardiac tamponade, and to obtain fluid samples for diagnostic evaluation. The fluid should be quantified and characterized. If the etiology of the effusion is not known, then a sample of the fluid should be submitted for fluid analysis and cytology. Serious complications associated with pericardiocentesis are rare. Complications include cardiac puncture, arrhythmias, and laceration of the tumor or coronary artery, resulting in intrapericardial hemorrhage.

Long-term follow-up of idiopathic chronic pericardial effusion.

A large idiopathic chronic pericardial effusion can be defined as a collection of pericardial fluid that persists for more than three months and has no apparent cause. We conducted a prospective study of the natural history and treatment of this disorder. Between 1977 and 1992, we prospectively evaluated and enrolled patients with large idiopathic chronic pericardial effusion. We performed pericardiocentesis in most of the patients. We performed pericardiectomy when large pericardial effusion reappeared after pericardiocentesis. Follow-up ranged from 18 months to 20 years (median, 7 years). During the study period, we evaluated a total of 1108 patients with pericarditis, 461 of whom had large pericardial effusion. Twenty-eight of these patients (age range, 7 to 85 years; median, 61) had large idiopathic chronic effusion and were included in the study. The duration of effusion ranged from 6 months to 15 years (median, 3 years). At the initial evaluation, 13 patients were asymptomatic. Overt tamponade was found in eight patients (29 percent). Therapeutic pericardiocentesis, performed in 24 patients, was followed by the disappearance of or marked reduction in the effusion in 8. Five of the 24 patients underwent early pericardiectomy, and in 11 large pericardial effusion reappeared. Cardiac catheterization, performed in 16 patients, showed elevated intrapericardial pressure (4.75+/-3.79 mm Hg) and reduced transmural pressure (1.0+/-2.50 mm Hg) before pericardiocentesis. Both of these abnormalities in pressure improved significantly after pericardiocentesis. Pericardiectomy, performed in 20 patients, yielded excellent long-term results. At the end of the follow-up period, 10 patients had died, but none had died from pericardial disease. Large idiopathic chronic pericardial effusion is well tolerated for long periods in most patients, but severe tamponade can develop unexpectedly at any time. Pericardiocentesis alone frequently results in the resolution of large effusions, but recurrence is common and pericardiectomy should be considered whenever a large effusion recurs after pericardiocentesis.

Pathophysiology of Cardiac Tamponade

C ardiac tamponade is always life threatening and nearly always requires urgent and precise therapeutic intervention. It is perhaps unique in that appreciation of its pathophysiologic state is essential to precise diagnosis and rational treatment. Since the 19th century, investigations in experimental animals provided a basic understanding that has been continually refined by recent investigators to the point where an integrated picture of its macrophysiologic condition emerges. This review covers the resultant concepts. Procedural details of investigations can be found in the references (thus, for example, the text omits the relative merits of catheters vs flat balloons for intrapericardial pressure determination).

Right heart ischemia: Pathophysiology, natural history, and clinical management

Right ventricular (RV) ischemia occurs in 50% of patients with acute inferior myocardial infarction, and may result in severe hemodynamic compromise associated with poor clinical outcome. Acute right coronary artery (RCA) occlusion proximal to the RV branches results in right ventricular free wall (RVFW) dysfunction. The ischemic, dyskinetic RVFW exerts mechanically disadvantageous effects on biventricular performance. Depressed RV systolic function leads to a decrease in transpulmonary delivery of left ventricular (LV) preload, resulting in diminished cardiac output. The ischemic right ventricle is stiff, dilated, and volume dependent, resulting in pandiastolic RV dysfunction and septally-mediated alterations in LV compliance, which are exacerbated by elevated intrapericardial pressure. Under these conditions, RV pressure generation and output are dependent on LV-septal contractile contributions, governed by both primary septal contraction and paradoxical septal motion. When the culprit coronary lesion is distal to the right atrial (RA) branches, augmented RA contractility enhances RV performance and optimizes cardiac output. Conversely, more proximal occlusions result in ischemic depression of RA contractility, which impairs RV filling, thereby resulting in further depression of RV performance and more severe hemodynamic compromise. Bradyarrhythmias limit the output generated by the rate-dependent noncompliant ventricles. Patients with right ventricular infarction and hemodynamic compromise often respond to volume resuscitation and restoration of a physiological rhythm. Vasodilators and diuretics should generally be avoided. In some, parenteral inotropic stimulation may be required. The right ventricle appears to be relatively resistant to infarction and has a remarkable ability to recover even after prolonged occlusion. Therefore, the term RV infarction appears to be somewhat of a misnomer, for in most patients a substantial proportion of acute RV dysfunction represents ischemic but viable myocardium. Although RV performance improves spontaneously even in the absence of reperfusion, recovery of function may be slow and associated with high in-hospital mortality. Reperfusion enhances the recovery of RV performance and improves the clinical course and survival of patients with ischemic RV dysfunction.

Hemodynamic Responses to Dobutamine, Hydralazine and Sodium Nitroprusside Following Pentastarch Infusion during Cardiac Tamponade in Dogs

Background : Cardiac tamponade results in a hemodynamic disorder associated with decreased cardiac output and blood pressure. To improve cardiac output in a subject with cardiac tamponade, cardiotonic drugs and vasodilators with blood volume expander can be used. The purpose of this study was to observe the hemodynamic effects of cardiotonic drugs and vasodilators following administration of plasma expander in the dogs with cardiac tamponade. Method : Three groups of dogs were studied during the induced cardiac tamponade. Following infusion of pentastarch, group I received dobutamine by dripping of 10ug/kg/min, followed by injection of 20ug/kg/min, group II received hydralazine (20 mg, 40 mg) and group III received sodium nitroprusside (5ug/kg/min, 10 g/kg/min). The heart rate, blood pressure, cardiac output and pulmonary arterial occluded pressure were measured. The atrial transmural pressure was calculated by subtracting intrapericardial pressure from mean atrial pressure. Results : Cardiac output was increased in the groups I and II, but mean arterial pressure was increased in only the group I. Atrial transmural pressure was not changed in all three groups. Conclusion : The most pronounced hemodynamic improvements during the cardiac tamponade is observed in group I with pentastarch-dobutamine combination. (Korean J Anesthesiol 1998; 35: 852∼860)

Severe right ventricular dysfunction following pericardiocentesis for cardiac tamponade

The accumulation of fluid in the pericardium in an amount sufficient to cause severe obstruction to blood inflow to the ventricles results in cardiac tamponade. In this condition, relief of intrapericardial pressure by pericardiocentesis usually dramatically improves cardiac output, and can be lifesaving. We report a case of a patient with malignant cardiac tamponade in which cardiogenic shock developed after pericardiocentesis due to severe right ventricular dysfunction.

Pleural and pericardial pressures limit fetal right ventricular output.

The chest wall, lungs, and pericardium limit diastolic filling of the left ventricle in the fetus, neonate, and adult. To determine the effect that these tissues have on the fetal right ventricle (RV), we studied six fetal lambs (142 days of gestation) Pregnant ewes were anesthetized (ketamine and alpha-chloralose), and the fetuses were partially delivered by cesarean section. Fetuses were instrumented to record RV stroke volume, RV end-diastolic pressure (Prved), intrapericardial pressure (Pip), and pleural pressure. Prved was varied between 2 and 20 mm Hg under three conditions: initially with a closed chest and a closed pericardium (CCCP); subsequently with an open chest (chest wall and lungs retracted) and a closed pericardium (OCCP); and finally after the chest wall, lungs, and pericardium were retracted (OCOP). At equal Prved, stroke volume increased substantially when the chest wall and lungs were retracted from the heart and increased further on subsequent retraction of the pericardium (eg, at Prved of 9 mm Hg, stroke volume increased from 1.2 +/- 0.2 mL [mean +/- SEM] in the CCCP condition to 2.9 +/- 0.4 and 4.2 +/- 0.3 mL in the OCCP and OCOP conditions, respectively, P < or = .05). The limitation of stroke volume in the CCCP and OCCP conditions occurred because Pip increased in an almost one-to-one fashion as Prved increased; as a consequence, RV preload (RV end-diastolic transmural pressure, Prved minus Pip) was relatively unchanged. The chest wall-lung combination and the pericardium each significantly constrain the fetal RV and together limit RV stroke volume.

Can pleural effusions cause tamponade-like effects?

Experimental studies have confirmed the clinical impression that large bilateral pleural effusions are able to raise the pressure in an otherwise hemodynamically insignificant pericardial effusion to a level sufficient to produce right ventricular diastolic collapse (RVDC). The hemodynamic consequences of this syndrome are not as severe as when the intrapericardial pressure is raised to the same level by excess intrapericardial fluid in the absence of pleural effusions. RVDC caused by excess pleural fluid with a minor pericardial effusion is a false positive indication for pericardial fluid drainage. Thoracentesis is more appropriate.

Effects of dobutamine and norepinephrine on oxygen availability in tamponade-induced stagnant hypoxia: a prospective, randomized, controlled study.

To explore the effects of dobutamine and norepinephrine on the global cardiovascular response and on the relationship between oxygen uptake (VO2) and oxygen delivery (DO2) during an acute reduction in blood flow associated with tamponade. Prospective, randomized, controlled acute intervention study. University intensive care unit (ICU) laboratory. Twenty healthy, anesthetized mongrel dogs, weighing 19 to 28 kg. Six dogs served as control, seven dogs were given 10 micrograms/kg/min of dobutamine and another seven dogs were given 1 microgram/kg/min of norepinephrine. Data were collected at graded incremental levels of intrapericardial pressure. VO2 was derived from expired gas analysis and DO2 was calculated from the product of thermodilution cardiac index and arterial oxygen content. In each animal, two catheters were inserted into the pericardium to induce tamponade by saline infusion and to measure the intrapericardial pressure. The critical Do2 value, below which VO2 decreased, was found at 9.4 +/- 1.3 mL/kg/min in the control animals. When DO2 decreased to below this critical value, lactic acidosis developed. Dobutamine and norepinephrine, at the dose that was administered, significantly increased cardiac index and DO2. Critical DO2 was slightly higher in the treated than in the control animals (12.1 +/- 1.6 mL/kg/min in dobutamine and 13.2 +/- 0.9 mL/kg/min in norepinephrine, NS). VO2 at critical DO2 was significantly higher in the treated groups than in the control group (7.7 +/- 1.1 mL/kg/min in the dobutamine group and 7.9 +/- 0.9 mL/kg/min in the norepinephrine group vs. 5.4 +/- 0.4 mL/kg/min in control, both p < .01). There was no significant difference in the critical oxygen extraction ratio and the slope of the supply-dependent line between the three groups. In dobutamine-treated animals, cardiac index, DO2, and VO2 were better maintained for any intrapericardial pressure than in the other groups. Critical intrapericardial pressure, at which VO2 started to decrease, was significantly higher in the dobutamine-treated group than in the control group (13.8 +/- 2.3 vs. 9.3 +/- 1.2 mm Hg, p < .05). At critical DO2, the mean blood lactate concentration was also lower in the dobutamine-treated animals than in the other animals (2.1 +/- 0.3 vs. 4.1 +/- 0.7 mmol/L in control and 3.8 +/- 0.4 mmol/L in the norepinephrine group, both p < .05). During low-flow states associated with tamponade, both dobutamine and norepinephrine at the dose used increased cardiac index, DO2, and VO2, but dobutamine delayed the onset of tissue hypoxia by further increasing blood flow and oxygen availability. In the conditions of the present study, neither agent significantly influenced the oxygen extraction capabilities of the body.

Biliary tract pathology in patients with AIDS.

We report a patient who presented to our hospital with unusual symptoms of non-specific complaints and uncontrolled hypertension. Acute cardiac tamponade was suspected from cardiomegaly on routine chest x-ray and confirmed with an echocardiogram. Analysis of the pericardial fluid and other laboratory data ruled out all the common causes except for hypothyroidism as a cause of cardiac tamponade. Tamponade results from increased intrapericardial pressure caused by the accumulation of pericardial fluid. The rapidity of fluid accumulation is a greater factor in the development of tamponade than absolute volume of the effusion. Hypothyroidism is a well-known cause of pericardial effusion. However, tamponade rarely develops owing to a slow rate of accumulation of pericardial fluid. The treatment of hypothyroidic cardiac tamponade is different from other conditions. Thyroxine supplementation is all that is necessary. Rarely, pericardiocentesis is needed in a severely symptomatic patient.

Acute pericardial distension in pigs: effect of fluid conductance on body surface electrocardiogram QRS size.

Pericardial effusion has long been associated with low voltage of the surface electrocardiogram and its clinical utility is well known. The cause of this reduced QRS voltage has usually been attributed to short circuiting of the impulses by the pericardial fluid, but its precise mechanism has not been clearly elucidated. Therefore, we investigated this phenomenon by instilling various fluids with different resistances in increasing volumes into the pericardial space to finally produce acute cardiac tamponade. Acute cardiac tamponade was produced 65 times in 25 closed chest pigs with a mean weight of 57(SEM 1.2) kg. A sufficient quantity (mean = 200 ml) of plasma, saline, blood, and blood with varying packed cell volume was introduced into the pericardial space in 60 ml increments to decrease systemic and pulmonary pressures to 50% of control to produce cardiac tamponade. At that point intrapericardial pressure had increased to 15-20 mm Hg. Resistivity values for the instilled fluids are 150 omega-cm for blood, 60 omega-cm for plasma, and 50 omega-cm for saline. Mean limb and precordial lead QRS voltage fell significantly, with no significant differences among these fluids. Electrocardiograph recordings from a unipolar electrode catheter in the right ventricle showed an increase in R wave voltage, but body surface recordings of stimuli introduced into the right atrium via a bipolar electrode catheter showed no amplitude change. In considering possibilities such as internal shunting of cardiac currents by intrapericardial fluid, distance of the heart from body surface electrodes, and change in cardiac position, the results are best explained by a reduction of cardiac volume and size during cardiac tamponade. This conclusion confirms Brody's hypothesis.

Pleural effusion as a cause of right ventricular diastolic collapse.

We hypothesized, after seeing several suggestive clinical examples, that a process leading to a large bilateral pleural effusion in the presence of an otherwise insignificant pericardial effusion could result in right ventricular diastolic collapse (RVDC) as seen by two-dimensional echocardiography. This noninvasive marker for hemodynamically significant cardiac tamponade occurs when pericardial fluid is under pressure. Therefore, RVDC resulting from a large pleural effusion would represent a false-positive indication of cardiac tamponade caused by excessive pericardial fluid. Seven spontaneously breathing dogs were chronically instrumented to measure ascending aortic, right atrial, intrapericardial, intrapleural, left atrial, and pulmonary artery pressures and cardiac output. Intravascular volume was adjusted before each experiment to the euvolemic range with saline solution. The onset of RVDC was observed in each animal by two-dimensional echocardiography during seven paired episodes of tamponade induced by infusions of warm saline into the pericardial space alone and, after drainage of the pericardial fluid and complete recovery, into the pleural space in the presence of a small pericardial effusion. The onset of RVDC occurred at the same intrapericardial (8.17 versus 9.47 mm Hg) and right atrial (7.41 versus 7.46 mm Hg) blood pressures regardless of whether it was produced by an intrapericardial or an intrapleural effusion but began in expiration during the former and in inspiration during the latter. Intrapericardial pressure increased in the same manner as intrapleural pressure during intrapleural saline infusion. Nevertheless, cardiac output and aortic blood pressure were better preserved, and at the onset of RVDC, the pulmonary artery systolic blood pressure was higher (p less than 0.0001) and the degree of pulsus paradoxus lower (p less than 0.01) with intrapleural infusion. These results indicate that a large bilateral pleural effusion can elevate intrapericardial pressure sufficiently to cause RVDC and, perhaps, lead to misdirected therapy of an otherwise insignificant pericardial effusion.

Effects of external constraint on the fetal left ventricular function curve

To determine if external ventricular constraint significantly limits fetal left ventricular (LV) stroke volume and can thus account for the plateau of the fetal ventricular function curve, we studied nine fetal lambs (142 to 144 days' gestation) after partial delivery by cesarean section (halothane anesthetic). LV stroke volume (electromagnetic flow probe), LV end-diastolic pressure, and external ventricular constraint (intrapericardial pressure [liquid-filled balloon]) were measured over a range of end-diastolic pressures under two conditions: with a closed chest and closed pericardium and with an open chest and open pericardium. Stroke volume recorded during open chest and open pericardium exceeded those recorded during closed chest and closed pericardium at any given end-diastolic pressure ( p < 0.01). Decreases in external ventricular constraint significantly increased LV transmural pressure (preload) and substantially increased fetal LV stroke volume. Thus the plateau of the fetal ventricular function curve was largely a result of external ventricular constraint limiting LV preload, not necessarily a result of myocyte immaturity.

Penetrating cardiac trauma: Management strategy based on 129 surgical emergencies over 2 years

Between 1986 and 1988, 129 patients with stab wounds to the heart were referred from the emergency room of our institution for a thoracic surgical procedure. Multiple entrance wounds of the heart were present in 12 patients, and through-and-through stab wounds were encountered in another 10. The overall hospital mortality rate was 8.5% ( 11 / 129 ), which includes a 54% mortality rate for the 13 patients undergoing emergency room thoracotomy. These patients were pulseless and unconscious either on arrival (n = 8) or soon thereafter (n = 5). Cardiopulmonary bypass was not used during the primary operation, although 7 patients underwent subsequent intracardiac repair with bypass without hospital mortality. Important aspects of our preoperative management strategy include: (1) aggressive transfusion to improve the central venous pressure/intrapericardial pressure gradient; (2) rapid drainage of the pleural and pericardial spaces to reduce intrapericardial pressure; (3) empirical partial correction of metabolic acidosis with sodium bicarbonate; and (4) emergency operation without unnecessary cardiac imaging. Patients suspected of having penetrating cardiac trauma and cardiac tamponade are best managed by aggressive primary intervention and immediate operation.

Alterations in transesophageal pulsed Doppler indexes of filling of the left ventricle after pericardiotomy

The impact of pericardial constraint on patterns of left ventricular filling was measured by transesophageal pulsed Doppler echocardiography in 30 patients undergoing elective nonvalvular cardiac surgery. Peak early left ventricular filling velocity increased from 0.52 ± 0.11 to 0.56 ± 0.15 m/s (p < 0.05) and early left ventricular filling fraction increased from 60 ± 9% to 65 ± 9% (p < 0.005) after pericardiotomy.The study group was retrospectively subdivided into two groups based on the prepericardiotomy mean right atrial pressure, an index of intrapericardial pressure and hence pericardial constraint. In 13 patients with a mean right atrial pressure <6 mm Hg, no significant changes in early left ventricular filling were evident after pericardiotomy. In 17 patients with a mean right atrial pressure ≥6 mm Hg indicative of a greater degree of pericardial constraint before pericardiotomy, significant increases in peak early filling velocity (0.52 ± 0.13 to 0.57 ± 0.19 m/s, p < 0.05), peak early filling rate (4.29 ± 0.67 to 4.66 ± 0.86 stroke volume/s, p < 0.05) and early left ventricular filling fraction (57 ± 7% to 63 ± 8%, p < 0.001) were measured after pericardiotomy.Thus, the pericardium does constrain early left ventricular filling and its effects are more pronounced in patients with an elevated right atrial pressure.

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.

The pericardium facilitates pressure work in the eel heart

An in siru perfused eel (Anguilla dieffenbachü) Gray 1842) heart was used to investigate the role of the pericardium in cardiac function. Hearts with intact pericardia were compared with hearts in which the pericardia were either punctured or opened completely. Cardiac function was assessed at low and high adrenaline levels by determining: maximum cardiac output; maximum sustainable output pressure; power output under maximal filling and output pressures; and maximum power output. Puncturing a small hole in the pericardium equalizing ambient and intrapericardial pressures had little effect on cardiac function and performance. Opening the pericardium, thereby fully exposing the chambers of the heart, severely limited the heart's ability to do pressure work. This effect was reversed at high adrenaline concentrations. Flow related work, and maximum power output levels were maintained after opening the pericardium.

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

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. 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. 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.

Quantitative relation between increased intrapericardial pressure and Doppler flow velocities during experimental cardiac tamponade

To establish whether a quantitative relation exists between pericardial pressure and respiratory variation in intracardiac blood flow velocities, a spontaneously breathing closed chest canine model of pericardial tamponade was created. In seven dogs, pericardial pressure was sequentially increased in stages from a mean of -4 +/- 1 to 10 +/- 2 mm Hg while aortic and pulmonary Doppler flow velocities, pleural pressure changes (respiratory effort), blood pressure and cardiac output were measured. The variation in the Doppler-detected peak transaortic velocity (AV) during inspiration (IV) increased linearly from -5 +/- 3% at baseline (pericardial pressure -4 mm Hg) to -32 +/- 9% at a pericardial pressure of 10 mm Hg [IVAV = -2 (pericardial pressure)--13.1; r = 0.78, p less than 10(-6)]. The inspiratory variation in the peak transpulmonary velocity increased from 13 +/- 3% at baseline to 71 +/- 19% at a pericardial pressure of 10 mm Hg. The inspiratory variation in the pulmonary Doppler peak velocity (IVPV) was dependent on both pericardial pressure and degree of respiratory effort [IVPV = 3.8 (pericardial pressure) + 2.6 (respiratory effort) + 10.9; r = 0.88, p less than 10(-8)]. Thus, quantitative relations exist between increases in intrapericardial pressure and increases in inspiratory variation of peak aortic and pulmonary flow velocities. Additionally, pulmonary artery flow velocity is influenced more than aortic velocity by intrathoracic pressure.

Spectrum of hemodynamic changes in cardiac tamponade

To investigate the pathophysiology of cardiac tamponade, the hemodynamics of 77 consecutive patients with >150 ml of pericardial effusion were studied. Patients were classified into 3 groups based on the equilibration of intrapericardial with right atrial and pulmonary arterial wedge pressures (mm Hg): group I (n = 16), intrapericardial pressure was less than right atrial and pulmonary arterial wedge pressures; group II (n = 13), intrapericardial pressure was equilibrated with right atrial but not pulmonary arterial wedge pressures; group III (n = 48), intrapericardial pressure was equilibrated with right atrial and pulmonary arterial wedge pressures. Pericardiocentesis produced the following changes: group I—significant (p < 0.03) decreases in intrapericardial pressure (7 ± 2 mm Hg), right atrial pressure (3 ± 2 mm Hg), pulmonary arterial wedge pressure (2 ± 2 mm Hg), and the inspiratory decrease in arterial systolic pressure (3 ± 4 mm Hg) but no significant change in cardiac output; group II—significant (p < 0.02) decreases in intrapericardial pressure (11 ± 5 mm Hg), right atrial pressure (6 ± 4 mm Hg), pulmonary arterial wedge pressure (4 ± 5 mm Hg), and inspiratory decrease in arterial systolic pressure (8 ± 7 mm Hg), and increase in cardiac output (1.1 ± 1.2 liters/min); group III—significant (p < 0.001) decreases in intrapericardial pressure (16 ± 7 mm Hg), right atrial pressure (9 ± 4 mm Hg), pulmonary arterial wedge pressure (8 ± 5 mm Hg), inspiratory decrease in arterial systolic pressure (17 ± 11 mm Hg), and increase in cardiac output (2.8 ± 1.5 liters/min). The changes after pericardiocentesis in all parameters were significantly (p < 0.05) greater in group III than in groups i or II except for the change in right atrial pressure, which was not significantly different in groups II versus III. The changes after pericardiocentesis indicate pericardial effusion caused the greatest abnormalities in group III but also caused significant abnormalities of pressure and flow in group II and of pressure alone in group I. Because hemodynamic alterations were noted in all groups, increasing in severity from groups I to III, it is concluded that cardiac tamponade is not an “all-or-none” phenomenon, and the severity of hemodynamic derangement rather than its presence or absence should be assessed in patients with pericardial effusion.