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81 Cards in this Set

  • Front
  • Back
Frank-starling mechanism says:
longer lengths of sarcomere enhance contractility but there is a optimal sarcomere length for the most forceful contraction
Atrial vs Ventricular myocytes?
atrial myocytes are smaller and less structure than ventricles and have ANP granules released from vesicles upon distension
Supplies apex?
LAD
Supplies anterior 2/3 of septum
LAD
supplies anterior wall of LV?
LAD
supplies lateral wall of LV?
left circumflex aa
supplise posterior 1/3 of septum?
right coronary aa
supplies posterior basal wall of LV?
right coronary artery
supplies RV free wall?
right coronary artery
coronary aa blood flow maximum during:
diastole
Chamber changes due to age?
LA enlargement and LV cavity decreases in size
What are lambl excrescences?
small filiform processes on closure lines of aortic and mitral valves
What is PORC D?
five principle mechanisms of cardiac dysfunction.
What does PORC D stand for?
Pump failure, Obstruction to blood flow, Regurgitation, Conduction defects, Distruption of continuity of circulatory system
Pathogenesis of heart pump failure?
either sytolic of diastolic due to underlying pathology
Types of systolic dysfunction?
IHD, HTN or volume overload, DCM
(increased work)
Types of diastolic dysfunction?
LV Hypertrophy, amyloidosis, myocardial fibrosis, constrictive pericarditis
(impairment of filling)
inability of the heart to pump blood at a high enough rate to meet metabolic demands
heart failure
the ability to pump blood at a rate enough to meet metabolic requirements but only at an elevated filling pressure
heart failure
acute causes of ventricular filling impairment?
pericarditis of tamponade
example of low CO heart failure
AV fistula
example of high CO heart failure
anemia
rapid adjustments in response to hemodynamic overload or impaired myocardial contractility?
RAAS, ANP, NE release, frank starling
Two stimuli for cardiac hypertrophy:
volume overload and pressure overload.
causes the largest hypertrophy of the heart:
aortic regurg
concentric hypertrophy
seen in pressure overload and may end with reduction in cavity diameter
hypertrophy with dilation:
volume overload where wall thickness may not even change but there is enlargement of nuclei and cytoplasm
Pathogenesis of why hypertrophy leads to cardiac failure
increased myofiber size decreases capillary density and causes increase in intercapillary distance
extension of normal myocardial growth with minimal or no deleterious effects
physiology hypertrophy
causes of LH failure
ischemia, HTN, valvular diseases, cardiomyopathies
most common cause of right heart failure
left heart failure
how does sleep apnea affect heart?
causes pulmonary hypoxia and shunting to cause pulmonary HTN and cor pulmonale
changes seen in systemic hypertensive heart disease?
LV enlargement without dilation which causes stiffness (working against high pressures)

also atrial enlargement
cause of acute cor pulmonale
PE
cuase of chronic cor pulmonale
primary pulm HTN or emphysema
What usually causes ischemic heart disease?
usually its secondary to coronary artery disease
What usually causes ischemic heart disease?
usually its secondary to coronary artery disease
ischemia without death of heart muscle
angina pectoris
ischemia without death of heart muscle
angina pectoris
what are MACS
the clinical syndromes of ischemic heart disease.
what are MACS
the clinical syndromes of ischemic heart disease.
What does MACS stand for
The clinical syndromes of IHD:
MI
Angina pectoris
Chronic IHD without heart failure
Suddent cardiac death
What does MACS stand for
The clinical syndromes of IHD:
MI
Angina pectoris
Chronic IHD without heart failure
Suddent cardiac death
What initial event causes IHD?
upredictable and abrupt conversion of a plaque into unstable atherothrombotic lesion
What initial event causes IHD?
upredictable and abrupt conversion of a plaque into unstable atherothrombotic lesion
Causes symptomatic ischemia induced by exercise:
narrowing of coronary aa of >75%
Causes symptomatic ischemia induced by exercise:
narrowing of coronary aa of >75%
amount of stenosis that will cause inadequate coronary flow at rest
>90%
amount of stenosis that will cause inadequate coronary flow at rest
>90%
Why does waking up in the morning cause an MI?
awakening causes adrenergic stimulation which my initiate acute plaque change
Why does waking up in the morning cause an MI?
awakening causes adrenergic stimulation which my initiate acute plaque change
Four steps to occlusion in IHD?
1) fixed obstruction
2) acute plaque change
3) thrombosis
4) vasoconstriction
Four steps to occlusion in IHD?
1) fixed obstruction
2) acute plaque change
3) thrombosis
4) vasoconstriction
what causes angina pectoris?
transient myocardial ischemia without cellular necrosis
what causes angina pectoris?
transient myocardial ischemia without cellular necrosis
angina that resonds to rest and nitroglycerin?
Stable/typical variant
Angina that occurs at rest and responds to nitroglycerin and CCBs?
Prinzmetal or variant pattern
Angina with progressive increasing frequency and often at rest and prolonged duration?
Unstable or crescendo pattern
Pattern of angina with high risk for MI?
unstable/screscuendo because it implies distruption of plaque with superimposed thrombus already
myocardial necrosis due to ischemia?
MI aka heart attack
risk factors for MI?
Old men with HTN that smoke and have diabetes
What are common causes of 10% of MIs not caused by acute plaque changes?
emboli or cocaine abuse
What occurs within 60 seconds of ischemia onset?
loss of contractility
What occurs within 20-40 minutes of ischemia onset?
irreversible damage with coagulative necrosis
What is a complication of MI?
arrhythmias induced by myocardial irritability from the infarct can lead to sudden death
Types of infarcts caused by MI?
transmural or subendocardial (furthest form coronary arteries)
Most transmural infarcts involve ___
left ventricle
most common coronary arteries involved with MIs:
LAD: 50%
RCA: 40%
LCA: 20%
What is tetrazolium stain?
stain that will show pale areas of infarct 2-3 hrs post occurance
red-blue color after MI
necrosis 24 hrs post infarct
yellow tan after MI
1-10 days which indicates neutrophil and macrophage involvement
hyperemic peripheral zone with central yell-tan post MI
scar formation (granulation tissue and collagen deposition) 10-14 days post MI
when does a scar form post MI?
>2 weeks
Reperfusion injury is usually due to:
nosocomial:
thrombolytic therapies
balloon angioplasties
bypass grafting
when is reperfusion helpful?
within 3-4 hrs to limit the extent of ischemia
Reperfusion injury due to:
oxygen radicals and microvascular injury
Complications of MI?
cardiogenic shock/pump failure due to contractile dysfunction
-arrhythmias
- myocardial rupture
- mural thrombus, aneurysm, muscle dysfunction
What is a patient at risk for 3-7 days post MI?
myocardial rupture
elderly patients with progressive heart failure as a consequence if ischemic myocardial damage
chronic ischemic heart disease (occurs in 1/2 of all transplant pts)
enlarged heart with LV hypertrophy, coronary AS, scars, and overall diffuse myocardial dysfunction
chronic ischemic heart disease (ischemic cardiomyopathy)
What is sudden cardiac death?
death within one hour after symptom onset caused by LETHAL ARRHYTHMIA, usually a complication of IHD but can be caused by other things