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40 Cards in this Set
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- Back
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differentiate SV/EDV ratio (EF) in systolic vs. diastolic dysfunction
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systolic dysfunction - decreased EF due to decreased SV with increased EDV
diastolic - normal/increased EF because EDV is decreased |
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what does an increase in preload due to SV and EDV
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increased preload increases both EVD and SV (due to ventricular stretch)
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what does increased contractility due to SV and EDV
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increased contractility causes increased SV with decreased EDV
*EDV is lower because ESV is lower from increased contractility |
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how does an increase in afterload affect venous return
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increased afterload causes decreased SV and therefore decreased venous return
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what is used to measure: preload, contractility, and afterload
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preload - EDV
afterload - EDP contractility - EF |
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what can artificially elevated the PAWP beyond the actual value of LVEDP
*PAWP is used to measure the LVEDP |
mitral stenosis
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contrast the cellular remodeling involved in pressure vs. volume overloaded states
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volume overloaded - ventricular dilatation to increased EDV and therefore SV
pressure overloaded - ventricular hypertrophy to decrease the afterload and increase the SV |
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how do myocytes that underwent ventricular dilatation eventually fail
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the stretch eventually reaches it limit and EDP increases more than SV, there is also an increase in afterload due to increased radius and thinner ventricular wall. Lastly the dilatated myocytes overstretch the myofibrils causing decreased contractiliy
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what is cardiomyopathy of overload
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increased cell death in newly hypertrophied myocytes that underwent eccentric or concentric hypertrophy, this causes more cells to undergo hypertrophy to compensate and a vicious cycle develops.
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what two receptors are responsible for ventricular remodeling
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B receptors
ATN II receptors |
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what are the beneficial and adverse effects of sinus tachycardia in systolic dysfunction
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benefit - increase CO and contractility initially
adverse effect - decreased filling time and increased energy demand |
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reverse treppe phenomenon
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the treppe phenomenon is tachycardia causing increased contractility due increased Ca entry; however when the HR is high enough this reverses and actually decreases contractility
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what is cephalization in an x-ray
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blood being redistributed to to better ventilated upper lobes from edematous lower lobes
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an increase in what starling force is associated with cardiogenic pulmonary edema
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increased hydrostatic pressure in the pulmonary arteries secondary to increased LVEDP
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what are the benefits of ACEI/ARBs in patient with cardiac dysfunction
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1. decrease cardiac remodeling by ATN II and Aldosterone
2. decrease Na and H20 reaborption, this leads to decreased afterload and preload |
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differentiate V1 and V2 receptors
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V1 - found on endothelial cells, causes vasocontriction and increases afterload and preload
V2 - found in collecting ducts and stimulation increases H20 reabsorption |
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what three things causes release of natriuretic peptides
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1. atrial distention
2. ventricular distention 3. vascular distention |
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what is used diagnostically to differentiate dyspnea caused by heart failure vs. lung disease
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BNP is found in high concentrations in heart failure, not lung disease
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what does SV increase with increased EDV
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increased stretch causes increased affinity of troponin C for calcium, also increases passive elastic forces built-up by titin with increased elastic recoil
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what happens to B1-recepivitytors on the heart during chronic sympathetic nervous system hyperactivity
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receptors are phosphorylated and digested by proteolytic enzymes released by lysosomes, protective by limiting the effects of sympathetic hyperactivity
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what is the initial benefit in ventricular dilatation
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increased SV by increasing EDV, however afterload increases and may offset any benefits
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what ventricular remodeling occurs after ventricular dilatation
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eccentric hypertrophy decreases afterload by increasing the thickness of ventricular wall, eventually fails itself due to myocyte dysfunction
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what two drugs retard cell loss from apoptosis and necrosis by inhibiting maladaptive growth
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B-blockers
ACE inhibitors |
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what receptors are known to mediate dyspnea in LV failure
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J receptors (interstitial juxtacapillary receptors)
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what is the earliest physical manifestation of systolic dysfunction
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sinus tachycardia
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differentiate gradual vs. acute onset dyspnea on exertion
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acute - suggests heart failure
chronic - suggests chronic lung disease |
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why do patients develop orthopnea of paroxysmal nocturnal dyspnea
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incrased ventricular EDP due to increased preload (venous return) from lower extremities or interstitial compartment
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effects of ATN II on: blood vessel, kidney, heart, adrenal gland, brain
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blood vessel - vasoconsriction
kidney - sodium and water retention heart - cellular hypertrophy and apoptosis adrenal gland - aldosterone secretion brain - vasopressin secretion |
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chemical inducers associated with myocyte apoptosis
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NO
oxygen free radicals TNF-a ATN II catecholamines calcium overload |
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top three causes for LV failure
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1. CAD
2. HTN heart disease 3. valvular (aortic/mitral) |
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where is chymase found
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cardiac mast cells
converts ATN I --> ATN II in heart |
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cardiomyopathy characterized by LV diastolic dysfunction with elevated EF
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hypertrophic cardiomyopathy
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cardiomyopathy characterized by simultaneous biventricular failure with systolic dysfunction
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congestive cardiomyopathy
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cardiomyopathy with both LV and RV diastolic dysfunction occuring at the same time
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restrictive cardiomyopathy
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differentiate sarcomere organization between primary and secondary hypertrophic cardiomyopathy
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primary - myofiber disarray
secondary - organized sarcomere appearance (added in parallel or series) |
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differentiate the mechanism responsible for myocardial ischemia in hypertrophic vs. congestive cardiomyopathy
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hypertrophic - thickened, fibrotic ventricular wall leading to decreased coronary artery perfusion, causes ischemic in situation with higher demand for oxygen
congestive - RAAS activation causes increased afterload with increased oxygen demand to overcome the increased afterload |
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what causes the outflow obstruction in hypertrophic cardiomyopathy
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arterior leaflet of mitral valve coming in contract with the hypertrophied IV septum
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how would you distinguish the murmur heard in hypertrophic cardiomyopathy from aortic stenosis
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HCM - decreased LV volume causes increased murmur intensity
Aortic stenosis - decreased LV volume would decrease murmur intensity *valsalva is maneuver to decreased LV volume |
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pharmacologic therapies used in: HCM, congestive and restrictive cardiomyopathies
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HCM - B-blockers and Ca channel blockers to decrease contractility, HR, and myocardial oxygen consumption
congestive - B-blockers and ACE inhibitors to slow progression of cell loss restrictive - B-blockers to lower HR and increase filling time |
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lab finding useful for distinguishing restrictive cardiomyopathy from restrictive pericarditis
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increased BNP is present in restrictive cardiomyopathy
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