Robbis pg. 383-388 Flashcards
What do most MI patients die of?
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
What are some possible consequences following an acute MI?
- contractile dysfunction
- papillary muscle dysfunction
- right ventricular infarction
- myocardial rupture
- arrhythmias
T or F. Papillary muscles
rupture infrequently after MI
T, however, they often are dysfunctional and can be poorly contractile as a result of ischemia, leading to post infarct mitral regurgitation
How common is myocardial rupture?
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
What does ventricular septal rupture cause?
Ventricular septal rupture
creates a VSD with left-to-right shunting
When does rupture commonly occur after an MI?
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
What are some risk factors for rupture?
-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).
How common are arryhthmias associated with MI?
Approximately 90% of patients develop some form of rhythm
disturbance, with the incidence being higher in STEMIs vs non-STEMIs.
MI-associated arrhythmias include:
heart block of variable degree (including asystole), bradycardia,
supraventricular tachyarrhythmias, ventricular premature contractions or ventricular tachycardia, and ventricular fibrillation.
When is the risk of serious arrhythmias (e.g., ventricular fibrillation) greatest?
in the first hour and declines thereafter.
What are some other complications of MI?
- pericarditis
- chamber dilation
- mural thrombus
- ventricular aneurysm
- progressive late heart failure (chronic IHD)
What is pericarditis?
Transmural MIs can elicit a fibrinohemorrhagic
pericarditis; this is an epicardial manifestation of the underlying myocardial inflammation.
When does pericarditis occur?
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.
Why does chamber dilation occur following MI?
Because of the weakening of necrotic muscle, there may be disproportionate stretching, thinning, and dilation of the infarcted region (especially with anteroseptal infarcts).
Why would mural thrombus occur following MI?
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.
Large transmural
infarcts are associated with a higher probability of what?
cardiogenic shock, arrhythmias, and late CHF
Anterior transmural MIs are at greatest risk for what?
free wall rupture, expansion, formation of mural thrombi, and aneurysm formation.
Posterior transmural infarcts are more likely to be complicated by what?
serious conduction
blocks, right ventricular involvement, or both;
T or F. Overall, patients with anterior infarcts have a much worse clinical course than those with posterior
infarcts.
T.
What is ventricular remodeling?
Noninfarcted regions undergo hypertrophy and dilation; in combination with the scarring and thinning of the infarcted zone
Long-term prognosis after MI depends on many factors, the most important of which are:
left ventricular function
and the severity of atherosclerotic narrowing of vessels perfusing the remaining viable myocardium.
Chronic IHD, also called ischemic cardiomyopathy, is essentially what?
progressive heart failure secondary to ischemic myocardial damage.
In most instances, there is a history of previous MI
When does chronic IHD appear?
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.
Patients with chronic IHD typically exhibit what?
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.
Can myocytes regenerate?
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.
T or F. Besides self-renewal,
these cardiac stem cells generate all cell lineages seen
within the myocardium.
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.
Abnormalities in myocardial conduction can be sustained or sporadic (paroxysmal)
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.
How can arrhythmias manifest?
- tachycardia,
- bradycardia,
- an irregular rhythm with normal ventricular contraction,
- chaotic depolarization without functional ventricular contraction (ventricular fibrillation), or
- no electrical activity at all (asystole).
What is the most common cause of rhythm disorder?
Ischemic injury because of direct damage or due to the dilation of heart chambers with consequent alteration in conduction system firing
What is sudden cardiac death defined as?
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)
Note about SCD.
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!
What are the criteria for the diagnosis of systemic hypertensive heart disease?
(1) left ventricular hypertrophy in the absence of other cardiovascular pathology (e.g., valvular stenosis), and
(2) a history or pathologic evidence of hypertension.
In some patients, the disease comes to attention with the onset of what?
atrial fibrillation (secondary to left atrial enlargement) and/or CHF.
What are some microscopic changes that occur in HTN?
- nuclei of myocytes enlarge and the transverse diameter is increased
- hyperchromasia (boxcar nuclei) reflecting increased DNA
- intercellular fibrosis
What is the major gross difference between acute and chronic for pulmonale?
acute- the right ventricle usually only shows dilation
chronic- right ventricular hypertrophy is usually present
