Heart Failure Flashcards
what is heart failure in general
complex clinical syndrome
dysfunction of LV, RV or both
terminal stage of heart diasease
most characteristic symptom
easy fatigability
left sided heart failure
L ventricle does not deliver O2 rich blood = easy fatigablity and SOB
also inc BP in BV bet lungs and L ventricle = inc pressure to force fluid and blood out lungs = SOB
right sided heart failure
R ventricle in unable to contract enough to push blood into lungs
causes build up of blood in veins = edema
most common cause of HF
coronary artery disease
other causes of HF
high BP
DM
damage to valves
damage to heart muscle
poison or substance
lung disease
sleep apnea
medical tx of HF
diuretics: reduce swelling by inc urine
ACE inhibitors: allow BV to expand and dec BP preventing further damage
beta blockers: blocks effect of stress hormones
CABG
improves BF to heart muscle
heart valve reconstruction
improve BF through the hear
L ventricle reconstruction
remove damaged heart muscle
implanted ventricular assists device
LVAD - helps to pump blood
heart transplant
in extreme cases of HF
hemodynamic adaptations - inc ventricular end-diastolic volume and pressure
may tira after systole hence more blood volume in diastole = heart works more
hemodynamic adaptations - inc atrial volume and pressure
inc pressure on L side causes inc pressure in blood flow from R to L = more work
hemodynamic adaptations - inc atrial and ventricular contractility
starling’s law - inc volume will inc stretch
heart muscle will contract more since more blood to eject
hemodynamic adaptations - inc vol and pressure in adjacent venous system
dammed up IVC and SVC
neck veins and IVC engorged
liver congestion
venous congestion in LE
hemodynamic adaptations - inc capillary pressure and secondary transudation of fluid
too much pressure in capillary = fluid seeps into interstitial space
hemodynamic adaptations - inc interstitial and extracellular fulid volume
bipedal edema
gr 1: ankle
gr 2: knee
gr 3: thigh
gr 4: anasarca or entire body
hemodynamic adaptations - inc lymphatic flow from interstitial spaces
edema anywhere on the body
what warrants suspicion of heart failure
edematous from leg down
hemodynamic adaptations present in acute and chronic HF
acute: not all
chronic: 1-7
exp myocardial dysfunction and neurohormonal mechanisms
myocardial insult causes myocardial dysfunction
heart cannot empty inc load = reduced systemic perfusion
detected by kidneys - activation of RAS and ANS = adaptations
overly expressed RAS and ANS - growth and remodelling = ischemia or cell death in long term
compensatory mechanisms in HF
adrenergic system: catecholamines will inc HR and BP
RAS: inc blood vol
vasoconstrictions: to conserve blood
all will cause damage in long term, only helpful in acute
mechanical abnormalities in HF
pressure overload
volume overload
masyado madami laman sa loob di na ma pump out and may natitira
restriction of ventricular filling in HF
mitral stenosis - cannot fill L ventricle
constrictive pericarditis - di ma ffill kase maga less space
LVH - muscle gets thick so less space to fill
endomyocardial fibrosis - fibrotic tissue does not expand and contract effectively
primary myocardial disease
myocardial muscle is weak
congenital - duchenne’s
secondary myocardial disease
CAD
DM - metabolic
amphetamines, chemo - drugs
iron deposition - metals
scleroderma - CT disease
neuro disease
inherited disease
common etiology
AMI
prolonged CV stress - HTN, valve disease
toxins
infection
idiopathic
acute heart failure
1-2 wks lang tas chronic na basta wala na adaptations
MC - AMI; rapid sx
inadequate organ perfusion - large part of myocardium
sudden cardiac decompensation
CO, BP and HR go gown fast
results if only a small part of myocardium is damaged
heart attack
chronic HF
adaptive mech are gradually activated
sx manifest mildly kaya able to adapt
cardiac hypertrophy
pt usually disregards and is able to adapt to sx
L sided HF if disregarded can lead to R sided HF
stable but can decompensate with precipitating factors
discuss progression of HF
usually one sided - L
biventricular in the long run: L-R
R sided HF to L is rare
d/t ventricular interdependence - enlarged sided compresses other side
low output HF
typical HF
pump failure - weak
dec CO - vasoconstriction as compensation
vasoconstriction - cold, clammy and pale hands
- oliguria
- low pulse pressure - diff of < 40 mmHg
- widened O2 diff
high ouput HF
normal ejection - >4L/min/m2
unable to meet metabolic demand
less common
assoc c hyperkinetic circulatory state
- anemia, thyrotoxicosis, pregnancy, pagets, AV fistula
vasodilation: warm and flushed
- bounding pulse
- normal or dec O2 diff
backward HF
R sided HF d/t L sided HF
inc pressure in L side causes backward transmission
pulmonary HTN
dec CO
inadequate perfusion
forward HF
inadequate CO in forward direction
under perfusion of brain
- dizzy and confuse
- fatigue and weak
sodium and water rentention
systolic heart failure
typical pump failure
d/t chronic contractile dysfunction:
- myocardial necrosis
- acute depression of inotropy
inadequate forward CO
diastolic HF
filling phase is abnormal - more subtle
reduced ventricular compliance
LV fibrosis
acute reduction in diastolic relaxation
causes pulmonary or systemic congestion
HF ejection fractions
HFrEF: < 40%
HFmEF: 40-49%
HFpEF: > 50%
normal: 55%
< 50% - HF
2D Echo
stages of HF
A: high risk for HF but s structural or sx
B: c structural but s sx
C: c structural and prior or current sx
D: refractory
clinical manifestations of HF
SOB
PND
orthopnea
fatigue and weakness
nocturia and oliguria
edema
arrhytmias
NYHA classification
1: no limitation
2: slight; ordinary activity cause sx
3: marked; less than ordinary activity causes sx
4: sx at rest worsents c any activity
exercise prescription in HF
usually class 1-3
mod to vigorous aerobic for 30-40 mins at 3x a wk
60-70% HRR
5-10 mins until 30 mins
