Respiration and the Cardio-vascular system
The effect of Respiration on the cardio-vascular system
The heart and great vessels are within the chest, and consequently are subject to the changes in intrathoracic pressure associated with respiration. The effects are relatively mild in the normal subject. These effects are easily observed at the beside as sinus arrhythmia, splitting of the second heart sound, and by small variations in the systolic blood pressure. Certain produce marked fluctuations in blood pressure with respiration: detection is essential for appropriate diagnosis and treatment. A review of this interaction physiology and pathophysiology is useful to emphasize the cardiovascular system as a complete circuit, separation the transient effects from the steady-state effects, and to clarify the concepts of venous return and cardiac output.
In the steady-state, venous return and cardiac output are identical in volume per minute, although cyclical changes with respiration may affect one more than the other transiently. Considerations of a complete circuit also require that the changes in output of the right ventricle must be accounted for in the return to the left ventricle within a short time (1-2 beats). Similarly, the left ventricular output must be accounted for in the systemic venous return in a steady-state, although the transportation lag is substantially longer for the systemic transient changes in the left ventricular output may be delayed several seconds, and are generally more damped in appearance in the systemic venous return.
Certain definitions are descriptions are important to consider before analyzing the effects of respiration on the cardiovascular system. First, it is helpful to bear in mind two types of vascular pressures. In analyzing the flow of blood around the circuit, the intravascular pressure relative to atmospheric pressure is used in determining pressure gradients. In considering the diameter of a cardiovascular chamber, the distending pressure must be considered. This is also called the transmural pressure, and is simply the internal pressure minus the pressure outside the wall. The transmural pressure should not be used in considering flow or pressure drop across part of the vascular bed. The transmural pressure is vital in determining the filling of cardiac chambers.
A. NORMAL RESPIRATION
Pleural Pressure The force that lowers the intrathoracic pressure with inspiration is produced by inspiratory muscles, primarily the diaphragm and thoracic skeletal musculature. The inspiratory drop in pleural pressure is transmitted to all intrathoracic structures, including the heart and great vessels.
If there were no change of volume in these chambers, the pressure would be transmitted quite faithfully, but flow usually continues into and out of the chamber, so that the intravascular pressure with not precisely reflect the fluctuations in intrathoracic pressure. This transmission of the intrathoracic pressure in utilized clinically by measuring the intrathoracic pressure via an esophageal balloon.
Pericardial Pressure The pericardium forms the immediate milieu for the heart, and it transmits the pleural pressure accurately in its fluctuation with respiration, but as the heart fills, during diastole, the pericardial pressure will increase above the intrathoracic pressure. This difference is relatively small in the normal subject, but may be quite important in abnormal states, and when calculation ventricular function curves from filling pressure against stroke volume.
Venous Return The return of systemic blood to the right atrium is driven by pressure gradient from the systemic veins to the right atrium. The venous pressure outside the thorax is above atmospheric pressure and as he intrathoracic pressure fall with inspiration, the pressure gradient favoring flow into the thorax is enhanced.
Since the pulmonary artery (upstream of the pulmonary veins) and the left atrium and left ventricle (downstream of the pulmonary veins) are all subject to the intrathoracic pressure, there should be little, if any, direct effect of inspiration on the pulmonary veins. Most of the change in flow in the pulmonary veins with inspiration results from transmission of the output from the right ventricle. Studies timing this relationship have shown that the major flow pulse from the right ventricle appears in the pulmonary veins in the same cardiac cycle.
Consequently, the increased volume of the right ventricle with should appears in the pulmonary veins in the same cycle, and should be reflected increased left ventricular stroke volume after one or two beats. This is should be reflected in increased left ventricle would occur in the first one or two cardiac cycles after the onset of inspiration, since the lowest point in the right ventricular stroke volume cycle is just prior to the onset of inspiration.
The enhanced right ventricular stroke volume does account for a commonly observed auscultator finding. With inspiration, the normal healthy young subject will demonstrate splitting of the second heart sound at the pulmonic area. This reflects the relative increase in the right ventricular stroke volume, which requires a greater ejection time, thereby delaying the pulmonic closure beyond that of the aortic valve, sufficiently to produce audible separation of the two closing sounds. (The aortic closure always precedes the pulmonic in the normal subject).
Arterial Effects (Afterload) The intrathoracic blood vessels are exposed to the drop in pressure with inspiration of approximately 7 mmHg. For the left ventricle, the effective pump level drops by that amount, since the bulk of the systemic circulation is outside the chest, at atmospheric pressure. To maintain the same pressure in the peripheral circulation, an increase in pressure generated by contraction of the left ventricle would have to be developed. This slight increase in afterload for the left ventricle has relatively little effect on the stroke volume of the left ventricle under normal conditions of respiration and circulation, but does account for the slight respiratory fall in systolic blood pressure that can be easily measured in the normal subject. By contrast, the right ventricle ejects into the pulmonary circulation within is entirely within the thorax and therefore the right ventricle experiences no change in afterload.
Reflex Effects In healthy subject at rest, inspiration is associated with an acceleration of the heart rate, and a deceleration occurs with expiration. This phenomenon, sinus arrhythmia, occurs under conditions of vagal control over the cardiac pacemaker, via neural radiation from the respiratory centre in the medulla to the cardiovascular center. This has a major effect on stroke volume of the two ventricles, through changes in the filling interval for the ventricles. With inspiratory acceleration, the filling interval is diminished and the stroke volume for both ventricles becomes smaller. With sinus arrhythmia, the varying diastolic interval becomes the single most important determinant of the stroke volume, and effect of enhanced venous return are less obvious. When the subject is stressed, resulting in an increased sympathetic tone and diminished vagal tone, tachycardia results, and the variation of filling interval disappears. At that time, the effect on stroke volume of enhanced venous return to the right heart with inspiration is much more pronounced.
B. CARDIAC TAMPONADE
Pleural Pressure During tamponade normal respiration persists, and the wings of intrapleural pressure do not change significantly, an average of 7 mmHg. Thus, in tamponade, the phenomenon of pulsus paradoxus (a drop in systolic blood pressure with inspiration of greater than 10 mmHg) cannot be attributed to a direct transmission of intrathoracic pressure.
Pericardial Pressure The peak-to peak pressure change with respiration in the pericardium is exactly the same as the pleural pressure. However, since pericardium is distended with fluid, its overall pressure is substantially; elevated. This increased pressure reduces the transmural or distending pressure for the heart, and drastically interferes with filling of the two ventricles. The rise in pericardial pressure is not limitless, since all circulation will cease when the pericardial pressure rises above 20 mmHg. Near that point, all of the diastolic pressure throughout the heart will be similar, in both atria and both ventricles.
The pericardial effusion does not shield the heart from the changing intrathoracic pressure of respiration, which is superimposed on the high pressures due to the tamponade. The pericardial pressure will also fluctuate with the cardiac cycle, to a much greater extent than the normal, since the pericardium is quite full, and small changes in volume will produce large changes in pericardial pressure.
The pericardium is capable of a slow stretching, and if the fluid accumulates very slowly, the pressure will not necessarily rise, and sometimes a rather large effusion can be tolerated without tamponade and pulsus.
Venous Return A high rate atrial pressure, as the downstream pressure of the systemic circulation, has a markedly inhibiting effect on systemic venous return. This is the case in tamponade, and shock is usually present with very high venous pressure. The 7 mmHg. Drop with normal inspiration is effective in temporarily increasing venous return to the right heart. Since the stroke volume is markedly limited by the limited diastolic filling, the enhanced venous return will make an obvious improvement in the stroke volume of the right ventricle with inspiration. After 1-2 beats, that stroke volume will appear in the left ventricular output, but that increase will be delayed by 2-3 beats from the onset of inspiration, and therefore systolic blood pressure will be at its lowest during inspiration. The effect of inspiration on the pulmonary veins, as discussed under the normal circulation, is minimized by the fact that the pulmonary vein and the left heart are subjected to the same intrathoracic pressure. An earlier theory of pulsus paradoxus contended that the pulmonary veins actually pooled blood temporarily with inspiration, through an increased transmural pressure, whereas the left ventricle was shielded from the effects of inspiration by the pericardial effusion.
Another theory explaining pulsus paradoxus that remains popular is that the enhanced venous return to the right ventricle with inspiration successfully competes for the fixed volume available within the pericardium. With a fixed total volume, and increase in right ventricular filling would competitively inhibit left ventricular filling, leading to a decrease in the stroke volume which in turn would lead to low systolic pressure during inspiration that is characteristic of pulsus paradoxus. It has been shown in human subjects with tamponade that, indeed, the ventricular septum is displaced into the left ventricular cavity during inspiration. That this could also be attributed to a diminished left ventricular volume of the delayed effect of the expiratory decrease in right ventricular stroke volume. Arterial Effects (Afterload) Since the fall in pleural pressure with tamponade is the same as in the normal, increased afterload cannot reasonably explain the substantially greater all in systolic blood pressure. The slight increase in afterload for the left ventricle could have a negative effect on the left ventricular stroke volume, but both by percentage and by actual volume, the effect would be trivial.
Reflex Effects In tamponade, a shock-like state exists, and invariably there is tachycardia and generalized vasoconstriction, which probably involves the veins as well as the arteries. Without this reflex adjustment, the mean circulatory pressure could not be increased, and circulation would cease at as earlier point in the disorder.
C. OBSTRUCTED BREATHING
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.
D. POSITIVE PRESSURE BREATHING
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.
E. POSITIVE END–EXPIRATORY PRESSURE (PEE)
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.
F. CARDIOPULMONARY RESUSCITATION (CPR)
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
