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APPENDIX 2

Hemodynamic Maneuvers

Inspiration causes a decrease in intrathoracic pressure resulting in decreased

central venous pressure, increased venous return to the right atrium, increased
right ventricle stroke volume, decreased pulmonary vascular resistance,
decreased left atrial pressure and decreased aortic pressure.
Expiration associated with increased intrathoracic pressure and effects opposite of those observed with inspiration.
Change in posture rising from a recumbent position decreases venous return to
the heart; squatting from a standing position is associated with a simultaneous
increase in venous return and systemic vascular resistance and a rise in arterial
pressure.
The Valsalva maneuver is widely used to elicit well-defined hemodynamic
changes and is a simple test of complex autonomic reflex controls of cardiovascular function. Correct performance of a Valsalva maneuver results in 4 distinct
hemodynamic phases. It can be induced by multiple mechanisms including a
forced expiration against a closed glottis, straining during a bowel movement
or lifting weights during a breath hold. At the bedside, the patient should be
asked to attempt exhalation against a resistance or to simulate straining for
a bowel movement. These efforts should be maintained for approximately 30
seconds and then released.
These maneuvers result in a large rise in intrathoracic pressure which compresses the vessels within the chest cavity. There is initially a transient increase
in aortic pressure (Phase 1) due to aortic compression and increased cardiac
output due to enhanced left atrial blood flow. This increase in aortic pressure
causes a reflex bradycardia due to baroreceptor activation. Because the thoracic vena cava is also compressed, venous return to the heart is compromised,
resulting in a large fall in cardiac output within several seconds. This leads to
a secondary fall in aortic pressure (Phase 2), and as aortic pressure falls, the
baroreceptor reflex increases heart rate. When breathing is resumed, the release
of aortic compression results in a small, transient dip in arterial pressure and
a further reflex increase in heart rate (Phase 3). When compression of the vena
cava is removed, venous return suddenly increases causing a rapid rise in cardiac output several seconds later which leads to a transient increase in arterial
pressure (Phase 4). Sympathetic activation that occurred during Phase 2 leads
to arterial pressure greater than baseline because the systemic vascular resistance is increased. Heart rate reflexively decreases during Phase 4 in response
to the transient elevation in arterial pressure.
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294 Appendix

Summary of Hemodynamic Effects of Valsalva Maneuver

Phase 1 - transient increase in left ventricular output.
Phase 2 (straining phase) - decreased venous return, right and left ventricular volumes, stroke volumes, mean arterial pressure, and pulse pressure;
reflex increase in heart rate.
Phase 3 (release of Valsalva) brief phase with a further reduction in left
ventricular volume.
Phase 4 - increase in stroke volume and arterial pressure and reflex slowing
of heart rate

Handgrip sustained for 20 to 30 seconds leads to an increase in systemic vascular resistance, arterial pressure, cardiac output, and left ventricular volume
and filling pressure.
Muellers maneuver is forced inspiration against airway resistance. This
results in decreased intrathoracic pressure and increased LV afterload. In a
study of 10 normal subjects [1], the hemodynamic response to the Mueller
maneuver included:
r no change in aortic systolic and mean pressures
r decreased aortic diastolic pressure
r increased pulse pressure
r large decrease in mean right atrial pressure ( SE) decreased from 7 1 to
17 4 mm
r accentuation of right atrial x descent
r decrease in left ventricular end-diastolic pressure
r increase in systemic vascular resistance
r reduction in cardiac output and stroke volume
r no significant change in heart rate.
In another study of patients with systolic dysfunction, the Mueller maneuver
caused immediate increases in systolic left ventricular transmural pressure and
simultaneous reductions in blood pressure, stroke volume, and cardiac output.
These changes were proportional to the magnitude of the negative intrathoracic
pressure generated [2].

References
1 Condos WR, Latham RD, Hoadley SD, Pasipoularides A. Hemodynamics of the Mueller
maneuver in man: right and left heart micromanometry and Doppler echocardiography.
Circulation 1987;76:1020-1028
2 Hall MJ, Ando S, Floras JS, Bradley TD. Magnitude and time course of hemodynamic
responses to Mueller maneuvers in patients with congestive heart failure. J Appl Physiol
1998;85:14761484.