Electronic Supplemental Material

Effect of tidal volume, intrathoracic pressure and cardiac contractility on variations in pulse pressure, stroke volume and intrathoracic blood volume

Jaume Mesquida, MD, Hyung Kook Kim, MD, Michael R Pinsky, MD

Methods:

Arterial blood gases were monitored periodically, and corrections in acid-base balance during the surgical procedure were made by administration of intravenous sodium bicarbonate and changing the ventilatory frequency when needed. A standard lead II electrocardiogram was monitored for heart rate (HR). A flow-directed thermodilution catheter (Edwards LifeSciences, Irvine, CA), with its injection port 15 cm from the distal end, was placed in the pulmonary artery from a peripheral cut-down site. A high-fidelity pressure transducer-tipped catheter (PC-470, Millar, Houston, TX) was placed at the aortic root. A midline sternotomy was performed, and the heart was suspended in a pericardial cradle. A saline-filled polyethylene catheter was placed in the left atrium via its appendage. Electromagnetic flow probes were snugly placed around the aortic root and pulmonary arterial roots so that there was no movement of the probes during ventilation. The flow probe signals (Model 501, Carolina Medical, NC) were linear to ±5% over the range of flows studied and were synchronized with each other to minimize an electromagnetic crosstalk. Zero flow was taken as the diastolic plateau of the flow signals. The flow signals were matched to each other during a 15-s apneic period so that the summed volumetric values during the apneic period were equal for both RV and LV output. Stroke volume (SV) from either ventricle was derived by integrating the flow signal. Summed SVRV and SVLV were within 2±3% (mean±SD) of each other over a 1-min interval. Absolute SV was estimated using triplicate 3-ml iced-saline thermodilution cardiac-output determination during apnea. Recalibration of the outputs of the two flow probes was assessed periodically and in practice required no readjustment. The pericardium was reapproximated with multiple interrupted sutures and care was taken not to restrict normal diastolic filling as evidenced by no change in left atrial pressure. Intrathoracic pressure (ITP), estimated by juxtacardiac pleural pressure was measured with a 10x1.5 cm thin-walled polyvinyl chloride balloon attached to a polyethylene catheter sutured to the pleural side of the pericardium by a method previously described (12). Chest tubes (20 Fr) were positioned bilaterally to evacuate air and fluid from the thoracic cavity by continuous suction (-15 cmH2O). The position of all catheters was determined by palpation prior to closing the chest, and all vascular catheters were referenced to the midthorax. The sternum was reapproximated, and the left atrial catheter, pleural balloon catheter, and flow probe cables were exteriorized. The fascia and skin were closed in three layers to insure an airtight seal. The pleural space was evacuated of fluid and air by positive-pressure hyperinflation and suction through the chest tubes. No persistent air leaks were observed following surgery. The vascular catheters were connected to low-displacement transducers (Micron MP-15, Gould, Cleveland, OH), and the airway and pleural catheters connected to high fidelity transducers (Bell and Howell 4-3271, Cleveland, OH). The pulmonary artery catheter monitoring was done to maintain hemodynamic stability during the procedure. The transducers were calibrated using a mercury manometer. The pressure and flow signals were continuously recorded on an eight-channel recorder (Gould 2800, Cleveland, OH).

All vascular pressures were referenced to the mid-thoracic plane. The zero hydrostatic pressure of all catheters was determined at autopsy by exposing the catheter opening ports to air in situ during the autopsy. At the conclusion of the experiment, the animals were killed while under general anesthesia by intravenous injection of KCl. A limited necropsy was performed to define gross cardiopulmonary abnormalities and the positioning of all intrathoracic devices. No animal demonstrated pulmonary parenchymal consolidation or hemorrhage, and no tracheal mucosal lesions were identified.

Following the surgical procedure that took approximately 2 hours the animals were observed for a 30-min period to document hemodynamic stability. Fourteen animals were hemodynamically stable without subsequent hypotension, hypoxemia (PO2 >90 Torr), arrhythmias, or ongoing metabolic acidosis (pH between 7.3 and 7.4). Prior to starting the protocol, cardiac output was returned to pre-thoracotomy values by volume infusion (dextran, 6% wt/vol), which gave an apneic left atrial pressure relative to ITP (transmural left atrial pressure) of 6.1±0.6 mm Hg.