Valsalva is a great little test for assessing the reflex autonomic control of the cardiovascular system, both
sympathetic and vagal. It does so by modifying blood pressure, heart rate, and venous return—all as a result
of respiratory swings in intrathoracic pressures. It can be difficult to perform, though, and thus should always be well explained to the patient, especially the need to keep on straining until told to stop, and to breathe as quietly as possible after stopping straining. Valsalva consists of two major periods, comprising a total of four phases :
Period 1: a held (or strain) period. This is carried out by asking the patient to fully inspire and then
forcefully exhale against closed glottis for at least 10 seconds. It can be easily accomplished by having the
patient “bear down as if having a bowel movement,” or alternatively, by placing a fist onto the mid abdomen of a supine patient and then having him or her strain against it (it could even be accomplished more formally by having the patient blow for 10 seconds against an aneroid manometer at a constant pressure of 40 mmHg). Whatever the technique, the resulting strain causes an increase in intrathoracic pressure, a drop in venous return, a reduction in left ventricular diameter, and a fall in cardiac output. These can be quite dramatic (in fact, when first experimenting with Valsalva’s, Weber, in typical Teutonic fashion, managed to give himself a syncope and a seizure; then he recovered and wrote the paper). This “strain” comprises two phases:
Phase I: After onset of straining, systolic pressure increases (due to aortic compression), and heart rate decreases (due to reflex bradycardia from baroreceptor activation).
Phase II: Characterized instead by a drop in venous return because of straining-induced compression of the vena cava. This eventually leads to a fall in cardiac output, a secondary fall in aortic pressure (which therefore slowly returns to the baseline level), and a secondary increase in heart rate (still mediated by the baroreceptor reflex). During the rest of the straining period, the arterial mean and pulse pressures continue to slowly fall, and the heart rate continues to slowly increase.
Period 2: a release period. This is carried out by asking the patient to stop bearing down, or alternatively, by releasing the fist pressure on the abdomen. It also comprises two phases:
Phase III: As soon as straining is released (and the subject starts breathing again), there is a small
but transient drop in systolic pressure due to sudden loss of aortic compression. This, in turn, causes a further reflex acceleration of the heart rate.
Phase IV: When the vena cava compression completely resolves, venous return suddenly
increases. This causes a rapid rise in cardiac output, which, in turn, makes the systolic pressure overshoot above baseline values (due to increased systemic resistance from phase II sympathetic activation) and heart rate to drop (because of baroreceptor reflex).
This normal hemodynamic response to Valsalva can be quite altered in congestive heart failure.
sympathetic and vagal. It does so by modifying blood pressure, heart rate, and venous return—all as a result
of respiratory swings in intrathoracic pressures. It can be difficult to perform, though, and thus should always be well explained to the patient, especially the need to keep on straining until told to stop, and to breathe as quietly as possible after stopping straining. Valsalva consists of two major periods, comprising a total of four phases :
Period 1: a held (or strain) period. This is carried out by asking the patient to fully inspire and then
forcefully exhale against closed glottis for at least 10 seconds. It can be easily accomplished by having the
patient “bear down as if having a bowel movement,” or alternatively, by placing a fist onto the mid abdomen of a supine patient and then having him or her strain against it (it could even be accomplished more formally by having the patient blow for 10 seconds against an aneroid manometer at a constant pressure of 40 mmHg). Whatever the technique, the resulting strain causes an increase in intrathoracic pressure, a drop in venous return, a reduction in left ventricular diameter, and a fall in cardiac output. These can be quite dramatic (in fact, when first experimenting with Valsalva’s, Weber, in typical Teutonic fashion, managed to give himself a syncope and a seizure; then he recovered and wrote the paper). This “strain” comprises two phases:
Phase I: After onset of straining, systolic pressure increases (due to aortic compression), and heart rate decreases (due to reflex bradycardia from baroreceptor activation).
Phase II: Characterized instead by a drop in venous return because of straining-induced compression of the vena cava. This eventually leads to a fall in cardiac output, a secondary fall in aortic pressure (which therefore slowly returns to the baseline level), and a secondary increase in heart rate (still mediated by the baroreceptor reflex). During the rest of the straining period, the arterial mean and pulse pressures continue to slowly fall, and the heart rate continues to slowly increase.
Period 2: a release period. This is carried out by asking the patient to stop bearing down, or alternatively, by releasing the fist pressure on the abdomen. It also comprises two phases:
Phase III: As soon as straining is released (and the subject starts breathing again), there is a small
but transient drop in systolic pressure due to sudden loss of aortic compression. This, in turn, causes a further reflex acceleration of the heart rate.
Phase IV: When the vena cava compression completely resolves, venous return suddenly
increases. This causes a rapid rise in cardiac output, which, in turn, makes the systolic pressure overshoot above baseline values (due to increased systemic resistance from phase II sympathetic activation) and heart rate to drop (because of baroreceptor reflex).
This normal hemodynamic response to Valsalva can be quite altered in congestive heart failure.