Robbis pg. 383-388

Question 1

What do most MI patients die of?

Answer 1

arrhythmia within an hour of symptom onset, before

they receive appropriate medical attention. If they make it to the hospital, only 7% of patients die

Question 2

What are some possible consequences following an acute MI?

Answer 2

• contractile dysfunction
• papillary muscle dysfunction
• right ventricular infarction
• myocardial rupture
• arrhythmias

Question 3

T or F. Papillary muscles

rupture infrequently after MI

Answer 3

T, however, they often are dysfunctional and can be poorly contractile as a result of ischemia, leading to post infarct mitral regurgitation

Question 4

How common is myocardial rupture?

Answer 4

Rupture complicates only 1% to 5% of MIs but is frequently fatal when it occurs. Left ventricular free wall rupture is most common, usually resulting in rapidly fatal hemopericardium and cardiac tamponade

Question 5

What does ventricular septal rupture cause?

Answer 5

Ventricular septal rupture

creates a VSD with left-to-right shunting

Question 6

When does rupture commonly occur after an MI?

Answer 6

3 to 7 days after infarction—the time in the healing process when lysis of myocardial connective tissue is maximal and when much of the infarct has been converted to soft, friable granulation tissue

Question 7

What are some risk factors for rupture?

Answer 7

-60+
-anterior or lateral wall infarctions,
-female gender,
-lack of left ventricular hypertrophy, and
-first MI (as scarring
associated with prior MIs tends to limit the risk of myocardial tearing).

Question 8

How common are arryhthmias associated with MI?

Answer 8

Approximately 90% of patients develop some form of rhythm

disturbance, with the incidence being higher in STEMIs vs non-STEMIs.

Question 9

MI-associated arrhythmias include:

Answer 9

heart block of variable degree (including asystole), bradycardia,
supraventricular tachyarrhythmias, ventricular premature contractions or ventricular tachycardia, and ventricular fibrillation.

Question 10

When is the risk of serious arrhythmias (e.g., ventricular fibrillation) greatest?

Answer 10

in the first hour and declines thereafter.

Question 11

What are some other complications of MI?

Answer 11

• pericarditis
• chamber dilation
• mural thrombus
• ventricular aneurysm
• progressive late heart failure (chronic IHD)

Question 12

What is pericarditis?

Answer 12

Transmural MIs can elicit a fibrinohemorrhagic

pericarditis; this is an epicardial manifestation of the underlying myocardial inflammation.

Question 13

When does pericarditis occur?

Answer 13

Heralded by anterior chest pain and a pericardial friction
rub, pericarditis typically appears 2 to 3 days after
infarction and then gradually resolves over the next few days.

Question 14

Why does chamber dilation occur following MI?

Answer 14

Because of the weakening of necrotic muscle, there may be disproportionate stretching, thinning, and dilation of the infarcted region (especially with anteroseptal infarcts).

Question 15

Why would mural thrombus occur following MI?

Answer 15

With any infarct, the combination of attenuated myocardial contractility (causing stasis) and endocardial damage (causing a thrombogenic surface) can foster mural thrombosis, eventually
leading to left-sided thromboembolism.

Question 16

Large transmural

infarcts are associated with a higher probability of what?

Answer 16

cardiogenic shock, arrhythmias, and late CHF

Question 17

Anterior transmural MIs are at greatest risk for what?

Answer 17

free wall rupture, expansion, formation of mural thrombi, and aneurysm formation.

Question 18

Posterior transmural infarcts are more likely to be complicated by what?

Answer 18

serious conduction

blocks, right ventricular involvement, or both;

Question 19

T or F. Overall, patients with anterior infarcts have a much worse clinical course than those with posterior
infarcts.

Answer 19

T.

Question 20

What is ventricular remodeling?

Answer 20

Noninfarcted regions undergo hypertrophy and dilation; in combination with the scarring and thinning of the infarcted zone

Question 21

Long-term prognosis after MI depends on many factors, the most important of which are:

Answer 21

left ventricular function

and the severity of atherosclerotic narrowing of vessels perfusing the remaining viable myocardium.

Question 22

Chronic IHD, also called ischemic cardiomyopathy, is essentially what?

Answer 22

progressive heart failure secondary to ischemic myocardial damage.

In most instances, there is a history of previous MI

Question 23

When does chronic IHD appear?

Answer 23

In this setting, chronic IHD appears when the
compensatory mechanisms (e.g., hypertrophy) of residual
viable myocardium begin to fail. In other cases, severe
obstructive CAD can cause diffuse myocardial dysfunction
without frank infarction.

Question 24

Patients with chronic IHD typically exhibit what?

Answer 24

left ventricular dilation and hypertrophy, often with discrete areas of
gray-white scarring from previous healed infarcts

Invariably, there is moderate to severe atherosclerosis of the coronary arteries, sometimes with total occlusion.

Question 25

Can myocytes regenerate?

Answer 25

No. Increasing evidence,
however, points to the presence of bone marrow–
derived precursors—as well as a small resident stem cell
population within the myocardium—capable of repopulating the mammalian heart.

Question 26

T or F. Besides self-renewal,
these cardiac stem cells generate all cell lineages seen
within the myocardium.

Answer 26

T. Like all other tissue stem cells, they occur in very low frequency. They have a slow intrinsic rate of proliferation, which is greatest in neonates and decreases with age.

Question 27

Abnormalities in myocardial conduction can be sustained
or sporadic (paroxysmal)

Answer 27

Aberrant rhythms can be
initiated anywhere in the conduction system, from the SA node down to the level of an individual myocyte; they are
typically designated as originating from the atrium (supraventricular)
or within the ventricular myocardium.

Question 28

How can arrhythmias manifest?

Answer 28

• tachycardia,
• bradycardia,
• an irregular rhythm with normal ventricular contraction,
• chaotic depolarization without functional ventricular contraction (ventricular fibrillation), or
• no electrical activity at all (asystole).

Question 29

What is the most common cause of rhythm disorder?

Answer 29

Ischemic injury because of direct damage or due to the dilation of heart chambers with consequent alteration in conduction system firing

Question 30

What is sudden cardiac death defined as?

Answer 30

Sudden cardiac death (SCD) most commonly is defined
as sudden death, typically due to sustained ventricular
arrhythmias in individuals who have underlying structural
heart disease which may or may not have been symptomatic in the past.

The ultimate mechanism of SCD most often is a lethal arrhythmia (e.g., asystole or ventricular fibrillation)

Question 31

Note about SCD.

Answer 31

Of note, frank infarction need not occur; 80% to 90% of patients who suffer SCD but are successfully resuscitated do not show any enzymatic or ECG evidence of myocardial
necrosis—even if the original cause was IHD!

Question 32

What are the criteria for the diagnosis of systemic hypertensive heart disease?

Answer 32

(1) left ventricular hypertrophy in the absence of other cardiovascular pathology (e.g., valvular stenosis), and
(2) a history or pathologic evidence of hypertension.

Question 33

In some patients, the disease comes to attention with the onset of what?

Answer 33

atrial fibrillation (secondary to left atrial enlargement) and/or CHF.

Question 34

What are some microscopic changes that occur in HTN?

Answer 34

• nuclei of myocytes enlarge and the transverse diameter is increased
• hyperchromasia (boxcar nuclei) reflecting increased DNA
• intercellular fibrosis

Question 35

What is the major gross difference between acute and chronic for pulmonale?

Answer 35

acute- the right ventricle usually only shows dilation

chronic- right ventricular hypertrophy is usually present