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

Article Outline

• Abstract
• Methods
• Results
• Discussion
• References
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Abstract 

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.

Keywords:  Cardiac tamponade, intermittent positive-pressure ventilation, pulsed-wave Doppler, respiratory variation, transesophageal echocardiography, transmitral flow velocity

Bedside echocardiography has become a standard technique to confirm the clinical diagnosis of pericardial effusion and cardiac tamponade.¹, ², ³, ⁴, ⁵, ⁶, ⁷, ⁸ In addition to accurate detection of pericardial fluid collection by 2-dimensional echocardiography, pulsed-wave Doppler echocardiographic measurement of transvalvular flow velocity has been used to differentiate pericardial effusion and cardiac tamponade.⁹, ¹⁰, ¹¹, ¹², ¹³, ¹⁴

In the presence of tamponade, a number of changes in valvular flow velocity have been identified: an inspiratory increase in tricuspid flow, an inspiratory decrease in mitral flow, and an exaggerated (>25%) inspiratory-to-expiratory variation in transvalvular flow velocities.¹⁰, ¹¹, ¹²

These changes, termed respiratory variation, have been described in spontaneously breathing patients. Because positive-pressure ventilation has a different influence on intrathoracic pressure changes, it may produce a different pattern of respiratory variation in cardiac tamponade. In patients with constrictive pericarditis, for example, positive-pressure ventilation produces changes in mitral valve flow velocities that are opposite to those seen during spontaneous ventilation.¹⁵ Whether differences in respiratory variation also occur in patients with cardiac tamponade undergoing positive-pressure ventilation remains to be defined.

Cardiac tamponade is a potentially lethal complication after cardiac surgery and presents in 2% of patients in the immediate postoperative period² when many patients are still receiving mechanical ventilation. An accurate and timely diagnosis of cardiac tamponade is lifesaving; a reliable diagnostic method is therefore of paramount importance. Knowing that positive-pressure ventilation changes the hemodynamics of cardiac tamponade,¹⁶ this study sought to determine whether the exaggerated respiratory variation in mitral flow velocity that occurs during spontaneous ventilation would also be present during positive-pressure mechanical ventilation.

Because of the inherent difficulties in prospectively investigating these Doppler phenomena in critically ill patients receiving mechanical ventilation, a canine model was used to examine the effects of intermittent positive-pressure ventilation on transvalvular flow velocities in experimentally induced acute pericardial effusion and cardiac tamponade.

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Methods 

This study was approved by the Institutional Animal Care and Use Committee. (All animals used in these experiments received humane care in compliance with the “Principles of Laboratory Animal Care” formulated by the National Society for Medical Research and the “Guide for the Care and Use of Laboratory Animals” prepared by the National Academy of Sciences and published by the National Institutes of Health, NIH Publication No. 86-23, revised 1985.) Eleven male mongrel dogs, mean weight 22 kg (range, 20-27 kg), were studied. After induction of anesthesia with thiopental, 20 to 25 mg/kg, the animals were tracheally intubated and mechanically ventilated (ohio V5 airco; Ohmeda, Murray Hill, NJ) with 100% oxygen and halothane, 0.4 to 1.8 vol% to maintain adequate anesthetic depth. Inspiratory and end-tidal gas concentrations were measured continuously by infrared spectroscopy (datex model 254; Puritan Bennett Corporation, Wilmington, MA). Tidal volume (15 mL/kg) and respiratory rate (12/min) were chosen to maintain an arterial carbon dioxide tension (PaCO₂) in the normal range (36-44 mmHg) measured by blood gas analysis. Peak inspiratory pressure was 12 ± 5 cm H²O and inspiratory-to-expiratory ratio was 1 to 2. Limb electrocardiogram leads were attached. Hemodynamic monitoring was provided with a femoral artery catheter and a 5F pulmonary artery catheter (Baxter pediatric 5F, Baxter Healthcare Corporation, Irvine, CA) inserted via the right internal jugular vein. Systemic blood pressure, central venous pressure, and pulmonary artery pressure were measured at end-expiration with conventional fluid- filled catheters and transducers (Baxter Edwards reusable cable, model PX-1800; Baxter Healthcare Corporation, Irvine, CA), with the zero reference value assigned to the midthoracic level. Cardiac output was measured by thermodilution with 5 mL of room temperature saline injections synchronized to end-expiration. The average value of triplicate measures was determined.

Right thoracotomy was performed in the fifth intercostal space, and the right accessory lung lobe was removed to obviate acoustic interference during echocardiographic measurements. Transducer-tipped 5F pressure catheters (Millar Instruments, Inc, Houston, TX) were inserted in the right pleural space and through a 2-mm incision in the pericardium. Through a second 2-mm incision, an injection catheter was placed in the inferior part of the pericardium. The pericardium was sealed, a chest tube was placed, and the thorax was closed. The chest tube was placed under water seal at atmospheric pressure, when no more air could be aspirated from the thorax by suction. An additional 5F pressure catheter was inserted in the endotracheal tube to measure airway pressure. Changes in airway pressure were used to provide precise timing of the onset of inspiration and expiration.

Transesophageal echocardiography was performed with an HP sonos 1000 OR ultrasonograph (Hewlett Packard, Andover MA) and a Delft omniplane probe (Delft Instruments NV, the Netherlands) equipped with a 5.0-MHz transducer. From a standard long-axis, 4-chamber view, mitral flow velocities were measured by pulsed-wave Doppler echocardiography. A 5.25-mm sample volume was placed at the tips of the mitral valve leaflets in diastole. Simultaneous 2-dimensional echocardiography confirmed stability of the sample volume throughout the respiratory cycle. Electrocardiogram and airway pressure signals were recorded together with the Doppler tracings on videotape for off-line analysis.

After surgical preparation of every dog, blood gas analyses and blood oxygen saturation were performed on standard blood gas analyzers (IL 1600 series, Instrumentation Laboratories, Lexington, MA, and IL 482 co-oximeter; Instrumentation Laboratories, Lexington, MA) calibrated for dog blood, and ventilation was adjusted to normalize PaCO₂. Intravenous Ringer's lactate was given continuously at a rate of 5 mL/kg/h during surgical preparation and 1 mL/kg/h during the rest of the experiment.

Respiratory variables (arterial blood gas values, tidal volume, respiratory rate, airway, pleural pressures), hemodynamic variables (heart rate, arterial blood pressure, central venous pressure, pulmonary artery wedge pressure, cardiac output, pericardial pressure), and echocardiographic data were collected 30 minutes after completion of all surgical procedures as a control. Pericardial effusion was induced by slow instillation (over 20-30 minutes) of warm saline into the pericardium to the point when arterial pressure started to decrease. Then saline was slowly removed again to allow blood pressure to return to the baseline value. The instilled volume to produce this effusion without arterial blood pressure changes was 113 ± 22 mL (mean ± SD). To obtain cardiac tamponade, additional saline (total volume 187 ± 31 mL) was injected slowly into the pericardium until mean arterial blood pressure was reduced to 60% of control value. To relieve cardiac tamponade, pericardial saline was evacuated (removed volume 137 ± 42 mL) until no further fluid could be aspirated through the pericardial catheter. All respiratory, hemodynamic, and echocardiographic measurements were made at 4 time intervals: control, effusion, tamponade, and tamponade relief.

At the conclusion of the experiment, the animals were killed by an overdose of intravenous potassium chloride, necropsy was performed, and the correct position of the catheters and the presence of an intact pericardium were confirmed.

Echocardiographic data were analyzed off-line from videotape recordings with 5 cm/s calibrated scales. Because heart rate exceeded 110 beats/min in most dogs, mitral E and A waves merged, and therefore pulsed-wave Doppler values for mitral flow velocity describe the amplitude of a combined E-A wave. Flow velocities were measured in each dog at each stage (control, effusion, tamponade, tamponade relief) over 3 respiratory cycles. Baseline velocity was defined as the mean of the 3 beats before onset of inspiration for each respiratory cycle. Average values for baseline, maximal, and minimal flow velocity were calculated from 3 respiratory cycles for each animal at each experimental stage. Respiratory variation was defined as the difference between the maximal inspiratory velocity and minimal expiratory velocity, divided by baseline velocity, and expressed as a percentage.

Technically adequate echo Doppler studies with stable sample volume throughout the respiratory cycle could not be obtained for all 11 dogs at all measurement stages, so average values were calculated only for technically adequate recordings and are expressed as mean ± SD. All data are reported to provide the most reliable mean values for all variables. Paired t-tests were performed using only animals for which paired data were available.

Statistical analysis was performed by using SAS software (SAS Institute, Cary, NC). Repeated measures linear regression (Hotelling-Lawley Trace) was used to test for overall difference caused by treatment (control, effusion, tamponade, tamponade relief). Significance of differences between stages was determined by paired t-test with the Bonferroni adjustment for multiple comparisons.

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Results 

Hemodynamic values differed in the 4 experimental stages (control, effusion, tamponade, tamponade relief) (Table 1). The effusion stage was characterized by decreases in cardiac output and stroke volume and an increase in central venous pressure. Systemic arterial blood pressure remained stable during the effusion stage, consistent with the study design. During cardiac tamponade, arterial blood pressure (systolic, diastolic, mean), cardiac output, and stroke volume decreased significantly compared with baseline and effusion stages, whereas central venous pressure increased further. After tamponade relief, hemodynamic variables returned to values that were statistically indistinguishable from baseline. Pericardial pressure increased progressively with increasing pericardial fluid volume in the effusion and tamponade stages (Table 1).

Table 1. Hemodynamic variables

NOTE. n = number of dogs with complete data sets.

Abbreviations: HR, heart rate; SAP, systolic arterial pressure; DAP, diastolic arterial pressure; MAP, mean arterial pressure; CVP, central venous pressure; PAWP, pulmonary artery wedge pressure; SV, stroke volume; CO, cardiac output; Pper ins, inspiratory pericardial pressure; Pper exp, expiratory pericardial pressure.

Respiratory (airway pressure, pleural pressure) and blood gas (PO₂, PCO₂, pH) variables remained stable during the course of the experiment, with the exception of an increase in base deficit during tamponade as compared with the effusion stage (Table 2).

Table 2. Respiratory variables

NOTE. All data are mean ± SD.

Abbreviations: Paw ins, inspiratory airway pressure; Paw exp, expiratory airway pressure; Ppl ins, inspiratory pleural pressure, Ppl exp, expiratory pleural pressure; SO₂, hemoglobin saturation; BE, base excess.

The inspiratory-expiratory differences in pleural pressure and pericardial pressure were not significantly different during the 4 experimental stages (Fig 1).

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• Fig. 1. 

  Differences between inspiratory and expiratory airway, pleural, and pericardial pressures during each experimental stage. ▵Paw, inspiratory − expiratory airway pressure; ▵Ppl, inspiratory − expiratory pleural pressure; ▵Pper, inspiratory − expiratory pericardial pressure

Mitral valve flow velocities changed during pericardial effusion and cardiac tamponade. As pericardial pressure progressively increased, baseline, maximal, and minimal mitral valve flow velocities decreased. Evacuation of pericardial fluid resulted in mitral valve flow velocities returning to control values (Table 3). Variation in mitral flow velocity changed in each experimental stage. The greatest variation in mitral flow velocity during the respiratory cycle was seen in the control stage (36%) and decreased progressively to 29% at the pericardial effusion stage and to 16% (p < 0.05) during the cardiac tamponade stage (Table 3, Fig 2).

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• Fig. 2. 

  Respiratory variation in mitral flow velocity and pericardial pressure. Pper ins, inspiratory pericardial pressure, Pper exp = expiratory pericardial pressure. *p < 0.0125 compared with control. As pericardial pressure increases, respiratory variation in transmitral flow decreases.

Table 3. Changes in mitral flow velocity and respiratory variation at different experimental stages

NOTE. Respiratory variation equals mitral flow velocity (maximum-minimum)/baseline.

Three different patterns of mitral flow velocity changes during the respiratory cycle were observed in these experiments. One was characterized by an increase in flow velocity starting with the first beat after onset of inspiration, with maximal velocity reached during the inspiratory plateau, and a rapid decrease in velocity seen with the onset of expiration and minimal flow velocity reached later during expiration (Fig 3A).

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• Fig. 3. 

  Patterns of mitral inflow velocity during positive-pressure mechanical ventilation. Insp, onset of inspiration; exp, onset expiration. See text for more detail.

A second pattern showed a slight decrease in flow velocity during inspiration and a further decrease that reached a minimum during expiration (Fig 3B). The first pattern was seen in the control stage (6 of 11 experiments) and during effusion (8 of 10 experiments), whereas the second pattern was seen less frequently (5 of 11 control experiments, 2 of 10 effusion experiments). During cardiac tamponade, a third pattern of flow velocity changes was seen in all 9 animals: a small increase in mitral flow velocity during the first 2 inspiratory heartbeats and a return to baseline thereafter (Fig 3C). After tamponade was relieved, the same patterns of mitral flow velocity as in control and effusion stages could be identified again.

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Discussion 

Respiratory variation in mitral flow is a normal finding during mechanical ventilation, and this mitral flow variation is markedly attenuated as cardiac tamponade develops. These observations are important because they highlight the effects of positive-pressure ventilation on transvalvular flow velocity. Previous studies, which show that both pericardial effusion and cardiac tamponade increase respiratory variation in mitral flow velocity, have been performed only in subjects breathing spontaneously.¹⁰, ¹¹, ¹², ¹³ Similar to these studies, these data show that effusion and tamponade result in an overall decrease in mitral flow velocity from 45 cm/s to 39 cm/s to 27 cm/s (Table 3). However, as the cardiac compression increases, respiratory variation in mitral flow velocity decreases. This is the most important distinction between these results and those previously reported in spontaneously breathing subjects.

The model used in this study showed the expected hemodynamic changes of pericardial effusion and cardiac tamponade.¹⁶, ¹⁷, ¹⁸, ¹⁹, ²⁰, ²¹, ²², ²³ In pericardial effusion, the increases in pericardial volume (0-113 mL) and pericardial pressure (−2.9 to 4.1 mmHg) were accompanied by an increase in central venous pressure and decreases in stroke volume and cardiac output. Further pericardial fluid instillation to produce cardiac tamponade increased pericardial volume (113-187 mL) and pericardial pressure (4.1-9.2 mmHg), accompanied by greater increases in central venous pressure and marked decreases in arterial blood pressure, stroke volume, and cardiac output. After the pericardial fluid had been removed, pericardial pressure and hemodynamic variables returned to control values.

During positive-pressure ventilation, transvalvular flow velocity depends on many factors, including intravascular volume status, pleural pressure, airway pressure, atrial function, ventricular compliance, and the atrioventricular pressure gradient. In a normovolemic subject, positive-pressure ventilation will retard right atrial venous return and reduce right ventricular stroke volume. At the same time, blood flow from the pulmonary vascular bed into the left atrium will be augmented as lung inflation squeezes the pulmonary venous blood volume and propels it toward the left heart chambers.²⁴, ²⁵ This creates an initial increase in mitral flow velocity at the beginning of inspiration and a subsequent decrease when the reduced stroke volume from the right ventricle crosses the pulmonary vascular bed. In contrast, hypovolemic subjects with little pulmonary vascular volume reserve will show a decrease in mitral flow velocity during the inspiration phase of positive-pressure ventilation. The extent of hypovolemia determines how fast the mitral flow velocity normalizes after the onset of expiration. Because the intravascular volume state of the animals was likely to be normal or slightly reduced, (central venous pressure range, 6-13 mmHg, in control state), the 2 patterns of mitral flow velocity observed during the control and effusion stages were consistent with these known respiratory-circulatory interactions.

During cardiac tamponade, a single unique pattern of respiratory mitral flow variation was observed that was different from the 2 patterns seen in the 3 experimental stages with hemodynamic compensation (control, effusion, tamponade relief stages). This suggests that in subjects with cardiac tamponade receiving positive-pressure ventilation, the left ventricular filling gradient changes only slightly during the respiratory cycle, with a slight inspiratory increase in mitral flow velocity (27 cm/s at baseline, 30 cm/s during inspiration), followed by a small expiratory decrease (26 cm/s). Presumably, the severity of diastolic filling impairment caused by the compressive pericardial fluid collection is the predominant factor that limits cardiac performance, and respiratory variations in pleural and pericardial pressures have little impact on left heart filling, which is already critically compromised by the tamponade.

A number of limitations in this study must be considered. First, clinically significant tamponade may exist with a wide range in hemodynamic or echocardiographic signs. For example, blood pressure response to tamponade depends in part on the rate of fluid accumulation, state of the pericardium and myocardium, and degree of any pre-existing hypertension.¹ The results may not be applicable to situations of chronic or subacute accumulation of pericardial fluid. In addition, when tamponade results from hemopericardium, particularly in patients after cardiac surgery or chest trauma, it may be localized instead of circumferential.², ⁷, ²⁶ This localization may also result in different echocardiographic and hemodynamic findings.

Second, these experiments were conducted in an animal model. Although dogs have been used routinely as an experimental model for hemodynamic studies of cardiac tamponade¹⁹ compared with humans, dogs have an increased chest wall and lung compliance and a proportionally larger lung volume. However, the pattern of positive-pressure ventilation used in this study is similar to the pattern used in mechanically ventilated patients—a relatively large tidal volume and low respiratory rate. Furthermore, the airway pressure changes observed were slightly smaller than those seen typically in patients. Therefore, the magnitude of respiratory variation in mitral flow velocity seen clinically in patients may be even greater than that observed in the control state of this dog model. Indeed, preliminary data in anesthetized surgical patients receiving positive-pressure mechanical ventilation indicate that marked respiratory variation in transmitral flow velocity is a normal finding and is similar in magnitude to the respiratory flow variation seen in the control state in these experiments.²⁷ As a result, it is believed that the pattern of change in mitral flow variation seen in this experimental model of pericardial effusion and tamponade would be seen in patients with these conditions who are receiving positive-pressure mechanical ventilation.

The authors were not able to record hemodynamic data repeatedly during the respiratory cycle but only at end-expiration. Inspiratory and expiratory recordings of other hemodynamic variables, such as pulmonary artery wedge pressure, might have provided additional insight into the physiologic mechanisms underlying the observations. Furthermore, the authors were not able to obtain acceptable flow velocity measurements across the tricuspid valve because of poor angle alignment. Although these measurements would have allowed a more complete description of the echocardiographic changes during cardiac tamponade, in clinical settings, tricuspid Doppler flow measurements are of acceptable quality in only 30% of patients with cardiac tamponade and frequently the diagnosis of cardiac tamponade has relied on 2-dimensional echocardiography and variations in mitral flow velocity alone.²⁸ Time-velocity integrals of mitral and tricuspid flow allow better assessment of total flow compared with peak velocity measurements alone.¹⁰, ¹² However, because of the rapid heart rates seen in this dog model (Table 1), time velocity integrals were difficult to measure accurately and were not believed to be as precise as peak velocities.

In conclusion, intrathoracic pressure and lung volume changes caused by intermittent positive-pressure ventilation produce large variations in mitral flow velocities during the respiratory cycle. In contrast to observations during cardiac tamponade in subjects breathing spontaneously,¹⁰, ¹¹, ¹², ¹³ exaggerated respiratory variation in mitral flow velocity does not accompany cardiac tamponade in subjects receiving positive-pressure ventilation. In fact, respiratory variation is most pronounced during the control state and decreases as pericardial effusion and hemodynamically significant cardiac tamponade develop.

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