Pleural Pressure – With increased airway resistance, the fluctuations in pleural pressure are exaggerated over those of normal breathing. Expiratory obstruction may lead to active expiratory effort, and positive intrathoracic pressure, but since dynamic compression of the airway limits any increase in airflow, patients gain little benefit and rarely develop a positive pleural pressure greater than a few centimeters of water.
During as asthmatic attack there is also marked obstruction to inspiratory air flow, and these patients breathe at a high lung volumes in order to maintain airway patency. These factors combine to produce extremely negative pleural pressures, as much as ?40 cm H2O with inspiration.
Venous Return – The negative intrathoracic pressure will enhance venous return, but the effect is limited by collapse of the veins. Nevertheless, there will be an inspiratory increases in right ventricular stroke volume, which should appear after a couple of beats in the left ventricular stroke volume. Although the inspiratory-expiratory variation in venous return is exaggerated the mean cardiac output is not necessarily altered.
Arterial Effects (Afterload) – The left ventricle, subjected to an intrathoracic pressure of ?40 cm H2O during inspiration, has to pump uphill to maintain forward flow in the peripheral circulation. This very substantial afterload results in a transient reduction in the left ventricular stroke volume and a marked drop in systolic blood pressure.
Obstructed breathing thus causes marked pulsus paradoxus, which can be used clinically as an index of the severity of air flow impairment. The pulsus paradoxus of tamponade can easily be distinguished from obstructed breathing by the absence of respiratory distress.
Pleural Pressure – A mechanical ventilating device delivers a tidal volume at a positive airway pressure to inflate the lungs; deflation is by elastic recoil with an open airway at atmospheric pressure. At the end of exhalation, the lung volume (FRC) and pleural pressure are about the same as during spontaneous breathing. However during the inflation phase, the pleural pressure rises (becoming less negative or slightly positive).
Pericardial Pressure – The pericardial pressure will follow the pleural pressure fluctuations but may be at a slightly higher mean level. Cardiac pulsation will be super-imposed and may be of substantial magnitude, relative to the respiratory fluctuations.
Venous Return – As the pleural pressure rises, the pressure in the venae cavae ad right atrium will rise, and the venous return will fall. Consequently, the right ventricular stroke volume will fall during inflation. However, the pulmonary capillaries will be compressed by the increased alveolar size and pressure, and pulmonary venous flow will be enhanced. Thus, return to left atrium is increased, and the left ventricular stroke volume will actually be increased initially during the lung expansion. Within a few heart beats the decreased right ventricular output causes left ventricular output to fall, usually coincident with expiration. Accordingly the cycle of rising and falling left ventricular stroke volume is reversed from that of normal respiration.
Arterial Effects (Afterload) – Although the left ventricle theoretically is at a slight advantage with the positive pleural pressure, relative to the peripheral vasculature at atmospheric pressure, this slight reduction in afterload is more than offset by the hindrance of venous return to the right heart.
Reflex Changes – Positive pressure ventilation usually induces an increase in sympathetic tone so that the heart rate is somewhat increased and there is constriction of the capacitance vessels, the veins, which help maintain a higher venous pressure, allowing partial restoration of venous return. The steady-state cardiac output is usually diminished.
In some mechanically ventilated patients, improved alveolar oxygenation can be obtained by maintaining a positive airway pressure at all times, even during passive exhalation. The end-expiratory lung volume (FRC) is increased above the normal volume. The effects are essentially the same as with positive pressure ventilation, but the effects on cardiac output are substantially greater, since the pleural pressure is increased above normal throughout all phases of respiration. The continuing impairment of venous return results in a decrease in mean stroke volume of right and left ventricles. The usual clinical index of left ventricular filling, the left atrial or pulmonary wedge pressure, will be elevated due to the increased intrathoracic pressure even though left atrial transmural pressure, left atrial volume, and left ventricular end diastolic volume are all reduced.
The addition of 5-10 cm H2O of PEEP is well tolerated by patients with normal to high intravascular volume but can markedly reduce cardiac output if initial volume is low. PEEP of 15-20 cm H2O will reduce cardiac output by 20% or more in most patients unless added volume is given. In some cases continuous positive airway pressure (CPAP) is maintained while the patients breathes spontaneously. The end-expiratory pleural pressure will still be elevated but it will decreased with inspiration rather than increasing further so venous return is less compromised and cardiac output better maintained than with comparable levels of PEP and mechanical ventilation.
In patients with asystole, or ventricular fibrillation, cardiac output adequate to maintain cerebral and coronary circulation, can be maintained by external compression of the chest. It has generally been assumed that the effective mechanism was compression of the ventricles directly against the spine, forcing blood out into the aorta. This assumption rested on the fact that during cardiac surgery, with the chest open, the cardiac output could be maintained by massaging the heat directly. Recently however, observation of patients who fibrillated during cardiac catheterization have suggested an alternate explanation for maintaining forward flow. These conscious patients were asked to cough vigorously at 1 or 2 second intervals, and the cardiac output was maintained by this method for over one minute. Since the heart was fibrillating, and no external pressure was applied to the pericardium, it was concluded that the driving force was the marked increase in intrapleural pressure produced by the cough.
As has been shown with positive pressure ventilation, blood is expelled from the pulmonary veins into the heart, and apparently through the heart into the aorta with the sharp cough. The caval pressure is also elevated by this means, but the transport lag across the peripheral vascular bed allows the flow pulse to be effective, since the venous pressure dropped quickly, and its retrograde progress was impeded by the venous valves. It is now considered likely that compression of the pulmonary vasculature, rather than the ventricle, may be important aspect of external compression must be intermittent, allowing refill with elastic recoil before subsequent compression would be effective.
Dept. of Pulmonary Medicine, PGIMER, Chandigarh, India