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Respiration and the Cardio-vascular system

Prof. S. K. Jindal

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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).


Dept. of Pulmonary Medicine, PGIMER, Chandigarh, India

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