Вы находитесь на странице: 1из 12

Aortic stenosis differential diagnosis

Overview
Aortic stenosis must be differentiated from other cardiac or pulmonary causes of dyspnea,
weakness, and dizziness. Furthermore, when left ventricular outflow tract obstruction is present,
it is critical to identify whether the obstruction is subvalvular, valvular or supravalvular and
whether there is hypertrophic cardiomyopathy (HOCM) or not.
Differentiating Aortic Stenosis from other Diseases
Pulmonary Causes of Dyspnea
Aortic stenosis can be differentiated from pulmonary causes of dyspnea by the presence of:
A narrow pulse pressure
A harsh late-peaking systolic murmur heard best at the right second intercostal space with
radiation to the carotid arteries
A delayed slow-rising carotid upstroke (pulsus parvus et tardus)
[1]

Signs of heart failure on examination
Aortic Sclerosis
While a murmur may be heard in aortic sclerosis, there is no fusion of the commisures and no
significant obstruction to antegrade blood flow across the aortic valve. As a result, the S2 is
normal in aortic sclerosis and the carotid upstroke is normal (i.e. pulsus parvus et tardus is
absent).
Mitral Regurgitation
The murmur of aortic stenosis is harsh and best heard at the right second intercostal space while
the murmur of mitral regurgitation is blowing, soft and best heard at the apex.
Hypertrophic Obstructive Cardiomyopathy
In HOCM the murmur is dynamic and varies with maneuvers. Moreover, there is a bifid or spoke
and dome pattern of the carotid upstroke.
Valvular, Subvalvular and Supravalvular Aortic Stenosis
Differentiating Valvular Aortic Stenosis from Subvalvular Aortic Stenosis
Aortic insufficiency is more often present with subvalvular aortic stenosis (in 50% to 75% of
cases). Symptoms associated with subvalvular aortic stenosis begin earlier in life (in childhood
or adolescence) than symptoms associated with valvular aortic stenosis.
Differentiating Valvular Aortic Stenosis from Supravalvular Aortic Stenosis
Supravalvular aortic stenosis is an uncommon congenital anomaly caused by a narrowing in the
ascending aorta or by the presence of a fibrous diaphragm just above the aortic valve. It presents
in early adulthood. Although the aortic valve is not stenotic, doppler shows an increased pressure
gradient. 50% of patients with supravalvular aortic stenosis have a characteristically greater
pulse and systolic blood pressure in the right carotid and brachial arteries than in the left. The
systolic murmur is maximal below the right clavicle and radiates primarily to the right carotid
artery. There is not an ejection click nor a diastolic murmur.
The handgrip maneuever is performed by clenching one's fist forcefully for a sustained time
until fatigued. Variations include squeezing an item such as a rolled up washcloth.
Contents
1 Physiological Response
2 Cardiology
3 See also
4 References
Physiological Response
The handgrip maneuver increases afterload by squeezing the arterioles and increasing total
peripheral resistance.
[1]

Cardiology
Since increasing afterload will prevent blood from flowing in a normal forward path, it will
increase any murmurs that are due to backwards flowing blood.
[2]
This includes aortic
regurgitation (AR), mitral regurgitation (MR), and a ventricular septal defect (VSD).
Mitral valve prolapse: The click and the murmur of mitral valve prolapse are delayed because of
the increased left ventricular volume
Murmurs that are due to forward flowing of blood such as aortic stenosis, and hypertrophic
cardiomyopathy decrease in intensity.
Mitral stenosis: The diastolic murmur of mitral stenosis increases because of an increased heart
rate, blood pressure and cardiac output
[3][4]

The effect of reducing the intensity in forward flowing murmurs is much more evident in aortic
stenosis rather than mitral stenosis. The reason for this is that there is a larger pressure gradient
across the aortic valve.
[5]
A complementary maneuver for differentiating disorders is the
Valsalva maneuver, which decreases preload.

Handgripping maneuver Cardiac Finding
Increased murmur intensity
Aortic regurgitation
Mitral regurgitation
Ventricular septal defect
Mitral valve prolapse
Mitral stenosis
Decreased murmur intensity

Aortic stenosis
Hypertrophic cardiomyopathy
ACC/AHA guideline summary: Interventions used to alter the intensity of cardiac murmurs
Respiration
Right-sided murmurs typically increase with inspiration, while left-sided murmurs generally are
louder during expiration.
Valsalva maneuver
Most murmurs decrease in length and intensity during the Valsalva maneuver. Two exceptions
are the systolic murmur of hypertrophic cardiomyopathy (HCM), which usually becomes much
louder, and the systolic murmur of mitral valve prolapse (MVP), which becomes longer and
often louder. Following release of the Valsalva, right-sided murmurs tend to return to baseline
intensity earlier than left-sided murmurs.
Exercise
Murmurs caused by blood flow across normal or obstructed valves (eg, mitral or pulmonic
stenosis) become louder with both isotonic and submaximal isometric (handgrip) exercise.
Murmurs of mitral (MR) and aortic regurgitation (AR) and ventricular septal defect (VSD) also
increase with handgrip exercise.
Positional changes
Most murmurs diminish with standing due to reduced preload. However, the murmur of HCM
becomes louder, and the murmur of MVP lengthens and often is intensified. Similarly, most
murmurs become louder with prompt squatting (or usually passive leg raising), while the
murmurs of HCM and MVP typically soften and may disappear.
Post ventricular premature beat (VPB) or atrial fibrillation (AF)
Murmurs originating at normal or stenotic semilunar valves increase in intensity during the
cardiac cycle following a VPB or in the beat after a long cycle length in AF. In contrast, systolic
murmurs due to atrioventricular valve regurgitation do not change, become softer (papillary
muscle dysfunction), or become shorter (MVP).
Transient arterial occlusion
Transient external compression of both arms by bilateral cuff inflation to 20 mmHg greater than
peak systolic pressure augments the murmurs of MR, VSD, and AR, but not murmurs due to
other causes.
RESPIRATION Venous return to the right ventricle increases during normal inspiration
resulting in an increase in its volume. In contrast, inspiration causes a decrease in venous return
to the left ventricle and a reduction in its volume. These changes in venous return can alter the
intensity of murmurs and heart sounds, primarily those that originate from the right side of the
heart. (See "Auscultation of cardiac murmurs" and "Auscultation of heart sounds".)
During inspiration there is an increase in the splitting of S2 as A2 and P2 are separated.
Third (S3) and fourth (S4) heart sounds of right ventricular origin usually diminish with
expiration and increase with inspiration. An S3 and S4 originating from the left side of the heart
may increase with expiration and decrease with inspiration.
In tricuspid stenosis, the opening snap diminishes with expiration and increases with
inspiration. In contrast, the opening snap of mitral stenosis increases with expiration and
decreases with inspiration.
Pulmonary ejection sound of valvular origin decreases in intensity during inspiration.
Inspiration increases the intensity of murmurs originating from the right side of the heart,
including the diastolic murmurs of tricuspid stenosis and pulmonary regurgitation, the systolic
murmur of tricuspid regurgitation (Carvallo's sign), and the presystolic murmur of Ebstein's
anomaly.
In mitral valve prolapse, the inspiratory decrease in venous return to the left side of the heart
reduces left ventricular volume; the murmur and click occur earlier and may diminish.
ABRUPT STANDING Abrupt standing from the supine position decreases venous return to
the heart and, consequently, right and left ventricular diastolic volumes and stroke volumes
decline. There also may be a fall in arterial pressure and a reflex increase in heart rate. These
hemodynamic changes are associated with changes in the following murmurs:
Decrease in the intensity of the murmurs of pulmonary and aortic stenosis
Decrease in the intensity of the murmurs of mitral and tricuspid regurgitation
Earlier onset of the click and prolongation of systolic murmur of mitral valve prolapse
Decrease in the intensity of the systolic murmur in ventricular septal defect without significant
pulmonary hypertension
In hypertrophic cardiomyopathy, a decrease in left ventricular outflow size is associated with
an increase in the intensity of the ejection systolic murmur along with a decrease or unchanged
carotid pulse volume
SQUATTING Squatting from a standing position is associated with a simultaneous increase
in venous return (preload) and systemic vascular resistance (afterload) and a rise in arterial
pressure. This causes changes in the following murmurs:
Increased intensity of the murmur of mitral regurgitation due to the rise in afterload, which
favors the movement of blood in the left ventricle across the insufficient mitral valve rather than
entering the systemic circulation across the aortic valve.
In patients with mitral valve prolapse there is a delay in the onset of the click and a shortening
of the late systolic murmur. These changes reflect the delay in prolapse induced by the increase
in preload. However, as mitral regurgitation becomes more severe, the murmur may increase in
intensity with squatting because of the increase in afterload.
Increase in the magnitude of the left-to-right shunt in ventricular septal defect associated with
an increased intensity of the systolic murmur.
In patients with tetralogy of Fallot, the net effect of squatting is usually an increase in
pulmonary flow, which is associated with increased intensity of the pulmonary ejection systolic
murmur. (See "Pathophysiology, clinical features, and diagnosis of tetralogy of Fallot", section
on 'Cardiac auscultation'.)
Intensity of the diastolic murmur of aortic regurgitation increases due to augmented
regurgitation; intensity of the Austin-Flint murmur also may increase.
In hypertrophic cardiomyopathy, intensity of the ejection systolic murmur promptly declines
because of an increased left ventricular volume and arterial pressure, which increase the effective
orifice size of the outflow tract; the carotid pulse upstroke remains sharp, and the volume may
increase.
Intensity of the murmur of valvular aortic stenosis shows variable changes, depending upon the
type of hemodynamic response; a significant increase in systemic vascular resistance is
associated with a decreased intensity of the murmur, an increased left ventricular volume with
increased intensity of the murmur.
VALSALVA MANEUVER The hemodynamic changes resulting from a Valsalva maneuver
vary with the different phases.
During phase 1, with the onset of the maneuver, there is a transient increase in left ventricular
output.
During the straining phase, phase 2, there is a decrease in venous return, right and left
ventricular volumes, stroke volumes, mean arterial pressure, and pulse pressure; this is
associated with a reflex increase in heart rate.
During phase 3 (release of Valsalva), which only lasts for a few cardiac cycles, there is a
further reduction in left ventricular volume.
Phase 4 is characterized by an increase in stroke volume and arterial pressure and reflex
slowing of heart rate (the overshoot).
Analysis of changes in the intensity and character of the murmur during phase 2 of the Valsalva
maneuver is most useful and practical for the differential diagnosis.
The intensity of flow murmurs, murmurs of aortic and pulmonary stenosis, tricuspid and mitral
regurgitation, aortic and pulmonary regurgitation, and mitral and tricuspid stenosis decreases.
The volume of the carotid pulse also decreases.
The murmur of hypertrophic cardiomyopathy increases in intensity as the left ventricular
outflow size decreases with a decreased venous return. The carotid pulse volume also declines.
In mitral valve prolapse there is an early onset of the click and murmur due to the decrease in
left ventricular volume. The opposite effects are observed during phase 4.
HAND GRIP Sustained hand grip for 20 to 30 seconds leads to an increase in systemic
vascular resistance, arterial pressure, cardiac output, and left ventricular volume and filling
pressure. Hemodynamic changes during hand grip are variable and not always similar in all
patients. As an example, the increase in arterial pressure may be relatively greater than the
increase in heart rate or cardiac output. Thus, changes in intensity of murmurs are not always
predictable.
Hand grip is most useful in differentiating between the ejection systolic murmur of aortic
stenosis and the regurgitant murmur of mitral insufficiency. Intensity of the murmur of aortic
stenosis tends to decrease along with a decreased transvalvular pressure gradient, while the
severity and murmur of mitral regurgitation increase. Other murmurs change as follows:
Increased severity and murmur of aortic regurgitation
Increased left-to-right shunt in ventricular septal defect with an increased intensity of the
murmur
The diastolic murmur of mitral stenosis becomes accentuated because of an increased heart rate
In hypertrophic cardiomyopathy, intensity of the ejection systolic murmur softens due to an
increased left ventricular volume and arterial pressure
The click and the murmur of mitral valve prolapse are delayed because of the increased left
ventricular volume
POSTEXTRASYSTOLIC POTENTIATION If premature beats occur during the clinical
examination, analysis of changes in the intensity and character of the murmur during the
postextrasystolic (postectopic) beat can provide clues to the diagnosis of valvular heart disease.
The postectopic pause is associated with an increased ventricular volume; however, myocardial
contractility also increases due to postextrasystolic potentiation. In most circumstances, the
effect of increased contractility supersedes the effect of an increased ventricular volume,
resulting in the following changes:
Intensity of the ejection systolic murmur increases in aortic stenosis and hypertrophic
cardiomyopathy. Carotid pulse volume increases in the former and decreases or remains
unchanged in the latter. These findings in patients with hypertrophic cardiomyopathy reflect the
Brockenbrough sign (postextrasystolic potentiation resulting in increased left ventricular outflow
gradient and decreased or unchanged pulse pressure). (See "Hemodynamics of valvular disorders
as measured by cardiac catheterization", section on 'Hypertrophic cardiomyopathy'.)
The murmur of aortic regurgitation also may increase due to an increased arterial pressure that
augments the regurgitant flow.
Tricuspid regurgitation murmurs increase due to an increased right ventricular volume
The pansystolic murmur of mitral regurgitation, particularly of rheumatic origin, does not
usually change.
In mitral valve prolapse, postextrasystolic potentiation causes a rapid rate of ejection and,
therefore, an earlier onset of the click and the murmur.
AMYL NITRITE Amyl nitrite (a predominantly arteriolar dilator) was previously used as a
bedside pharmacologic maneuver [2-5], but its use is no longer recommended given the utility of
echocardiography for distinguishing various cardiac lesions.
INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials,
The Basics and Beyond the Basics. The Basics patient education pieces are written in plain
language, at the 5
th
to 6
th
grade reading level, and they answer the four or five key questions a
patient might have about a given condition. These articles are best for patients who want a
general overview and who prefer short, easy-to-read materials. Beyond the Basics patient
education pieces are longer, more sophisticated, and more detailed. These articles are written at
the 10
th
to 12
th
grade reading level and are best for patients who want in-depth information and
are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print
or e-mail these topics to your patients. (You can also locate patient education articles on a variety
of subjects by searching on patient info and the keyword(s) of interest.)
Basics topics (see "Patient information: Heart murmurs (The Basics)" and "Patient information:
Vagal maneuvers and their responses (The Basics)")
SUMMARY
Systemic venous return and pulmonary venous return change reciprocally with inspiration and
expiration. These changes alter certain heart sounds and murmurs, primarily those that originate
from the right side of the heart. (See 'Respiration' above.)
Systemic venous return and systemic arterial pressure change reciprocally with abrupt standing
and squatting. These changes alter certain heart sounds and murmurs such as the click and
murmur of mitral valve prolapse and the ejection systolic murmur in hypertrophic
cardiomyopathy. (See 'Abrupt standing' above and 'Squatting' above.)
The straining phase of the Valsalva maneuver induces a decrease in intensity of the murmur of
aortic stenosis and an increase in the intensity of the systolic ejection murmur of hypertrophic
cardiomyopathy. (See 'Valsalva maneuver' above.)
Hand grip induces an increase in systemic vascular resistance and tends to decrease the
intensity of the murmur of aortic stenosis and increase the intensity of the murmur of mitral
regurgitation. (See 'Hand grip' above.)
RESPIRATION Venous return to the right ventricle increases during normal inspiration
resulting in an increase in its volume. In contrast, inspiration causes a decrease in venous return
to the left ventricle and a reduction in its volume. These changes in venous return can alter the
intensity of murmurs and heart sounds, primarily those that originate from the right side of the
heart. (See "Auscultation of cardiac murmurs" and "Auscultation of heart sounds".)
During inspiration there is an increase in the splitting of S2 as A2 and P2 are separated.
Third (S3) and fourth (S4) heart sounds of right ventricular origin usually diminish with
expiration and increase with inspiration. An S3 and S4 originating from the left side of the heart
may increase with expiration and decrease with inspiration.
In tricuspid stenosis, the opening snap diminishes with expiration and increases with
inspiration. In contrast, the opening snap of mitral stenosis increases with expiration and
decreases with inspiration.
Pulmonary ejection sound of valvular origin decreases in intensity during inspiration.
Inspiration increases the intensity of murmurs originating from the right side of the heart,
including the diastolic murmurs of tricuspid stenosis and pulmonary regurgitation, the systolic
murmur of tricuspid regurgitation (Carvallo's sign), and the presystolic murmur of Ebstein's
anomaly.
In mitral valve prolapse, the inspiratory decrease in venous return to the left side of the heart
reduces left ventricular volume; the murmur and click occur earlier and may diminish.
ABRUPT STANDING Abrupt standing from the supine position decreases venous return to
the heart and, consequently, right and left ventricular diastolic volumes and stroke volumes
decline. There also may be a fall in arterial pressure and a reflex increase in heart rate. These
hemodynamic changes are associated with changes in the following murmurs:
Decrease in the intensity of the murmurs of pulmonary and aortic stenosis
Decrease in the intensity of the murmurs of mitral and tricuspid regurgitation
Earlier onset of the click and prolongation of systolic murmur of mitral valve prolapse
Decrease in the intensity of the systolic murmur in ventricular septal defect without significant
pulmonary hypertension
In hypertrophic cardiomyopathy, a decrease in left ventricular outflow size is associated with
an increase in the intensity of the ejection systolic murmur along with a decrease or unchanged
carotid pulse volume
SQUATTING Squatting from a standing position is associated with a simultaneous increase
in venous return (preload) and systemic vascular resistance (afterload) and a rise in arterial
pressure. This causes changes in the following murmurs:
Increased intensity of the murmur of mitral regurgitation due to the rise in afterload, which
favors the movement of blood in the left ventricle across the insufficient mitral valve rather than
entering the systemic circulation across the aortic valve.
In patients with mitral valve prolapse there is a delay in the onset of the click and a shortening
of the late systolic murmur. These changes reflect the delay in prolapse induced by the increase
in preload. However, as mitral regurgitation becomes more severe, the murmur may increase in
intensity with squatting because of the increase in afterload.
Increase in the magnitude of the left-to-right shunt in ventricular septal defect associated with
an increased intensity of the systolic murmur.
In patients with tetralogy of Fallot, the net effect of squatting is usually an increase in
pulmonary flow, which is associated with increased intensity of the pulmonary ejection systolic
murmur. (See "Pathophysiology, clinical features, and diagnosis of tetralogy of Fallot", section
on 'Cardiac auscultation'.)
Intensity of the diastolic murmur of aortic regurgitation increases due to augmented
regurgitation; intensity of the Austin-Flint murmur also may increase.
In hypertrophic cardiomyopathy, intensity of the ejection systolic murmur promptly declines
because of an increased left ventricular volume and arterial pressure, which increase the effective
orifice size of the outflow tract; the carotid pulse upstroke remains sharp, and the volume may
increase.
Intensity of the murmur of valvular aortic stenosis shows variable changes, depending upon the
type of hemodynamic response; a significant increase in systemic vascular resistance is
associated with a decreased intensity of the murmur, an increased left ventricular volume with
increased intensity of the murmur.
VALSALVA MANEUVER The hemodynamic changes resulting from a Valsalva maneuver
vary with the different phases.
During phase 1, with the onset of the maneuver, there is a transient increase in left ventricular
output.
During the straining phase, phase 2, there is a decrease in venous return, right and left
ventricular volumes, stroke volumes, mean arterial pressure, and pulse pressure; this is
associated with a reflex increase in heart rate.
During phase 3 (release of Valsalva), which only lasts for a few cardiac cycles, there is a
further reduction in left ventricular volume.
Phase 4 is characterized by an increase in stroke volume and arterial pressure and reflex
slowing of heart rate (the overshoot).
Analysis of changes in the intensity and character of the murmur during phase 2 of the Valsalva
maneuver is most useful and practical for the differential diagnosis.
The intensity of flow murmurs, murmurs of aortic and pulmonary stenosis, tricuspid and mitral
regurgitation, aortic and pulmonary regurgitation, and mitral and tricuspid stenosis decreases.
The volume of the carotid pulse also decreases.
The murmur of hypertrophic cardiomyopathy increases in intensity as the left ventricular
outflow size decreases with a decreased venous return. The carotid pulse volume also declines.
In mitral valve prolapse there is an early onset of the click and murmur due to the decrease in
left ventricular volume. The opposite effects are observed during phase 4.
HAND GRIP Sustained hand grip for 20 to 30 seconds leads to an increase in systemic
vascular resistance, arterial pressure, cardiac output, and left ventricular volume and filling
pressure. Hemodynamic changes during hand grip are variable and not always similar in all
patients. As an example, the increase in arterial pressure may be relatively greater than the
increase in heart rate or cardiac output. Thus, changes in intensity of murmurs are not always
predictable.
Hand grip is most useful in differentiating between the ejection systolic murmur of aortic
stenosis and the regurgitant murmur of mitral insufficiency. Intensity of the murmur of aortic
stenosis tends to decrease along with a decreased transvalvular pressure gradient, while the
severity and murmur of mitral regurgitation increase. Other murmurs change as follows:
Increased severity and murmur of aortic regurgitation
Increased left-to-right shunt in ventricular septal defect with an increased intensity of the
murmur
The diastolic murmur of mitral stenosis becomes accentuated because of an increased heart rate
In hypertrophic cardiomyopathy, intensity of the ejection systolic murmur softens due to an
increased left ventricular volume and arterial pressure
The click and the murmur of mitral valve prolapse are delayed because of the increased left
ventricular volume
POSTEXTRASYSTOLIC POTENTIATION If premature beats occur during the clinical
examination, analysis of changes in the intensity and character of the murmur during the
postextrasystolic (postectopic) beat can provide clues to the diagnosis of valvular heart disease.
The postectopic pause is associated with an increased ventricular volume; however, myocardial
contractility also increases due to postextrasystolic potentiation. In most circumstances, the
effect of increased contractility supersedes the effect of an increased ventricular volume,
resulting in the following changes:
Intensity of the ejection systolic murmur increases in aortic stenosis and hypertrophic
cardiomyopathy. Carotid pulse volume increases in the former and decreases or remains
unchanged in the latter. These findings in patients with hypertrophic cardiomyopathy reflect the
Brockenbrough sign (postextrasystolic potentiation resulting in increased left ventricular outflow
gradient and decreased or unchanged pulse pressure). (See "Hemodynamics of valvular disorders
as measured by cardiac catheterization", section on 'Hypertrophic cardiomyopathy'.)
The murmur of aortic regurgitation also may increase due to an increased arterial pressure that
augments the regurgitant flow.
Tricuspid regurgitation murmurs increase due to an increased right ventricular volume
The pansystolic murmur of mitral regurgitation, particularly of rheumatic origin, does not
usually change.
In mitral valve prolapse, postextrasystolic potentiation causes a rapid rate of ejection and,
therefore, an earlier onset of the click and the murmur.
AMYL NITRITE Amyl nitrite (a predominantly arteriolar dilator) was previously used as a
bedside pharmacologic maneuver [2-5], but its use is no longer recommended given the utility of
echocardiography for distinguishing various cardiac lesions.
INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials,
The Basics and Beyond the Basics. The Basics patient education pieces are written in plain
language, at the 5
th
to 6
th
grade reading level, and they answer the four or five key questions a
patient might have about a given condition. These articles are best for patients who want a
general overview and who prefer short, easy-to-read materials. Beyond the Basics patient
education pieces are longer, more sophisticated, and more detailed. These articles are written at
the 10
th
to 12
th
grade reading level and are best for patients who want in-depth information and
are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print
or e-mail these topics to your patients. (You can also locate patient education articles on a variety
of subjects by searching on patient info and the keyword(s) of interest.)
Basics topics (see "Patient information: Heart murmurs (The Basics)" and "Patient information:
Vagal maneuvers and their responses (The Basics)")
SUMMARY
Systemic venous return and pulmonary venous return change reciprocally with inspiration and
expiration. These changes alter certain heart sounds and murmurs, primarily those that originate
from the right side of the heart. (See 'Respiration' above.)
Systemic venous return and systemic arterial pressure change reciprocally with abrupt standing
and squatting. These changes alter certain heart sounds and murmurs such as the click and
murmur of mitral valve prolapse and the ejection systolic murmur in hypertrophic
cardiomyopathy. (See 'Abrupt standing' above and 'Squatting' above.)
The straining phase of the Valsalva maneuver induces a decrease in intensity of the murmur of
aortic stenosis and an increase in the intensity of the systolic ejection murmur of hypertrophic
cardiomyopathy. (See 'Valsalva maneuver' above.)
Hand grip induces an increase in systemic vascular resistance and tends to decrease the
intensity of the murmur of aortic stenosis and increase the intensity of the murmur of mitral
regurgitation. (See 'Hand grip' above.)