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CR - Heart failure + Circulatory Oedema (i) (intro (CO (increased by NA…
CR - Heart failure + Circulatory Oedema (i)
intro
lifetime development risk = 20% for Americans 40+ y/o
50% 5-yr survival after Dx of significant HF (same as CR carcinoma)
heart is unable to pump blood @ a rate sufficient to meet the metabolic demands of a tissue (insufficient CO)
complex clinical syndrome
causes
impaired ventricular filling
decreased EDV
sometimes due to arrhythmias - not enough filling time
can be due to poor venous return
impairment ejection (poor pump function)
CO
depends on
SV
amount of blood pumped out of ventricle per beat
depends on venous return (filling-FS mechanism), symp activity (vasoconstriction increases venous return + prevents pooling), pump ability (contractility), blood vol (increased salt + water retention)
HR
ANS influences SA node
beats/min
if too fast will impede dias filling
= SV x HR (L/min)
increased by NA
increased HR
increased contractility
alters vasc resistance
use inotropes in severe pump failure (hypoperfusion)
ANP increases Na renal excretion (serum biomarker for HF)
LHF + RHF can occur independently, but failure of one causes strain + eventual failure in the other side - global failure
Classification
pathologists use anatomical/morphological classifications
left
more common (thick muscle - needs more O2)
pul oedema (dyspnoea, tachypnoea)
right
cor pulmonale (due to pul hypertension due to lung disease)
clinicians use clinical classifications
reduced EF
preserved EF
acute vs chronic
Frank-Starling Mechanism
increased venous return
increased ventricular filling (EDV)
increased preload (stretching of cardiac myocyte prior to contraction
increased force of contraction
increased SV
(i.e. increased vol -> increased pumping)
compensation
SV, contractility, intravasc vol + venous return all increased by increased blood vol
CO increased by increasing HR
causes of LHF
ischaemic heart disease (e.g. atherosclerosis)
hypertension (increased peripheral resistance -> increased workload)
aortic/mitral valve diseases
myocardial diseases (myopathy, myocarditis-e.g. viral)
arrhythmia
(muscle failure -> pump failure)
Effects of LHF
congestion of pul venous circulation
oedema
decreased oxygenation
remove with diuretics
fluid in alveolar space
reduced air entry
dyspnoea on exertion, progresses to @ rest (or just sudden + severe if acute LHF, e.g. MI)
fatigue
reduced exercise tolerance
pul venous hypertension
back pressure - RHF
orthopnoea + PND (pul oedema gravitates from lung bases to all lobes, more shallow breaths when asleep)
cough
heavy wet lungs (normally 300g, up to 1kg now)
reduced CO
hypoperfusion
organ dysfunction
kidney: perceived dehydration -> RAAS activated -> further fluid rentention
brain: hypoxic encephalopathy if advanced
mesenteric/hepatic ishcaemia
cardiogenic shock if acute LHF, e.g. MI
appearance of LHF
macro
ventricle hypertrophied/dilated
left atrium may also be dilated due to mitral stenosis
increased risk of A fib + mural thrombus
micro
fibrosis due to infarcts
non-specific myocyte hypertrophy
inflamm of myocardium in myocarditis
Oedema
abnormal increase in interstitial fluid in tissue (outside cells)
non-inflamm causes
increased hydrostatic pressure/decreased oncotic pressure (fluid leaves vessels)
water + salt retention
lymphatic construction (fluid leaves lymphatics)
transudate (low protein)
pitting oedema (stays depressed)
Management
lifestyle: reduced salt + fluids to reduced intravasc vol
diuretics
ACE inhibitors to block RAAS
beta-blockers to decrease adrenergic tone
end stage: ICD, LVAD, transplant