Heart Failure

Front 1

definition of chf

Back 1

inability for heart to pump blood forward at sufficient enough rate to meet metabolic demands or ability to do so only at extremely high pressures

Front 2

etiologies of systolic dysfxn

Back 2

IMPAIRED CONTRACTILITY SECONDARY TO
mi
cardiac ischemia
mitral regurg or aortic insuff (--> fluid overload)
dilated cmp

INCREASED AFTERLOAD SECONDARY TO:
aortic stenosis, htn

Front 3

consequences of impaired systolic dysfxn

Back 3

decreased sv
or, if nml vr is maintained, diastolic chamber volume increases even more --> very high edv --> increased sv from increased preload, but edv will remain high b/c of systolic dysfxn
also leads to pulm edema

Front 4

etiologies of diastolic dysfxn

Back 4

IMPAIRED LV RELAXATION SECONDARY TO:
lvh, hcm, restrictive cmp, transient cardiac ischemia
OBX OF LV FILLING:
ms, pericardial constriction/tamponade

Front 5

which is more common systolic or diastolic dysfxn

Back 5

systolic (2/3 have this)

Front 6

what can cause sudden r-chf
what is the pathophysiology behind this

Back 6

if there is a sudden increase in rv afterload (like acute pe)

rv is thin-walled, highly compliant and ejects blood at low pressure
rv can accept wide range of filling volumes without change in filling pressure (v compliant)

Front 7

effects that r-chf has on left side of heart

Back 7

can lead to decrease in sv
if less blood is entering the la and lv, then there is decreased preload
decreased preload may --> decreased lv sv

Front 8

compensatory mechanisms seen in chf

Back 8

frank starling
neurohormonal alterations
raas activation
adh release

Front 9

explain the role of the frank-starling mechanism in compensating for chf

Back 9

heart shifts to lower starling curve, so at same preload (edp) there is less sv and co and incomplete lv emptying and increased preolad b/c of increased blood accumulation in lv
--> increased preload along same curve that is lower than a healthy person
as preload is increased in this person, only minor increase in sv (b/c at flat part of curve) and there are very elevated lv edp/edv --> pulmonary congestion

Front 10

what neurohormonal alterations are seen in chf compensation

Back 10

activation of adrenergic ns: decreased co is sensed by baroreceptors in carotid sinus and aortic arch --> cn ix and x are activated --> increased sympathetic outflow and decreased parasympathetic outfolw --> increasdd hr, contractility, and co --> increased bp
increased vasoconstriction is initially helpful b/c veins constrict --> increased vr --> increased preload --> increased sv

Front 11

why is raas activated in chf

Back 11

renin is released b/c there is decreased renal artery perfusion 2/2 decreased co
also, decreased na delivery to macula densa

Front 12

effects of ATII

Back 12

vasonconstriction
stimulates thrist --> increased h20 intake and aldo secretion
both --> increased intravascular volume --> increased co by increasing preload

Front 13

role of adh

Back 13

promotes h20 retention --> increased intravascular volume --> increased preload --> increased co
adh also leads to systemic vasoconstriction

Front 14

long term consequences of body's compensatory mechanisms

Back 14

increased circ volume --> pulm edema
increased art resistance lowers sv and co
increased hr --> increased metabolic demands
long standing sympathetic activation --> downregulation of b1 receptors --> decreased inotropic effects
AII and aldo --> fibrosis and remodeling

Front 15

what is anp

Back 15

storedin atrial cells, released when there is atrial distention

leads to excretion of na, h20, vasodilation, decreased renin secretion, ATII antag

Front 16

what is bnp

Back 16

not found in healthy heart, but produced when ventricular muscles are subjected to hemodynamic stress
close relationship btwn bnp and chf severity
leads to excretion of na, h20, vasodilation, decreased renin secretion, ATII antag

effects are beneficial but insufficient to overcome the body's effects

Front 17

why is ventricular hypertrophy considered a compensation mechanism

Back 17

helps to maintain contractile force and counteracts increased wall stress

Front 18

why is wall stress increased in chf

Back 18

lv dilation increases wall stress
or need to overcome increased afterload

Front 19

what things can precipitate acute sx of chf

Back 19

anything that increases metabolic demand (fever, infx), tachycardia (decreases vent filling time), bradycardia (decreases co), increased salt intake, anything that increases circulating volume (not taking diuretics, renal insuff)

Front 20

clinical manifestations of left sided failure

Back 20

when pulm ven p >20 --> transudaion of fluid into pulm interstitium and congestion of lung parenchyma --> decreased pulm compliance and increased work of breathing to move same volume of air
excess fluid in interstitium also compresses walls of bronchioles and alveoli --> increased airway resistance
decreased ms b/c less cerebral perf
decreased urine output by day, increased nocturia (from redistribution of blood to kidneys when supine)
orthopnea
pnd

Front 21

pathophys of orthopnea

Back 21

redistribution of blood from gravity dependent regions towards the lungs while supine

Front 22

pathophys of pnd

Back 22

2-3 hrs after laying down it occurs b/c gradual reabsorption into circulation of LE interstitial edema --> expansion of intravascular volume
--> increased vr to heart and lungs

Front 23

describe cheyne stokes respirations
why does it occur

Back 23

hyperventilation followed by periods of apnea
related to prolonged circulation time btwn lungs and respiratory centers in brain

Front 24

why do crackles occur

Back 24

popping open of small airways that were closed off by fluid before inspiration

Front 25

"cardiac asthma"

Back 25

compression of conducting airways from pulm congestion --> wheezing but NOT from asthma

Front 26

what la pressure is there when cephalization is seen on cxr

Back 26

>10 mm Hg

Front 27

pathophys behind cephalization

Back 27

when a pt is upright, blood normally is greatest at lung bases
Redist occurs when edema develops b/c edema is most prominent at bases --> compression of bv d/t hydrostatic pressure
blood flow is redirected to areas of less resistance

Front 28

what is seen on cxr is la pressure >20

Back 28

kerley b lines
poor visualization of bv

Front 29

what is seen on csr when la pressure >25-30

Back 29

alveolar pulmonary edema with opacification of air spaces

Front 30

what changes are seen on cxr when ra pressure is increased

Back 30

prominent azygous vein +/- pleural effusions

Front 31

medication classes used to treat chf

Back 31

diuretics
ace-i/arb
bb
inotropic meds
vasodilators (nitrates, hydralazine, ace-i, arb)
spironolactone

Front 32

effects of diuretics on chf

Back 32

decrease intravascular volume, which decreases preload and edp
this shifts pt to left on starling curve, not really reducing sv/co but decreasing sx of pulm congestion

Front 33

what precautions should be taken in pts on diuretics for chf

Back 33

don't overtreat: in pts with diastolic dysfxn, they require extra volume to help maintain co
in pts with systolic dysfxn, too much decrease in vr --> large drop in co (b/c pt will move to steep descending part of the curve)

Front 34

what benefits do arterial and "balanced" vasodilators have in chf

Back 34

increase sv while also decreasing edp
edp is decreased b/c of mroe complete lv emptying, so there is less blood in lv before diastole even starts

Front 35

what effect do nitrates have in chf

Back 35

they cause venodilation --> increased vr --> increased preload with very little effect on co

Front 36

how do nitrates effect the starling curve

Back 36

pt remains on same curve, but it shifts slightly to the left

has overall same outcome as diuretics do

Front 37

what effect does hydralazine have in chf

Back 37

decrease afterload --> increased sv and co
--> decreased edp and move up to different curve, shifting to left

Front 38

what effects do ace-i and arbs have in chf

Back 38

balanced vasodilation (equal dilation in art and ven), also promotes natriuresis (by decreasing aldosterone) --> decreased intravasc volume adn pulm congestion
preload and afterload are both decreased

Front 39

what added benefit is seen in ace-i that is not seen in arb use

Back 39

the bradykinin seems to have added positive effects on the heart

Front 40

effects of digitalis in chf

Back 40

digitalis enhances contractility, decreases cardiomeg, and increases co
decreases lvedp b/c of more complete emptyhing during systole

Front 41

when should beta blockers be used in chf

Back 41

after a pt has been asx for 2-4 weeks, and has NO signs of fluid overload during that time

Front 42

which bb are approved for use in chf

Back 42

carvedilol (b1, b2, a antag)
metoprolol

Front 43

when is spironolactone used in chf

Back 43

use in older pts with nyha class iii/iv, already on dig, diuretic, ace-i, and bb

should be used if pt has had sx related to chf at rest any time in the prior 2 months

Front 44

why is spironolactone beneficial

Back 44

it has been shown that chronic exposures to high levels of aldosterone --> cardiac fibrosis and remodeling

Front 45

what is the recommended regimen for tx of a pt with systolic chf

Back 45

1. ace-i and bb (unless there si recent deterioration); if sx persist, add dig
2, if ace-i not tolerated, switch to arb or hydralazine + isdn
3. pts wit nyha iv add spironolactone
4. implantable defib if indicated

Front 46

what should be avoided in pts with pure diastolic dysfxn

Back 46

DO NOT GIVE INOTROPES OR VASODILATORS, USE DIURETICS CAUTIOUSLY B/C LV RELIES ON HIGHER VOLUMES TO MAINTAIN CO