Changes in intrathoracic pressure can significantly affect cardiac performance, and also cause other serious health problems such as erectile dysfunction http://healthcaremall4you.com/natural-remedies-offered-by-canadian-healthcare-mall-for-erectile-dysfunction.html. Positive-pressure ventilation has been shown to decrease cardiac output, mainly due to the associated decrease in venous return, since cardiac output can be corrected by volume infusion. It has recently been demonstrated that left ventricular performance can also be significantly influenced by changes in intrathoracic pressure. Studies by Summer et al using a canine model and by Buda et al using human cardiac transplants and
patients with coronary arterial bypass grafts demonstrated that negative swings in intrathoracic pressure act to increase left ventricular afterload by increasing transmural left ventricular pressure. We asked the question: If negative intrathoracic pressure increases left ventriular afterload, will positive intrathoracic pressure act to unload the left ventricle, allowing stroke volume to improve in the presence of a constant left ventricular end-diastolic pressure and volume? Since forward blood flow can be generated in an asystolic human by increasing intrathoracic pressure during a paroxysm of coughing, we reasoned that if venous return could be maintained, then increasing intrathoracic pressure would augment a failing myocardium by decreasing its effective afterload. We have recently demonstrated that increasing intrathoracic pressure by the use of chest and abdominal binders in an artificially ventilated dog in acute ventricular failure improves left ventricular performance, as manifested by an increase in both cardiac output and left ventricular stroke work at any left: ventricular filling pressure. Further analysis of these data suggested that the augmentation involved a decrease in the effective left ventricular systolic pressure load and a decrease in left ventricular wall tension, making the left ventricle more efficient. To test this hypothesis clinically, we studied the effects of chest and abdominal binding during artificial ventilation, which we call phasic high intrathoracic pressure support (PHIPS), on patients with shock in the intensive care unit.
Materials and Methods
Seven patients in the medical intensive care unit of Johns Hopkins University Hospital, Baltimore, served as our subjects for this study. All subjects were gravely ill with severe shock either due to sepsis (four) or myocardial infarction (three). All were being treated aggressively with conventional fluid resuscitation and vasoactive drugs. Profiles of the patients are shown in Table 1. Criteria for entrance into this study included the following: (1) severe hypotension secondary to depressed cardiac output or peripheral vasodilation not responsive to volume loading and vasopressor therapy (or both); (2) dependency on a respirator; and (3) the presence of both a pulmonary arterial catheter and an arterial line. The protocol for this study was approved by the Johns Hopkins University Hospital Human Experimentation Committee, and all patients or their family members signed informed consents. The protocol involved the following additional items: insertion of an esophageal balloon (National catheter B5843) for measurement of esophageal pressure (Pes); the application to the chest and upper abdomen of standard abdominal elastic binders (Dale combo binder 0584-411); and an increase in the respirators delivered tidal volume to at least 15 ml/kg of body weight. For this study, all subjects were placed on controlled ventilation at a frequency of 20/min and an inspiration-expiration ratio of 3:7. No positive end-expiratory pressure was used.
The positioning of the esophageal balloon and the measurement of Pes were done in the manner of Milic-Emili et al. We used changes in Pes to estimate changes in intrathoracic pressure. Mean Pes was calculated by planimetry. Arterial pressure was continuously monitored. Mean arterial pressure was calculated as the diastolic arterial pressure plus one-third of the arterial pressure pulse and was closely correlated with an electronically measured mean arterial pressure. Transmural pulmonary arterial occlusion pressure was determined by electronic subtraction of the Pes from pulmonary arterial occlusion pressure. Transmural pulmonary arterial occlusion pressure was taken to represent the effective left ventricular filling pressure and did not vary significantly during the respiratory cycle despite large changes in Pes. All monitoring of vascular pressure and Pes was performed using transducers (Statham dB-23), and the pressure signals were recorded on a strip-chart recorder for subsequent analysis. Peak airway pressure in centimeters of water was recorded from the respirator. Transpulmonary pressure was estimated as peak airway pressure minus Pes. Cardiac output was estimated by thermodilution using a cardiac output computer (Edwards 9520) and triplicate injections of 10 ml of physiologic saline solution at 4°C. All injections of saline solution were performed at the end of expiration.
Arterial blood gas levels were monitored. Supplemental sodium bicarbonate was given to two patients (patients 2 and 3). Both patients required supplemental sodium bicarbonate prior to PH IPS, suggesting severe progressive metabolic acidosis. No adjustments were made in vasopressor therapy or intravascular volume status during the protocol.
The protocol consisted of measuring hemodynamic variables at the end of 20-minute periods of stabilization during three sequential steps. The first and third steps were the control runs, at which time the binders were loosely attached to the chest and abdomen and did not significantly affect Pes. The middle step consisted of a 20-minute run of PH IPS. In an attempt to increase intrathoracic pressure without increasing pulmonary vascular resistance or significantly compromising venous return, PHIPS was applied during constant-volume positive-pressure ventilation by tightening the chest and abdominal binders to increase mean Pes by approximately 5 mm Hg while maintaining transpulmonary pressure and transmural pulmonary arterial occlusion pressure constant. This was achieved by making the binders loose enough to not increase end-expiratory Pes, but tight enough to significantly increase end-expiratory Pes. In practice, this necessitated a relatively greater tension of the chest binder, presumably due to the inhibitory effects of the upper abdominal binder on venous return. We were unable to totally eliminate end-expiratory increases in Pes during PHIPS, suggesting that functional residual capacity during PHIPS was reduced when compared to control.
In an attempt to assess cardiac performance for routine clinical reasons, one patient (patient 4) was studied using a gated cardiac blood pool scan with radioactive ^technetium, which gave, through the profile of the time-activity curve, estimates of ejection fraction during both control runs and those with PHIPS. Using measurements of cardiac output and heart rate, the end-diastolic volume was also estimated as the stroke volume divided by the ejection fraction.
All patients tolerated PHIPS well, without deterioration in their hemodynamic status during that part of the protocol; however, upon removal of PHIPS, the condition of two patients rapidly deteriorated (patients 2 and 3), despite vigorous therapy. The reinstitution of PHIPS in one patient (patient 3) did momentarily improve the mean arterial pressure.
Statistical analysis was performed using a repeated-measures analysis of variance; and, unless otherwise stated, statistical significance reports are p<0.05.
Table 1—Profile cf Subjects
|Patient||Age, yr||Presumed Cause of Shock||UnderlyingPathology||Vasopressor and Dosage, iig/kg/min||Other Therapy|
|1||54||Gram-negative sepsis||Cirrhosis||Dopamine, 15||Antibiotics; corticosteroids|
|2||64||Septicemia||Diabetes mellitus||Dobutamine, 15||Digoxin; antibiotics; corticosteroids|
|3||62||Gram-negative sepsis||Cirrhosis||Dobutamine, 25||Digoxin; antibiotics|
|4||54||Cardiogenic||Coronary arterial disease||Dobutamine, 15||Furosemide|
|5||62||Septicemia||Cirrhosis||Dopamine, 25; and norepinephrine, 4||Furosemide|
|6||69||Cardiogenic||Coronary arterial disease||Dobutamine, 15||Furosemide; morphine sulfate|
|7||62||Cardiogenic||Coronary arterial disease||Dobutamine, 17; and dopamine, 10||Digoxin|