Pericardial Diseases

PHD MD Puschita Maria

Department of Internal Medicine and
Cardiology, Emergency County Hospital of
Arad
Vasile Goldis Western University of Arad

General characteristics
(Normal Pericardial Anatomy and Physiology)
1.Pericardium is the
membranous sac
surrounding the heart.
2. The pericardium consists
of two layers: visceral
layer and parietal layer.
3.There is about 50ml
pericardial fluid in the
pericardial cavity.

The normal functions of the pericardium

Maintaining an optimal cardiac shape.
Reducing friction between the beating
heart and adjacent structures.
Protecting the heart from other diseases
which are caused by the neighboring
organs: inflammation , TB, cancer etc.
Preventing the overfilling of the heart.

Classification of Pericardial Diseases

Congenital defect
Pericarditis
acute pericarditis
pericardial effusion
constrictive pericaditis.

Pericardial neoplasm
Pericardial cysts.

Triage in acute pericarditis

Clinical and echo evaluation
Is specific etiology highly
suspected or prevalent?
YES
Specific etiology search and
management

NO
Clinical poor prognostic
predictors?

YES
HIGH RISK CASES

NO
LOW RISK CASES

Admission to hospital
Etiology search
Empiric trial with NSAID

Outpatient treatment with NSAID

No Etiology search
Response to NSAID?

NO
MODERATE TO HIGH RISK

YES
LOW RISK PERICARDITIS

Admission to hospital
Etiology search

Outpatient follow-up
No Etiology search

 Stage I
everything is UP (i.e., ST elevation in almost all leads - see below)
Stage II
Transition ( i.e., "pseudonormalization").
Stage III
Everything is DOWN (inverted T waves).
Stage IV
Normalization

Acute pericarditis

Definition
Acute pericarditis is an inflammation
of the pericardium.

Etiology
The disease may be idiopathic or secondary to
other diseases, for example
Viral infection: coxsackievirus B, CMV
Bacterial infection: Staphylococcus sp, Streptococcus
sp, tubercle bacillus
Post-MI complications
Drugs
Malignancy
Collagen vascular disease

Pathology
Early stage
fibrous protein pericarditis

Progressive stage
Rapid effusive pericarditis acute cardiac tamponade
Chronic accumulation is accommodated by the expanding
pericardium
myopericarditis

Final result
The exudate was completely dissolved and absorbed
Organization calcification of pericardium constrictive
pericarditis

pathophysiology
Acute pericardial effusion

The pressure of the pericardial cavity

FV( filling volume) of the ventricular diastole

SV( stroke-volume)

BP

Clinical Manifestations
---fibrous protein pericarditis
Chest pain (Symptoms)
Position
retrosternal or
precordium, midsection

Character
sharp pain, dull pain,
compression

Worsen
deep breathing, cough,
and lying down.

Relieved
sitting and leaning
forward.

Pericardial friction rub

(Signs)
Both systole and
diastole
This finding is
diagnostic

Clinical Manifestations
---Pericardial effusion
Symptoms
Dispnea
Pressure symptoms
dry cough(bronchus)
hoarseness(laryngeal
nerve)
dysphagia
esophagus)

Signs
physical sign of the heart
tachycardia, indistinct heart
sounds
Ewart sign (consolidation of lower
lobe of left lung)

Hypotension
SBPpulse pressure
even paradoxical pulse.(there is
an exaggerated reduction of the
pulse >10mmHg during
inspiration)

Congestion of systemic
circulation
distended jugular vein
edema

Clinical Manifestations
---Cardiac tamponade
Acute Becks trilogy
Hypotension or shock
Distended jugular vein
Indistinct heart sounds

Subacute or chronic
venous pressure
congestion of systemic circulation
Kussmaul sign( dilation of jugular vein
during inspiration)

Laboratory findings
--- ECG
Stage I:ST segment elevation (concave upward not
convex) in all leads except avR and V1 without
reciprocal ST segment depression (which occurs in
MI) (Several hours later).
Stage II: ST segments return to baseline, the
initially upright T waves flatten (several days later)
Stage III:T waves invert (weeks later)
Stage IV:T waves revert to normal (weeks or
months later))
Other changes: Large effusion can cause both
reduced voltage and electrical alternans.

EKG of Acute pericarditis (Stage I)

Acute Pericarditis

51 years, man with acute onset sharp substernal

chest pain two days prior

ECG in Acute Pericarditis

EKG contrast the pattern of ST segment elevation characteristic of

acute pericarditis (a) with the normal variant (early repolarization)
pattern of ST segment elevation (b). The normal variant pattern is
associated with a normal or slow heart rate and has relatively tall R
waves and T waves in V4, V5, and V6. The ST segment elevation is
less than 25% of the T wave amplitude. In contrast, the acute

Acute inferior myocardial infarction

Laboratory findings
--- Chest x-ray film
Cardiac shadow has
an enlarged waterbottle appearance.
Clear lung field.
Cardiac shadow
changes with
postures.

Laboratory findings
---Echocardiography
This is the best
noninvasive
investigation
for confirming
diagnosis of a
pericardial
effusion

Laboratory findings
--- Pericardiocentesis
1.Pericardiocentesis can help to make diagnosis.
Fluid should be sent for culture and assay
Protein, glucose and LDH assays: LDH, glucose and protein
determine if fluid is a transudate or exudate;
Cytology and tumor marker: CEA, AFP, CA125 and so on;
ANA assay: if collagen vascular disease is suspected.

2. Pericardiocentesis can relieve the pressure of

pericardial cavity.

Diagnosis of Acute Pericarditis

Chest pain aggravated by coughing, inspiration,or

recumbency
Pericardial friction rub on auscultation
Charateristic EKG changes
Chest X-ray and UCG may find pericardial
effusion

Differential Diagnosis of Acute Pericarditis

Acute
idiopathic
pericarditis

Maligancy

Postpericar
diostomy
syndrome

Accompa
nied with
original
infection
lesion or
septemia

Frequently
caused by
metastatic
tumour

History of
cardiac injury
such as
operation,
myocardial
infarction,
may often
recurrent

seldom

High
fever

seldom

often

often

often

seldom

seldom

seldom

often

seldom

often

Tuberculous Purulent
pericarditis pericarditis

History of up
Accompanied
respiratory
tract infection with primary
Histrory acute onset
TB
often
recurrent

Fever

Constant
fever

Pericardi
obviously
al friction
occur early
rub
Chest
pain

Often
severely

Differential Diagnosis of Acute Pericarditis

Acute
idiopathic
pericarditis

Tuberculous
pericarditis

Leukocyte
count

Normal or
increase

Normal or
slightly
increase

Blood
culture

Volume of
pericardial
effusion

Characteris
tic

Purulent
Maligancy
pericarditis

Postpericardi
ostomy
syndrome

Significantl
y increase

Normal
or
slightly
increase

Normal or
slightly
increase

Little

Large

Large

Large

Medium

Grass
yellow or
hematic

Often
hematic

Purulent

Often
hematic

Often
serosity

Differential Diagnosis of Acute Pericarditis

Acute
Purulent
Tuberculous
idiopathic
pericard
pericarditis
pericarditis
itis
Classificati
on of
leukocyte

Bacteria

Treatment

Maliga Postperica
rdiostomy
ncy
syndrome
More
More
lymphocyte

More
lymphocyte

More
lymphocyte

More
neutrophil

None

Tubercle
bacillus may
be found

Purulent
bacteria

Anti-tubercle
bacillus

Treat
Antibiotic
original
or
diseases,
pericardi Perecardio
otomy
centesis

NSAIDs

lymphocyte

None

None

Steroid

Treatment
1.Etiology treatment

Bacterial infection
Viral infection
TB
Malignancy
Collagen vascular disease

2. Relieving pain and inflammation:

NSAIDs and steroids

3.If symptoms are severe, pericardiocentesis is

indicated to remove fluid.

Pericardial Effusion and

Cardiac Tamponade

Pericardial Effusion and

Cardiac Tamponade
Fluid can accumalte in the pericardium in any form of
pericardial disease
Transudate
Exudate

Serosanguineous: Idopathic, dialysis-related, neoplastic,

radiation induced, TB, coagulapaties
Bloody: Coagulopathies, trauma, rupture in MI and in aortic

dissection
Cardiac Tamponade is the most important complication of
fluid accumulation

Cardiac Tamponade
pathophysiology
Fluid accumulation within the pericardial
space resulting in
increased intracardiac pressure
progressive limitation of ventricular diastolic
filling
reduction of stroke volume and cardiac output

Cardiac Tamponade
The physiological effect depends on the rate of fluid
accumulation
Gradually the pericardium may strech and
accommodate > 2,000 ml

Acutely as little as 200 ml of accumulated fluid may

raise the intrapercardial pressure to cause
tamponade
JVD elevated (rarely not in low pressure tamponade)
B.P variable, paradoxical pulse (>10 mm HG )
Echocardiography
Treatment: fluids, pericardiocentesis, cardiac surgery.

Cardiac Tamponade
Becks Triad
Described in 1935 by thoracic surgeon
Claude S. Beck
3 features of acute tamponade
Decline in systemic arterial pressure
Elevation in systemic venous pressure (e.g.
distended neck vein)
A small, quiet heart

Etiologies of Cardiac Tamponade

malignancy
idiopathic pericarditis
uremia
acute myocardial
infarction
diagnostic procedures
with cardiac perforation
bacterial
tuberculosis

radiation
myxedema
dissecting aortic
aneurysm
post pericardiotomy
syndrome
systemic lupus
erythematosus
cardiomyopathy

Cardiac Tamponade
Early stage
mild to moderate elevation of central venous
pressure

Advanced stage
intrapericardial pressure
ventricular filling, stroke volume
hypotension
impaired organ perfusion

Cardiac Tamponade
Clinical Features
Symptoms
dyspnea, fatigue, agitation and restlessness,
syncope, shock, anuria

Physical examination
pulsus paradoxus
tachycardia
increased jugular venous pressure
hypotension

Cardiac Tamponade
Pulsus Paradoxus
tamponade without
pulsus

atrial septal defect

severe aortic stenosis
aortic insufficiency
left ventricular
dysfunction
LVH with LVEDP
decreased
intravascular volume
(low-pressure
tamponade)

pulsus without
tamponade

COPD
RV infarct
pulmonary embolism
effusive constrictive
pericarditis
restrictive
cardiomyopathy
extreme obesity
tense ascites

Cardiac Tamponade
Central Venous Pressure
X - descent
descent of the base in systole

Y - descent
occurs as the tricuspid valve opens and ventricular filling
begins from the high-pressure right atrium
in constrictive pericarditis, filling is truncated in early to mid
diastole
in tamponade, filling is restricted throughout diastole

Kussmauls Sign
in constriction, venous return increases with inspiration and
a high right atrial pressure resists filling resulting in an
increased JVP

Central Venous Pressure

Cardiac Tamponade

Constrictive Pericarditis

presence of a rapid Y-descent argues against cardiac tamponade

Cardiac Tamponade
Pulsus Paradoxus

an exaggerated drop in SBP with inspiration (>10mmHg)

Lateral CXR of a person with

chronic calcified pericarditis due to
TB
A cystic mass
B calcified pericardium

Pericardial Effusion

Pressure Readings in Cardiac Tamponade

The aortic pressure and right atrial pressure are recorded

during quiet breathing in a patient with cardiac
tamponade. The marked fall in arterial pressure that
occurs during inspiration is a paradoxical pulse. The
decrease in pulse pressure, defined as the difference
between systolic and diastolic pressures, that
accompanies the fall in systolic pressure indicates that left
ventricular stroke volume decreases during inspiration.
Central venous pressure, as indicated by the right atrial
pressure, also falls during inspiration.

Cardiac Tamponade
Dignostic Evaluation
Chest x-ray
usually requires > 200 ml of fluid
cannot distin guish between pericardial effusion
and cardiomegly

Echocardiography
standard for diagnosing pericardial effusion
convenient, highly reliable, cost effective
false positives (M-mode)- left pleural effusion,
epicardial fat, tumor tissue, pericardial cysts

ECG in Pericardial Effusion

Diffuse low voltage
amount of fluid
electrical conductivity of the fluid

Electrical alternans
alternating amplitude of the QRS
produced by heart swinging motion
also seen in PSVT, HTN, ischemia

ECG: Pericardial Effusion

The electrocardiogram (V2 lead) from a patient with pericardial effusion

caused by malignant melanoma reveals a low voltage and electrical
alternans.

Cardiac Tamponade
Echocardiographic Diagnosis
Pericardial effusion
highly reliable

Cardiac tamponade
RA and RV diastolic collapse
reduced chamber size
distension of the inferior vena cava
exaggerated respiratory variation of the
mitral and tricuspid valve flow velocities

Pericardial Effusion-Echocardiography

Pericardial effusion is seen in the two-dimensional echocardiogram as an echofree space outside the cardiac chambers. Two characteristic sites are lateral to the
left ventricle in the apical four-chamber view (shown here) and posterior to the left
ventricle in the parasternal long-axis view (see Figure 3b).

RA and RV diastolic collapse

early diatole

systole

late
diastole

CT Scan: Pericardial Effusion

A chest CT scan of a patient with pericardial effusion, pericardial fluid appears

less dense than the heart and is separated from the myocardium by epicardial fat
in some areas.

Echocardiogram: Pericardial Effusion

The echocardiogram demonstrates that the heart moves forward (F) and backward
(B) within the effusion on alternate beats, thus producing the alternation of the
QRS axis characteristic of electrical alternans. The heart also moves with
inspiration (Insp) and expiration (Exp), which accounts for a change in anterior
wall motion with every two cardiac cycles.

Differential Diagnosis of Cardiac Tamponade vs. Chronic Constrictive Pericarditis

Differences between the central venous pulse contours characteristic of cardiac

tamponade (left) and chronic constrictive pericarditis (right) provide the basis for
differential diagnosis. The pressure contour in a patient with pericardial effusion
and tamponade has a prominent systolic dip (X) but little or no diastolic
deflection. The central venous pulse pattern in a patient with chronic constrictive
pericarditis displays an M or W contour consisting of both systolic dip (X) and
diastolic dip (Y), the Y descent being more prominent.

Constriction vs. Tamponade

TAMPONADE
Low cardiac output state
JVD present
NO Kussmauls sign
Equalized diastolic
pressures
RA: blunted y descent
Decreased heart sounds

CONSTRICTION
Low cardiac output state
JVD present
Kussmauls sign
Equalized diastolic
pressures
RA: rapid y descent
Pericardial knock

Constriction vs. Tamponade

TAMPONADE
CONSTRICTION
Pulsus paradoxus:
Pulsus paradoxus:
Present
Absent
Echo/MRI:
Echo/MRI:
Normal systolic function Normal systolic function
Large effusion
No effusion
RA & RV compression Pericardial thickening
Treatment:
Treatment:
Pericardiocentesis
Pericardial stripping

CT Scan in Chronic Constrictive Pericarditis

In this CT scan of the chest of a patient with chronic constrictive pericarditis, the
dense layer on the anterior surface of the heart represents thickened and partially
calcified pericardium.

Cardiac Tamponade
Treatment Options
Nonsurgical
pericardiocentesis

blind
ECG guided
Echo guided
CT guided

balloon
pericardiotomy

Surgical
subxiphoid
video-assisted
thoracoscopy
pericardialperitoneal
pericardial window
pericardiectomy

Cardiac Tamponade
Pericardiocentesis
Diagnostic tap
usually not indicated
rarely have positive cytology or infection that
can be diagnosed

Therapeutic drainage
indicated for significant elevation of the
central venous pressure

Cardiac
Pericardial Window
Tamponade
Balloon dilatation of a needle
pericardiostomy
subxyphoid surgical pericardiostomy
video-assisted thoracoscopy with localized
pericardial resection
anterolateral thoracotomy with parietal
pericardial resection

Cardiac
Tamponade
Localized
and Low Pressure
Localized tamponade
due to loculated pericardial effusion
Low pressure tamponade
due to relative intravascular volume
depletion

Clinical Features That Differentiate Constrictive Pericarditis from Amyloidosis and

Idiopathic Restrictive Cardiomyopathy

Clinical Feature

Constrictive
Pericarditis

Cardiac
Amyloidosis

Idiopathic
Restrictive
Cardiomyopathy

Early diastolic sound (S3 or pericardial knock)

Frequent

Occasional

Occasional

Late diastolic sound (S4)

Rare

Frequent

Frequent

Atrial enlargement

Mild or absent

Marked

Marked

Atrioventricular or intraventricular conduction defect

Rare

Frequent

Frequent

QRS voltage

Normal or low

Low

Normal or high

Mitral or tricuspid regurgitation

Rare

Frequent

Frequent

Paradoxical pulse

Frequent but usually

mild
Usual

Rare

Rare

Rare

Rare

Exaggerated variation in mitral and tricuspid flow

velocity with respiration, out of phase

Endocarditis
Infective endocarditis is defined as an
infection of the endocardial surface of the
heart, which may include one or more
heart valves, the mural endocardium, or a
septal defect

 Endocarditis can be broken down into the

following categories:
Native valve (acute and subacute) endocarditis
Prosthetic valve (early and late) endocarditis

Endocarditis related to intravenous drug use

Native valve endocarditis (acute

and subacute)
Native valve acute endocarditis usually
has an aggressive course. Virulent
organisms, such as Staphylococcus
aureus and group B streptococci, are
typically the causative agents of this type
of endocarditis.

 Subacute endocarditis usually has a more

indolent course than the acute form.
Alpha-hemolytic streptococci or
enterococci, usually in the setting of
underlying structural valve disease,
typically are the causative agents of this
type of endocarditis.

Prosthetic valve endocarditis (early

and late)
Early prosthetic valve endocarditis occurs
within 60 days of valve implantation.
Staphylococci, gram-negative bacilli, and
Candida species are the common infecting
organisms.

Prosthetic valve endocarditis (early

and late)
Late prosthetic valve endocarditis occurs
60 days or more after valve implantation.
Staphylococcus epidermidis, alphahemolytic streptococci, and enterococci
are the common causative organisms.

Endocarditis related to intravenous

drug use
Endocarditis in intravenous drug abusers
commonly involves the tricuspid valve. S aureus
is the most common causative organism
Infective endocarditis generally occurs as a
consequence of nonbacterial thrombotic
endocarditis, which results from turbulence or
trauma to the endothelial surface of the heart.

Endocarditis
Increased mortality rates are associated with
increased age, infection involving the aortic
valve, development of congestive heart failure,
central nervous system (CNS) complications,
and underlying disease
Affects men more than women (2:1 ratio)
Affects all age groups - however, 50% of cases
in adults over age 50

Endocarditis
Most common symptoms - fever (90% of cases)
and chills
Anorexia, weight loss, malaise, headache,
myalgias, night sweats, shortness of breath,
cough, or joint pains are common complaints
Dyspnea, cough, and chest pain are common
complaints of intravenous drug users who have
infective endocarditis

Endocarditis
Primary cardiac disease may present with
signs of congestive heart failure due to
valvular insufficiency
Heart murmurs are heard in approximately
85% of patients

Endocarditis
One or more classic signs of infective endocarditis are found
in as many as 50% of patients. They include the following:
Petechiae - Common but nonspecific finding
Splinter hemorrhages - Dark red linear lesions in the
nailbeds
Osler nodes - Tender subcutaneous nodules usually
found on the distal pads of the digits
Janeway lesions - Nontender maculae on the palms and
soles
Roth spots - Retinal hemorrhages with small, clear
centers; rare and observed in only 5% of patients.

splinter hemorrhages and purpuric papules on the

foot of a 10 year old boy with acute bacterial
endocarditis

Splinter hemorrhages(Panel A) are normally seen under the fingernails.

They are usually linear and red for the first two to three days and brownish
thereafter.
Panel B shows conjunctival petechiae.
Osler's nodes (Panel C)are tender, subcutaneous nodules, often in the pulp
of the digits or the thenar eminence.
Janeway's lesions (Panel D) are nontender, erythematous, hemorrhagic, or
pustular lesions, often on the palms or soles

Endocarditis
baseline studies, such as a complete blood count
(CBC), electrolytes, creatinine, BUN, glucose, and
coagulation panel
Blood cultures: Two sets of cultures have >90%
sensitivity when bacteremia is present. Three sets
of cultures improve sensitivity and may be useful
when antibiotics have been administered previously

Endocarditis
Echocardiogram

Transthoracic echocardiography has a sensitivity of

approximately 60%. Transesophageal
echocardiography has a sensitivity of more than 90%
for valvular lesions

Endocarditis
Empiric antibiotic therapy is chosen based
on the most likely infecting organisms.
Native valve disease usually is treated
with penicillin G and gentamicin for
synergistic treatment of streptococci

Endocarditis
Patients with a history of IV drug use may
be treated with nafcillin and gentamicin to
cover for methicillin-sensitive
staphylococci.

Endocarditis
Infection of a prosthetic valve may include
methicillin-resistant Staphylococcus
aureus; thus, vancomycin and gentamicin
may be used, despite the risk of renal
insufficiency

Endocarditis
Rifampin also may be helpful in patients
with prosthetic valves or other foreign
bodies; however, it should be used in
addition to vancomycin or gentamicin.

Endocarditis
prophylaxis against infective endocarditis in patients at
higher risk. Patients at higher risk include those with the
following conditions:
Presence of prosthetic heart valve
History of endocarditis

History of rheumatic heart disease

Congenital heart disease with a high-pressure
gradient lesion
Mitral valve prolapse with a heart murmur

Endocarditis
prophylaxis in patients before they undergo procedures
that may cause transient bacteremia, such as the
following:
Ear, nose, and throat (ENT) procedures associated
with bleeding, including dental manipulations and
nasal packing
Incision and drainage of an abscess
Anoscopy and Foley catheter placement when a
urinary tract infection is present or suspected

Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (2014)

Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (2014)

Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (2014)

Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (2014)

Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (2014)

Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (2014)

Myocarditis

Myocarditis
Inflammation of the myocardium
May be the result of systemic disorder or
infectious agent ...usually follows an upper
resp infection
Pericarditis frequently accompanies
myocarditis
Drug induced, cytotoxic agents,also,
cocaine

Myocarditis
Bacterial cases include;
Corynebacterium diphtheriae, Neisseria
meningitides, Mycoplasma pneumoniae, and
B-hemolytic streptococci

Viral etiologies include;

coxsackie B, echovirus, influenza,
parainfluenza, Epstein-Barr, and HIV

Myocarditis -clinical features

Systemic signs/symptoms (fever,
tachycardia, myalgias, headache, and
rigors)
chest pain due to coexisting pericarditis
pericardial friction rub in cases of
concomitant pericarditis
In severe cases - symptoms of
progressive heart failure (CHF, pulmonary
rales, pedal edema, etc.)

Diagnosis
Nonspecific ECG changes, atrioventricular
block, prolonged QRS duration, or ST
segment elevation (in cases of
accompanying pericarditis)
normal chest x-ray
cardiac enzymes may be elevated
Differential diagnosis includes cardiac
ischemia or infarction, valvular disease
and sepsis

Treatment
Supportive care
If bacterial cause suspected, antibiotics
are appropriate
Myocardial biopsy may reveal
inflammatory pattern
Many cases spontaneously resolve others
progress to dilated cardiomyopathy

Course
questionnaire

QUESTION 1
A 46-year-old man is evaluated in the emergency department for a 3-day history of progressively worsening
dyspnea on exertion to the point that he is unable to walk more than one block without resting. He has had
sharp intermittent pleuritic chest pain and a nonproductive cough with myalgias and malaise for 7 days and
has had orthostatic dizziness for 2 days. He is taking no medications.
On physical examination, temperature is 37.7 C (99.9 F), blood pressure is 88/44 mm Hg, pulse is
125/min, and respiration rate is 29/min; BMI is 27. Oxygen saturation on ambient air is 95%. Pulsus
paradoxus is 15 mm Hg. Estimated central venous pressure is 10 cm H2O. Cardiac examination discloses
muffled heart sounds with no rubs. Lung auscultation reveals normal breath sounds and no crackles. There
is 2+ pedal edema. Blood pressure and heart rate are unchanged after a 500-mL intravenous normal saline
challenge.
Twelve-lead electrocardiogram shows sinus tachycardia, diffuse low voltage, and no ST-segment shifts.
Echocardiogram shows a large circumferential pericardial effusion, right ventricular and atrial free wall
diastolic collapse, normal left ventricular systolic function, and an ejection fraction of 70%. Chest radiograph
shows an enlarged cardiac silhouette and no pulmonary infiltrates.

What is the most appropriate treatment?

A. Dobutamine
B. Levofloxacin and tobramycin
C. Pericardiocentesis
D. Surgical pericardiectomy

Correct Answer: C. Pericardiocentesis

This is likely cardiac tamponade. Physical examination reveals tachycardia, reduced blood pressure, distended jugular veins,
elevated pulsus paradoxus (>10 mm Hg), and an unremarkable lung examination. This constellation of signs should always
raise the possibility of cardiac tamponade but is not pathognomonic. Other acute conditions, such as pulmonary embolism or
myocardial infarction, could account for these findings. However, cardiac tamponade is confirmed by echocardiography,
specifically by a pericardial effusion with associated right atrial and ventricular free wall diastolic collapse. In addition, this
patient presents with symptoms consistent with an infectious illness. A viral pericarditis is the most likely source. The
definitive treatment for this patients hemodynamic derangement is pericardiocentesis, which is typically performed via a
percutaneous route but may be performed surgically if indicated.
Cardiac tamponade is typically caused by a circumferential pericardial effusion, but a loculated pericardial effusion also can
cause tamponade, particularly in patients with prior cardiac surgery. The rapidity of fluid accumulation, rather than the
absolute size of an effusion, is the major determinant of developing tamponade. Thus, a small but rapidly developing effusion
may cause tamponade, whereas a large but slowly accumulating effusion may not.
Wrong answers:
A. Dobutamine: vigorous LV function on TTE, unlikely to be of benefit. Aggressive IVF are indicated, which were given.
B. Levofloxacin and tobramycin: findings more consistent with tamponade than septic shock.
D. Surgical pericardiectomy: would be appropriate treatment for constrictive pericarditis after 3 months of conservative
mgmt

QUESTION 2
A 45-year-old man is evaluated for a 6-month history of progressive dyspnea on exertion and lower-extremity
edema. He can now walk only one block before needing to rest. He reports orthostatic dizziness in the last 2
weeks. He denies chest pain, palpitations, or syncope. He was diagnosed 15 years ago with non-Hodgkin
lymphoma, which was treated with chest irradiation and chemotherapy and is now in remission. He also has
type 2 diabetes mellitus. He takes furosemide (80 mg, 3 times daily), glyburide, and low-dose aspirin.
On physical examination, he is afebrile. Blood pressure is 125/60 mm Hg supine and 100/50 mm Hg standing;
pulse is 90/min supine and 110/min standing. Respiration rate is 23/min. BMI is 28. There is jugular venous
distention and jugular venous engorgement with inspiration. Estimated central venous pressure is 15 cm H 2O.
Cardiac examination discloses diminished heart sounds and a prominent early diastolic sound but no gallops
or murmurs. Pulmonary auscultation discloses normal breath sounds and no crackles. Abdominal examination
shows shifting dullness, and lower extremities show 3+ pitting edema to the level of the knees. The remainder
of the physical examination is normal.
BUN 40 mg/dL, Cr 2.0 mg/dL, ALT 130 U/L, AST 112 U/L, Albumin 3.0 g/dL, UA negative for protein,
Whats the most likely diagnosis?
A. Cirrhosis
B. Constrictive pericarditis
C. Nephrotic syndrome
D. Systolic heart failure

Correct Answer: B. Constrictive pericarditis

This patient has symptoms and signs of heart failure. The physical examination is notable for findings of right heart failure
(jugular venous distention, peripheral edema) in the absence of left heart failure (clear lung fields, absence of gallop). The
most important physical examination findings are a Kussmaul sign (accentuated jugular venous pressure during inspiration)
and an early diastolic sound (pericardial knock). These findings help to confirm constrictive pericarditis as the most likely
diagnosis.
Constrictive pericarditis is characterized by thickened, fibrotic, and adherent pericardium that restrains ventricular diastolic
expansion, leading to impaired filling. Orthostatic hypotension may occur as an adverse effect from excessive diuresis in
patients with constrictive pericarditis, as seen in this patient, who was being treated with a high dosage of furosemide.
Constrictive pericarditis is a well-known complication of chest irradiation therapy and may occur 10 to 15 years after exposure.
Mediastinal radiation therapy results in approximately a three-fold increase in the risk of cardiac death. Most deaths are due to
myocardial infarction, and the remainder are due to heart failure, constrictive pericarditis, cardiomyopathy, or valvular heart
disease.

Wrong answers:
A. Cirrhosis: Cirrhosis with portal hypertension could account for this patients peripheral edema and ascites. However, it
would not explain the elevated right heart pressures, orthostatic hypotension, pericardial knock, or Kussmaul sign. In addition,
the patient does not have any cutaneous findings of chronic liver disease such as gynecomastia, spider angioma, or palmar
erythema. The elevated aminotransferase levels reflect passive hepatic congestion and are a feature of constrictive
pericarditis.
C. Nephrotic syndrome: Nephrotic syndrome is a reasonable consideration in a patient with diabetes mellitus,
hypercholesterolemia, hypoalbuminemia, and peripheral edema. However, the absence of proteinuria excludes this diagnosis.
In addition, nephrotic syndrome would not explain the jugular venous distention, pericardial knock, or orthostatic hypotension.
D. Systolic heart failure: Systolic heart failure can explain many of the patients findings, including dyspnea on exertion,
elevated central venous pressure, and peripheral edema. However, systolic failure is also associated with crackles on
pulmonary auscultation and an S3, which are absent in this patient. Furthermore, murmurs characteristic of mitral regurgitation
and tricuspid regurgitation are frequently associated with systolic failure but are absent in this patient. Systolic failure cannot
explain the pericardial knock or Kussmaul sign.

QUESTION 3
A 34-year-old woman is evaluated for sharp intermittent pleuritic chest pain that has persisted for 1 week. The
pain is worse when she lies down in the supine position. She has had no fever, chills, cough, or weight loss.
She had acute viral pericarditis 6 months ago that was treated initially with ibuprofen, but when she failed to
respond after 3 days, a 10-day tapering dosage of prednisone was instituted, leading to resolution of clinical
symptoms. She has a 10-year history of essential hypertension, and she takes hydrochlorothiazide and
potassium chloride.
On physical examination, temperature is normal, blood pressure is 98/54 mm Hg, pulse is 99/min, and
respiration rate is 20/min. Cardiac examination discloses a pericardial friction rub at the lower left sternal
border but no gallops. Pulmonary auscultation reveals normal breath sounds and no crackles. There is no
jugular venous distention and no chest-wall tenderness. Laboratory studies reveal a serum creatinine level of
1.0 mg/dL (76.3 mol/L). EKG is performed. CXR shows normal sized cardiac silhouette and clear lung fields.
Whats the most appropriate treatment?
A. Colchicine
B. High dose aspirin
C. High dose ibuprofen
D. Prednisone

Correct answer: A. Colchicine

This young patient has a history of acute viral pericarditis and presents with pleuritic chest pain and a pericardial friction rub.
The likely diagnosis is recurrent pericarditis. The ST-segment elevation on the electrocardiogram is concave upward and PRsegment depression is present, further supporting the diagnosis. Prior treatment of acute viral pericarditis with prednisone
predisposes to recurrent pericarditis. Because of its efficacy, colchicine has emerged as the treatment of choice for acute
bouts of recurrent pericarditis and can be useful in the prevention of recurrences. Treatment duration is 6 months.
Treatment of pericarditis with colchicine is an off-label use. Colchicine is contraindicated in patients with chronic kidney
disease. However, this patient has no signs of chronic kidney disease.
Wrong answers:
B. High dose aspirin: High-dose aspirin and NSAIDs are first-line agents for the treatment of an initial episode of viral or
idiopathic pericarditis. However, high-dose aspirin therapy is less effective in the treatment of recurrent pericarditis and is
complicated by gastrointestinal adverse effects with long-term use.
C. High dose ibuprofen: High-dose NSAIDs, such as ibuprofen, are useful adjuncts to colchicine therapy in the treatment of
recurrent pericarditis, but are less effective as first-line agents in the treatment of recurrent bouts of pericarditis.
D. Prednisone: The use of systemic corticosteroids early in the course of acute pericarditis is associated with an increased
frequency of relapse, as was seen in this patient. Corticosteroids are considered third-line agents for refractory cases of
recurrent pericarditis.

QUESTION 4
A 58-year-old man presents to the emergency department within 4 hours of worsening pleuritic chest pain,
which has become progressively more severe. Ten days ago, he had an acute anterior ST-elevation
myocardial infarction and underwent successful thrombolytic therapy within 2 hours of the onset of symptoms.
He has a history of hypertension. Medications include metoprolol, clopidogrel, simvastatin, aspirin, and
isosorbide mononitrate.
On physical examination, temperature is 37.9 C (100.2 F), blood pressure is 110/70 mm Hg, pulse is
60/min, and respiration rate is 18/min. There is no jugular venous distention. Cardiac examination discloses a
two-component pericardial friction rub but no murmurs or gallops. Crackles are heard on pulmonary
auscultation. There is no pedal edema.
ESR 60 mm/hr, WBC 12,000/mcL, BUN 15 mg/dL, Cr 1.0 mg/dL
Twelve-lead electrocardiogram during an episode of chest pain shows normal sinus rhythm with diffuse,
concave, upward 1.0- to 1.5-mm ST-segment elevation and 1-mm PR-segment depression in leads II, III, and
aVF.
Whats the most appropriate treatment?
A. Colchicine
B. High dose aspirin
C. High dose ibuprofen
D. Prednisone

Correct answer: B. High dose aspirin

The correct diagnosis in this middle-aged man is acute pericarditis associated with postmyocardial infarction syndrome, or
Dressler syndrome. Postmyocardial infarction syndrome develops several weeks (rarely within a week) to months after an
ST-elevation myocardial infarction and is characterized by pleuritic chest pain, pericardial friction rub, fever, leukocytosis,
and, sometimes, pleural effusion or pulmonary infiltrates. This is distinguished from infarction pericarditis, which is
characterized by a pericardial friction rub with or without chest pain and typically occurs within 1 to 2 days of the
myocardial infarction. On electrocardiogram, acute pericarditis is characterized by diffuse ST-segment elevation that is
characteristically concave upward (as opposed to downward, as in the case of a myocardial infarction) and PR-segment
depression, which is nearly pathognomonic for pericarditis.
Anti-inflammatory therapy is the mainstay of treatment for pericarditis. Treatment with aspirin is preferred over NSAIDs if
an acute myocardial infarction is the cause of acute pericarditis because its antiplatelet effects are beneficial and
because of a prevailing concern that NSAIDs may promote ventricular rupture by impairing myocardial scar
formation. Although animal data support this proposition, no definite proof for this concern exists in humans. However,
expert opinion supports avoidance of these agents in this setting until further evidence is available.
Wrong answers:
A. Colchicine: Colchicine is an effective drug in the treatment of acute bouts of recurrent pericarditis. In addition, colchicine
added to aspirin has been reported to be more effective than aspirin alone in the treatment of a first episode of idiopathic
acute pericarditis. However, its efficacy in the treatment of acute pericarditis in the setting of myocardial infarction has not
been firmly established. Colchicine therapy has no specific role in the treatment of patients after myocardial infarction. Thus,
it would not be the best choice in this patient.
C. High dose ibuprofen: See above.
D. Prednisone: Corticosteroids such as prednisone may promote the development of recurrent pericarditis and should be
avoided if possible in the treatment of acute pericarditis. They should be considered only in patients who are refractory to or
have contraindications for the use of all alternative agents (aspirin, NSAIDs, and colchicine).

QUESTION 5
An 85-year-old woman is admitted to the coronary care unit following successful thrombolytic therapy for an acute anterior
wall ST-elevation myocardial infarction (STEMI). Prior to the myocardial infarction she had been active without any medical
problems and was taking no medications. Blood pressure is 120/70 mm Hg and heart rate is 90/ min. There is no jugular
venous distention and no cardiac murmurs. The lung fields are clear and there is no peripheral edema. Medications started
in the hospital are aspirin, low-molecular-weight heparin, intravenous nitroglycerin, and oral metoprolol. The
electrocardiogram shows Q waves in the anterior leads with upsloping ST segments.
On hospital day 3, the patient experiences acute onset of respiratory distress, and her systolic blood pressure falls to 80
mm Hg. Her oxygen saturation remains at 80% despite the administration of 100% oxygen by face mask. She is given
dopamine and intravenous furosemide. On physical examination, blood pressure is 96/40 mm Hg, pulse rate is 100/min,
and respiration rate is 28/min. Findings include jugular venous distention, crackles throughout both lung fields, and a grade
4/6 systolic murmur associated with a thrill. A pulmonary artery catheter is placed via the right internal jugular vein. The
pulmonary capillary wedge pressure tracing shows prominent v waves.

Whats the best immediate treatment option?

A. Mitral valve repair
B. Pericardiocentesis
C. Pulmonary artery thrombectomy
D. Ventricular septal defect repair

Correct answer: D. Ventricular septal defect repair

Mechanical complications occur in roughly 0.1% of patients with ST-elevation myocardial infarction (STEMI) and usually
occur 2 to 7 days after infarction. Late complications following STEMI include cardiogenic shock, ventricular septal defect,
mitral regurgitation, free wall rupture, and left ventricular thrombus. This patients progressive hypotension, respiratory
distress, and new systolic murmur and thrill suggest either ischemic mitral regurgitation or a ventricular septal defect. Either
mitral regurgitation or a ventricular septal defect can result in a prominent v wave in the pulmonary capillary wedge pressure
tracing. However, only a ventricular septal defect results in the step-up in oxygen saturation from the right atrium to
the right ventricle seen in this patient. Following echocardiography to confirm the diagnosis, this patient should undergo
emergent surgery to repair the defect. Although treatment for a ventricular septal defect is emergent surgery, in-hospital
mortality remains high at approximately 60%.
Wrong answers:
A. Mitral valve repair would be the correct answer for a patient with severe ischemic mitral regurgitation.
B. Pericardiocentesis: Pericardial tamponade from rupture of the left ventricular free wall usually leads to sudden
hypotension and death. Ventricular free wall rupture typically occurs 1 to 4 days after acute myocardial infarction; rarely, it
occurs up to 3 weeks after myocardial infarction. Patients usually present with cardiovascular collapse, tamponade, or
pulseless electrical activity.
C. Pulmonary artery thrombectomy: A massive pulmonary embolism may produce cardiovascular collapse and hypoxemia
but cannot explain the new systolic murmur, left heart failure, prominent v wave, and step-up of oxygen saturation.
Therefore, a pulmonary artery thrombectomy is not indicated.

QUESTION 6
A 42-year-old man is hospitalized for progressively worsening dyspnea on exertion for 6 months, now occurring with minimal
activities. He has had frequent episodes of dyspnea at rest, progressive fatigue, leg edema, and a 9.1-kg (20.0-lb) weight
gain over the last 4 weeks. He reports symptoms of three-pillow orthopnea and nocturnal dyspnea but does not have chest
pain, palpitations, syncope, or cough. There is no family history of sudden cardiac death. He has no other medical problems.
His medications are metoprolol, disopyramide, and furosemide.
On physical examination, temperature is normal, blood pressure is 100/50 mm Hg, pulse is 48/min, and respiration rate is
28/min. Jugular venous distention is noted, with brisk carotid upstrokes. Estimated central venous pressure is 10 cm H2O.
Cardiac examination reveals an S3 gallop at the apex and a grade 3/6 midsystolic murmur along the lower left sternal border
that accentuates with a Valsalva maneuver and diminishes with a hand-grip maneuver. Pulmonary examination discloses
dullness to percussion in the posterior lung fields at the bases, crackles in the basilar posterior lung fields, and no wheezing.
The lower extremities show 3+ edema.
Hb 13.5 g/dL, WBC 8300/mcL, BUN 50 mg/dL, Cr 2.0 mg/dL, Albumin 4.0 g/dL, iron studies WNL, TSH 2.5 mU/L, BNP 2045
Twelve-lead electrocardiogram shows sinus bradycardia, left atrial enlargement, and left ventricular hypertrophy.
Echocardiogram shows hyperdynamic left ventricular systolic function, a left ventricular ejection fraction of 80%, asymmetric
septal hypertrophy, left ventricular dynamic outflow obstruction with a peak gradient of 144 mm Hg, left ventricular diastolic
dysfunction, and left atrial enlargement. Septal thickness is 26 mm. Chest radiograph discloses no infiltrates, an enlarged
cardiac silhouette, and small pleural effusions.
Whats the most appropriate treatment?
A. Carvedilol
B. Implantable cardioverter-defibrillator
C. Permanent pacemaker
D. Surgical septal myectomy

Correct answer: D. Surgical septal myectomy

This young man presents with progressively worsening dyspnea and New York Heart Association (NYHA) functional class
III symptoms. Biventricular heart failure is evident by symptoms (dyspnea, fatigue, weight gain) and signs (jugular venous
distention, S3 gallop, crackles, peripheral edema). Echocardiography confirms a hypertrophic obstructive cardiomyopathy
(HOCM) with diastolic dysfunction, marked septal hypertrophy, and a severe outflow tract obstruction. The patients heart
failure has been refractory to aggressive medical therapy, including negative inotropic and chronotropic agents and
diuretics. Surgical septal myectomy should be considered in patients with outflow obstruction who are NYHA
functional class III or IV and whose symptoms are refractory to medical therapy. Septal myectomy has been
beneficial in improving symptoms of heart failure and may lead to a better prognosis. Thus, this patient who is
refractory to medical therapy with no significant comorbidities should undergo surgical septal myectomy.
Wrong answers:
A. Carvedilol: Beta blockers are useful, however pt is already on metoprolol.
B. An implantable cardioverter-defibrillator is not indicated in this patient with no significant predictors of sudden cardiac
death.
C. Permanent pacemaker: Ventricular pacing reduces the vigor of left ventricular septal contraction by causing an
asynchronous or disorganized pattern of contraction. This reduces left ventricular outflow tract obstruction in HOCM.
However, permanent pacing has not shown long-term benefit in improving heart failure in patients with HOCM. Thus, this
approach is not the best treatment choice.

QUESTION 7
A 40-year-old black man is hospitalized for heart failure. He has had fatigue and progressive dyspnea on exertion for 12
months, pedal edema for 6 months, paroxysmal nocturnal dyspnea for 3 months, and recent onset of orthostatic
lightheadedness. These symptoms have worsened over the past week, prompting the hospitalization. He has a history of
sickle cell anemia with frequent painful hemolytic crises and numerous blood transfusions. Medications are furosemide,
metolazone, diltiazem, lisinopril, hydroxyurea, and folic acid.
On physical examination, temperature is normal, blood pressure is 115/70 mm Hg supine and 80/50 mm Hg standing, pulse
is 90/min supine and 122/min standing, and respiration rate is 30/min. Oxygen saturation on ambient air is 95%. There is
jugular venous distention that worsens with inspiration. Cardiac examination discloses a right-sided S4 gallop, no pericardial
friction rub, and a grade 2/6 holosystolic murmur at the lower left sternal border. Pulmonary auscultation reveals normal
breath sounds and faint bibasilar crackles. The abdomen is distended with shifting dullness. There is 3+ lower extremity
edema to the level of the knees.
Hb 8 g/dL, ferritin 650 ng/mL, iron 512 mcg/dL, transferrin saturation 78%
Twelve-lead electrocardiogram shows normal sinus rhythm and normal QRS voltage. Echocardiogram shows severe biatrial
enlargement, normal left ventricular wall thickness, a left ventricular ejection fraction of 70%, normal ventricular cavity size,
and restrictive left ventricular filling without respiratory variation in peak filling velocity. Endomyocardial biopsy is positive for
iron deposits.
Whats the most appropriate treatment?
A. Heart transplant
B. Increase the dosage of furosemide
C. Iron chelation
D. Phlebotomy

Correct answer: C. Iron chelation

This patient has signs and symptoms of heart failure, particularly of the right side of the heart (peripheral edema, jugular
venous distention, and Kussmaul sign or inspiratory increase in jugular venous distention). Disproportionate involvement of
the right side of the heart should always raise the suspicion for restrictive cardiomyopathy, particularly in a patient at risk for
iron overload. This patients iron studies confirm an acquired iron-overload state, or acquired hemochromatosis.
Hemochromatosis is the only cause of restrictive cardiomyopathy that is potentially reversible by medication
therapy that induces regression of symptoms. Because the body lacks an intrinsic method of increasing elimination of
excessive iron, therapeutic methods are needed. Restrictive cardiomyopathy from iron overload may improve with removal
of iron by chelation therapy in iron-overload states, such as lifelong transfusion-dependent anemias. Iron chelation therapy
is indicated only in patients who cannot tolerate phlebotomy therapy, such as those with significant anemia. Iron
chelation therapy would be the most appropriate treatment in this patient.
Wrong answers:
A. Heart transplant has been used with variable results for treatment of refractory cases of restrictive cardiomyopathy due to
hereditary hemochromatosis. Heart transplant has not been studied and is not of proven benefit in restrictive
cardiomyopathy from acquired hemochromatosis. In addition, in this setting the ongoing need for blood transfusions would
subject the transplanted heart to iron deposition.
B. Increase the dosage of furosemide: Diuretic therapy plays a major role in the symptomatic treatment of patients with
restrictive cardiomyopathy. Importantly, because of these patients pathophysiologic dependence on maintaining higher
atrial pressures (preload) to achieve adequate ventricular filling, excessive diuresis often results in orthostatic hypotension
by lowering atrial pressures. This patient has evidence of orthostatic hypotension that is probably related to his diuretic
therapy. Thus, increasing furosemide (a loop diuretic) would not be the best treatment for this patient.
D. Phlebotomy: Phlebotomy would exacerbate anemia in patients with sickle cell anemia, and thus is not a feasible
treatment option.

QUESTION 8
A 35-year-old black woman is admitted to the hospital after experiencing two episodes of syncope in the same
day. The episodes were brought on by standing, with abrupt loss of consciousness for 5 minutes. There were
no prodromal symptoms and the episodes were nonexertional. She had no associated nausea, vomiting,
diaphoresis, or postictal confusion. She has had a 12-month history of chest pain, cough, and dyspnea.
Exercise thallium stress testing done 2 months ago demonstrated patchy uptake of radionuclide throughout
the ventricular myocardium and no demonstrable ischemia. Her mother died suddenly at age 45 years.
On physical examination, the patient is afebrile, blood pressure is 110/60 mm Hg without orthostasis, pulse is
65/min, and respiration is unlabored at a rate of 16/min. Yellowish-brown maculopapular lesions are present
around the lips and eyelids. Jugular veins are distended. Pulmonary auscultation reveals faint scattered
expiratory wheezes. Cardiac examination discloses normal heart sounds with no murmurs or gallops. Trace
pedal edema is noted.
Twelve-lead electrocardiogram shows sinus rhythm, first-degree atrioventricular block, and left bundle branch
block. Chest radiograph shows hilar lymphadenopathy and scattered interstitial infiltrates. Twenty-four-hour
electrocardiographic monitoring shows frequent premature ventricular ectopic beats and nonsustained
ventricular tachycardia. Endomyocardial biopsy discloses noncaseating granulomata.
Whats the most appropriate management option?
A. Amiodarone
B. Cardiac magnetic resonance imaging
C. Electrophysiologic study
D. Implantable cardioverter-defibrillator placement
E. Implantation of permanent pacemaker

QUESTION 9
A 20-year-old female college student is evaluated at the student health center to establish care. She had no
major medical problems prior to college, and there is no family history of cardiovascular disease.
On physical examination, blood pressure is 110/60 mm Hg and pulse is 70/min. S 1 and S2 are normal and
there is an S4 present. There is a harsh grade 2/6 midsystolic murmur heard best at the lower left sternal
border. The murmur does not radiate to the carotid arteries. A Valsalva maneuver increases the intensity of
the murmur; moving from a standing position to a squatting position, performing a passive leg lift while
recumbent, and performing isometric handgrip exercises decrease the intensity. Rapid upstrokes of the
carotid pulses are present. Blood pressures in the upper and lower extremities are equal.
Whats the most likely diagnosis?
A. Aortic coarctation
B. Bicuspid aortic valve
C. Hypertrophic cardiomyopathy
D. Mitral valve prolapse
E. Ventricular septal defect

Correct answer: C. Hypertrophic cardiomyopathy

This patient has a systolic murmur. The most common diagnoses to consider in the differential diagnosis include a primary valve source, such as
a bicuspid aortic valve, aortic stenosis, mitral valve prolapse, and a benign murmur. Other cardiac abnormalities associated with a systolic
murmur include hypertrophic cardiomyopathy, ventricular septal defect, and aortic coarctation.
In this patient, the physical examination is most consistent with hypertrophic cardiomyopathy. The systolic murmur of hypertrophic
cardiomyopathy is caused by turbulent flow and obstruction in the left ventricular outflow tract from the thickened interventricular septum. In
severe cases, systolic anterior motion of the mitral valve apparatus into the left ventricular outflow tract contributes to the systolic murmur. If
mitral valve leaflet coaptation is affected, there may be concurrent mitral regurgitation. The stand-to-squat maneuver and passive leg lift
transiently increase venous return (preload), which increases left ventricular chamber size and volume. As a consequence, there is
less relative obstruction and turbulence in the left ventricular outflow tract, decreasing murmur intensity. The Valsalva maneuver and
the squat-to-stand maneuver transiently decrease venous return, with the septum and anterior mitral leaflet brought closer together.
Turbulent flowand the murmurare increased. Handgrip exercise increases afterload and decreases the relative pressure gradient
across the left ventricular outflow tract, so murmur intensity for hypertrophic cardiomyopathy is decreased. Transthoracic
echocardiography can confirm a diagnosis of hypertrophic cardiomyopathy.
Wrong answers:
A. Aortic coarctation in an adult is characterized by hypertension and a continuous or late systolic murmur that may be heard over the back.
Because pulses distal to the aortic obstruction are decreased, aortic coarctation is also associated with abnormal differences in upper and lower
extremity blood pressures. The carotid upstroke is normal in coarctation.
B. Bicuspid aortic valve:The murmur of aortic stenosis is an early systolic murmur that often radiates superiorly, toward the carotid arteries.
Hypertrophic cardiomyopathy is associated with rapid upstrokes of the carotid arteries, helping to distinguish it from aortic stenosis (of either a
bicuspid or tricuspid aortic valve), which is associated with a carotid artery pulsation that has a slow up-rise and is diminished in volume.
D. Mitral valve prolapse: The murmur associated with mitral valve prolapse and regurgitation is a holosystolic to late systolic murmur that is
apically located and associated with a midsystolic click. In a patient with mitral valve prolapse, the Valsalva maneuver moves the click murmur
complex earlier in systole and may increase the intensity of the murmur. Similarly, decreased preload (smaller left ventricular chamber size)
increases systolic buckling of the valve leaflets, and the murmur lengthens or intensifies. The carotid upstroke is normal in mitral valve prolapse.
E. Ventricular septal defect: The murmur associated with a ventricular septal defect is a harsh systolic murmur located parasternally that radiates
to the right sternal edge and may be associated with a palpable thrill but no change in the carotid artery pulsation. Maneuvers that increase
afterload, such as isometric handgrip exercise, increase the left-sided murmurs of mitral regurgitation and ventricular septal defect.