Shock

Front 1

CHF definition

Back 1

heart is unable to pump blood at a rate commensurate w/ body's requirements, or can do so only from an elevated filling P

Front 2

CHF sx (4)

Back 2

dyspnea, fatigue, exercise intolerance, swelling

Front 3

CHF stages

Back 3

A -> high risk pts (HTN, diabetes, CAD, fam hx, cardiotoxic drugs); B -> structural HD w/o sx (LVH, MI, low LVEF, dilatation, valvular dis); C -> prior/current sx; D -> refractory

Front 4

CHF classes

Back 4

I = asymptomatic; II = sx w/ moderate-strenous extertion; III = with mild exertion; IV = at rest

Front 5

CHF w/ gender and age

Back 5

in younger pts, more M > F; in older pts, almost =

Front 6

men vs women diff in heart structure

Back 6

women have less compliant hearts

Front 7

systolic vs diastolic HF (6)

Back 7

systolic = decr LVEF (failure to contract) = younger (30-70 yo) men with eccentric LVH (dilated volume b/c decr LVEF), S3 gallop, previous MI; diastolic = normal (40%+) LVEF (failure to relax) = elderly women with concentric LVH (normal volume), S4 gallop, assoc w/ HTN, obesity, diab, lung dis, dialysis

Front 8

sx due to volume overload (9)

Back 8

pulmonary congestion -> cough, dyspnea, SOB when supine (orthopnea), SOB while asleep (PND); visceral congestion: abd bloating, swelling, early satiety, anorexia; peripheral edema

Front 9

signs of volume overload (6)

Back 9

JVD, peripheral edema, ascites, anasarca (gen swelling), displaced/diffuse apex (eccentric hypertophy in systolic HF), gallop rhythm (S3 = systolic, S4 = diastolic)

Front 10

RWT in eccentric vs concentric hypertrophy vs normal

Back 10

RWT > .45 in concentric (thick walls, same cavity); RWT < or = .34 in eccentric (same walls, larger cavity) -- RWT = .34 in normal heart = 2 x WT/LVID (diameter)

Front 11

eccentric vs concentric hypertrophy in response to what?

Back 11

eccentric in response to volume overload (renal dysfn, valvular regurg); concentric in response to P overload (HTN, aortic stenosis)

Front 12

which type of hypertrophy can you feel on exam?

Back 12

eccentric -> changes overall shape of heart (football -> basketball)

Front 13

which hypertrophy can lead to mitral regurgitation?

Back 13

eccentric hypertrophy -> leads to globular remodeling and distortion of the mitral valve -> regurgitation

Front 14

evolution of diastolic HF

Back 14

stenosis (for example) increases afterload, so LV must hypertrophy (concentric) to accomodate greater P; this increased thickness decreases compliance (which is already lower in women, where diastolic HF is predominant), and less diastolic filling occurs -> diastolic HF

Front 15

evolution of systolic HF

Back 15

MI causes failure of systolic ejection -> decr LVEF -> incr volume load -> eccentric hypertrophy -> poss mitral regurgitation -> more volume overload -> more eccentric hypertrophy

Front 16

NE levels in CHF

Back 16

NE signal of how activated the SNS is -> higher NE levels assoc. w/ decr survival

Front 17

HF sx due to cytokines (5)

Back 17

fatigue, anorexia, muscle wasting, remodeling, anemia of chronic dis

Front 18

HF sx due to what factors (4)

Back 18

volume overload, adrenergic overdrive, cytokine secretion, RAAS activation

Front 19

how does myocyte protect itself from SNS activation in CHF? (3)

Back 19

downregulate beta receptors; beta2 uncouples from Gs; Gi upregulated

Front 20

which natriuretic peptide is used for dx CHF?

Back 20

BNP -> released by ventricles in response to stretch (high volume overload in CHF -> high LVEDP -> high BNP release)

Front 21

drugs to affect RAAS system

Back 21

ACE inhibitors (prevent angiotensin conversion, prevent bradykinin breakdown); ARBs (angiotensin II receptor blockers -> affect angiotensin II w/o affecting bradykinin, so no sx due to elev bradykinin like cough); aldosterone antagonists

Front 22

when to use ARBs

Back 22

don't give unless pt can't tolerate ACE-I (i.e. they get a cough due to high bradykinin) -> ACEI is first line

Front 23

African-Americans and HF

Back 23

have more vasoconstriction vs other races -> tx w/ vasodilators

Front 24

cardiac resynchronization therapy indications (3)

Back 24

used to counteract LBBB: need symptomatic HF, LVEF < 35%, QRS > 120 msec

Front 25

Laplace

Back 25

tension on wall = P x R / h

Front 26

how dilated can LV get normally to incr SV? (how much can it increase preload)

Back 26

140% of normal LVEDV

Front 27

how much can LV increase EF to incr SV? (due to incr inotropic state)

Back 27

up to 80-90%

Front 28

normal LV - how much can it increase its SV?

Back 28

180%

Front 29

short term adaptation to increase SV?

Back 29

LV can increase SV up to 180% by incr preload up to 140% and incr LVEF up to 80-90%

Front 30

normal LV mass

Back 30

71 g/m2

Front 31

large LV mass

Back 31

143 g/m in men, 102 g/m in women

Front 32

chronic volume overload example (5)

Back 32

aortic regurgitation, mitral regurgitation, ventricular septal defect, anemia, renal dysfn

Front 33

chronic pressure overload example (2)

Back 33

aortic stenosis, HTN (although has aspects of volume overload)

Front 34

pressure overloads cause what hypertrophy? volume overloads cause what hypertrophy?

Back 34

pressure = concentric; volume = eccentric

Front 35

HTN: eccentric vs concentric hypertrophy in regards to age, sex, BP, SVR, CO, blood volume

Back 35

eccentric: younger, women, have high CO and high circulating volume; concentric: older, men, have high BP and high SVR

Front 36

myoctye enlargement in eccentric and concentric hypertrophy

Back 36

myoctye length increases in eccentric hypertrophy; myoctye diameter increases in concentric hypertrophy

Front 37

hypertrophy causes what change in mitochondrial volume to myofibrillar volume?

Back 37

7% decr in the ratio of mitochondrial volume to myofibrillar volume

Front 38

how do capillaries change in hypertrophy?

Back 38

total capillary length increases only slightly, but each capillary incr in size

Front 39

hypertrophy time line

Back 39

myocardial prot synth incr w/in 3 hrs after incr P/V load; LV mass increases rapidly and plateaus at new level in 10 days

Front 40

abnormal systolic performance in hypertrophy (2)

Back 40

decr active tension for given end-diastolic fiber length, decr in max velocity of shortening of hypertrophied muscle

Front 41

abnormal diastolic performance in hypertrophy (4)

Back 41

P overload (concentric hypertrophy): intrinsic shift of passive filling of ventricle to the steeper portion of LV diastolic PV relationship -> slope of PV curve becomes steeper due to wall thickening --- at any volume, diastolic P is elevated in concentric hypertrophy (can lead to diastolic HF); V overload (eccentric hypertrophy): rightward shift of PV curve w/ slightly incr diastolic Ps due to incr cavity volume, however this is combined w/ shallower steepening of PV curve due to incr mass and slight incr in wall thickness; stiffness of walls increases due to collagen deposition and cross-linking; active relaxation is compromised due to changes in SERCA (prolonged uptake of Ca into SR during diastole)

Front 42

is there a maximal hypertrophy?

Back 42

likely -> inability of the coronary circulation to provide adequate blood flow --- we see fibrosis in extensively hypertrophied myocardium

Front 43

how does gas and substrate exchange alter in hypertrophy?

Back 43

increase intercap distance (capillary prolif doesn't commensurate w/ incr myocyte mass); incr in collagen deposition and cross-linking