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40 Cards in this Set

  • Front
  • Back
differentiate SV/EDV ratio (EF) in systolic vs. diastolic dysfunction
systolic dysfunction - decreased EF due to decreased SV with increased EDV
diastolic - normal/increased EF because EDV is decreased
what does an increase in preload due to SV and EDV
increased preload increases both EVD and SV (due to ventricular stretch)
what does increased contractility due to SV and EDV
increased contractility causes increased SV with decreased EDV
*EDV is lower because ESV is lower from increased contractility
how does an increase in afterload affect venous return
increased afterload causes decreased SV and therefore decreased venous return
what is used to measure: preload, contractility, and afterload
preload - EDV
afterload - EDP
contractility - EF
what can artificially elevated the PAWP beyond the actual value of LVEDP
*PAWP is used to measure the LVEDP
mitral stenosis
contrast the cellular remodeling involved in pressure vs. volume overloaded states
volume overloaded - ventricular dilatation to increased EDV and therefore SV
pressure overloaded - ventricular hypertrophy to decrease the afterload and increase the SV
how do myocytes that underwent ventricular dilatation eventually fail
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
what is cardiomyopathy of overload
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.
what two receptors are responsible for ventricular remodeling
B receptors
ATN II receptors
what are the beneficial and adverse effects of sinus tachycardia in systolic dysfunction
benefit - increase CO and contractility initially
adverse effect - decreased filling time and increased energy demand
reverse treppe phenomenon
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
what is cephalization in an x-ray
blood being redistributed to to better ventilated upper lobes from edematous lower lobes
an increase in what starling force is associated with cardiogenic pulmonary edema
increased hydrostatic pressure in the pulmonary arteries secondary to increased LVEDP
what are the benefits of ACEI/ARBs in patient with cardiac dysfunction
1. decrease cardiac remodeling by ATN II and Aldosterone
2. decrease Na and H20 reaborption, this leads to decreased afterload and preload
differentiate V1 and V2 receptors
V1 - found on endothelial cells, causes vasocontriction and increases afterload and preload
V2 - found in collecting ducts and stimulation increases H20 reabsorption
what three things causes release of natriuretic peptides
1. atrial distention
2. ventricular distention
3. vascular distention
what is used diagnostically to differentiate dyspnea caused by heart failure vs. lung disease
BNP is found in high concentrations in heart failure, not lung disease
what does SV increase with increased EDV
increased stretch causes increased affinity of troponin C for calcium, also increases passive elastic forces built-up by titin with increased elastic recoil
what happens to B1-recepivitytors on the heart during chronic sympathetic nervous system hyperactivity
receptors are phosphorylated and digested by proteolytic enzymes released by lysosomes, protective by limiting the effects of sympathetic hyperactivity
what is the initial benefit in ventricular dilatation
increased SV by increasing EDV, however afterload increases and may offset any benefits
what ventricular remodeling occurs after ventricular dilatation
eccentric hypertrophy decreases afterload by increasing the thickness of ventricular wall, eventually fails itself due to myocyte dysfunction
what two drugs retard cell loss from apoptosis and necrosis by inhibiting maladaptive growth
ACE inhibitors
what receptors are known to mediate dyspnea in LV failure
J receptors (interstitial juxtacapillary receptors)
what is the earliest physical manifestation of systolic dysfunction
sinus tachycardia
differentiate gradual vs. acute onset dyspnea on exertion
acute - suggests heart failure
chronic - suggests chronic lung disease
why do patients develop orthopnea of paroxysmal nocturnal dyspnea
incrased ventricular EDP due to increased preload (venous return) from lower extremities or interstitial compartment
effects of ATN II on: blood vessel, kidney, heart, adrenal gland, brain
blood vessel - vasoconsriction
kidney - sodium and water retention
heart - cellular hypertrophy and apoptosis
adrenal gland - aldosterone secretion
brain - vasopressin secretion
chemical inducers associated with myocyte apoptosis
oxygen free radicals
calcium overload
top three causes for LV failure
1. CAD
2. HTN heart disease
3. valvular (aortic/mitral)
where is chymase found
cardiac mast cells
converts ATN I --> ATN II in heart
cardiomyopathy characterized by LV diastolic dysfunction with elevated EF
hypertrophic cardiomyopathy
cardiomyopathy characterized by simultaneous biventricular failure with systolic dysfunction
congestive cardiomyopathy
cardiomyopathy with both LV and RV diastolic dysfunction occuring at the same time
restrictive cardiomyopathy
differentiate sarcomere organization between primary and secondary hypertrophic cardiomyopathy
primary - myofiber disarray
secondary - organized sarcomere appearance (added in parallel or series)
differentiate the mechanism responsible for myocardial ischemia in hypertrophic vs. congestive cardiomyopathy
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
what causes the outflow obstruction in hypertrophic cardiomyopathy
arterior leaflet of mitral valve coming in contract with the hypertrophied IV septum
how would you distinguish the murmur heard in hypertrophic cardiomyopathy from aortic stenosis
HCM - decreased LV volume causes increased murmur intensity
Aortic stenosis - decreased LV volume would decrease murmur intensity
*valsalva is maneuver to decreased LV volume
pharmacologic therapies used in: HCM, congestive and restrictive cardiomyopathies
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
lab finding useful for distinguishing restrictive cardiomyopathy from restrictive pericarditis
increased BNP is present in restrictive cardiomyopathy