Effects of Respiration on Blood Pressure in Normal Subjects
The effects ofrespiration on the level ofblood pressure in the normal must be understood in relation to the changes in the respiratory variations of the intrathoracic pressures as well as the venous return. On inspiration, there is generally a lower systolic pressure compared to the end of expiration. The intrathoracic pressure falls on inspiration, which helps to augment venous return to the heart. The inspiratory expansion of the lungs, by increasing its pulmonary venous capacity, accommodates for the extra volume of blood returned to the right side on inspiration and the consequent increase in right ventricular output. The increased venous return on inspiration is therefore not immediately available to the left heart. In fact, the return to the left heart may slightly decrease on inspiration, the expanded lungs holding the extra volume for at least a few cardiac cycles. By that time the expiratory phase usually occurs. The intrathoracic pressure on expiration becomes relatively more positive. The aorta being an intrathoracic structure, these changes in the intrathoracic pressures will also affect the aortic pressure. There is generally a fall in the systolic blood pressure with normal inspiration, and the magnitude of this fall is about 5-10 mm. This is a result ofboth the fall in intrathoracic pressure and the effect ofthe expanded lungs holding the extra venous return, thereby diminishing the return to the left heart and therefore its output. The opposite occurs on expiration—the intrathoracic pressure rises and the lungs contract in volume by exhaling air—and this aids in increased pulmonary venous inflow to the left side, increasing the stroke output. The net effect leads to an increased arterial pressure on expiration. In the normal, the expansion of the right ventricle on inspiration does not usually result in shift of the interventricular septum to the left since the normal pericardium does not limit physiological changes in ventricular volumes (34).
In the normal, the effect of this inspiratory fall in the systolic blood pressure is not detectable by palpation of the arterial pulse. However, the magnitude of the inspiratory fall in the blood pressure can be easily assessed by blood pressure cuff at the bedside. When the cuff is being slowly deflated to detect the onset ofthe Korotkoff sounds, careful observation will reveal that initially the Korotkoff sounds are audible only at the end of expiration. With each inspiration they will be seen to become inaudible. The level of the blood pressure at the end of expiration when the Korotkoff sounds begin to be heard must be first noted. With further cuff deflation, however, it will be observed that the Korotkoff sounds are audible throughout both inspiration and expiration. The level of the blood pressure at which this begins to happen must be noted next. The difference between the two systolic levels, namely the number of mmHg to which the cuff needed to be deflated (i.e., when Korotkoff sounds no longer remain inaudible on inspiration), gives the magnitude of the inspiratory fall in the blood pressure.
In cardiac tamponade, there is an exaggeration of the normal inspiratory fall in the systolic blood pressure leading to a truly definable pulsus paradoxus. The fall in the stroke volume of the heart and consequently the systolic blood pressure despite the increased venous return to the heart caused by inspiration is the paradox that led to this term. In fact, in significant cardiac tamponade, the palpation of the arterial pulse may reveal that its amplitude is less or the pulse may not even be felt on inspiration. This of course is not the case in the normal. The mechanism of this exaggerated fall in the blood pressure on inspiration is attributable to the compressive effect of the fluid in the pericardial space, which is under high pressure. In cardiac tamponade, all four chambers of the heart are as if boxed in this tight pericardial space. In the absence of pre-existing cardiac disease, the pressures in the right and the left atria, the intrapericardial pressures, as well as the right and left ventricular diastolic pressures are all elevated to the same level. In extreme cases of tamponade, the thinner-walled structures like the right ventricle are compressed more completely than the thicker-walled left ventricle. When inspiration increases the venous return to the right heart as in normals, the expansion of the right ventricle within this enclosed tight pericardial space will ofnecessity push the interventricular septum to the left side, thereby further diminishing the left heart filling and its compliance. This will lead to decreased left ventricular output. The septal bulge on inspiration to the left side can in fact be demonstrated in echocardiograms of patients with tamponade.
Because the pericardium is attached to the diaphragm, the descent of the diaphragm with inspiration may also pull on the pericardium, thereby altering its global shape to a more spindle-like shape. This physically can lead to further rise in the intrapericardial pressure. The effects of the inspiratory fall in the intrathoracic pressures as well as the effects of the inspiratory expansion of the lungs and pulmonary venous pooling leading to diminished left heart filling, mentioned above in the normal, are also still operative in patients with cardiac tamponade. The net effect of these changes on the left heart filling as well as the intrathoracic pressures will cause a greater fall in the left ventricular stroke output and the blood pressure on inspiration. The opposite changes occur on expiration, leading to a higher arterial pressure on expiration. The effect of the inspira-tory pulmonary venous pooling is even more dramatic when the left ventricular stroke output is already diminished due to the tamponade.
The blood pressure cuff is used in the same manner as mentioned above to determine the magnitude of fall in mmHg due to pulsus paradoxus. The pulsus paradoxus by blood pressure measurement must exceed 15 mmHg to be considered significant.
In the presence of significant elevations of the left ventricular diastolic pressures resulting from pre-existing cardiac disease, cardiac tamponade does not cause pulsus paradoxus. The raised diastolic pressures offer greater resistance to the compressive effects of the intrapericardial pressures. Cardiac tamponade also does not lead to pulsus paradoxus in two other conditions, namely aortic regurgitation and atrial septal defect. In the former, the extra source of left ventricular filling due to the aortic regurgitation keeps the left ventricular volumes from falling, thereby preventing the respiratory fluctuations in left heart filling. Similarly in atrial septal defect, the left-to-right shunt accommodates for respiratory changes in venous return, thereby preventing a fall in left heart filling during inspiration (35-43).
Conditions Other Than Cardiac Tamponade With Pulsus Paradoxus Constrictive Pericarditis
In constrictive pericarditis, pulsus paradoxus is much less common than in cardiac tamponade. It is more common in the effusive subacute type of constriction than in chronic cases. Pulsus paradoxus is absent in chronic cases because of poor transmission of the intrathoracic pressures to the cardiac chambers as a result of thickened and fibrosed and sometimes calcified pericardium. When pulsus paradoxus is seen, it is probably a result of a combination of two factors, namely the septal shift to the left and the increased pulmonary venous pooling on inspiration. The diaphragmatic pull on the pericardium on inspiration is also unlikely to be operative on a thickened and scarred pericardium (38).
Bronchial Asthma and Chronic Obstructive Pulmonary Disease
The exaggerated swings in intrathoracic pressures may be directly transmitted to the aorta, affecting the systolic and the diastolic pressures with very little change in the stroke volume or the pulse pressure. In the presence of significant airways obstruction, there is marked increase in the intrathoracic pressures during expiration caused by the intercostal muscles to overcome the airways obstruction. This elevated intrathoracic pressure is directly transmitted to the aorta, raising the expiratory pressure in the aorta. Thus, there is an expiratory gain in blood pressure rather than the usual inspiratory fall in the normal. The net effect on the blood pressure is the same.
In some patients with hypovolemic shock, pulsus paradoxus may be noted (44). This is a result of an exaggerated effect of the inspiratory pulmonary venous pooling on the already diminished stroke volume. The change in the percentage of the stroke volume is higher compared to the normal individuals with normal cardiac output.
Similarly, the reduced capacity of the pulmonary arterial bed because of embolic obstruction in the presence of the normal pulmonary venous bed may also lead to an accentuated effect of the inspiratory pulmonary venous pooling on the left ventricular stroke volume (45).
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