Heart failure, also called congestive
heart failure, is a life-threatening
condition in which the heart can no
longer pump enough blood to the rest
of the body.
Alternative Names
CHF; Congestive heart failure
Causes, incidence, and risk factors
Heart failure is almost always a
chronic, long-term condition, although
it can sometimes develop suddenly.
This condition may affect the right
side, the left side, or both sides of the
heart.
As the heart's pumping action is lost,
blood may back up into other areas of
the body, including the:
• Gastrointestinal tract, arms,
and legs (right-sided heart
failure)
• Liver
• Lungs (left-sided heart failure)
Heart failure results in a lack of oxygen
and nutrition to organs, which
damages them and reduces their
ability to function properly. Most areas
of the body can be affected when both
sides of the heart fail.
The most common causes of heart
failure are:
• Coronary artery disease
• High blood pressure
Other structural or functional causes of
heart failure include:
• Cardiomyopathy
o Dilated cardiomyopathy
o Hypertropic
cardiomyopathy
o Restrictive
cardiomyopathy
• Congenital heart disease
• Heart valve disease
• Heart tumor
• Lung disease
Heart failure becomes more common
with advancing age. You are also at
increased risk for developing heart
failure if you are overweight, have
diabetes, smoke cigarettes, abuse
alcohol, or use cocaine.
Symptoms
• Cough
• Decreased alertness or
concentration
• Decreased urine production
• Difficulty sleeping
• Fatigue, weakness, faintness
• Irregular or rapid pulse
• Loss of appetite, indigestion
• Nausea and vomiting
• Neck veins that stick out
• Need to urinate at night
• Sensation of feeling the heart
beat (palpitations)
• Shortness of breath with
activity, or after lying down for
a while
• Swelling of the abdomen
• Swelling of feet and ankles
• Weight gain
Infants may sweat during feeding (or
other activity).
Some patients with heart failure have
no symptoms. In these people, the
symptoms may develop only with
these conditions:
• Abnormal heart rhythm
(arrhythmias)
• Anemia
• Hyperthyroidism
• Infections with high fever
• Kidney disease
Signs and tests
A physical examination may reveal the
following:
• Fluid around the lungs (pleural
effusion)
• Irregular heartbeat
• Leg swelling (edema)
• Neck veins that stick out (are
distended)
• Swelling of the liver
Listening to the chest with a
stethoscope may reveal lung crackles
or abnormal heart sounds. Blood
pressure may be normal, high, or low.
The following tests may reveal heart
swelling or decreased heart function:
• Cardiac MRI
• Chest CT scan
• Chest x-ray
• ECG, which may also show
arrhythmias
• Echocardiogram
• Heart catheterization
• Nuclear heart scans
This disease may also alter the
following test results:
• Blood chemistry
• BUN
• Complete blood count
• Creatinine
• Creatinine clearance
• Liver function tests
• Serum uric acid
• Serum sodium
• Urinalysis
• Urinary sodium
Treatment
If you have heart failure, your doctor
will monitor you closely. You will have
follow up appointments at least every
3 to 6 months and tests every now and
then to check your heart function. For
example, an ultrasound of your heart
(echocardiogram) will be done once in
awhile to see how well your heart
pumps blood with each beat.
You will need to carefully monitor
yourself and help manage your
condition. One important way to do
this is to track your weight on a daily
basis. Weight gain can be a sign that
you are retaining fluid and that the
pump function of your heart is
worsening. Make sure you weigh
yourself at the same time each day
and on the same scale, with little to no
clothes on.
Other important measures include:
• Take your medications as
directed. Carry a list of
medications with you wherever
you go.
• Limit salt intake.
• Don’t smoke.
• Stay active. For example, walk
or ride a stationary bicycle.
Your doctor can provide a safe
and effective exercise plan
based on your degree of heart
failure and how well you do on
tests that check the strength
and function of your heart. DO
NOT exercise on days that your
weight has gone up from fluid
retention or you are not feeling
well.
• Lose weight if you are
overweight.
• Get enough rest, including after
exercise, eating, or other
activities. This allows your heart
to rest as well. Keep your feet
elevated to decrease swelling.
Here are some tips to lower your salt
and sodium intake:
• Look for foods that are labeled
“low-sodium,” “sodium-free,”
“no salt added,” or “unsalted.”
Check the total sodium content
on food labels. Be especially
 careful of canned, packaged,
and frozen foods. A nutritionist
can teach you how to
understand these labels.
• Don’t cook with salt or add salt
to what you are eating. Try
pepper, garlic, lemon, or other
spices for flavor instead. Be
careful of packaged spice
blends as these often contain
salt or salt products (like
monosodium glutamate, MSG).
• Avoid foods that are naturally
high in sodium, like anchovies,
meats (particularly cured
meats, bacon, hot dogs,
sausage, bologna, ham, and
salami), nuts, olives, pickles,
sauerkraut, soy and
Worcestershire sauces, tomato
and other vegetable juices, and
cheese.
• Take care when eating out.
Stick to steamed, grilled,
baked, boiled, and broiled foods
with no added salt, sauce, or
cheese.
• Use oil and vinegar, rather than
bottled dressings, on salads.
• Eat fresh fruit or sorbet when
having dessert.
Your doctor may consider prescribing
the following medications:
• ACE inhibitors such as captopril,
enalapril, lisinopril, and ramipril
to open up blood vessels and
decrease the work load of the
heart
• Diuretics including thiazide,
loop diuretics, and potassium-
sparing diuretics to help rid
your body of fluid and sodium
• Digitalis glycosides to increase
the ability of the heart muscle
to contract properly and help
treat some heart rhythm
disturbances
• Angiotensin receptor blockers
(ARBs) such as losartan and
candesartan to reduce the
workload of the heart; this class
of drug is especially important
for those who cannot tolerate
ACE inhibitors
• Beta-blockers such as such as
carvedilol and metoprolol,
which are particularly useful for
those with a history of coronary
artery disease
If you have sudden (acute) heart
failure, you may be admitted to the
hospital. Treatment may involve:
• Oxygen
• Medicines given through a vein,
including dobutamine or
milrinone, which help the heart
pump blood
• A medication called nesiritide
(Natrecor) to help dilate blood
vessels
Swan-Ganz catheterization may be
needed in some cases. If excessive
fluid has gathered around the sac
surrounding the heart (pericardium),
pericardiocentesis will be done.
Severe heart failure may require the
following treatments:
• Thoracentesis to remove excess
fluid
• Implanted devices such as the
intra-aortic balloon pump (IABP)
and the left ventricular assist
device (LVAD)
These devices can be life-saving, but
they are not permanent solutions.
Patients who become dependent on
circulatory support will need a heart
transplant.
Heart failure symptoms may be
improved with biventricular pacemaker
or cardiac resynchronization therapy.
Ask your provider if you are a
candidate for this type of treatment.
• circulatory collapse)
Possible side effects of medications
include:
 • Cough
• Digitalis toxicity
• Gastrointestinal upset (such as
nausea, heartburn, diarrhea)
• Headache
• Light-headedness and fainting
• Low blood pressure
• Lupus reaction
• Muscle cramps
Calling your health care provider
Call your health care provider if
weakness, increased cough or sputum
production, sudden weight gain or
swelling, or other new or unexplained
symptoms develop.
Go to the emergency room or call the
local emergency number (such as 911)
if you experience severe crushing
chest pain, fainting, or rapid and
irregular heartbeat (particularly if
other symptoms accompany a rapid
and irregular heartbeat).
Prevention
Follow your health care provider's
treatment recommendations and take
all medications as directed.
Keep your blood pressure , heart rate,
and cholesterol under control as
recommended by your doctor. This
may involve exercise, a special diet,
and medications.
Other important treatment measures:
• Do not smoke.
• Do not drink alcohol.
• Reduce salt intake.
• Exercise as recommended by
your health care provider.
PERICARDITIS
Acute pericarditis
Definition
Acute pericarditis is an inflammatory
process involving the pericardium that
results in a clinical syndrome with the
triad of chest pain, pericardial friction
rub, and changes in the
electrocardiogram (ECG). 1
Prevalence
Acute pericarditis is the admitting
diagnosis in 0.1% of hospital
admissions. It occurs more commonly
in men than in women.
Causes
The most common form of acute
pericarditis is idiopathic, which
accounts for about 90% of cases (Box
1). 2 Other common causes include
infection, renal failure, myocardial
infarction (MI), 3 malignancy, radiation,
and trauma. 4 These are discussed in
more detail later.
Box 1: Common Causes of
Pericarditis and Pericardial
Effusion
Idiopathic
Infectious—bacterial, viral, fungal, HIV
Myocardial infarction
Radiation
Postoperatively after open heart
surgery
Chest trauma—blunt, sharp
Malignancy
• Primary—mesothelioma,
angiosarcoma
• Metastatic—lung, breast, bone,
lymphoma, melanoma
Collagen vascular diseases—
rheumatoid arthritis, SLE
Metabolic—uremia, hypothyroidism
Pharmacologic—penicillin, phenytoin,
procainamide, hydralazine, minoxidil,
cromolyn sodium, methysergide,
doxorubicin
HIV, human immunodeficiency virus;
SLE, systemic lupus erythematosus.
Signs and Symptoms
Symptoms
The most common symptom of acute
pericarditis is severe, sharp,
retrosternal chest pain, often radiating
to the neck, shoulders, or back.
Positional changes are characteristic,
with worsening of the pain in the
supine position and with inspiration,
and improvement with sitting upright
and leaning forward. Other symptoms
may occur, reflecting the underlying
disease.
Physical Examination Findings
A scratchy, grating, high-pitched
friction rub (“squeak of leather of a
new saddle”) caused by fibrinous
deposits in the pericardial space (Fig.
1) with three components—atrial
systole, ventricular systole, and early
ventricular diastole—is classic. It is
best heard during inspiration at the left
lower sternal border, with the patient
leaning forward. The rub may
disappear with the development of an
effusion and impending cardiac
tamponade.
Specific Types of Acute
Pericarditis
Idiopathic Pericarditis.
The cause of acute pericarditis is often
difficult to establish, and idiopathic
pericarditis remains the most common
diagnosis.
Viral Pericarditis.
Coxsackievirus B virus and echovirus
are the most common viruses, and a
fourfold increase in antiviral titers is
required for the diagnosis. Patients
often experience a prodrome of an
upper respiratory tract infection. The
prognosis of viral pericarditis is good,
the course is usually self limited, and
patients may be treated on an
outpatient basis.
Purulent Pericarditis.
Before the antibiotic era, pneumonia
was the prime cause of purulent
pericarditis. Currently, causes include
thoracic surgery, chemotherapy,
immunosuppression, and
hemodialysis. Presentation is usually
acute with high fevers, chills, night
sweats, and dyspnea, but the classic
findings of chest pain or friction rub
are rare. Cardiac tamponade occurs
frequently (42% to 77% of patients in
select series), and mortality is high. If
purulent pericarditis is suspected,
hospital admission with immediate
pericardiocentesis and intravenous
broad-spectrum antibiotics are
mandatory, followed by early surgical
drainage. Findings on pericardial fluid
analysis include a high protein level
(more than 6 g/dL), low glucose level
(lower than 35 mg/dL), and very high
leukocyte count (6,000 to
240,000/mm3). 5
Tuberculous Pericarditis.
This occurs in 1% to 2% of cases of
pulmonary tuberculosis.
Immunocompromised or human
immunodeficiency virus (HIV)–positive
patients are at increased risk. 6
Nonspecific symptoms such as
dyspnea, fever, chills, and night
sweats develop slowly, and a friction
rub or chest pain is often absent. The
ECG is usually unrevealing, but the
chest radiograph may be most useful
when findings of pulmonary
tuberculosis are present (Figs. 2 and
3). A patient with suspected or
diagnosed pericardial tuberculosis
should be hospitalized, and
antituberculous therapy (e.g., rifampin,
isoniazid, streptomycin, ethambutol)
started promptly.
Analysis of the pericardial fluid shows
high specific gravity, very high protein
level (often more than 6 g/dL), and
predominantly lymphocytic cells. A
pericardial biopsy with acid-fast bacilli
polymerase chain reaction testing is
recommended for all patients with
suspected tuberculous pericarditis.
However, a normal pericardial biopsy
does not exclude the diagnosis.
Uremic and Dialysis-Associated
Pericarditis.
Uremic pericarditis occurs in 6% to
10% of patients with advanced renal
failure before the initiation of
hemodialysis; blood urea nitrogen
levels usually exceed 60 mg/dL. The
typical ST-segment elevation on the
ECG usually is absent. A large
hemorrhagic effusion caused by
impaired platelet function is common,
although tamponade is rare. Dialysis-
associated pericarditis is caused by
fluid overload, and the fluid is usually
serous. With both forms, initiation or
intensification of hemodialysis is
indicated, usually leading to
improvement in 1 to 2 weeks. 7,8
Postmyocardial Infarction
Pericarditis.
This is a common complication (25% to
40% of patients with MI) and occurs
early, within 3 to 10 days after the MI.
Its development correlates with the
extent of necrosis, is more frequent
with anterior than inferior infarcts, and
is associated with a higher 1-year
mortality rate and incidence of
congestive heart failure. 9
The diagnosis of post-MI pericarditis
requires symptoms or a new
pericardial friction rub; a pericardial
effusion alone is nonspecific. In
addition to the typical ST elevation
seen with acute pericarditis that may
be difficult to differentiate from the
actual MI in this setting, findings on
the ECG are persistently positive T
waves more than 2 days post-MI or
normalization of previously inverted T
waves. 10
Postcardiac Injury Syndrome.
Dressler's syndrome typically occurs 2
to 3 weeks after MI or open heart
surgery. An autoimmune component
and possibly a latent viral infection are
believed to be responsible. The fully
expressed syndrome consists of
pleuritic chest pain, fever,
leukocytosis, and a pericardial friction
rub. Pleural effusions or pulmonary
infiltrates may be seen.
Malignancy.
Pericarditis associated with
malignancy is caused mostly by
metastatic disease. Bronchogenic or
breast carcinoma, Hodgkin's disease,
and lymphoma are common (Fig. 4);
primary mesothelioma and
angiosarcoma are rare. Diagnosis is
based on analysis of pericardial fluid
cytology, which has a sensitivity
ranging from 70% to 90% and a
specificity of up to 95% to 100%. 1
Radiation Pericarditis.
Recent or remote mediastinal radiation
may cause pericarditis at any time
from weeks to months after the
exposure.
Pericarditis associated with
malignancy is caused mostly by
metastatic disease. Bronchogenic or
breast carcinoma, Hodgkin's disease,
and lymphoma are common (Fig. 4);
primary mesothelioma and
angiosarcoma are rare. Diagnosis is
based on analysis of pericardial fluid
cytology, which has a sensitivity
ranging from 70% to 90% and a
specificity of up to 95% to 100%. 1
Radiation Pericarditis.
Recent or remote mediastinal radiation
may cause pericarditis at any time n
from weeks to months after the Resolutio Flattenin
exposure. 2 Days Resolution
n g
Days-
The diagnosis of acute pericarditis 3 week Inversion
remains a clinical s
diagnosis based on Days-
history, physical 4 week Upright
examination, and the s
ECG. Other imaging
studies, including
computed tomography
(CT), magnetic resonance Table 2: Electrocardiographic
imaging (MRI), and Differentiation of Acute
echocardiography, may Pericarditis and
be used in select cases to Myocardial Infarction
investigate the
pericardium. Acute Acute
Paramet
Electrocardiography Pericarditi Myocardial
er
s Infarction
Diffuse in I,
The ECG in acute pericarditis has four
II, and III
consecutive stages ( Table 1 ). Stage Focal—vascular
Originating
1, characterized by diffuse ST territory
ST from S wave
elevation, is the most useful stage for Originating
elevation Concave
the diagnosis of acute pericarditis (Fig. from R wave
Lead V6—ST-
6). The distinction between pericarditis Convex
T amplitude
and acute MI is difficult at times, but
>0.24 mm
there are several clues (Table 2). 12
Present;
Troponin levels may be elevated in up
reciprocal
to 50% of patients with pericarditis ST
Lead aVR changes to ST
but, in the absence of myocarditis, the depressio
only elevation
prognosis remains unchanged. 13 n
according to
territory
Leads aVR,
Rare changes if
PR V1—
atrial infarction
Table 1: Stages of Acute segment elevation
is present
Pericarditis by frequent
Electrocardiography
ST Chest Radiography
Stag PR
Time Segmen T Wave
e Segment
t The chest radiograph may be entirely
1 HoursDiffuse Upright • Lead normal unless there is a pericardial
elevation s effusion causing cardiomegaly (Fig. 7)
aVR, or changes caused by an underlying
V1— disease.
eleva
tion Echocardiography

• All An episode of acute pericarditis that

other responds well to therapy may be
s— followed clinically. Indications for
depr echocardiography are symptoms
essio persisting for longer than 1 to 2 weeks,
the presence of hemodynamic
abnormalities, clinical suspicion of a
large or increasing pericardial effusion,
or recent cardiac surgery.
Treatment
Most cases of acute pericarditis are
uncomplicated and self limited and
may be treated on an outpatient basis.
Indications for an imaging modality,
hospital admission, or both include
clinical suspicion of a large effusion,
hemodynamic instability, severe pain
or other symptoms, suspicion of a
serious underlying condition, or any
other signs or symptoms of clinical
instability or impending deterioration.
Medical Management
Treatment of the underlying disease is
the mainstay of therapy. 14
Nonsteroidal anti-inflammatory drugs
(NSAIDs) can be used for relief of pain,
with agents such as indomethacin and
aspirin having similar efficacy. 15
Ibuprofen may be started at a dose of
400 mg every 8 hours and increased
for symptom relief. 15 Ketorolac
tromethamine may be used as a
parenteral agent for relief of
symptoms. 16 NSAIDs are
contraindicated in the early period
(less than 7 to 10 days) after MI (may
predispose to cardiac rupture), and
aspirin should be used instead.
If pericarditis recurs (20% to 30% of
patients) or response to NSAIDs is
poor, prednisone may be started at
high doses and then tapered over 3
weeks. Use of steroids in acute
pericarditis may promote a recurrence.
17
As with NSAIDs, steroids should be
avoided in post-MI pericarditis because
there is an increased incidence of
myocardial wall rupture.
Colchicine may be effective for
persistent or refractory cases of
Dressler's syndrome and idiopathic
pericarditis. 18,19 The COPE trial found
that colchicine in addition to aspirin
reduces the recurrence of pericarditis
from 32.3% to 10.7%. 20 If not
mandatory, anticoagulants should be
avoided during the acute phase of
pericarditis to reduce the risks of
bleeding and tamponade.
Pericardiectomy
Indications for pericardiectomy include
the development of pericardial
constriction and, rarely, recurrent
pericarditis. Pericardiectomy is the
most definitive procedure, with almost
no recurrence; the 30-day
perioperative mortality rate is about
5%.
Outcomes
Patients with uncomplicated acute
pericarditis should have regular follow-
up after the initial visit to ensure
resolution of symptoms and rule out
the development of constrictive
symptoms.
Back to Top
Pericardial effusion
Definition
Pericardial effusion is defined as an
increased amount of pericardial fluid.
Cause
The most common causes of large
pericardial effusions (see Box 1) are
malignancy (25% of cases), infection
(27%), collagen vascular disease
(12%), and chest radiation (14%). 21,22 A
pericardial effusion is the most
common cardiovascular manifestation
of acquired immunodeficiency
syndrome and is associated with a
worse outcome. 23–25
Pathophysiology
The pericardial sac normally contains
15 to 30 mL of fluid; it can hold 80 to
200 mL of fluid acutely and even up to
2 L if the fluid accumulates slowly. The
development of tamponade depends
on the rate of accumulation rather
than on the volume of the effusion.
Typically, signs of right ventricular
diastolic failure develop first, followed
by left-sided symptoms. As the
understanding of tamponade has
evolved, it has been shown that
cardiac hemodynamics can be altered
early, because fluid accumulates
without clinical evidence of
tamponade. 26
Signs and Symptoms
Symptoms
Symptoms arise from the compression
of surrounding structures (lung,
stomach, phrenic nerve) or diastolic
heart failure and include chest
pressure or pain, dyspnea, and
nausea, abdominal fullness, and
dysphagia. Phrenic nerve irritation
may cause hiccup.
Physical Examination Findings
With a small effusion, the physical
examination is unremarkable. Larger
effusions cause muffled heart sounds
and, rarely, Ewart's sign (dullness to
percussion, bronchial breath sounds,
and egophony below the angle of the
left scapula). With increasing volume
of the effusion, signs and symptoms of
cardiac tamponade may occur.
Diagnosis
Electrocardiography
Low voltage and electrical alternans
(Fig. 8) may be seen if the effusion is
large.
Chest Radiography
Cardiomegaly occurs if there is more
than 250 mL of fluid in the pericardial
sac (see Fig. 7). Displacement of the
pericardial lining more than 2 mm
away from the lower heart border is
best seen on lateral film. 27,28
Echocardiography
A pericardial effusion causes an echo-
free space between visceral and
parietal pericardium; the extent of the
space defines the size of the effusion (
Table 3 ). Large effusions may produce
the picture of a “swinging heart”.
Although echocardiography is the
imaging modality of choice for
diagnosing a pericardial effusion, it
may miss small loculated effusions.
Table 3: Sizing of Pericardial
Effusion by
Echocardiography
Size Small Medium Large
Volume
<100 100-500 >500
(mL)
Localizatio Localize CircumferentiaCircumferentia
n d l l
Width (cm) <1 1-2 >2
Magnetic Resonance Imaging and
Computed Tomography
CT is the best imaging modality for
assessing the pericardium itself, being
slightly superior to MRI in spatial
resolution. Both are superior to
echocardiography in detecting
loculated effusions.
Laboratory Tests
Laboratory analysis in a patient with a
pericardial effusion should include a
complete blood count, chemistry
panel, and erythrocyte sedimentation
rate. Further testing should be done
according to clinical suspicion.
Analysis of Pericardial Fluid
Pericardiocentesis should be
performed for diagnostic purposes if
the cause is unclear or if malignancy,
tuberculous, fungal, or bacterial
infection is suspected. Therapeutic
pericardiocentesis should be disease
performed for large effusions that are Specific
increasing in size or those causing gravity >1.015 <1.015
pretamponade or tamponade. (g/mL)
Total
The initial inspection should assess protein >3.0 <3.0
whether the fluid is hemorrhagic, (g/dL)
purulent, or chylous. A red blood cell Fluid-to-
count higher than 100,000/mm3 is serum
>0.5 <0.5
suggestive of trauma, malignancy, or protein
pulmonary embolism (rare). Chylous ratio
fluid implies injury to the thoracic duct Fluid-to-
by trauma or infiltration. The fluid serum >0.6 <0.6
should be sent for a cell count, Gram LDH ratio
stain, culture, cytology, acid-fast Fluid-to-
bacilli, determination of glucose, serum
<1.0 >1.0
protein, and lactate dehydrogenase glucose
(LDH) levels, and specific gravity. The ratio
parameters listed in Table 4 have a
high sensitivity for differentiating LDH, lactate dehydrogenase
exudates versus transudates. An
elevated protein level higher than 6.0 Treatment
g/dL often indicates tuberculous,
purulent, or parapneumonic effusion. The medical management of
An isolated increased fluid LDH level pericardial effusion is based on
(higher than 300 U/dL) with a normal treating the underlying cause. 29
serum LDH level is most likely caused Diuretics may help decrease the
by malignancy. A low pericardial fluid intensity of fluid overload symptoms if
glucose level (lower than 60 to 80 present. Effusions causing
mg/dL) may be caused by pretamponade or tamponade require
parapneumonic, rheumatoid, immediate drainage. Volume
tuberculous, or malignant effusion. expansion and inotropic support may
However, no diagnostic test of be used for hemodynamic stabilization
pericardial fluid is specific for effusion pending drainage. In the immediate
associated with postpericardiotomy postoperative setting, surgical
syndrome, radiation or uremic management and open drainage are
pericarditis, hypothyroidism, or preferred because of the high
trauma. The overall diagnostic yield of incidence of loculated effusions.
pericardial fluid analysis and biopsy is
low (about 20%), emphasizing the
importance of clinical history and Pericardiocentesis
examination. 5
Echocardiographically guided
Table 4: Pericardial Effusion: pericardiocentesis is safe and
Exudate Versus effective. Indications for
Transudate pericardiocentesis include a large
effusion with hemodynamic
Paramet compromise or tamponade, or for
Exudate Transudate
er diagnostic purposes.
Cause Malignancy Radiation
Infectious,
Uremia Surgical Treatment
parainfectious
Postpericardiotom Hypothyroidis
y syndrome m Percutaneous Balloon
Collagen vascular Trauma Pericardiotomy.
This is the least invasive of the surgical
procedures. It is used mostly for
neoplastic effusion with a poor
prognosis as a palliative treatment
option. The success rate for relieving
reaccumulation of pericardial fluid is
85% to 92% at 30 days. It may be
performed in the catheterization
laboratory under fluoroscopy using a
balloon-dilating catheter.
Subxyphoid Pericardiostomy.
This procedure, known as a
“pericardial window,” may be done
under local anesthesia. It has a high
success rate, with few complications,
and recurrence of fluid accumulation is
rare.
Outcomes
After drainage, follow-up
echocardiography to rule out
reaccumulation and constrictive
physiology should be performed in all
patients. Cardiac tamponade may
develop with large or rapidly
accumulating effusions. 30
Back to Top
Cardiac tamponade
Definition
Cardiac tamponade occurs when fluid
accumulation in the finite pericardial
space causes an increase in pressure,
with subsequent cardiac compression
and hemodynamic compromise.
Prevalence
Of patients with large pericardial
effusions, 25% to 30% develop
tamponade. 31
Pathophysiology
The elevated intrapericardial pressure
leads to progressive limitation of
mostly early diastolic ventricular filling,
resulting in low cardiac output. 32,33
Signs and Symptoms
Symptoms
Symptoms resulting from decreased
cardiac output and congestion include
dyspnea, chest discomfort, weakness,
restlessness, agitation, drowsiness,
oliguria, and anorexia. If the
tamponade develops acutely as a
complication of an acute MI (free wall
rupture) or trauma, the presentation is
usually catastrophic, with sudden
death or shock and high mortality
(Figs. 9 and 10).
Physical Examination Findings
The combination of the classic findings
known as Beck's triad (hypotension,
jugular venous distention, and muffled
heart sounds) occurs in only 10% to
40% of patients. Tachycardia,
tachypnea, and hepa tomegaly are
common. Pulsus paradoxus is defined
as an inspiratory decline in systolic
blood pressure of more than 10 mm
Hg resulting from compression and
poor filling of the left ventricle caused
by increased venous return to the right
side of the heart. Pulsus paradoxus is
nonspecific and insensitive and may
occur with extracardiac disease, such
as severe chronic obstructive
pulmonary disease or asthma. 34
Diagnosis
Electrocardiography
The ECG may be unremarkable.
Abnormal findings on ECG include
electrical alternans (see Fig. 8), low
voltage, and changes associated with
acute pericarditis (see Fig. 6).
Transthoracic Echocardiography
Usually, a moderate-size or large
pericardial effusion is present and
leads to increasing compression and
subsequent diastolic compression of
the cardiac chambers, usually in the
sequence right atrium–right ventricle–
left atrium. The most sensitive finding
for tamponade physiology on the
echocardiogram is inferior vena cava
plethora, with absent inspiratory
collapse. Right ventricle inversion is
the most accurate finding for
diagnosis. Other less specific findings
include excessive respiratory
variations in diastolic mitral valve
inflow, which is analogous to pulsus
paradoxus.
Right Heart Catheterization
The most typical finding of right heart
catheterization is equalization of mean
right atrial, right ventricular and
pulmonary artery diastolic, and mean
pulmonary capillary wedge pressures.
Differential Diagnosis
The symptoms of pericardial
tamponade may mimic those of right-
sided heart failure, right ventricle
infarction, constrictive pericarditis, and
pulmonary embolism. However, with
the use of echocardiography and right
heart catheterization, these may be
easily distinguished.
Treatment
Patients with pretamponade and
tamponade require immediate hospital
admission and prompt pericardial
drainage by pericardiocentesis. The
drain catheter may be left in place for
up to 48 hours if drainage is slow or re-
accumulation likely. If follow-up
echocardiography documents fluid re-
accumulation, a pericardial window
should be considered, because the
infection risk associated with a
pericardial drain increases after 48
hours. 35 Pending drainage, intravenous
fluid expansion and inotropic support
may be used for hemodynamically
unstable patients.
Back to Top
Pericardial constriction
Definition
Constrictive pericarditis refers to an
abnormal thickening of the
pericardium, resulting in impaired
ventricular filling and decreased
cardiac output.
Cause
Most cases are idiopathic, although a
history of acute or chronic pericarditis
may occasionally be elicited.
Pathophysiology
The initiating event causes a chronic
inflammatory pericardial process,
resulting in fibrinous thickening,
calcification of the pericardium (Fig.
11; also see Figs. 2 and 3), and
limitation of intrapericardial volume.
This leads to impaired ventricular
filling and decreased cardiac output.
Ultimately, right and then left
ventricular heart failure develop.
Distinguishing heart failure caused by
constrictive physiology from diastolic
restrictive physiology is a classic
diagnostic dilemma.
igns and Symptoms
Clinical Symptoms
Symptoms are often vague and their
onset is insidious; they include
malaise, fatigue, and decreased
exercise tolerance. With progression of
constriction, symptoms of right-sided
heart failure (e.g., peripheral edema,
nausea, abdominal discomfort, ascites)
become apparent and usually precede
signs of left-sided failure (e.g.,
exertional dyspnea, orthopnea,
paroxysmal nocturnal dyspnea).
Physical Examination Findings
Increased ventricular filling pressures
cause jugular venous distention and
Kussmaul's sign, (absent inspiratory
decline of jugular venous distention),
which is sensitive but nonspecific for
constriction. 36 Auscultation reveals
muffled heart sounds and occasionally
a characteristic pericardial knock (60
to 200 milliseconds after the second
heart sound), caused by sudden
termination of ventricular inflow by the
encasing pericardium.
Constrictive Effusive Pericarditis
This entity consists of a tense
pericardial effusion in the presence of
pericardial constriction, and both
tamponade and constrictive signs and
symptoms are present. Therapy
includes pericardiocentesis initially,
followed by pericardiectomy for long-
term management. 37
Diagnosis
Electrocardiography
The ECG does not show specific
findings, but low voltage may be seen.
Laboratory Test Findings
Brain natriuretic peptide (BNP) is a
serum biomarker that may help
distinguish constrictive pericarditis
from restrictive cardiomyopathy.
Despite elevated filling pressures in
both conditions, levels of BNP are
significantly higher in restrictive
cardiomyopathy. 38
Chest Radiography
Pericardial calcifications (see Figs. 2
and 3), pleural effusions, and biatrial
enlargement may be noted on the
chest radiograph.
Echocardiography
This is the best imaging modality for
assessing hemodynamic parameters
noninvasively. M-mode
echocardiography is useful to look for
flattening of the left ventricular free
wall. Two-dimensional
echocardiography shows septal
bounce and inferior vena cava plethora
with absent inspiratory collapse, as
well as the effects of increased
pericardial pressure on the relatively
low-pressure right atrial and right
ventricular chambers. Doppler
echocardiographic findings have the
highest sensitivity and specificity for
detecting constrictive physiology.
Excessive respiratory variations in
transmitral, transtricuspid, pulmonary
venous, and hepatic vein flow are
characteristic. 39,40 More recently
developed echocardiographic
modalities such as tissue Doppler
imaging have enhanced the ability to
discriminate between restriction and
constriction. 41
Right Heart Catheterization
Direct pressure measurements are
performed if there is doubt about the
diagnosis. M- or W-shaped atrial
pressure waveforms and “square root”
or “dip-and-plateau” right ventricular
pressure waveforms reflect impaired
ventricular filling. Because of the fixed
and limited space within the thickened
and stiff pericardium, end-diastolic
pressure equalization (typically within
5 mm Hg) occurs between these
cardiac chambers. Pulmonary artery
systolic pressures are usually normal
in pericardial constriction; higher
pulmonary pressures suggest a
restrictive cardiomyopathy.
Magnetic Resonance Imaging and
Computed Tomography
CT is the imaging modality of choice to
evaluate the pericardium, being
slightly superior to MRI in spatial
resolution. Pericardial calcifications
may easily be identified on CT.
Although the finding of thickened
pericardium on the CT or MRI is
specific for constriction, up to 18% of
patients with constriction confirmed by
other modalities may not have
pericardial thickening (see Fig. 11). 42
Treatment
Medical treatment is difficult and does
not affect the natural progression or
prognosis of the disease. Diuretics and
a low-sodium diet may be tried for
patients with mild to moderate (New
York Heart Association [NYHA] Class I
or II) symptoms or contraindications to
surgery. 43 For most patients,
pericardiectomy is advised, with 80%
to 90% of patients experiencing
improvement and 50% complete relief
of symptoms. The 30-day
perioperative mortality rate averages
5% to 10%. 44,45
Outcomes
Recurrence following surgery is caused
mainly by incomplete resection.
Without surgical treatment,
biventricular failure develops.
Transient Constrictive Pericarditis
In a minority of patients, constrictive
pericarditis may resolve with medical
therapy, without surgical intervention.
Although most cases are caused by
prior cardiovascular surgery, there
may be other causes, with the
exception of radiation. In select cases,
a trial of medical therapy has been
reported to be useful in the early
stages of pericardial constriction. 46
Summary
• Acute pericarditis manifests
with the triad of acute chest
pain, changes on the ECG, and
a pericardial rub. Ninety
percent of cases are idiopathic,
with troponin levels being
elevated in about 50% of cases.
NSAIDs should be used for most
patients, except post-MI
pericarditis, with steroids as an
additional option for primary
treatment. Steroids may
increase the recurrence rate of
pericarditis. Colchicine may
reduce the recurrence of
pericarditis.
• Cardiac tamponade is a clinical
diagnosis made by
documenting pulsus paradoxus,
jugular venous distention, and
muffled heart sounds in the
presence of a pericardial
effusion. The signs depend on
the volume of fluid in the
pericardial sac and the rate at
which the fluid accumulates.
Echocardiography can confirm
the diagnosis at an early stage
and help with the drainage of
the effusion.
• Pericardial constriction results
from an abnormal thickening of
the pericardium that causes an
impairment of diastolic filling.
The diagnosis can be made by
noting hemodynamic
derangements on
echocardiography and a
thickening of the pericardium
on CT or MRI. About 20% of
patients will not demonstrate
thickening of the pericardium
by CT. The treatment of choice
is surgical excision of the
pericardium. In a minority of
patients, transient constriction
can occur, which may respond
to medical management.
Pericarditis is a condition in which the
sac-like covering around the heart
(pericardium) becomes inflamed.
See also: Bacterial pericarditis
Causes, incidence, and risk factors
Pericarditis is usually a complication of
viral infections, most commonly
echovirus or coxsackie virus. Less
frequently, it is caused by influenza or
HIV infection.
Infections with bacteria can lead to
bacterial pericarditis (also called
purulent pericarditis). Some fungal
infections can also produce
pericarditis.
In addition, pericarditis can be
associated with diseases such as:
• Autoimmune disorders
• Cancer (including leukemia)
• HIV infection and AIDS
• Hypothyroidism
• Kidney failure
• Rheumatic fever
• Tuberculosis
Other causes include:
• Heart attack (see post-MI
pericarditis)
• Injury (including surgery) or
trauma to the chest,
esophagus, or heart
• Medications that suppress the
immune system
• Myocarditis
• Radiation therapy to the chest
Often the cause of pericarditis remains
unknown. In this case, the condition is
called idiopathic pericarditis.
Pericarditis most often affects men
aged 20-50. It usually follows
respiratory infections. In children, it is
most commonly caused by adenovirus
or coxsackie virus.
Symptoms
• Ankle, feet and leg swelling
(occasionally)
• Anxiety
• Breathing difficulty when lying
down
• Chest pain, caused by the
inflamed pericardium rubbing
against the heart
o May radiate to the neck,
shoulder, back or
abdomen
o Often increases with
deep breathing and lying
flat, and may increase
with coughing and
swallowing
o Pleuritis type: a sharp,
stabbing pain
o Usually relieved by
sitting up and leaning
forward
• Dry cough
• Fatigue
• Fever
• Need to bend over or hold the
chest while breathing
Signs and tests
When listening to the heart with a
stethoscope, the health care provider
can hear a sound called a pericardial
rub. The heart sounds may be muffled
or distant. There may be other signs of
fluid in the pericardium (pericardial
effusion).
If the disorder is severe, there may be:
• Crackles in the lungs
• Decreased breath sounds
• Other signs of fluid in the space
around the lungs (pleural
effusion)
If fluid has built up in the pericardial
sac, it may show on:
• Chest MRI scan
• Chest x-ray
• ECG
• Echocardiogram
• Heart MRI or heart CT scan
• Radionuclide scanning
These tests show:
• Enlargement of the heart
• Signs of inflammation
 • Scarring and contracture of the
pericardium (constrictive
pericarditis)
Other findings vary depending on the
cause of pericarditis.
To rule out heart attack, the health
care provider may order serial cardiac
marker levels (CK -MB and troponin I).
Other laboratory tests may include:
• Blood culture
• CBC
• C-reactive protein
• Erythrocyte sedimentation rate
(ESR)
• HIV serology
• Pericardiocentesis, with
chemical analysis and
pericardial fluid culture
• Tuberculin skin test
reatment
The cause of pericarditis must be
identified, if possible.
Medications include:
• Analgesics for pain
• Antibiotics for bacterial
pericarditis
• Antifungal medications for
fungal pericarditis
• Aspirin or a nonsteroidal anti-
inflammatory drug (NSAID)
such as ibuprofen for
inflammation of the
pericardium
• Corticosteroids such as
prednisone
• Colchicine
• Diuretics to remove excess fluid
in the pericardial sac
If the buildup of fluid in the
pericardium makes the heart function
poorly or produces cardiac tamponade,
it is necessary to drain the fluid from
the sac. This procedure, called
pericardiocentesis, may be done using
an echocardiography-guided needle or
a minor surgery.
If the pericarditis is chronic, recurrent,
or causes constrictive pericarditis,
cutting or removing part of the
pericardium may be recommended.
Expectations (prognosis)
Pericarditis can range from mild cases
that get better on their own to life-
threatening cases. The condition can
be complicated by significant fluid
buildup around the heart and poor
heart function.
The outcome is good if the disorder is
treated promptly. Most people recover
in 2 weeks to 3 months. However,
pericarditis may come back.
Complications
• Arrhythmias
• Cardiac tamponade
• Constrictive pericarditis, which
may develop into heart failure
Calling your health care provider
Call your health care provider if you
experience the symptoms of
pericarditis. This disorder can be life-
threatening if untreated.
Prevention
Many cases are not preventable.
Myocarditis is an inflammation of the
heart muscle that decreases the
strength of the heart to pump blood
normally. It can be caused by:
• An infection — Many
infections have been associated
with myocarditis. Some of the
more likely germs include:
o Viral infections — A
common cause of
myocarditis. Although
many different viruses
can cause myocarditis,
coxsackievirus B is the
most common culprit in
the United States. Other
viruses that can cause
myocarditis include
echovirus, influenza
(flu), Epstein-Barr,
rubella, varicella
(chickenpox), mumps
and the hepatitis
viruses. Often the
person has no preceding
symptoms of a cold,
cough, nasal congestion
or rash and only o Chagas' disease —
becomes aware of the
infection when heart
failure occurs.
o HIV infection — About
10% of people with HIV
develop myocarditis,
either because HIV
directly invades the
heart muscle or because
the patient's weakened
immune system makes
the heart muscle more
susceptible to attack by
other infections.
o Bacteria — Rarely,
myocarditis is a
complication of
endocarditis, an
infection of the heart
valves and the lining o Lyme myocarditis —
inside the heart's
chambers caused by
bacteria. Some of the
bacteria responsible for
myocarditis include
Staphylococcus aureus,
enterococci and
Corynebacterium
diphtheriae (the cause
of diphtheria). In about
25% of people with
diphtheria, a toxin
(poison) produced by C.
diphtheriae bacteria
causes a form of
myocarditis that leads to
a flabby, stretched-out
heart muscle. Because
the flabby, enlarged
heart cannot pump
blood efficiently, severe
heart failure may
develop within the first
week of illness.
This infection, caused by
the protozoan
Trypanosoma cruzi, is
transmitted by an insect
bite. In the United
States, myocarditis
caused by Chagas'
disease is most common
among travelers to or
immigrants from Central
and South America. In
up to one-third of people
with Chagas' disease, a
form of chronic (long-
term) myocarditis
develops many years
after the first infection.
This chronic myocarditis
leads to significant
destruction of heart
muscle with progressive
heart failure.
Lyme disease, an
infection caused by the
tick-borne bacterium
Borrelia burgdorferi,
causes myocarditis or
 other heart problems in
about 10% of patients.
• Toxic substances and
certain medications —
Myocarditis also can be caused
by overuse of alcohol, radiation,
chemicals (hydrocarbons and
arsenic) and certain drugs.
• Other agents — Myocarditis
also can be caused by alcohol,
radiation, chemicals
(hydrocarbons and arsenic),
and drugs, including
doxorubicin (Adriamycin,
Rubex), cyclophosphamide
(Cytoxan, Neosar), emetine,
chloroquine (Aralen) and
sulfonamides (Gantanol,
Gantrisin, Thiosulfil Forte,
Urobak). A recent study also
showed that severe emotional
stress can produce heart failure
that startsabruptly, with
evidence of inflammation of
heart muscle.
• Inflammatory diseases —
This includes systemic lupus
erythematosus (SLE or lupus)
and other autoimmune
diseases, sarcoidosis, and
thyrotoxicosis (a very
overactive thyroid).
Another type of myocarditis is peri-
partum cardiomyopathy. For
unexplained reasons, some women in
the very last phase of pregnancy or
soon after delivery of the baby develop
poor heart muscle function. This
condition is unusual.
Symptoms
The symptoms of myocarditis depend
on the cause and severity. For
example, many people with
uncomplicated myocarditis caused by
coxsackievirus don't have any
symptoms, and their only sign of heart
inflammation is a temporary abnormal
result on an electrocardiogram (EKG),
a test that measures the heart's
electrical activity. Other people have
fever, chest pain, cardiac arrhythmias
(abnormally fast, slow or irregular
heartbeats), sudden loss of
consciousness (syncope) or signs of
heart failure (shortness of breath, leg
swelling).
Diagnosis
Your doctor will suspect myocarditis
based on your medical history and
symptoms. To confirm the diagnosis,
your doctor will examine you, paying
special attention to your heart. This
will be followed by an EKG, a chest X-
ray and blood tests. Your doctor will
likely order an echocardiogram to see
how well the heart is pumping.
In some patients, your doctor may
order tests to determine if a virus or
other infectious agent is the cause.
These tests in include blood tests and
attempts at isolating certain types of
viruses from stool, throat washings or
other body fluids.
Expected Duration
How long myocarditis lasts depends on
the cause and on the patient's general
health. For example, in many typically
healthy adults with uncomplicated
coxsackievirus B myocarditis,
symptoms can start to improve over a
couple weeks. In other cases, the heart
takes a few months to recover.
Sometimes, the damage to the heart
muscle is permanent and heart failure
persists after the inflammation has
resolved.
Prevention
Myocarditis caused by infections can
theoretically be avoided by practicing
good hygiene, especially washing your
hands often. Diphtheria myocarditis
can be prevented by undergoing
diphtheria immunization, and HIV can
be prevented by following safe sex
practices and avoiding intravenous
drug use. Myocarditis caused by
insect-borne Chagas' disease can be
prevented by using effective
insecticides in Latin American
countries where the illness is common.
Treatment
Treatment of myocarditis depends on
the cause and severity. For example,
people with only mild viral myocarditis
may be allowed to rest at home. They
will be advised not to smoke or to
drink alcohol, and they will need to
limit strenuous activities until an EKG
test is normal.
People with myocarditis that causes
heart failure or cardiac arrhythmias
will be treated in a hospital. There they
will receive one or more of the
following:
• Oxygen
• Medication or a pacemaker to
treat or prevent cardiac
arrhythmias
• Medication, including diuretics
and vasodilators, to treat heart
failure
• Nonsteroidal anti-inflammatory
drugs (NSAIDs) to relieve pain
• Anticoagulants to prevent blood
clots
• Antibiotics, usually given
intravenously, to treat bacterial
myocarditis or Lyme disease
• Diphtheria antitoxin and
antibiotics to treat diphtheria
myocarditis
• Glucocorticoid medication to
treat autoimmune diseases and
sarcoidosis.
When To Call a Professional
Call your doctor immediately if you
have moderate or severe chest pain,
even if you think that you are too
young to be having heart problems.
People of any age can get the chest
pain of myocarditis, with or without
other symptoms (fever, shortness of
breath, abnormal heartbeat, leg
swelling).
Prognosis
In many people with uncomplicated
viral myocarditis, the illness goes away
on its own, and any myocarditis-
related EKG abnormalities eventually
disappear. However, more severe
forms of myocarditis can cause
permanent damage to the heart
muscle.
Endocarditis, also called infective
endocarditis, is an infection and
inflammation of the heart valves and
the inner lining of the heart chambers,
which is called the endocardium.
Endocarditis occurs when infectious
organisms, such as bacteria or fungi,
enter the bloodstream and settle in the
heart. In most cases, these organisms
are streptococci ("strep"),
staphylococci ("staph") or species of
bacteria that normally live on body
surfaces. The infecting organism
enters the bloodstream through a
break in the skin caused by a skin
disorder or injury; a medical or dental
procedure; or a skin prick, especially
among intravenous drug users.
Depending on the aggressiveness
(virulence) of the infecting germ, the
heart damage caused by endocarditis
can be swift and severe (acute
endocarditis) or slower and less
dramatic (subacute endocarditis).
• Acute endocarditis - Acute
endocarditis most often occurs
when an aggressive species of
skin bacteria, especially a
staphylococcus, enters the
bloodstream and attacks a
normal, undamaged heart
 valve. Once staph bacteria
begin to multiply inside the
heart, they may send small
clumps of bacteria called septic
emboli into the bloodstream to
spread the infection to other
organs, especially to the
kidneys, lungs and brain.
Intravenous (IV) drug users are
at very high risk of acute
endocarditis, because
numerous needle punctures
give aggressive staph bacteria
many opportunities to enter the
blood through broken skin.
Dirty drug paraphernalia
increases the risk. If untreated,
this form of endocarditis can be
fatal in less than six weeks.
• Subacute endocarditis - This
form of endocarditis most often
is caused by one of the viridans
group of streptococci
(Streptococcus sanguis,
mutans, mitis or milleri) that
normally live in the mouth and
throat. Streptococcus bovis or
Streptococcus equinus also can
cause subacute endocarditis,
typically in patients who have
some form of gastrointestinal
cancer, usually colon cancer.
Subacute endocarditis tends to
involve heart valves that
already are damaged in some
way, and it usually is less likely
to cause septic emboli than
acute endocarditis. If untreated,
subacute bacterial endocarditis
can worsen for as long as one
year before it is fatal.
Endocarditis strikes approximately
19,000 people in the United States
each year, with 2,000 deaths. Men
develop endocarditis more often than
women, and the illness is more
common among people who have one
or more of the following risk factors:
• A congenital (present at birth)
malformation of the heart or a
heart valve, or mitral valve
prolapse with mitral valve
regurgitation
• A heart valve damaged by
rheumatic fever or by age-
related valve thickening with
calcium deposits
• An implanted device in the
heart (pacemaker wire, artificial
heart valve)
• A history of IV drug use
• A chronic (long-term) medical
condition that weakens the
immune system (alcoholism,
diabetes, cancer with
chemotherapy)
In about 20% to 40% of patients who
do not have artificial heart valves and
who do not use intravenous drugs, no
heart problem can be identified that
would increase their risk of
endocarditis. In the 10% to 20% of
endocarditis patients who have
artificial heart valves, infections that
follow within 60 days of valve surgery
often are caused by a staphylococcus,
while endocarditis that occurs later
most frequently is caused by a
streptococcus.
Symptoms
Symptoms of acute endocarditis
include:
• High fever
• Chest pain
• Shortness of breath
• Cough
• Small broken blood vessels
(hemorrhages) on the palms
and soles of the feet
If severe heart damage causes shock,
the patient may collapse suddenly;
have a rapid pulse; and have pale, cool
skin.
Symptoms of subacute endocarditis
include:
 • Low-grade fever (less than
102.9 degrees Fahrenheit)
• Chills
• Night sweats
• Pain in muscles and joints
• A persistent tired feeling
• Headache
• Shortness of breath
• Poor appetite
• Weight loss
• Small, tender nodules on the
fingers or toes
• Tiny broken blood vessels on
the whites of the eyes, the
palate, inside the cheeks, on
the chest, or on the fingers and
• Echocardiography - In this
toes
Diagnosis
Your doctor will review your medical
history with particular attention to
possible risk factors for endocarditis,
including congenital heart disease,
rheumatic fever, an artificial heart
valve or pacemaker, a history of IV
drug use, and a history of chronic
illness. Your doctor also will ask
whether you have ever been told that
you have a heart murmur and whether
you have had any recent medical or
dental procedure in which bacteria
might have had an opportunity to
entire your bloodstream (dental
scaling, periodontal surgery,
professional teeth cleaning,
bronchoscopy, certain diagnostic tests
of the genitourinary tract,
colonoscopy).
Your doctor will examine you, and will
check for fever; skin symptoms of
endocarditis (tiny hemorrhages in the
skin, tender nodules on finger and
toes); and a heart murmur, which
indicates possible heart valve damage.
Additional testing includes:
• Serological tests - These are
• Blood cultures - In these
tests, several blood samples
will be drawn over a 24-hour
period. These blood samples
will be added to culture bottles
that contain special nutrients to
aid bacterial growth. If bacteria
are living in your bloodstream,
they will grow inside the culture
bottles in the laboratory. Once
bacteria grow, the specific
species can be identified, and it
can be tested for its sensitivity
to various types of antibiotics.
Results of this testing will help
your doctor select the specific
antibiotic that will work best to
treat endocarditis.
test, sound waves are used to
outline the structure of the
heart, the heart chambers and
heart valves. By using
echocardiography, your doctor
can check for abnormal growths
that contain infecting
organisms (vegetations) inside
the heart. He or she also can
look for abscesses inside the
heart and for signs of damage
to natural or artificial heart
valves. The best type of
echocardiography for
evaluating heart valves is
transesophageal
echocardiography, in which a
tube is inserted through your
mouth, allowing images of the
heart to be obtained from just
behind it. This test may be
recommended if the diagnosis
remains uncertain after
conventional echocardiography.
Transesophageal
echocardiography is also a
much better test for evaluating
artificial heart valves.
blood tests that look for
evidence of increased immune
system activity, which is a sign
of infection. These tests may be
helpful when blood cultures do
 not show bacterial growth,
which happens in a small
percentage of patients.
Expected Duration
Symptoms of acute endocarditis
usually begin suddenly and get worse
quickly. It is an infection that can
develop dramatically over a few days.
Subacute endocarditis develops more
slowly, and its milder symptoms can
be present for weeks or months before
the illness is suspected.
Prevention
If you are at high risk of endocarditis
because of a damaged heart valve or
other medical problem, tell your doctor
and dentist. To prevent endocarditis,
your doctor and dentist may prescribe
antibiotics before you have any
medical or dental procedure in which
bacteria have a chance of entering
your blood. Antibiotics usually are
given to people with artificial valves,
people who had endocarditis in the
past and people with other high-risk
conditions. People with mitral valve
prolapse and many milder conditions
generally do not need antibiotics.
In general, antibiotics are given one to
two hours before a high-risk
procedure, and up to eight hours
afterward. Before a dental procedure,
an antiseptic mouth rinse also can be
used, especially one containing
chlorhexidine or povidone-iodine.
You also can help to prevent
endocarditis by avoiding IV drug use.
Treatment
When endocarditis is caused by a
bacterial infection, it usually is treated
with two to six weeks of antibiotics,
such as penicillins, cephalosporins,
gentamicin (Garamycin, Gentamar, G-
Mycitin) or vancomycin (Vancocin).
The type of antibiotic and the length of
therapy depend on the results of the
blood cultures. In most cases,
antibiotic treatment is given
intravenously (through a vein) while
you are hospitalized. However, certain
highly motivated patients who have
Streptococcus viridans endocarditis
and stable heart function can be
treated at home.
In patients with the following
conditions, the infected heart valve
must be replaced surgically.
• Damage to the aortic or mitral
valve that is severe enough to
cause backflow of blood
through the valve
(regurgitation) with heart
failure
• Valve dysfunction and
persistent infection after 7 to
10 days of appropriate
antibiotic therapy
• Abnormal growth of
organisms(vegetation) larger
than 10 millimeters (seen on
echocardiography) clinging to a
heart valve
• Endocarditis caused by a
fungus rather than bacteria –
Fungal endocarditis often
responds poorly to intravenous
antifungal medications.
When To Call a Professional
Call your doctor whenever you
experience symptoms of acute or
subacute endocarditis, especially if you
have a history of heart valve damage,
a known heart murmur or an
implanted device in your heart
(artificial valve or pacemaker wire).
Prognosis
With prompt diagnosis and proper
medical treatment, about 90% of
patients with bacterial endocarditis
recover. Those whose endocarditis
affects the right side of the heart
usually have a better outlook than
those with left-side involvement. In
cases in which endocarditis is caused
by fungi, the prognosis is usually
worse than for bacterial endocarditis.
Some possible complications of
endocarditis include:
• Congestive heart failure
• Floating blood clots, called
emboli, in the bloodstream that
lodge in the brain, lungs or
coronary arteries
• Kidney problems
If acute endocarditis remains
untreated, it can be fatal in less than
six weeks. Untreated subacute
endocarditis can cause death within
six weeks to one year.
Central venous pressure (CVP)
describes the pressure of blood in the
thoracic vena cava, near the right
atrium of the heart. CVP reflects the
amount of blood returning to the heart
and the ability of the heart to pump
the blood into the arterial system.
It is a good approximation of right
atrial pressure,[1] which is a major
determinant of right ventricular end
diastolic volume. (However, there can
be exceptions in some cases.)[2]
Measurement
Normal CVP can be measured from two
points of reference:
• Sternum: 0-5 cm H2O
• Midaxillary line: 5-10 cm H2O
CVP can be measured by connecting
the patient's central venous catheter
to a special infusion set which is
connected to a small diameter water
column. If the water column is
calibrated properly the height of the
column indicates the CVP.
In most progressive intensive care
units in the U.S., specialized monitors
are available to continuously measure
CVP as well as other hemodynamic
values.
Normal values are 2-8 mmHg
Factors affecting CVP
Factors which increase CVP include:
• Hypervolemia
• forced exhalation
• Tension pneumothorax
• Heart failure
• Pleural effusion
• Decreased cardiac output
• Cardiac tamponade
Factors which decrease CVP include:
• Hypovolemia
• Deep inhalation
• Distributive shock
Coronary artery bypass surgery, also
coronary artery bypass graft
(CABG) surgery, and
colloquially heart bypass or
bypass surgery is a surgical
procedure performed to
relieve angina and reduce
the risk of death from
coronary artery disease.
Arteries or veins from
elsewhere in the patient's
body are grafted to the
coronary arteries to bypass
atherosclerotic narrowings
and improve the blood
supply to the coronary
circulation supplying the
myocardium (heart muscle).
This surgery is usually
performed with the heart
stopped, necessitating the
usage of cardiopulmonary
bypass; techniques are
available to perform CABG on
a beating heart, so-called
"off-pump" surgery.
Terminology
There are many variations on
terminology, in which one or more of
'artery', 'bypass' or 'graft' is left out.
The most frequently used acronym for
this type of surgery is CABG
(pronounced 'cabbage'),[5] pluralized as
CABGs (pronounced 'cabbages'). More
recently the term aortocoronary
bypass (ACB) has come into popular
use. CAGS (Coronary Artery Graft
Surgery, pronounced phonetically)
should not be confused with Coronary
Angiography (CAG).
Arteriosclerosis is a common arterial
disorder characterized by thickening,
loss of elasticity, and calcification of
arterial walls, resulting in a decreased
blood supply.
Atherosclerosis is a common arterial
disorder characterized by yellowish
plaques of cholesterol, lipids, and
cellular debris in the inner layer of the
walls of large and medium-sized
arteries.
[edit] Number of bypasses
The terms single bypass, double
bypass, triple bypass, quadruple
bypass and quintuple bypass refer to
the number of coronary arteries
bypassed in the procedure. In other
words, a double bypass means two
coronary arteries are bypassed (e.g.
the left anterior descending (LAD)
coronary artery and right coronary
artery (RCA)); a triple bypass means
three vessels are bypassed (e.g. LAD,
RCA, left circumflex artery (LCX)); a
quadruple bypass means four vessels
are bypassed (e.g. LAD, RCA, LCX, first
diagonal artery of the LAD) while
quintuple means five. Bypass of more
than four coronary arteries is
uncommon.
A greater number of bypasses does
not imply a person is "sicker," nor does
a lesser number imply a person is
"healthier."[6] A person with a large
amount of coronary artery disease
(CAD) may receive fewer bypass grafts
owing to the lack of suitable "target"
vessels. A coronary artery may be
unsuitable for bypass grafting if it is
small (< 1 mm or < 1.5 mm depending
on surgeon preference), heavily
calcified (meaning the artery does not
have a section free of CAD) or
intramyocardial (the coronary artery is
located within the heart muscle rather
than on the surface of the heart).
Similarly, a person with a single
stenosis ("narrowing") of the left main
coronary artery requires only two
bypasses (to the LAD and the LCX).
However, a left main lesion places a
person at the highest risk for death
from a cardiac cause.[citation needed]
The surgeon reviews the coronary
angiogram prior to surgery and
identifies the lesions (or "blockages")
in the coronary arteries. The surgeon
will estimate the number of bypass
grafts prior to surgery, but the final
decision is made in the operating room
upon examination of the heart.
Indications for CABG
Several alternative treatments for
coronary artery disease exist. They
include:
• Medical management (anti-
anginal medications plus
statins, antihypertensives,
smoking cessation, tight blood
sugar control in diabetics)
• Percutaneous coronary
intervention (PCI)
Both PCI and CABG are more effective
than medical management at relieving
symptoms,[7] (e.g. angina, dyspnea,
fatigue). CABG is superior to PCI for
some patients with multivessel CAD[8][9]
The Surgery or Stent (SoS) trial was a
randomized controlled trial that
compared CABG to PCI with bare-metal
stents. The SoS trial demonstrated
CABG is superior to PCI in multivessel
coronary disease.[8]
The SYNTAX trial was a randomized
controlled trial of 1800 patients with
multivessel coronary disease,
comparing CABG versus PCI using
drug-eluting stents (DES). The study
found that rates of major adverse
cardiac or cerebrovascular events at
12 months were significantly higher in
the DES group (17.8% versus 12.4%
for CABG; P=0.002). [9] This was
primarily driven by higher need for
repeat revascularization procedures in
the PCI group with no difference in
repeat infarctions or survival. Higher
rates of strokes were seen in the CABG
group.
The FREEDOM (Future
Revascularization Evaluation in
Patients With Diabetes Mellitus—
Optimal Management of Multivessel
Disease) trial will compare CABG and
DES in patients with diabetes. The
registries of the nonrandomized
patients screened for these trials may
provide as much robust data regarding
revascularization outcomes as the
randomized analysis.[10]
A study comparing the outcomes of all
patients in New York state treated with
CABG or percutaneous coronary
intervention (PCI) demonstrated CABG
was superior to PCI with DES in
multivessel (more than one diseased
artery) coronary artery disease (CAD).
Patients treated with CABG had lower
rates of death and of death or
myocardial infarction than treatment
with a coronary stent. Patients
undergoing CABG also had lower rates
of repeat revascularization.[11] The New
York State registry included all
patients undergoing revascularization
for coronary artery disease, but was
not a randomized trial, and so may
have reflected other factors besides
the method of coronary
revascularization.
The 2004 ACC/AHA CABG guidelines
state CABG is the preferred treatment
for:[12]
• Disease of the left main
coronary artery (LMCA).
• Disease of all three coronary
vessels (LAD, LCX and RCA).
• Diffuse disease not amenable
to treatment with a PCI.
The 2005 ACC/AHA guidelines further
state: CABG is the likely the preferred
treatment with other high-risk patients
such as those with severe ventricular
dysfunction (i.e. low ejection fraction),
or diabetes mellitus.[12]
Prognosis
Prognosis following CABG depends on
a variety of factors, but successful
grafts typically last around 10–15
years. In general, CABG improves the
chances of survival of patients who are
at high risk (meaning those presenting
with angina pain shown to be due to
ischemic heart disease), but
statistically after about 5 years the
difference in survival rate between
those who have had surgery and those
treated by drug therapy diminishes.
Age at the time of CABG is critical to
the prognosis, younger patients with
no complicating diseases have a high
probability of greater longevity. The
older patient can usually be expected
to suffer further blockage of the
coronary arteries.
Procedure (Simplified)
1. The patient is brought to the
operating room and moved on
to the operating table.
2. An anaesthetist places a variety
of intravenous lines and injects
an induction agent (usually
propofol) to render the patient
unconscious.
3. An endotracheal tube is
inserted and secured by the
anaesthetist or assistant (e.g.
respiratory therapist or nurse
anaesthetist) and mechanical
ventilation is started.
4. The chest is opened via a
median sternotomy and the
 heart is examined by the
surgeon.
5. The bypass grafts are
harvested - frequent conduits
are the internal thoracic
arteries, radial arteries and
saphenous veins. When
harvesting is done, the patient
is given heparin to prevent the
blood from clotting.
6. In the case of "off-pump"
surgery, the surgeon places
devices to stabilize the heart.
7. If the case is "on-pump", the
surgeon sutures cannulae into
the heart and instructs the
perfusionist to start
cardiopulmonary bypass (CPB).
Once CPB is established, the
surgeon places the aortic cross-
clamp across the aorta and
instructs the perfusionist to
deliver cardioplegia to stop the
heart.
8. One end of each graft is sewn
on to the coronary arteries
beyond the blockages and the
other end is attached to the
aorta.
9. The heart is restarted; or in
"off-pump" surgery, the
stabilizing devices are
removed. In some cases, the
Aorta is partially occluded by a
C-shaped clamp, the heart is
restarted and suturing of the
grafts to the aorta is done in
this partially occluded section
of the aorta while the heart is
beating.
10. Protamine is given to reverse
the effects of heparin.
11. The sternum is wired together
and the incisions are sutured
closed.
12. The patient is moved to the
intensive care unit (ICU) to
recover. After awakening and
stabilizing in the ICU
(approximately 1 day), the
person is transferred to the
cardiac surgery ward until
ready to go home
(approximately 4 days).
Minimally Invasive CABG
Alternate methods of minimally
invasive coronary artery bypass
surgery have been developed in recent
times. Off-pump coronary artery
bypass surgery (OPCAB) is a technique
of performing bypass surgery without
the use of cardiopulmonary bypass
(the heart-lung machine). Further
refinements to OPCAB have resulted in
minimally invasive direct coronary
artery bypass surgery (MIDCAB), a
technique of performing bypass
surgery through a 5 to 10 cm incision.
Conduits used for bypass
The choice of conduits is highly
dependent upon the particular surgeon
and institution. Typically, the left
internal thoracic artery (LITA)
(previously referred to as left internal
mammary artery or LIMA) is grafted to
the left anterior descending artery and
a combination of other arteries and
veins is used for other coronary
arteries. The right internal thoracic
artery (RITA), the great saphenous
vein from the leg and the radial artery
from the forearm are frequently used.
The right gastroepiploic artery from
the stomach is infrequently used given
the difficult mobilization from the
abdomen.
[edit] Graft patency
Grafts can become diseased and may
occlude in the months to years after
bypass surgery is performed. Patency
is a term used to describe the chance
that a graft remain open. A graft is
considered patent if there is flow
through the graft without any
significant (>70% diameter) stenosis
in the graft.
Graft patency is dependent on a
number of factors, including the type
of graft used (internal thoracic artery,
radial artery, or great saphenous vein),
the size or the coronary artery that the
graft is anastomosed with, and, of
course, the skill of the surgeon(s)
performing the procedure. Arterial
grafts (e.g. LITA, radial) are far more
sensitive to rough handling than the
saphenous veins and may go into
spasm if handled improperly.
Generally the best patency rates are
achieved with the in-situ (the proximal
end is left connected to the subclavian
artery) left internal thoracic artery with
the distal end being anastomosed with
the coronary artery (typically the left
anterior descending artery or a
diagonal branch artery). Lesser
patency rates can be expected with
radial artery grafts and "free" internal
thoracic artery grafts (where the
proximal end of the thoracic artery is
excised from its origin from the
subclavian artery and re-anastomosed
with the ascending aorta). Saphenous
vein grafts have worse patency rates,
but are more available, as the patients
can have multiple segments of the
saphenous vein used to bypass
different arteries.
Veins that are used either have their
valves removed or are turned around
so that the valves in them do not
occlude blood flow in the graft. LITA
grafts are longer-lasting than vein
grafts, both because the artery is more
robust than a vein and because, being
already connected to the arterial tree,
the LITA need only be grafted at one
end. The LITA is usually grafted to the
left anterior descending coronary
artery (LAD) because of its superior
long-term patency when compared to
saphenous vein grafts.[13][14]
[edit] Sternal Precautions
Patients undergoing coronary artery
bypass surgery will have to avoid
certain things for eight to 12 weeks to
reduce the risk of opening the incision.
These are called sternal precautions.
First, patients need to avoid using their
arms excessively, such as pushing
themselves out of a chair or reaching
back before sitting down. To avoid this,
patients are encouraged to build up
momentum by rocking several times in
their chair before standing up. Second,
patients should avoid lifting anything
in excess of 5-10 pounds. A gallon
(U.S.) of milk weighs approximately 8.5
pounds, and is a good reference point
for weight limitations. Finally, patients
should avoid overhead activities with
their hands, such as reaching for
sweaters from the top shelf of a closet
or reaching for plates or cups from the
cupboard.
[edit] Complications
People undergoing coronary artery
bypass are at risk for the same
complications as any surgery, plus
some risks more common with or
unique to CABG.
[edit] CABG associated
• Postperfusion syndrome
(pumphead), a transient
neurocognitive impairment
associated with
cardiopulmonary bypass. Some
research shows the incidence is
initially decreased by off-pump
coronary artery bypass, but
with no difference beyond three
months after surgery. A
neurocognitive decline over
time has been demonstrated in
people with coronary artery
disease regardless of treatment
(OPCAB, conventional CABG or
medical management).
However, recent research
suggests that the cognitive
decline is not caused by CABG
but is rather a consequence of
vascular disease.[15]
• Nonunion of the sternum;
internal thoracic artery
harvesting devascularizes the
sternum increasing risk.
• Myocardial infarction due to
embolism, hypoperfusion, or
graft failure.
• Late graft stenosis, particularly
of saphenous vein grafts due to
 atherosclerosis causing
recurrent angina or myocardial
infarction.
• Acute renal failure due to
embolism or hypoperfusion.
• Stroke, secondary to embolism
or hypoperfusion.

[edit] General surgical

• Infection at incision sites or

sepsis.
• Deep vein thrombosis (DVT)
• Anesthetic complications such
as malignant hyperthermia.
• Keloid scarring
• Chronic pain at incision sites
• Chronic stress related illnesses
• Death

[edit] Randomized Controlled Trial

(RCT) including Placebo

While there have been a handful of

RCTs[8][9] comparing CABG with other
surgical procedures, an exhaustive
review of the medical literature
reported in 2002 found no RCT had
ever been conducted to demonstrate
the efficacy of CABG to that of
placebo.[16] In fact, as Daniel Moerman
has pointed out the combined results
of two RCTs comparing an earlier
surgical procedure for angina -
bilateral internal mammary artery
ligation (BIMAL) - to a sham surgery
clearly show that patients
"experienced significant subjective
improvement," with both BIMAL (67%
substantial improvement) and the
sham procedure (82% substantial
improvement).[17] Surgery as a
meaningful experience (placebo effect)
was most likely the cause of
improvement for patients in both of
these studies with the sham surgical
procedure actually proving slightly
more effective.