Cardiovascular

Physiology
Describe what is happening at each point of the following curve?

The graph above depicts the left ventricular pressure and volume during the cardiac cycle.
Together these graphs can be used to plot the various phases of the cardiac cycle. First, on the
left, is atrial systole. In this phase, blood is forcefully expelled from the atria into the ventricles
causing the slight increase in ventricular pressure and volume seen on the far left of the graph.
Next the mitral valve closes causing a slight depression of the ventricular pressure curve (marked
as point A above). The ventricle then begins to contract. The segment between points A and B
corresponds to isovolumetric contraction. During this time the ventricular pressure increases but
the ventricular volume remains the same because the aortic and mitral valves are closed.
When the ventricular pressure exceeds the diastolic systemic blood pressure the aortic valve
opens (point B). Now the ventricular volume begins to decrease sharply as blood is expelled. The
left ventricular pressure continues to increase between points B and C until the systolic maximum
blood pressure is reached.
When these two values are equal, the aortic valve closes (point C). Isovolumetric relaxation
occurs between points C and D. The ventricle relaxes and both the aortic and mitral valves are
closed. At point D, the mitral valve opens, initiating the phase of diastolic filling.

Which of the following causes the changes depicted by the following
curves?
a) Excessive hydration
b) Acute hemorrhage
c) Chronic anemia
d) Myocardial infarction
e) Anaphylaxis

Which of the following causes the changes depicted by the following
curves?
a) Excessive hydration
b) Acute hemorrhage
c) Chronic anemia
d) Myocardial infarction
e) Anaphylaxis

The graph above combines cardiac and vascular function curves. The
cardiac function curve, labeled as cardiac output (CO) illustrates the Frank-
Starling effect.
The Frank-Starling effect states that as cardiac muscle is increasingly
stretched, the cardiac output increases (up to a limit). This is essentially a
length-tension relationship. This relationship reaches its limit at the flat
portion of the curve.
The vascular function curve, labeled venous return, gives the mean
systemic pressure where it intersects with the x axis and the total
peripheral resistance (TPR) with its slope. Increases in blood volume shift
this graph to the right and increases in the TPR decrease the slope of the
curve (in part due to the increased afterload in the systemic circulation).

The dashed lines depict decreased cardiac output and unchanged
venous return (unchanged blood volume and TPR). An isolated
decrease in cardiac output indicates decreased contractility that is not
the result of decreased preload (because the venous return line is
unchanged). This indicates either the action of a negative inotropic
drug or injury to the myocardium inhibiting contraction, such as a
myocardial infarction.

(Choice A) Excessive hydration or a blood transfusion would increase the
blood volume; shift the venous return graph to the right and change the
cardiac output from point A to point B. Because there is more volume in
the right atrium, the right atrial pressure is also elevated.
(Choice B) Acute hemorrhage would cause a sharp decrease in the
circulating blood volume and would shift the venous return curve to the
left.
(Choice C) Chronic anemia causes an increase in cardiac output in an effort
to meet the metabolic demands of the tissues. This causes an increase in
the slope of the cardiac output graph.
(Choice E) Anaphylaxis causes widespread venous and arteriolar dilatation
along with increased capillary permeability and third-spacing of fluids. This
results in a serious drop in venous return.

Which of the following is most likely to increase as a result of the
change shown by the dashed line?
a) Ventricular Preload
b) End-diastolic pressure
c) Ventricular afterload
d) End-systolic volume
e) Ejection fraction
Which of the following is most likely to increase as a result of the
change shown by the dashed line?
a) Ventricular Preload
b) End-diastolic pressure
c) Ventricular afterload
d) End-systolic volume
e) Ejection fraction
The ventricular pressure-volume loop depicts the relationship between pressure
and volume in the left ventricle during systole and diastole. Left ventricular
contraction ejection, relaxation and refilling are represented as follows:






The dashed loop reflects an increase in cardiac contractility and stroke volume as
evidenced by the increased ejection volume and higher systolic pressure
generated.


Increased ventricular preload would be represented by widening of
the ventricular pressure-volume loop to the right, corresponding to
an increased intra ventricular volume during diastolic filling. End-
diastolic pressure would be increased by an increased preload.

Ventricular afterload is increased when there is increased systemic
blood pressure against which the ventricle must pump. The
ventricular pressure-volume loop would show elevated pressures
during the isovolumetric ventricular contraction phase before the
aortic valve opens.

End-systolic volume would be increased in states of decreased cardiac
contractility: the ventricular pressure-volume loop would be
narrowed by shifting the isovolumetric relaxation line to the right.

If an arteriovenous shunt is created by a particular injury, what would
most likely result in which of the following changes of the left
ventricular pressure-volume loop?

If an arteriovenous shunt is created by a particular injury, what would
most likely result in which of the following changes of the left
ventricular pressure-volume loop? Answer = B










Arteriovenous (AV) shunts result from the formation of AV fistulas. An AV fistula is
an abnormal communication between an artery and a vein that bypasses the
capillary beds, which are the major source of resistance in the vascular system.
Thus AV shunts allow blood under arterial pressure to directly enter the venous
system. AV fistulas can be congenital or acquired (e.g. secondary to penetrating
injuries or iatrogenically created for the purpose of dialysis access). In patients
with an AV fistula, physical exam will reveal a pulsatile mass with a thrill on
palpation.
Auscultation reveals a constant bruit over the site.
Pressure-volume loops represent the relationship between pressure and volume
in the left ventricle during systole and diastole. AV shunts increase cardiac
preload by increasing the rate and volume of blood flow back to the heart. This
increase in the diastolic ventricular volume causes elongation of the diastolic
filling segment (bottom line) on the ventricular pressure-volume loop. Loop B
reflects these changes.

(Choice A) This graph represents an increase in cardiac contractility.
Increased contractility generates higher systolic blood pressures and
causes an increased volume of blood to be ejected from the ventricles
as compared to baseline.
(Choice C) This graph represents increased afterload. Afterload is the
pressure against which the heart must pump to force blood into the
systemic circulation. The loop is taller because elevated pressures are
required in this state, and it is narrower because the ventricle cannot
eject as much volume in the face of an increased afterload. Thus
stroke volume is decreased.
(Choice D) This graph represents decreased preload.

Which of the following pairs of pre-medication (solid curve) and post-
medication (dashed curve) left ventricular pressure/volume
relationships best represents the effects of nitroprusside in this
patient?
Which of the following pairs of pre-medication (solid curve) and post-
medication (dashed curve) left ventricular pressure/volume
relationships best represents the effects of nitroprusside in this
patient? Answer = E
Nitroprusside is a short-acting balanced venous and arterial
vasodilator. As such it decreases left ventricular (LV) preload and
afterload, allowing an adequate cardiac output to be delivered at a
lower LV end diastolic pressure (LVEDP). Of the choices given, only
graph E shows a decrease in both LVEDP (preload) and mean systolic
intraventricular pressure (afterload) without a reduction in stroke
volume.

(Choice A) Here the preload is unchanged. The dashed LV
pressure/volume curve reflects an increase in cardiac contractility.
Nitroprusside decreases preload and afterload but does not directly
alter cardiac contractility.
(Choice B) Here the preload is increased.
(Choice C) Here both the preload and afterload have increased, while
the end systolic volume and stroke volume have decreased.
(Choice D) While this graph appropriately depicts decreased preload,
nitroprusside infusion would also reduce afterload to maintain
adequate cardiac output.

Describe the phases depicted by the following diagram
This pressure-volume loop depicts the relationship between pressure and volume
in the left ventricle during systole and diastole. Left ventricular contraction
ejection, relaxation and refilling are shown as follows:
1. Isovolumetric contraction: This phase of the cardiac cycle begins with the
closure of the mitral valve at point
A. During this period of time the left ventricle is contracting and intraventricular
pressure is increasing, but no blood is leaving the ventricle because both the
aortic and mitral valves are closed. The pressure in the left ventricle continues to
increase until the systemic diastolic blood pressure is reached and the aortic valve
opens at point B.
Ventricular ejection: This phase of the cardiac cycle is represented by the curved
line between points B and Con the graph. This phase begins with the opening of
the aortic valve at point B and represents the period of time where blood is
actively squeezed out of the ventricle and into the systemic circulation.

Isovolumetric relaxation: This phase of the cardiac cycle is represented by the line
between points C and D on the above graph. This phase begins with closure of
the aortic valve at point C. The pressure in the ventricle decreases during this
time, but no blood enters or leaves the ventricle because both the aortic and
mitral valves are closed.
Ventricular filling: This phase is represented by the line between points D and A
on the above graph. This phase begins with the opening of the mitral valve at
point D, and during this time blood fills the ventricles.
The patient described above most likely has mitral stenosis. The opening snap
results from the abrupt halting of motion of the stenotic mitral valve leaflets
during mitral valve opening. Mitral valve opening is represented by point D on the
above graph. The diastolic rumbling murmur is the result of turbulent blood flow
through the stenotic mitral valve during left atrial contraction. Prior rheumatic
carditis is the most common cause of mitral stenosis.

A 43-year-old man is rushed to the emergency room following repeated
episodes of coffee ground-appearing emesis. He has a blood pressure
of 70/40 mmHg, a heart rate of 130/mm, and his extremities are cool
to the touch. Immediate infusion of 2L of normal saline is expected to
increase:
a) Total peripheral resistance
b) Ventricular muscle contraction velocity
c) End-diastolic sarcomere length
d) Heart rate
e) Diastolic ventricular compliance

A 43-year-old man is rushed to the emergency room following repeated
episodes of coffee ground-appearing emesis. He has a blood pressure
of 70/40 mmHg, a heart rate of 130/mm, and his extremities are cool
to the touch. Immediate infusion of 2L of normal saline is expected to
increase:
a) Total peripheral resistance
b) Ventricular muscle contraction velocity
c) End-diastolic sarcomere length
d) Heart rate
e) Diastolic ventricular compliance

This patient is most likely experiencing a brisk upper gastrointestinal bleed.
Coffee ground emesis suggests the presence of blood in the vomitus that has
been exposed to gastric acid. The coffee ground color of the blood is caused by
the oxidation of heme iron.
The patients clinical presentation indicates that he has lost a considerable
amount of blood and is experiencing hypovolemic shock. The human body can
sustain a normal blood pressure and cardiac output with blood losses of up to
10% of the circulating blood volume. After this point the sympathetic nervous
system is activated leading to constriction of the arteriolar and venous beds as
well as stimulation of the heart.
Constriction of the arteriolar beds serves to increase total peripheral resistance
and maintain end organ pressure. It also serves to shunt blood away from the
extremities and skin and toward the vital organs (hence the patients cool
extremities). Constriction of the venous circulation increases blood return to the
heart, thereby assisting in maintaining preload.
Finally, stimulation of the heart results in increased contractility and heart
rate. Despite these actions of the sympathetic system, progressive bleeding
will lead to a drop in blood pressure.
In the treatment of hypovolemic shock the most important intervention
other than identifying and eliminating the source of bleeding is rapid
infusion of blood products and crystalloid solutions like normal saline. In a
patient with hypovolemic shock the intravascular volume is low and the
sympathetic system is maximally stimulated thus administration of
vasopressors is of little benefit beyond a small temporary effect in some
cases.
By infusing intravenous fluids one can immediately increase the
intravascular volume and ventricular preload. The preload increase extends
the end diastolic sarcomere length in the ventricular myocardium
increasing stroke volume and cardiac output.

(Choices A and B) In a patient with hypovolemic shock total peripheral
resistance and contraction velocity are high due to sympathetic activation.
Administration of fluids will reduce sympathetic activation and decrease
both of these parameters.
(Choice D) Fluid resuscitation of the hypovolemic patient will cause the
heart rate to decrease.
(Choice E) The diastolic ventricular compliance is unaffected by crystalloid
infusions. Compliance is affected by pathologic processes acting on the
heart itself such as amyloid cardiomyopathy and hypertrophic
cardiomyopathy two processes that decrease compliance. Dilated
cardiomyopathies increase ventricular compliance.


Murmurs
A 38 year old female is being evaluated for progressive exertional dyspnea.
The cardiac catheterization data are obtained. Left ventricular end-diastolic
pressure 10 mmHg (normal 3 -12 mmHg). Left ventricular peak systolic
pressure 110 mmHg (normal 100 -140 mmHg), Pulmonary capillary wedge
pressure 36 mmHg (normal <12mmHg). Which of the following is the most
likely cause of this patients symptoms?
a) Mitral stenosis
b) Aortic stenosis
c) Dilated cardiomyopathy
d) Restrictive cardiomyopathy
e) Cardiac tamponade

A 38 year old female is being evaluated for progressive exertional dyspnea.
The cardiac catheterization data are obtained. Left ventricular end-diastolic
pressure 10 mmHg (normal 3 -12 mmHg). Left ventricular peak systolic
pressure 110 mmHg (normal 100 -140 mmHg), Pulmonary capillary wedge
pressure 36 mmHg (normal <12mmHg). Which of the following is the most
likely cause of this patients symptoms?
a) Mitral stenosis
b) Aortic stenosis
c) Dilated cardiomyopathy
d) Restrictive cardiomyopathy
e) Cardiac tamponade

The pulmonary capillary wedge pressure (PCWP) is the pressure in a
pulmonary artery distal to the point of its occlusion by an inflated
intravascular balloon.
Because there is no significant blood flow towards the left atrium (LA)
beyond this point of occlusion, the pressure at the tip of the wedged
pulmonary artery catheter becomes nearly equal to the LA pressure.
During normal diastole, the LA pressure is nearly equal to the left
ventricular (LV) pressure since the open mitral valve offers minimal
resistance to flow between the two chambers. In this patient, cardiac
catheterization reveals a LA end-diastolic pressure (LAEDP) that is
significantly greater than the LVEDP. This abnormal pressure gradient
implies increased resistance flow between the LA and LV, i.e. mitral
stenosis.
(Choice B) Isolated aortic stenosis would cause elevation of the left
ventricular peak systolic pressure. It could also elevate both the PCVVP and
the LVEDPI but these two values would remain approximately equal.
(Choice C) Dilated cardiomyopathy would reduce the left ventricular peak
systolic pressure and elevate the PCWP and LVEDP. The PCWP and LVEDP
would remain approximately equal.
(Choice D) Restrictive cardiomyopathy causes diastolic dysfunction and
similar elevations of the PCVVP and LVEDP. The PCWP and LVEDP would
remain approximately equal.
(Choice E) In the absence of mitral stenosis, tamponade would elevate the
PCWP and LVEDP to the same degree, keeping them equal.


A 53-year-old male presents to your office with difficulty breathing and
increasing fatigue. He has been sleeping in a recliner chair to relieve his
shortness of breath. His past medical history is significant for a myocardial
infarction two months ago. On cardiac auscultation, a diastolic sound is
heard when the patient lies in the left lateral decubitus position. Which of
the following is most likely to accentuate this physical examination finding?
a) Valsalva maneuver
b) Expiration
c) Standing
d) Furosemide injection
e) Amyl nitrite inhalation

A 53-year-old male presents to your office with difficulty breathing and
increasing fatigue. He has been sleeping in a recliner chair to relieve his
shortness of breath. His past medical history is significant for a myocardial
infarction two months ago. On cardiac auscultation, a diastolic sound is
heard when the patient lies in the left lateral decubitus position. Which of
the following is most likely to accentuate this physical examination finding?
a) Valsalva maneuver
b) Expiration
c) Standing
d) Furosemide injection
e) Amyl nitrite inhalation

This patient presents with signs and symptoms of heart failure. Heart failure can result
from a variety of pathogenic processes. Repeated bouts of myocardial ischemia are the
most common cause.
In heart failure resulting from systolic dysfunction the ejection fraction is decreased and
the heart is left with a considerable end-systolic volume within the ventricles. An 53, or
ventricular gallop heart sound is commonly heard in patients with left ventricular failure
(this can be a normal variant in healthy children and adolescents). The 33 heart sound is
a low frequency sound that occurs immediately following 32 during the phase of rapid
passive ventricular filling. It results from blood rushing into a partially filled ventricle or
into a very stiff ventricle in patients with restrictive cardiomyopathy.
The 33 is best appreciated with the bell of the stethoscope pressed lightly against the
skin in the region of the ventricular apex. (The bell is well-suited to detect low frequency
sounds while the diaphragm is best for hearing high-pitched sounds like S1 and S2.)
Having the patient lie in the left lateral decubitus position makes it easier to hear 53.
Having the patient exhale completely while in this position can make the sound even
more audible by decreasing the volume of the lungs and bringing the heart closer to the
chest wall.

(Choices A and C) The Valsalva maneuver (bearing down against a closed glottis)
and the standing position can be used to differentiate between the various
causes of a systolic murmur in the left heart. Both maneuvers decrease venous
return to the heart thereby reducing left ventricular volume and blood pressure.
The murmurs associated with mitral valve prolapse and hypertrophic
cardiomyopathy become more audible and those associated with aortic stenosis
become less audible. Squatting and Valsalva release (maneuvers that increase
venous return) have the opposite effect.
(Choice D) Furosemide injection causes brisk diuresis. The volume reduction
would likely lessen the intensity of the 33 sound.
(Choice E) Amyl nitrite inhalation causes vasodilatation and decreased blood
pressure. It would have the same effect as the Valsalva maneuver on the
murmurs of mitral prolapse hypertrophic cardiomyopathy and aortic stenosis.

A 46 year old patient is referred to the cardiology department after a
primary care physician hears a murmur on cardiac auscultation. Physical
examination reveals bounding femoral pulses and carotid pulsations that are
accompanied by head-bobbing. This patient most likely suffers from:
a) Mitral stenosis
b) Aortic stenosis
c) Tricuspid Regurgitation
d) Mitral Regurgitation
e) Aortic Regurgitation
f) Pulmonary Stenosis
A 46 year old patient is referred to the cardiology department after a
primary care physician hears a murmur on cardiac auscultation. Physical
examination reveals bounding femoral pulses and carotid pulsations that are
accompanied by head-bobbing. This patient most likely suffers from:
a) Mitral stenosis
b) Aortic stenosis
c) Tricuspid Regurgitation
d) Mitral Regurgitation
e) Aortic Regurgitation
f) Pulmonary Stenosis
This patients physical exam findings are classic for aortic
regurgitation (AR). In patients with AR, there is a large left ventricular
stroke volume (LVSV) a large regurgitant SV, and a large pulse
pressure. The left ventricular end diastolic volume is also increased
due to the incompetent aortic valve. Bounding femoral and carotid
pulses marked by abrupt distention and quick collapse (water-
hammer pulses) are the result of the large pulse pressure. Some
patients exhibit head-bobbing with carotid pulsations (de Musset
sign) due to transfer of momentum from the large left ventricular
stroke volume (LVSV) to the head and neck.

(Choice A) In isolated mitral stenosis (MS), left ventricular diastolic
pressures are usually near-normal. though pressures proximal to the
stenotic mitral valve are typically elevated. Since the left ventricular end-
diastolic volume is not elevated, stroke volume and pulse pressures are
usually near-normal.
(Choice B) Aortic stenosis causes delayed, prolonged carotid pulses (pulsus
parvus et tardus). Systolic vibrations or a carotid shudder (thrill) may also
be present. (Choices C and F) Neither tricuspid regurgitation nor
pulmonary stenosis causes the pattern of physical findings described
above.
(Choice D) Mitral regurgitation increases the LVSV but does not increase
the volume of blood ejected into the aorta. This patients physical
examination findings are the result of an abnormally large volume of blood
being ejected into the aorta.

A thrombus originating in the deep veins of the lower extremities is
most likely to cause a stroke in a patient with which of the following
physical findings?
a) Splitting of S1 that is accentuated on inspiration
b) Ejection-type systolic murmur that increases on standing
c) Diastolic decrescendo-type murmur that decreases following amyl
nitrite inhalation
d) Presystolic murmur that disappears with atrial fibrillation
e) Splitting of S2 that does not change with respiration
A thrombus originating in the deep veins of the lower extremities is
most likely to cause a stroke in a patient with which of the following
physical findings?
a) Splitting of S1 that is accentuated on inspiration
b) Ejection-type systolic murmur that increases on standing
c) Diastolic decrescendo-type murmur that decreases following amyl
nitrite inhalation
d) Presystolic murmur that disappears with atrial fibrillation
e) Splitting of S2 that does not change with respiration
A patent connection between the right and left atria is a defect that would make a
paradoxical embolism possible. Paradoxical emboli originate in the venous system, but
cross over into the arterial circulation (bypassing the lungs) via an abnormal connection
between the right and left heart. Wide splitting of S2 that does not vary with respiration
can result from an atrial septal defect (ASD) a defect that would permit a paradoxical
embolism.
(Choice A) Assuming the patient had no S4 gallops or aortic ejection click, a split S1
accentuated on inspiration would indicate delayed closure of the tricuspid valve. This
could be caused by a right bundle branch block and need not indicate any abnormal
connection between the right and left cardiac chambers.
(Choice B) A systolic ejection murmur (SEM) generally refers to a mid-systolic crescendo-
decrescendo murmur, most commonly the result of aortic stenosis. Hypertrophic
obstructive cardiomyopathy may also cause SEM. When in the upright position, venous
return to the heart is decreased and the left ventricular enddiastolic volume and stroke
volume are reduced, increasing the SEM of hypertrophic obstructive cardiomyopathy.
Neither of these lesions by themselves would permit a paradoxical embolus.
(Choice C) An early diastolic decrescendo murmur is characteristic of aortic
regurgitation (AR). Inhaled amyl nitrite produces marked vasodilatation,
resulting in reduction of systemic arterial pressure and decreasing this
regurgitant murmur. Isolated AR does not result in an abnormal right-to-
left heart connection that would permit paradoxical embolism.
(Choice D) Presystolic accentuation occurs when the intensity of a
diastolic murmur becomes louder just prior to S1 or when a diastolic
murmur appears just prior to S1. A presystolic (late diastolic) murmur can
result from mitral or tricuspid valve stenosis and/or physiologically
increased blood flow across these valves. Presystolic accentuation occurs
due to atrial contraction. Atrial fibrillation could eliminate an
atrioventricular valve stenotic murmur by removing the atrial contraction
during late diastole. However, tricuspid and/or mitral stenosis alone would
not permit a paradoxical embolus.


A 73-year-old Caucasian male presents to your office following repeated
episodes of exertional dyspnea. Physical examination reveals a cardiac
murmur. The patient is referred to cardiologist or further evaluation. Cardiac
catheterization is performed and the findings are shown on the slide below.
Which of the time points indicated on the slide best corresponds to the peak
of the murmur intensity in this patient?
a) A
b) B
c) C
d) D
e) E
f) F


A 73-year-old Caucasian male presents to your office following repeated
episodes of exertional dyspnea. Physical examination reveals a cardiac
murmur. The patient is referred to cardiologist or further evaluation. Cardiac
catheterization is performed and the findings are shown on the slide below.
Which of the time points indicated on the slide best corresponds to the peak
of the murmur intensity in this patient?
a) A
b) B
c) C
d) D
e) E
f) F


The hemodynamic profile shows an abnormal pressure gradient
between the left ventricle (LV) and the aorta (Ac) during systole (see
arrows in graph below), indicating significant aortic stenosis (AS).

The intensity of the murmur of AS is directly related to the magnitude
of the LV-toaorta pressure gradient. Thus the murmur in this patient
would be loudest at point B and less intense at point A.
(Choices A and C) The murmur of AS is a systolic ejection-type
crescendodecrescendo murmur that starts after the first heart sound,
following the opening of the aortic valve (time A). It typically ends
before the A2 component of the second heart sound (time C). At
times A and C, the left ventricular and aortic pressures are nearly
equal so that a murmur due to flow across the aortic valve would be
unlikely at these points.
(Choices D and E) These points occur during diastole, when the aortic
valve is closed and the mitral valve is open. There is no abnormally
elevated pressure gradient between the left atrium and left ventricle,
consistent with normal unobstructed diastolic filling of the left
ventricle. Since turbulent flow due to a high pressure gradient is
generally required to produce a murmur the patient would not have a
murmur at times D or E.
(Choice F) This time point corresponds to atrial contraction just prior
to ventricular systole. There is no abnormally elevated pressure
gradient between the left atrium and left ventricle consistent with
normal unobstructed filling of the left ventricle.


A 52-year-old Caucasian male presents to your office for a routine
checkup. He says that some cardiac problems were detected during his
previous visit to the doctor. Physical examination reveals a holosystolic
murmur at the apex that radiates to the axilla. Which of the following is
the best indicator of the severity of this patients problem?
a) Holosystolic murmur intensity
b) Presystolic component of the murmur
c) S2 to opening snap (OS) time interval
d) Presence of audible S3
e) Presence of audible S4

A 52-year-old Caucasian male presents to your office for a routine
checkup. He says that some cardiac problems were detected during his
previous visit to the doctor. Physical examination reveals a holosystolic
murmur at the apex that radiates to the axilla. Which of the following is
the best indicator of the severity of this patients problem?
a) Holosystolic murmur intensity
b) Presystolic component of the murmur
c) S2 to opening snap (OS) time interval
d) Presence of audible S3
e) Presence of audible S4

Under most modern clinical circumstances, the anatomy and severity of mitral
regurgitation (MR) are best delineated by2D and Doppler echocardiography. Among
auscultator findings, the best indicator of a high regurgitant volume indicating severe MR
with left ventricular volume overload is the presence of a left ventricular S3 gallop. A left
ventricular (LV) S3 gallop reflects an increased rate of filling of the LV during mid diastole.
It can be heard as a consequence of MR and in this condition reflects the relatively high
volume of regurgitant flow which is recycled back into the LV during diastole.
(Choice A) If the volume of left ventricular blood pumped backed into the left atrium
during systole, or regurgitant volume, is used as a measure of severity of mitral
regurgitation (MR), then one might expect the murmur of MR to become louder as
regurgitant volume increased. However, this would only apply to an anatomically fixed
effective regurgitant orifice (ERO). In the clinical setting, patients with higher regurgitant
volumes may also have larger EROs, such that systolic transvalvular flow resistance and
the degree of turbulence in the regurgitant jet (which accounts for the intensity of the
murmur of MR) may not be strongly correlated with regurgitant volume.

(Choice B) The murmur of mitral regurgitation is either holosystolic or, in some
cases of mitral valve prolapse, midsystolic. In some cases of severe MR, a diastolic
rumble produced by a high rate of flow across a normal sized diastolic mitral
orifice may be heard. The latter amounts to a functional murmur (relative mitral
stenosis) but is a less reliable finding with a high regurgitant volume than is the
presence of an S3. (Choice C) The S2 to opening snap interval is a diastolic
interval between the second heart sound (specifically A2) and the tensing of a
stenotic mitral valve. It is a parameter of mitral stenosis, not mitral regurgitation.
(Choice E) In a patient with mitral regurgitation, a left ventricular S4 gallop would
most likely be a sign of left heart failure, indicating LV dilatation and the reaching
of the limit of LV compliance during end diastole. However, many patients with
severe MR have not yet developed left sided heart failure. In the latter group of
patients, a left sided S3 would be a more likely finding on cardiac auscultation
than a left sided S4.

A 32-year-old Asian female presents to your office complaining of easy
fatigability and exertional dyspnea. Cardiac auscultation reveals an extra
diastolic sound and a diastolic murmur at the apex. You suspect mitral
stenosis. Cardiac catheterization findings are given on the slide below. Which
of the following corresponds to the opening snap (OS) timing in this patient?
a) A
b) B
c) C
d) D
e) E

A 32-year-old Asian female presents to your office complaining of easy
fatigability and exertional dyspnea. Cardiac auscultation reveals an extra
diastolic sound and a diastolic murmur at the apex. You suspect mitral
stenosis. Cardiac catheterization findings are given on the slide below. Which
of the following corresponds to the opening snap (OS) timing in this patient?
a) A
b) B
c) C
d) D
e) E

The opening snap (OS) in patents with mitral stenosis is an early diastolic
sound due to tensing of the abnormal mitral valve (MV) leaflets after the
valve cusps have completed their opening excursion. This occurs shortly
after the mitral valve opens, when left ventricular pressure drops below
left atrial pressure.
From the graph above, it can be seen that the higher the early diastolic left
atrial pressure the closer the opening snap will tend to be to point B, which
corresponds to the A2 component of the heart sound.
The A2-OS interval is inversely correlated with the severity of mitral
stenosis. The more severe the stenosis, the higher the steady state left
atrial pressure in early diastole and the shorter the A2-OS interval
(Choice A) This point corresponds to the opening of the aortic valve at the end of
isovolumetric ventricular contraction in early systole, when the left ventricular pressure
exceeds the aortic pressure.
(Choice B) Point B corresponds to the closure of the aortic valve at the end of systole,
producing the A2 component of the second heart sound. The aortic valve closes as soon
as left ventricular pressure drops below the aortic pressure.
(Choice D) This is a random point in diastole, when the mitral valve is already maximally
open and ventricular filling is progressing. Note that there is a significant gradient of
pressure between the left atrium and left ventricle during diastole, consistent with mitral
stenosis. Under normal conditions, diastolic left atrial and left ventricular pressures are
nearly equal.
(Choice E) Point E roughly corresponds to the onset of atrial contraction during late
ventricular diastole. The mitral valve is still maximally open. Note the increase in the
gradient of pressure between the left atrium and left ventricle produced by atrial
contraction. This can cause presystolic accentuation of the diastolic murmur of mitral
stenosis.

A 12-year-old Caucasian male is found to have a wide, fixed splitting of the
second heart sound (S2) on routine physical examination. He denies any
symptoms. If present, the congenital heart disease in this patient may
require surgical repair to prevent irreversible changes in the:
a) Right ventricle
b) Right atrium
c) Left ventricle
d) Left atrium
e) Pulmonary vessels
f) Coronary vessels

A 12-year-old Caucasian male is found to have a wide, fixed splitting of the
second heart sound (S2) on routine physical examination. He denies any
symptoms. If present, the congenital heart disease in this patient may
require surgical repair to prevent irreversible changes in the:
a) Right ventricle
b) Right atrium
c) Left ventricle
d) Left atrium
e) Pulmonary vessels
f) Coronary vessels

Wide fixed splitting of S2 that does not vary with respiration is a characteristic
auscultatory finding of an atrial septal defect (ASD). ASD creates a left-to-right
shunt because of the high pressure in the left atrium. The result is increased
blood flow through the pulmonary artery.
The muscular pulmonary arteries may develop laminated medial hypertrophy
that can become so severe overtime as to increase the pulmonary vascular
resistance above the total systemic vascular resistance. At this point the original
left-to-right intracardiac shunt reverses, and flow becomes right-to- left.
This switch to right-to-left shunting manifests as late-onset cyanosis, with
clubbing and polycythemia. Eisenmenger syndrome is the name for reversal of
shunt flow through a congenital cardiac defect that occurs as a result of chronic
pulmonary hypertension. Overtime the pulmonary vascular sclerosis becomes
irreversible and closure of the cardiac septal defect can no longer be
hemodynamically tolerated by the right ventricle.

(Choices A and B) Pulmonary hypertension produced by an ASD could
result in right ventricular hypertrophy and right atrial enlargement.
However, these changes are not necessarily irreversible. If the
pulmonary hypertension is corrected, the right heart can revert to a
more normal morphology.
(Choices C and D) Left ventricular failure is uncommon in patients
with ASD. Left atrial enlargement can be present due to volume
overload but the main changes are in the right side of the heart.

A 72-year-old Caucasian male has a presystolic sound on cardiac auscultation
that immediately precedes the first heart sound and is best heard when the
patient turns to his left side and holds his breath. The patients blood
pressure is 150/90 mmHg and his heart rate is 74 beats per minute and
regular. He has a long history of hypertension and evidence of extensive
calcinosis around the mitral and aortic valves on chest x-ray. The extra sound
is most likely due to:
a) Increased flow velocity through the aortic valve
b) Restricted motion of the aortic valve cusps
c) Restricted motion of the mitral valve cusps
d) Papillary muscle tension after the rapid filling of the ventricles
e) Increased stiffness of the left ventricular wall

A 72-year-old Caucasian male has a presystolic sound on cardiac auscultation
that immediately precedes the first heart sound and is best heard when the
patient turns to his left side and holds his breath. The patients blood
pressure is 150/90 mmHg and his heart rate is 74 beats per minute and
regular. He has a long history of hypertension and evidence of extensive
calcinosis around the mitral and aortic valves on chest x-ray. The extra sound
is most likely due to:
a) Increased flow velocity through the aortic valve
b) Restricted motion of the aortic valve cusps
c) Restricted motion of the mitral valve cusps
d) Papillary muscle tension after the rapid filling of the ventricles
e) Increased stiffness of the left ventricular wall

An S4 gallop (also known as an atrial sound or atrial gallop) is a presystolic sound on
cardiac auscultation that immediately precedes S1. A left-sided S4 is heard best at the
cardiac apex with the patient in the left lateral decubitus position, and a rightsided S4 is
heard best along the lower left sternal border (the tricuspid area) with the patient in the
supine position.
An S4 is heard when there is a sudden rise in end diastolic ventricular pressure caused by
atrial contraction against a ventricle that has reached the limit of its compliance. Thus, an
S4 may be present in any condition that causes a stiff ventricle. Degenerative mitral
annular calcification or aortic valve calcification can be associated with chronically
elevated LV pressures and systemic hypertension. This patient probably has left
ventricular hypertrophy (LVH) associated with hypertensive heart disease. LVH reduces
ventricular compliance and can cause diastolic dysfunction.
A normal atrial contraction is required to generate an S4. (Choice A) This would tend to
produce the murmur of aortic stenosis, an ejectiontype murmur that occurs during
systole (after S1 and before A2).
(Choice B) Restricted motion of the aortic valve cusps might be associated with an
aortic ejection click, aortic stenosis, and/or aortic regurgitation. In any event, the
extra sound(s) produced would occur after S1, during systole.
(Choice C) Restricted motion of the mitral valve cusps could result in abnormal
diastolic sounds, like an opening snap and/or a murmur of mitral stenosis (MS).
The opening snap would occur early in diastole. Pre-systolic accentuation (due to
atrial contraction) of an otherwise inaudible murmur of MS could explain the
extra sound heard in this patient. However, isolated MS is generally associated
with normal or reduced left ventricular pressures making degenerative mitral
annular calcification as seen in this patient less likely.
(Choice D)The papillary muscles are not placed under increased tension during
diastolic ventricular filling. They are tensed during ventricular systole, after S1.


A 33-year-old Hispanic female who recently emigrated from Mexico is brought to
the ER with severe shortness of breath and hemoptysis. She is treated with
diuretics, and begins to feel better. However, she develops rightsided hemiparesis
soon after. Based on the history and initial physical examination, you suspect mitral
stenosis is responsible. Which of the following findings suggests an associated
lesion or another diagnosis in this patient?
a) Right ventricular dilation
b) Increased systolic pulmonary artery pressure
c) Increased pulmonary capillary wedge pressure
d) Tricuspid regurgitation
e) Increased diastolic left ventricular pressure
f) Reduced pulmonary compliance
A 33-year-old Hispanic female who recently emigrated from Mexico is brought to
the ER with severe shortness of breath and hemoptysis. She is treated with
diuretics, and begins to feel better. However, she develops rightsided hemiparesis
soon after. Based on the history and initial physical examination, you suspect mitral
stenosis is responsible. Which of the following findings suggests an associated
lesion or another diagnosis in this patient?
a) Right ventricular dilation
b) Increased systolic pulmonary artery pressure
c) Increased pulmonary capillary wedge pressure
d) Tricuspid regurgitation
e) Increased diastolic left ventricular pressure
f) Reduced pulmonary compliance
In isolated mitral stenosis (MS) diastolic pressures in the left ventricle (LV) are usually
near normal. Only pressures proximal to the stenotic mitral valve would be markedly
elevated.
When a patient with suspected MS is also found to have an increased LV end diastolic
pressure, the presence of an additional lesion is likely. Possibilities include rheumatic
involvement of the aortic valve (which typically causes combined aortic stenosis and
regurgitation), or infective endocarditis superimposed on an aortic valve deformed by
chronic rheumatic heart disease (RHD).
In patients with RHDI the mitral valve alone is the sole site of involvement in 65% to 70%
of cases. Both the mitral and aortic valves are affected in about 25% of cases. This
patients right-sided hemiparesis may have arisen from an embolic stroke complicating
isolated MS (via atrial dilatation, atrial mural thrombosis and thromboembolism) or from
an aortic valve vegetation generated by endocarditis. (Choice A) Right ventricular
dilatation is found in mitral stenosis that is severe enough to cause significant pulmonary
hypertension.
(Choice B) This finding would be expected in isolated mitral stenosis severe enough to cause
significant pulmonary hypertension via backward transmission of elevated left atrial pressure.
(Choice C) This finding would be expected in isolated mitral stenosis (MS) severe enough to cause
a significant elevation of left atrial pressure. A properly measured pulmonary capillary wedge
pressure reflects the left atrial transmural pressure at end diastole, which is elevated in MS, even
though left ventricular end diastolic transmural pressure (LVEDP) may be normal. Note that the
wedge pressure does not reflect LVEDP in patients with MS.
(Choice D) Tricuspid regurgitation may occur as a complication of severe isolated mitral stenosis,
as a consequence of right ventricular dilatation due to pulmonary hypertension.
(Choice F) Reduced pulmonary vascular compliance may complicate long-standing pulmonary
hypertension induced by isolated mitral stenosis. Pulmonary vascular endothelial dysfunction and
reactive vasoconstriction can result from pulmonary hypertension. Chronic pulmonary
hypertension can also cause reactive hypertrophy in the walls of pulmonary vessels (pulmonary
vascular sclerosis). Both of these processes reduce pulmonary vascular compliance.

A 46-year-old Caucasian female presents to your office because of easy
fatigability and exertional dyspnea. Auscultation of the heart reveals a
diminished first heart sound and an apical holosystolic murmur radiating to
the axilla. Lungs have bibasilar crackles. There is no elevation of jugular
venous pressure or peripheral edema. Which of the following would most
likely increase forward-toregurgitant volume ratio in this patient?
a) Decreasing left ventricular preload
b) Increasing left ventricular contractility
c) Decreasing left ventricular afterload
d) Decreasing heart rate
e) Increasing left ventricular volume

A 46-year-old Caucasian female presents to your office because of easy
fatigability and exertional dyspnea. Auscultation of the heart reveals a
diminished first heart sound and an apical holosystolic murmur radiating to
the axilla. Lungs have bibasilar crackles. There is no elevation of jugular
venous pressure or peripheral edema. Which of the following would most
likely increase forward-to-regurgitant volume ratio in this patient?
a) Decreasing left ventricular preload
b) Increasing left ventricular contractility
c) Decreasing left ventricular afterload
d) Decreasing heart rate
e) Increasing left ventricular volume

This patient has clinical features suggestive of mitral regurgitation with left sided heart failure. In
a patient with mitral regurgitation, some of the blood in the left ventricle is pumped forward
through the aortic valve and is considered the forward stroke volume (FSV) while some is forced
backwards through the incompetent mitral valve into the left atrium and is considered the
regurgitant stroke volume (RSV).
If the systolic retrograde flow resistance between the LV and LA, the preload (LV end diastolic
volume) and the contractility remain the same, the amount of blood that flows forward and
backward is determined by the left ventricular afterload (or systolic intraventricular pressure).
The lower the average LV afterload, the lower will be the average systolic pressure gradient
driving regurgitant flow into the LA and the lower will be the RSV. Moreover, FSV will be
increased. This will increase the forward-to-regurgitant volume ratio. Thus arterial vasodilator
therapy, which acts to decrease LV afterload, tends to decrease RSV and increase FSV in patients
with MR.
(Choice A) LV preload reduction might decrease the regurgitant flow fraction if the degree of
mitral valve incompetence was LV end diastolic volume dependent (eg. in dilated
cardiomyopathy) or if the reduction in LV preload was also accompanied by a slight decrease in LV
afterload. However these effects on the regurgitant flow fraction would generally be
quantitatively less than that of a significant reduction of afterload.

(Choice B) For a fixed anatomical degree of mitral valve incompetence producing mitral
regurgitation (MR) and at a given left ventricular preload, an increase in LV contractility
would tend to increase LV afterload. The latter would tend to increase the fraction of
each LV stroke volume going into regurgitant flow. Thus an isolated increase in LV
contractility would tend to increase MR. Partly for this reason some experts recommend
chronic beta blocker therapy for patients with significant MR.
(Choice D) A primary decrease in heart rate (HR) would tend to increase LV end diastolic
volume (preload). In the new steady state after recruitment of cardiovascular reflexes to
maintain forward LV output and mean systemic arterial pressure LV afterload might not
be significantly changed. Moreover in some cases of MR where LV dilatation alone
maybe responsible the fraction of regurgitant flow can increase as the LV dilates further
(as preload is increased). Under these conditions a primary decrease in heart rate could
decrease the forward to regurgitant LV output ratio.
(Choice E) Presumably this choice means increasing LV end diastolic volume or preload.
As explained above increasing LV preload does not significantly alter steady state LV
afterload, the major determinant of the degree of mitral regurgitation. Moreover LV
dilatation alone can contribute to or worsen MR.

A 63-year-old Caucasian male presents to the emergency department with severe
dyspnea, orthopnea and fatigue. He suffered a myocardial infarction six months
ago, and has not been compliant with his medications since that time. On exam, his
blood pressure is 170/100 mmHg and his heart rate is 100 beats per minute.
Auscultation reveals crackles at the lung bases, an S3 gallop, and a Il/VI holosystolic
murmur over the apex. After initial treatment with diuretics and vasodilators the
patients condition improves significantly. The next morning, there are no
appreciable gallops or murmurs on cardiac exam. The murmur heard at
presentation is likely explained by:
a) Thickened and deformed mitral valve cusps
b) Heavily calcified mitral annulus
c) Increased flow rate through the aortic valve
d) Ruptured chorda tendineae
e) Functional mitral regurgitation

A 63-year-old Caucasian male presents to the emergency department with severe
dyspnea, orthopnea and fatigue. He suffered a myocardial infarction six months
ago, and has not been compliant with his medications since that time. On exam, his
blood pressure is 170/100 mmHg and his heart rate is 100 beats per minute.
Auscultation reveals crackles at the lung bases, an S3 gallop, and a Il/VI holosystolic
murmur over the apex. After initial treatment with diuretics and vasodilators the
patients condition improves significantly. The next morning, there are no
appreciable gallops or murmurs on cardiac exam. The murmur heard at
presentation is likely explained by:
a) Thickened and deformed mitral valve cusps
b) Heavily calcified mitral annulus
c) Increased flow rate through the aortic valve
d) Ruptured chorda tendineae
e) Functional mitral regurgitation

This patients symptoms of dyspnea and orthopnea together with bibasilar
crackles are consistent with high pulmonary venous pressure and
pulmonary edema in the dependent lung. The holosystolic murmur heard
over the cardiac apex is suggestive of mitral regurgitation (MR). An 33
gallop reflects an increased left ventricular filling rate during mid diastole,
and can be heard as a consequence of MR.
Treatment with a diuretic tends to reduce left ventricular (LV) preload and
therefore decreases the LV end diastolic volume (EDV). Since the patients
murmur and gallop disappeared following the reduction of LVEDVI his MR
was most likely functional that is, due to transient hemodynamic factors
causing LV dilatation and/or papillary muscle ischemia rather than due to a
fixed mitral valve lesion.
Acute LV dilatation can sufficiently separate otherwise normal mitral
valve leaflets to permit functional regurgitation. The most common
anatomical abnormality producing mitral regurgitation is myxomatous
degeneration (mitral valve prolapse). Afterload reduction with a
vasodilator decreases the average intraventricular systolic pressure
required to generate a given stroke volume and would tend to reduce
MR due to any cause.
(Choice A) Thickened and deformed mitral valve cusps are fixed
anatomical lesions that typically result from chronic rheumatic heart
disease. For this reason, these lesions are usually only found in older
individuals (who may not have had access to antibiotics while young).
Mitral stenosis is the usual result.

(Choice C) Mitral annular calcification, consisting of degenerative calcific
deposits in the fibrous ring of the mitral valve, generally does not impair
valvular function. There is associated regurgitation or stenosis only in rare
instances. Mitral annular calcification is most common in women older
than 60, individuals with a history of myxomatous degeneration of the
mitral valve, and individuals with chronically elevated left ventricular (LV)
pressures. Furthermore, whereas the patient in the vignette had mitral
regurgitation that was eliminated by a reduction in LV size (which also
decreases the mitral valve radius), the radius is fixed in patients with a
calcified mitral valve annulus.
(Choice D) An increased rate of flow through the aortic valve could produce
a functional murmur of aortic stenosis, which would be a systolic ejection
type murmur heard best over the aortic area (right upper sternal border).


(Choice E) Chordae tendineae rupture producing severe mitral
regurgitation (MR) is a complication of bacterial endocarditis, and less
frequently of connective tissue diseases or acute myocardial infarction.
When papillary muscle or chordae rupture occurs in association with
myocardial infarction, it is usually an early complication of the Ml (i.e.
occurring within 10 days).
The MR of the patient in the vignette appears to have been precipitated by
medication non-compliance which caused an acute hemodynamic change.
Thus endocarditis and connective tissue disease are more remote
possibilities. Additionally, the murmur of MR due to chordae rupture may
not be completely eliminated by pharmacological manipulations. Chordae
rupture results in fixed anatomic (versus reversible functional) MR.

A 34-year-old immigrant from South Asia presents to your office complaining
of heart palpitations that are particularly prominent at night. He also notes
that with moderate exertion, he experiences head pounding accompanied
by involuntary head bobbing. He remembers being diagnosed with a heart
murmur years before, but he cannot recall the type and has never received
any treatment. Based on this patients history, you suspect:
a) Restricted left ventricular filling
b) Impaired left ventricular contractility
c) Left ventricular outflow obstruction
d) Systolic-diastolic hypertension
e) Widening of the pulse pressure

A 34-year-old immigrant from South Asia presents to your office complaining
of heart palpitations that are particularly prominent at night. He also notes
that with moderate exertion, he experiences head pounding accompanied
by involuntary head bobbing. He remembers being diagnosed with a heart
murmur years before, but he cannot recall the type and has never received
any treatment. Based on this patients history, you suspect:
a) Restricted left ventricular filling
b) Impaired left ventricular contractility
c) Left ventricular outflow obstruction
d) Systolic-diastolic hypertension
e) Widening of the pulse pressure

This patient complains of nocturnal palpitations and head pounding with
exertion. Palpitations may result from forceful ventricular contractions
ejecting large stroke volumes, and head pounding can be due to unusually
high amplitude pulsations of the intracranial arteries with each heartbeat.
In voluntary head bobbing can be a sign of a widened pulse pressure (recall
that pulse pressure = peak systolic arterial pressure end diastolic arterial
pressure). The most likely cause of a repetitive, widened pulse pressure
together with unusually large LV stroke volumes and a heart murmur is
aortic regurgitation (AR).
(Choice A) Restriction of left ventricular (LV) filling would result in a
reduced LV end diastolic volume (reduced preload). At a given level of
contractility, this would cause a reduction in stroke volume. Lower stroke
volumes result in lower pulse pressures, whereas this patients symptoms
and signs suggest a high pulse pressure.

(Choice B) Impaired left ventricular contractility would cause a
reduction in stroke volume for a given preload, resulting in lower
pulse pressures.
(Choice C) Left ventricular outflow tract obstruction, as can result
from aortic stenosis or hypertrophic cardiomyopathy, could cause a
murmur but would tend to reduce stroke volume and thus pulse
pressure.
(Choice D) Combined systolic and diastolic hypertension is not
necessarily accompanied by an abnormally large pulse pressure or
murmur.

A 54-year-old Caucasian female presents to your office with exertional
dyspnea and fatigue. She also describes nocturnal episodes of dyspnea and
orthopnea. After initial evaluation cardiac catheterization was performed
that reveals the following findings (see the diagram below).
The pressure tracings shown in the diagram are most consistent with which
of the following?
a) Aortic stenosis
b) Aortic regurgitation
c) Mitral stenosis
d) Mitral regurgitation
e) Normal findings

A 54-year-old Caucasian female presents to your office with exertional
dyspnea and fatigue. She also describes nocturnal episodes of dyspnea and
orthopnea. After initial evaluation cardiac catheterization was performed
that reveals the following findings (see the diagram below).
The pressure tracings shown in the diagram are most consistent with which
of the following?
a) Aortic stenosis
b) Aortic regurgitation
c) Mitral stenosis
d) Mitral regurgitation
e) Normal findings

This patient presents with nonspecific symptoms consistent with an
inadequate ability to increase cardiac output during exertion as well
as elevated pressures in the pulmonary circulation resulting in a
degree of pulmonary edema. The v wave corresponding to left atrial
filling during the patients cardiac catheterization is abnormal. See
graph below.

Note that the peak v wave pressure corresponding to maximal left atrial filling
just prior to the opening of the mitral valve (arrowheads) is elevated. These
abnormalities are indicative of mitral regurgitation, with abnormal retrograde
filling of the left atrium during ventricular systole.
(Choice A) The major hemodynamic finding in a patient with aortic stenosis
would be a pressure difference (gradient) between the left ventricle and the
aorta in the interval delimited by points A and B on the graph in the explanation
under (Choice D). A corresponds to opening of the aortic valve and B corresponds
to its closure. Left ventricular pressure would be significantly higher than aortic
pressure during the A-B interval.
(Choice B) Aortic regurgitation would tend to elevate both the left ventricular (LV)
and left atrial diastolic pressures above their normal values. However the contour
of the left atrial pressure tracing relative to the LV pressure curve would not be
significantly alteredas it is altered in this patient.
(Choice C) Mitral stenosis affects the hemodynamic profile during
cardiac catheterization as shown below.
Note the pressure gradient between the left atrium and left ventricle
during diastole (arrows).
(Choice E) Only the aortic and left ventricular pressure tracings in this
patient have a grossly normal relationship.

A 44-year-old Caucasian male is successfully treated for infective
endocarditis with a long course of antibiotics. Echocardiographic
evaluation reveals significant aortic regurgitation as a consequence of
the infection. Which of the following is the major hemodynamic
compensation for this valvular abnormality?
a) Increase in left ventricular afterload
b) Increase in left ventricular preload
c) Concentric left ventricular hypertrophy
d) Sustained increase in heart rate
e) Decrease in aortic elasticity

A 44-year-old Caucasian male is successfully treated for infective
endocarditis with a long course of antibiotics. Echocardiographic
evaluation reveals significant aortic regurgitation as a consequence of
the infection. Which of the following is the major hemodynamic
compensation for this valvular abnormality?
a) Increase in left ventricular afterload
b) Increase in left ventricular preload
c) Concentric left ventricular hypertrophy
d) Sustained increase in heart rate
e) Decrease in aortic elasticity

In a patient with relatively acute aortic regurgitation, the major hemodynamic adaptation to
maintain cardiac output is an increase in the left ventricular end diastolic volume (EDV). Assuming
no acute decrease in contractility, this preload increase allows forward LV stroke volume (FSV) in
the new steady state to remain adequate, although reduced from normal.
(Choice A) Left ventricular (LV) afterload is already increased in acute aortic regurgitation (AR),
and is associated with a greatly increased LV total stroke volume and a widened pulse pressure. A
further increase in afterload would increase the regurgitant stroke volume and further decrease
the LV forward stroke volume (FSV), thereby further reducing cardiac output. This is why medical
stabilization of patients with severe acute AR may include administration of a vasodilator
(nitroprusside) in addition to an intravenous positive inotropic agent (dopamine or dobutamine).
The vasodilator decreases after load in order to improve the FSV.
(Choice C) Aortic regurgitation subjects the left ventricle (LV) to volume overload, not pressure
overload. The adaptation to volume overload is eccentric hypertrophy, i.e. chamber dilation (due
to increased end diastolic volume, EDV) with predominantly in series synthesis of new
myocardial sarcomeres. Concentric hypertrophy, the response to pressure overload, involves in
parallel deposition of new sarcomeres, which produces net ventricular wall thickening and a
reduction in ventricular chamber size (decreased EDV). Pressure overload may occur in aortic
stenosis or systemic hypertension.

(Choice D) This patients relatively acute aortic regurgitation (AR) would
decrease the left ventricular forward stroke volume. The acute
compensatory response to maintain cardiac output would include an
increase heart rate. Patients with acute AR are usually tachycardic and
poorly tolerant of lower heart rates.
However this answer choice describes a sustained increase in heart rate. As
the heart of a patient who survives acute AR adapts to volume overload,
increased left ventricular end diastolic volume (LVEDV) and eccentric LV
hypertrophy result in progressive increases in LV forward stroke volume.
Heart rate therefore returns toward normal in chronic AR, so that sustained
tachycardia is not the major final hemodynamic compensation.
(Choice E) A decrease in aortic elasticity would tend to increase afterload.
An increase in afterload would further decrease net left ventricular
(cardiac) output.

A 45-year-old Caucasian female is hospitalized with exertional dyspnea and
fatigue. She recently emigrated from Eastern Europe and has no significant
past medical history. Her blood pressure is 110/80 mmHg and her heart rate
is 90 beats per minute and regular. You suspect mitral stenosis. Which of the
following is the best indicator of the severity of stenosis?
a) Diastolic murmur intensity
b) Presystolic accentuation of the murmur
c) S2-to-opening snap time interval
d) Audible S3
e) Audible S4
A 45-year-old Caucasian female is hospitalized with exertional dyspnea and
fatigue. She recently emigrated from Eastern Europe and has no significant
past medical history. Her blood pressure is 110/80 mmHg and her heart rate
is 90 beats per minute and regular. You suspect mitral stenosis. Which of the
following is the best indicator of the severity of stenosis?
a) Diastolic murmur intensity
b) Presystolic accentuation of the murmur
c) S2-to-opening snap time interval
d) Audible S3
e) Audible S4
The best auscultatory indicator of the severity of mitral stenosis (MS) is the length
of the interval between A2 and the opening snap (OS). The shorter the interval
the more severe the stenosis. The OS occurs due to tensing of the mitral valve
(MV) leaflets after the valve cusps have completed their opening excursion. The
more thickened and fibrotic the MV the earlier this tensing occurs. The A2-OS
interval is also inversely correlated with mean diastolic left atrial pressure. (In
modern practice the standard for the diagnosis and determination of MS severity
is measurement of mean transvalvular pressure gradients via 2-D Doppler
echocardiography).
(Choice A) Although the intensity of the diastolic rumble of mitral stenosis (MS)
may increase as the degree of MS increases this sign is a less reliable indicator of
MS severity. This is because the transmission of the flow murmur at a given
transvalvular pressure gradient varies among patients depending upon thoracic
anatomy. The diastolic rumble is heard best at the cardiac apex (mitral area) with
the bell of a stethoscope.
(Choice B) There is presystolic accentuation of the murmur of mitral stenosis (MS)
because of the increased transvalvular flow associated with left atrial contraction.
This accentuation is heard across a range of MS severity. More significant than
the degree of presystolic accentuation is its presence or absence. When MS
becomes severe enough to precipitate atrial fibrillation, presystolic accentuation
of the MS murmur disappears.
(Choices D and E) Left-sided SS and/or S4 gallops are generally absent in mitral
stenosis (MS), since left ventricular filling is subnormal to normal. When MS is
severe enough to produce pulmonary hypertension, patients may develop
rightsided heart failure, with dilatation of the right ventricle (RV) and its annulus
and possible secondary tricuspid or pulmonic regurgitation. Tricuspid and
pulmonic regurgitation might cause a right-sided S3 and/or S4. However these EN
gallops would only arise when the maximal degree of MS had been reached and
thus are poor indicators of the severity of less serious MS.


A 52-year-old Caucasian male presents to your office with two week history
of progressive fatigue and exertional dyspnea. He brings with him the report
from a recent cardiac catheterization (shown below). Cardiac auscultation
reveals a murmur that is best heard when the patient sits up and leans
forward. Which of the time points pictured below corresponds to the peak
murmur intensity?
a) A
b) B
c) C
d) D
e) E

A 52-year-old Caucasian male presents to your office with two week history
of progressive fatigue and exertional dyspnea. He brings with him the report
from a recent cardiac catheterization (shown below). Cardiac auscultation
reveals a murmur that is best heard when the patient sits up and leans
forward. Which of the time points pictured below corresponds to the peak
murmur intensity?
a) A
b) B
c) C
d) D
e) E

Cardiac catheterization shows a hemodynamic profile consistent with
aortic regurgitation (AR). Note the high peaking left ventricular and
aortic pressures during systole and the steep diastolic decline in aortic
pressure. A normal catheterization report is shown below for
purposes of comparison:

The peak intensity of an AR murmur occurs after closure of the
incompetent aortic valve, at the point when the pressure gradient
between the aorta and the left ventricle is at its maximum i.e. time C.
(Choice A) This time point corresponds to the opening of the aortic
valve during systole. The murmur of aortic stenosis would be heard
best here.
(Choice B) This point corresponds to the closure of the aortic valve.
The A2 heart sound is heard here. At this instant there is not yet
regurgitant flow from the aorta to the left ventricle, so no murmurs
are audible.

(Choice D) Time point D occurs in mid-diastole. The murmur of AR
might be heard here, as there is a pressure gradient between the
aorta and left ventricle (LV). However the intensity of the murmur
would be less than at time C because the magnitude of the gradient is
less. Because the AR murmur decreases in intensity with the falling
aortic pressure, it is a decrescendo diastolic murmur.
(Choice E)Time E marks the onset of left atrial contraction at the end
of ventricular diastole. If the murmur of AR were still audible at this
time, its intensity would be further reduced by the increase in left
ventricular end diastolic pressure.