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Cardio Quiz 1a

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eem8u's version from 2016-12-05 02:25

Heart Failure

definition- heart failure: clinical *syndrome* - any structural or functional cardiac disorder that IMPAIRS the ventricle’s ability to fill or eject blood
Question Answer
prevalence1/5 U.S. americans
cardiac output - definition / normal valuevolume of blood ejected from the ventricle per minute (5L/min)
cardiac output - equationCO = SV x HR
3 key mediators of Stroke volume1) contractility 2) preload 3) after load
preload - defined /measurementventricular wall tension @ end of diastole (FILLING), measured by end-diastolic V or P
afterload - defined / measurementventricular wall tension DURING CONTRACTION - systolic ventricular (or arterial pressure) -- against which the heart must pump...
contractilityproperty of heart muscle that accounts for changes in strength of contraction **INDEPENDENT OF PRELOAD AND AFTERLOAD**
S1/S2 correspond toMV (mitral @ end of filling) and AV (at end of ejection) CLOSING
axis of the FRANK STARLING CURVEstroke volume/cardiac output vs LV end diastolic PRESSURE or VOLUME
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Physiology of Heart Failure
Question Answer
s1 soundLV contraction - mitral valve closing
s2 soundejection ends, A-V valve closes
steep vs narrow ESPVR (end systolic p-v relationship)steep = increase CONTRACTILITY (wider loop)
ejection fraction - defined, normal rangefraction of end-diastolic Vol ejected / normal = 55%-75%
***HFrEF (reduced) vs HFpEF (preserved)(EF<45%, HFrEF) / (EF≥45%, HFpEF)
2 causes for HF w/ reduced ejection fraction1) impaired contractility 2) increased afterload
***1 cause for HF w/ preserved ejection fractionimpaired diastolic filling
ESPVR in HFrEFREDUCED slope (shift down/right) = (decreased contractility/systolic dysfunction)
ESPVR in HFpEFSAME slope
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****Compensatory mechanisms for Heart Failure
Question Answer
explain frank-starling mechanismrespond to decreased contractility by increase in preload (i.e. LV end diastolic volume or P — but this ONLY works up to a point) **see drawing**
***how does hypertrophy help the failing ventricle? and in what condition?**in increased AFTERLOAD wall stress** increasing wall thickness decreases afterload
***calculate wall stresswall stress = ( pressure x radius / 2x thickness)
ventricular hypertrophy - concentric vs eccentric growthConcentric = new sarcomeres in parallel with old (**increased wall thickness**) / ECCENTRIC = new sarcomeres in SERIES with old (chamber dilation and increased wall thickness)
***ventricular hypertrophy - **conditions** for concentric vs eccentricconcentric - Pressure overload (aortic stenosis/uncontrolled hypertension) / eccentric - VOLUME overload (mitral regurgitation)
name three neurohormonal mech.1) increased sympathetic 2) renin-angiotensin 3) Antidiuretic hormone (see slide 25)
decreased C.O. - sympathetic NS response (3)INCREASE Symp NS response via 1) direct UP contractility >> UP SV 2) direct UP heart rate = UP C.O 3) vasoconstriction **review why up vasoconstriction = up CO
how does arteriolar vs venous constriction affect C.O arteriolar — DOWN CO/ venous - increases venous return to heart —> increase SV —> increase SV
2 possible side effects of increase venous return to heart 1) peripheral edema 2) pulm congestion
decreased C.O. - Renin-Angiotensin system (2)1) increase vasoconstriction (renin cleaves angiotensiogen >> angiotensin I > ACE makes it angiotensin II) 2) increase circulating volume (via ACE, increases aldosterone) >> increasing preload
decreased C.O. - Antidiuretic hormone effect (1)increases circulation volume (released from pituitary — increase na/h20 retention and THIRST)
how does sympathetic NS increase contractilityb1 receptors @ heart ventricles
***calculate Blood pressureMAP = CO x TPR
memorize

Heart Failure II - Clinical components

Clinical Classifications of Heart Failure
Question Answer
by Ejection Fraction - reduced vs preservedRed = (<45%) or Preserved (≥45%)
by magnitude of symptomsNew York Heart Association (NYHA)
by presence of structural heart diseasestages of chronic HF — American College of Cards
NYHA Ino physical activity limitation
NYHA IIslight activity limitation (walking up stairs quickly)
NYHA IIImarked limitation (slowly walking up stairs)
NYHA IVsevere limitation (even at rest)
Stage A of Chronic HFat risk (e.g. hypertension)
Stage B of Chronic HFstructural heart disease (e.g. HTN and CONCENTRIC hypertrophy
Stage C of Chronic HFpatient w/ current or PRIOR HF-symptoms & structural heart disease
Stage D of Chronic HFstructural heart disease & refractory sx **despite tx** (in need of maximal intervention, ex transplant)
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Signs and symptoms of HF
Question Answer
what mediates the Frank-starling response to LOW SVdecrease ventricular emptying >> increase ventricular EDV (preload)
what mediates the hypertrophic response to LOW SVincreased wall stress & neurohormonal activation
1 negative consequence of compensatory mechanismincrease atrial pressure (b/c of increase end diastolic vol in ventricle and myocardial hypertrophy) >> Pulmonary congestion and peripheral edema
mechanism of dyspneaincrease pulmonary venous congest >> transudate
mechanism of dulled mental status (in HFrEF)decrease cerebral perfusion
mechanism of paroxysmal nocturnal dyspneagradual reabsorption into circulation of lower extremity interstitial edema > pulmonary congestion
mechanism of diaphoresisneurohormonal activation
mechanism of lower extremity coolnesscompensatory vasoconstriction (MAP = CO x TPR)
mechanism of JVDelevated systemic venous press
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Diagnosis of HF
Question Answer
evidence of HF on CXR (4)1- cardiomegaly / 2- cephalization (redistribution of blood flow to apices b/c of interstitial edema 3- Kerley B lines 4- diffuse alveolar edema/air bronchograms (due to transudation) (see 5.11/5.12)
***describe Kerley B linesf.uid in interlobular space — faint lines (5.12)
use echocardiogram (ultrasound) to measureleft ventricular EF (for preserved vs reduced)
creatinine clearance/GFR changes in HFreduced b/c of renal hypo perfusion = cardiorenal syndrome
serum sodium changes in HFreduced because of hypervolemia (hypervolemic hyponatremia)
4 diseases to rule out in test for HFthyroid, CT disease, HIV/AIDS, hemochromatosis
***BNP (B-type Natriuretic peptide)**usually high** secreted by cardiomyocyte stretch to *decrease PVR/induce natriuresis*
normal BNP indicatesgood for ruling out HF in dyspneic patients
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Treatment
Question Answer
key principle to tx of HFrEFprevent DECOMPENSATION / tx of precipitating factors
metabolic condition that can exacerbate HF (3)(all increase metabolic demands) Hyperthyroidism, anemia, infection
conditions that increase circulating volume (4)excessive fluid intake / excessive sodium (limit to 1.5-2 g daily) / renal failure / *****NSAID’s ***
how do NSAIDS increase volumeconstrict afferent arterioles in kidney (prostaglandins normally dilate
condition increasing afterload (2)HTN, OTC decongestants (eg phenylephrine)
conditions impairing contractility (2)alcohol / ***negative inotrope meds (verapamil, diltiazem)
3 medication classes with MORTALITY benefit in HFrEFsome beta blockers / ACE-i and A-ii receptor blockers / aldosterone ANTAGONISTS
beta blockers w/ mortality benefit (4)bisoproplol, carvedilol, metoroplol, succinate
aldosterone antagonists w/ mortality benefit (2)spironolactone, eplerenone
threshold for ICD (cardioverter-defrib)LVEF≤35%
? criteria and LOCATION for cardiac resynch. therapy devisea (QRS>120 msec and “LBBB” pattern)/ leads in RA, RV/ coronary sinus /
LVAD-mechanism and 2-year survival ratesinternal pump (bypasses heart) / 75%
1 and 5 year post-transplant survival rates88 / 71
medical tx w/ mortality benefit in HFpreserved EF**NONE** - tx is underlying co-morbidity (usually HTN)
2 factors to consider in tx of ACUT HFpulmonary congestion / Low perfusion
memorize