Cardiac, Thoracic, and Vascular: Heart Flashcards
Heart: Anatomy
- Coronary circulation begins at the sinus of Valsalva,
where the right and left coronary arteries (RCA, LCA)
arise. The left main artery branches into the left anterior
descending and the left circumflex arteries. The left
anterior descending artery supplies the anterior of the
left ventricle, the apex of the heart, the intraventricular
septum, and the portion of the right ventricle that bor-
ders the intraventricular septum (Fig. 17-1). The left
circumflex artery travels in the groove separating the
left atrium and ventricle and gives off marginal
branches to the left ventricle. The RCA travels between
the right atrium and ventricle to supply the lateral
portion of the right ventricle (Fig. 17-2). The posterior
descending artery (PDA) comes from the RCA in 90%
of patients and supplies the arteriovenous node.
Patients whose PDA arises from the RCA are termed
right dominant. If the PDA arises from the left circum-
flex, the system is left dominant.
The aortic valve is located between the left ventricle
and the aorta. It usually has three leaflets, which form
three sinuses. One sinus gives rise to the RCA, another
to the LCA, and the third forms the noncoronary sinus.
The mitral valve is located between the left atrium and
ventricle. It normally has two leaflets, with the anterior
protruding farther across the valve. Chordae tendineae
attach the leaflets to the papillary muscles, which in
turn serve to tether the leaflets to the ventricular wall.
Congenital Heart Disease (Part 1)
- Approximately 0.6% of live births will be compli-
cated by congenital heart defects. This risk more than
doubles in subsequent siblings. Most cases are sporadic,
although there are well-known associations of genetic
syndromes and congenital heart defects. These include
atrioventricular canal defects in children with Down
syndrome, coarctation of the aorta in children with
Turner’s syndrome, and supravalvular aortic stenosis
in children with William’s syndrome.
Congenital heart defects are best understood by
the pathophysiology they cause, either congestive
heart failure or cyanosis. Most anomalies fit into one
of these categories.
Congenital Heart Disease (Part 2)
- Congestive heart failure can be caused either by a
left-to-right shunt or an obstructive lesion. Left-
to-right shunts result in a certain fraction of blood
leaving the left side of the heart to the right side,
increasing pulmonary pressure and necessitating large
volume of left ventricular output to satisfy peripheral
demands. Among these lesions are patent ductus arte-
riosus, in which the normal fetal connection between
the pulmonary artery and aorta is not obliterated at
birth. Depending on the size of the communication,
it can cause severe failure. Premature infants with
pulmonary compromise and/or children with an audi-
ble murmur should undergo closure , which can be achieved via catheter-based therapies.
Congenital Heart Disease (Part 3)
- Atrial and ventricular septal defects also result in left-
to-right shunting. Patients with atrial septal defects clas-
sically have a second heart sound in which the split is
of fixed duration. Over time such patients can develop
pulmonary hypertension, right and left ventricular fail-
ure, and atrial arrhythmias. Most atrial septal defects
can be closed using percutaneous methods. Ventricular
septal defects may present in a similar fashion with pul-
monary hypertension and congestive heart failure, cul-
minating in Eisenmenger syndrome when the shunt
reverses to a right-to-left shunt, causing cyanosis. These
lesions should be fixed.
Congenital Heart Disease (Part 4)
- Atrioventricular canal defects are complicated lesions
involving the atrial and ventricular septae and the
atrioventricular valves. When diagnosed, these lesions
should be fixed. In its extreme form, a single arterial
trunk arises from a joined ventricular chamber; this is
termed a truncus arteriosus.
Congenital Heart Disease (Part 5)
- Obstructive lesions can also cause congestive heart
failure. Aortic stenosis most commonly occurs as a
result of a bicuspid aortic valve, but can also occur at
the supravalvular or subvalvular location, or as a result
of subvalvular ventricular hypertrophy, termed
hypertrophic muscular subaortic stenosis. Although
many procedures may be used to treat this condition,
of particular interest is the Ross operation, which
involves transposing the pulmonary valve to the aortic
position and using a prosthetic graft for a new pul-
monary valve.
Congenital Heart Disease (Part 6)
- Mitral stenosis commonly occurs in association
with other congenital heart defects. Pulmonic stenosis
is often mildly symptomatic and is generally treated
with percutaneous methods. The most common obstructive
lesion in children is coarctation of the aorta. This occurs when the aorta becomes narrowed, usually just
after the takeoff of the left subclavian artery (Fig. 17-3). Often, blood flow to the lower extremities will depend on a patent ductus arteriosus, closure of which can cause
severe heart failure. Because of the risk of endocarditis,
severe hypertension, congestive heart failure, and stroke,
these lesions are repaired.
Congenital Heart Disease (Part 7)
- Right-to-left shunts occur when deoxygenated
blood makes its way into the peripheral circulation;
this is also referred to as cyanotic heart disease. The most
common cause is Tetralogy of Fallot (Fig. 17-4). This
abnormality has four components: ventricular septal
defect, pulmonic stenosis, right ventricular hypertro-
phy, and an overriding aorta.
- Tricuspid atresia prevents flow from the right atrium
to the right ventricle, and instead, deoxygenated blood
traverses an atrial septal defect into the left atrium.
Other lesions that can cause a right-to-left shunt include
pulmonic atresia, transposition of the great arteries, and
total anomalous pulmonary venous connection.
Coronary Artery Disease: Epidemiology
- Atherosclerosis of the coronary arteries is the most
common cause of mortality in the United States,
responsible for one third of all deaths. Approximately
5 million Americans have coronary artery disease,
which is five times more prevalent in men than in
women. Risk factors include hypertension, family his-
tory, hypercholesterolemia, smoking, obesity, dia-
betes, and physical inactivity.
Coronary Artery Disease: Pathophysiology
- Coronary artery stenosis is a gradual process that begins
in the second decade. When the lumen decreases to
75% of the native area, the lesion becomes hemody-
namically significant.
Coronary Artery Disease: History
- Patients with ischemic heart disease usually complain
of substernal chest pain or pressure that may radiate
down the arms or into the jaw, teeth, or back. Typically,
the pain occurs during periods of physical exertion or
emotional stress. Episodes that are reproducible and
resolve with rest are termed stable angina. If the pain
occurs at rest or does not improve with rest, is new and
severe, or is progressive, it is termed unstable angina
and suggests impending infarction. Presentation can be
variable, with patients complaining of indigestion, nau-
sea, vomiting, diaphoresis, cough, new onset arrhyth-
mia, syncope, and, in older adult patients, confusion or
delirium. Ischemic heart disease can also be asympto-
matic, classically in patients with diabetes.
Coronary Artery Disease: Physical Examination
- The patient may have evidence of peripheral vascular
disease, including diminished pulses. Signs of ventric-
ular failure, including cardiomegaly, congestive heart
failure, an S3 or S4, or murmur of mitral regurgita-
tion (MR), may occur.
Coronary Artery Disease: Diagnostic Evaluation
- Electrocardiogram (ECG) may show signs of ischemia
or an old infarct. A chest radiograph may show an
enlarged heart or pulmonary congestion. An exercise
stress test is sensitive in identifying myocardium at risk.
These areas can be localized using nuclear medicine
scans, including thallium imaging. Echocardiography is
extremely useful in evaluating myocardial function and
valvular competence. Angiography is the gold standard
for identifying lesions in the coronary arteries, assessing
their severity, and planning operative intervention.
Coronary Artery Disease: Treatment
- Patients with severe disease of the left main artery or
with severe disease in the three major coronary arteries
have decreased mortality after coronary artery bypass
surgery. Pain is reliably relieved in greater than 85% of patients.
* Surgical options include bypass using the internal mam-
mary arteries or saphenous veins. Internal mammary
bypass is preferred because of higher patency rates.
Percutaneous coronary interventions include bal-
loon angioplasty and stent placement. Despite the
tremendous volume of procedures performed in the
United States, the exact indications for interventions
re not well known. A large study in 2005 in the
New England Journal of Medicine by Hannon et al. demon-
strated that in patients with two or more diseased
vessels, stents were associated with an increased need
for further procedures and increased mortality com-
pared with bypass grafting. Because early mortality
was higher with bypass grafting, care must be indi-
vidualized to the patient.
One common problem with coronary stents is
in-stent restenosis. Benefits of drug-eluting stents, which
elaborate various substances including sirolimus and
paclitaxel, remain unclear.
- It is important to note that nearly all risk factors
for coronary artery disease are modifiable before and
after an event. Preventive medicine used to aggressively
lower blood pressure and cholesterol, combined with
diet and exercise regimens, is critical.
Aortic Stenosis: Etiology
- Aortic stenosis (AS) can present early in life—for exam-
ple, when the valve is unicuspid—but more commonly
occurs in the older population. A congenitally bicuspid
valve usually causes AS by the time the patient reaches
70 years of age. Other causes include rheumatic fever,
which results in commissural fusion and subsequent
calcification, and degenerative stenosis, in which calcifi-
cation occurs in the native valve (see Color Plate 13).
Aortic Stenosis: Pathophysiology
- The initial physiologic response to AS is left ventric-
ular hypertrophy to preserve stroke volume and
cardiac output. Left ventricular hypertrophy and
increasing resistance at the level of the valve result in
decreased cardiac output, pulmonary hypertension,
and myocardial ischemia
Aortic Balloon Pumps and Ventricular Assist Devices
- In patients with markedly decreased cardiac output
insufficient to sustain end organ perfusion, an intra-
aortic balloon pump may be useful to decrease after-
load, increase coronary perfusion, decrease myocardial
oxygen demand, and increase cardiac output (Figs. 17-5
and 17-6). These are temporary devices, generally placed
via a femoral approach. Correct placement is critical.
Occlusion of the left subclavian artery during infla-
tion must be avoided, and proximal location above
the renal arteries is also critical. Vascular complications,
including arterial thrombosis and embolism, must be
constantly checked for and may necessitate balloon
removal.
- When medical therapy and intra-aortic balloon
pumps are insufficient to provide adequate cardiac out-
put, left ventricular assist devices may be used. These
are divided into pulsatile flow pumps and nonpulsatile
flow pumps, which use axial or centrifugal flow. These
pumps can be used in the short term, generally in
patients with temporary heart failure. These patients are
expected to improve, and a common indication is post-
cardiotomy syndrome. Left ventricular assist devices
can also be useful longer term as a bridge to transplan-
tation. Thromboembolism, bleeding, and infection are
common complications.
