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81 Cards in this Set
- Front
- Back
Frank-starling mechanism says:
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longer lengths of sarcomere enhance contractility but there is a optimal sarcomere length for the most forceful contraction
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Atrial vs Ventricular myocytes?
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atrial myocytes are smaller and less structure than ventricles and have ANP granules released from vesicles upon distension
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Supplies apex?
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LAD
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Supplies anterior 2/3 of septum
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LAD
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supplies anterior wall of LV?
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LAD
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supplies lateral wall of LV?
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left circumflex aa
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supplise posterior 1/3 of septum?
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right coronary aa
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supplies posterior basal wall of LV?
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right coronary artery
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supplies RV free wall?
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right coronary artery
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coronary aa blood flow maximum during:
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diastole
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Chamber changes due to age?
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LA enlargement and LV cavity decreases in size
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What are lambl excrescences?
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small filiform processes on closure lines of aortic and mitral valves
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What is PORC D?
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five principle mechanisms of cardiac dysfunction.
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What does PORC D stand for?
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Pump failure, Obstruction to blood flow, Regurgitation, Conduction defects, Distruption of continuity of circulatory system
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Pathogenesis of heart pump failure?
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either sytolic of diastolic due to underlying pathology
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Types of systolic dysfunction?
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IHD, HTN or volume overload, DCM
(increased work) |
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Types of diastolic dysfunction?
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LV Hypertrophy, amyloidosis, myocardial fibrosis, constrictive pericarditis
(impairment of filling) |
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inability of the heart to pump blood at a high enough rate to meet metabolic demands
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heart failure
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the ability to pump blood at a rate enough to meet metabolic requirements but only at an elevated filling pressure
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heart failure
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acute causes of ventricular filling impairment?
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pericarditis of tamponade
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example of low CO heart failure
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AV fistula
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example of high CO heart failure
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anemia
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rapid adjustments in response to hemodynamic overload or impaired myocardial contractility?
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RAAS, ANP, NE release, frank starling
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Two stimuli for cardiac hypertrophy:
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volume overload and pressure overload.
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causes the largest hypertrophy of the heart:
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aortic regurg
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concentric hypertrophy
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seen in pressure overload and may end with reduction in cavity diameter
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hypertrophy with dilation:
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volume overload where wall thickness may not even change but there is enlargement of nuclei and cytoplasm
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Pathogenesis of why hypertrophy leads to cardiac failure
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increased myofiber size decreases capillary density and causes increase in intercapillary distance
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extension of normal myocardial growth with minimal or no deleterious effects
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physiology hypertrophy
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causes of LH failure
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ischemia, HTN, valvular diseases, cardiomyopathies
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most common cause of right heart failure
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left heart failure
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how does sleep apnea affect heart?
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causes pulmonary hypoxia and shunting to cause pulmonary HTN and cor pulmonale
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changes seen in systemic hypertensive heart disease?
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LV enlargement without dilation which causes stiffness (working against high pressures)
also atrial enlargement |
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cause of acute cor pulmonale
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PE
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cuase of chronic cor pulmonale
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primary pulm HTN or emphysema
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What usually causes ischemic heart disease?
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usually its secondary to coronary artery disease
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What usually causes ischemic heart disease?
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usually its secondary to coronary artery disease
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ischemia without death of heart muscle
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angina pectoris
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ischemia without death of heart muscle
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angina pectoris
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what are MACS
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the clinical syndromes of ischemic heart disease.
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what are MACS
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the clinical syndromes of ischemic heart disease.
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What does MACS stand for
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The clinical syndromes of IHD:
MI Angina pectoris Chronic IHD without heart failure Suddent cardiac death |
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What does MACS stand for
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The clinical syndromes of IHD:
MI Angina pectoris Chronic IHD without heart failure Suddent cardiac death |
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What initial event causes IHD?
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upredictable and abrupt conversion of a plaque into unstable atherothrombotic lesion
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What initial event causes IHD?
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upredictable and abrupt conversion of a plaque into unstable atherothrombotic lesion
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Causes symptomatic ischemia induced by exercise:
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narrowing of coronary aa of >75%
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Causes symptomatic ischemia induced by exercise:
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narrowing of coronary aa of >75%
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amount of stenosis that will cause inadequate coronary flow at rest
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>90%
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amount of stenosis that will cause inadequate coronary flow at rest
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>90%
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Why does waking up in the morning cause an MI?
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awakening causes adrenergic stimulation which my initiate acute plaque change
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Why does waking up in the morning cause an MI?
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awakening causes adrenergic stimulation which my initiate acute plaque change
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Four steps to occlusion in IHD?
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1) fixed obstruction
2) acute plaque change 3) thrombosis 4) vasoconstriction |
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Four steps to occlusion in IHD?
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1) fixed obstruction
2) acute plaque change 3) thrombosis 4) vasoconstriction |
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what causes angina pectoris?
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transient myocardial ischemia without cellular necrosis
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what causes angina pectoris?
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transient myocardial ischemia without cellular necrosis
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angina that resonds to rest and nitroglycerin?
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Stable/typical variant
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Angina that occurs at rest and responds to nitroglycerin and CCBs?
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Prinzmetal or variant pattern
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Angina with progressive increasing frequency and often at rest and prolonged duration?
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Unstable or crescendo pattern
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Pattern of angina with high risk for MI?
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unstable/screscuendo because it implies distruption of plaque with superimposed thrombus already
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myocardial necrosis due to ischemia?
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MI aka heart attack
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risk factors for MI?
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Old men with HTN that smoke and have diabetes
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What are common causes of 10% of MIs not caused by acute plaque changes?
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emboli or cocaine abuse
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What occurs within 60 seconds of ischemia onset?
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loss of contractility
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What occurs within 20-40 minutes of ischemia onset?
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irreversible damage with coagulative necrosis
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What is a complication of MI?
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arrhythmias induced by myocardial irritability from the infarct can lead to sudden death
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Types of infarcts caused by MI?
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transmural or subendocardial (furthest form coronary arteries)
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Most transmural infarcts involve ___
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left ventricle
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most common coronary arteries involved with MIs:
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LAD: 50%
RCA: 40% LCA: 20% |
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What is tetrazolium stain?
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stain that will show pale areas of infarct 2-3 hrs post occurance
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red-blue color after MI
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necrosis 24 hrs post infarct
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yellow tan after MI
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1-10 days which indicates neutrophil and macrophage involvement
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hyperemic peripheral zone with central yell-tan post MI
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scar formation (granulation tissue and collagen deposition) 10-14 days post MI
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when does a scar form post MI?
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>2 weeks
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Reperfusion injury is usually due to:
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nosocomial:
thrombolytic therapies balloon angioplasties bypass grafting |
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when is reperfusion helpful?
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within 3-4 hrs to limit the extent of ischemia
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Reperfusion injury due to:
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oxygen radicals and microvascular injury
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Complications of MI?
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cardiogenic shock/pump failure due to contractile dysfunction
-arrhythmias - myocardial rupture - mural thrombus, aneurysm, muscle dysfunction |
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What is a patient at risk for 3-7 days post MI?
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myocardial rupture
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elderly patients with progressive heart failure as a consequence if ischemic myocardial damage
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chronic ischemic heart disease (occurs in 1/2 of all transplant pts)
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enlarged heart with LV hypertrophy, coronary AS, scars, and overall diffuse myocardial dysfunction
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chronic ischemic heart disease (ischemic cardiomyopathy)
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What is sudden cardiac death?
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death within one hour after symptom onset caused by LETHAL ARRHYTHMIA, usually a complication of IHD but can be caused by other things
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