11/14 Heart Failure - Almendral Flashcards
heart failiure
result of myocardial muscle dysfx or loss
- can be systolic, diastolic, or mixed → leads to neurohormonal and circulatory abnormalities
- progressive, often fatal
- stabilization → myocardial dysvx and remodeling may improve (spontaneous or as consequence of tx
symptoms:
- fluid retention
- shortness of breath
- fatigue, esp on exertion’
severity of sx can vary substantially during course of disease
course of HF
NYHA functional classes
vs
stages of heart failure
functional classes can move up and down
stages only move in one direction
Stage A-D
A: high risk for HF without structural heart disease or sx
- HTN
- atherosclerotic HD
- diabetes
- obesity
- metabolic syndrome
- family hx of cardiomyopathy
B: structural heart disease without devpt of HF
- prior MI
- depressed LV ejection fraction
- LVH
- asymptomatic valvular HD
C: structural heart disease with CURRENT OR PRIOR symptoms
D: end-stage HF
refractory sx requiring special intervention like:
- inotropes
- LVAD
- transplant
- hospice
normal EF
EF = ejection fraction = fraction of blood ejected by ventricle relative to its end diastolic volume
normal EF > 50-60%
cardiac output
CO = SV * HR
heart rate
- influenced by SNS and PSNS
stroke volume
- influenced by preload, contractility, afterload
- incr preload → incr stretch → incr SV
- incr afterload → more impedance to flow → decr SV
- contractility: indep of preload/afterload, influenced by chem/neurohormonal factors
heart failure
distinguish between factors that cause preserved IF and reduced EF
preserved EF
-
impaired diastolic filling
- LVH
- restrictive CM
- myocardial fibrosis
- transient ischemia
- pericardial constriction
- tamponade
reduced EF
-
incrased afterload
- aortic stenosis
- severe HTN
-
impaired contractility
- CAD
- chronic volume overload
- dilated CM
HF with reduced EF
(HFrEF)
LVEF < 40-50%
- dereased capacity to eject blood
- due to decr contractility
- myocyte loss
- incr fibrosis
- abnormal systolic fx
HF with preserved EF
(HFpEF)
LVEF > 5%
abnormal diastolic fx due to :
- incr stiffness (passive)
- impaired relaxation (active)
incr diastolic pressures are transmitted retrograde to pulmonary and systemic veins → HF sx
RV failure
RV is thin-walled and more compliant
- accepts wide rane of volumes without significant change in filling pressures
- ejects to low resistance system (pulmo circuit) → not used to high afterload!
- most common cause of RV failure = LV failure
- other causes: lung processes (COPD, PE, etc)
symptoms of right sided failure:
- leg edema
- abdominal bloating
- ascites
compensatory mechanisms in heart failure
-
Frank-Starling mechanism
- decr contractility → decr SF → incr LV end diastolic volume → incr stretch → incr contractility!
-
Neuro-hormonal activation
- components:
- sympathetic nervous system (SNS)
- renin-angiotensin-aldosterone system (RAAS)
- anti-diuretic hormone (ADH)
- serves to maintain perfusion to vital organs by effecting:
- incr SVR
- incr intravastular volume
- acute effects = good, chronic effects = deleterious
- incr volume → congestion
- incr vasoconstriction → incr afterload → decr CO
- incr Ang II and incr aldosterone → incr cytokines, fibroblasts → cardiac fibrosis
- components:
-
Natriuretic peptides (ANP, BNP)
- respond to stretch →
- incr Na and water excretion!
- promotes vasodil
- inhibits renin secretion
- good mech but usually not sufficient :(
- respond to stretch →
-
Ventricular hypertrophy and remodeling
- reduces wall stress and maintains contractlity
- myocardial hypertrophy + ECM deposition → incr wall thickness (reduction in wall stress)
- incr thickness → incr stiffness → incr diastolic pressure
neurohormonal activation:
SNS activity
role of SNS in HF is to increase activity
incr SNS, decr PSNS output to heart and periphery
- incr HR, incr contractility, incr vasoconstriction
- alpha receptor distribution in periphery aids with peripheral vasoconstriction → maintenance of central perfusion!
neurohormonal activation:
RAAS activity
- decrease in CO → decr renal perfusion → incr reninrenin cleave antiogensinogen to Ang I, which can then be converted into Ang II [ACE[
- Angiotensin II
- potent vasoconstrictor (incr SVR)
- thirst stimulator
- incr aldosterone →incr Na retention → incr volume
neurohormonal activation:
ADH activity
- ADH is secreted by posterior pituitary
- mediated by arterial baroreceptor and AngII
- fx: incr water retention in distal nephron
sx of left sided HF
- congestion
- low output
sx of right sided HF
physical findings in…
L sided HF
R sided HF
left sided HF
- cardiac cachexia, tachypnea, tachycardia
- rales, decreased breath sounds
- diffuse apical impulse
- S3/S4, mitral regurg murmur
- weak pulse
right sided HF
- RV heave
- right sided S3/S4
- incr JVD, hepatic enlargement
- ascites, leg edema
diagnostic studies in HF
chest film
CXR
- upper zone vascular redistribution
- pleural effusions
- cardiomegaly
see others in slide
management of HFrEF
tx (medication) for HFrEF
- sx relief
- ID of underlying cause
- recog of precipitant for HF decompensation
- long-term modulation of neuro-hormonal response
- prolong survival
- diuretics
- vasodilators
- inotropes
- beta-blockers
- aldosterone antagonists
HFrEF tx:
diuretics
mechanism: water and Na elimination
- decr intravascular volume
- decr diastolic volume → decr congestion
*use judiciously! overdiuresis can lower CO even more
most potent = loop diuretics
less potent, additive = thiazides
HFrEF tx:
vasodilators
venous vasodilators (ex. nitrates)
- incr venous capacitance
- decr LV preload
arteriolar vasodilators (ex. hydralazine, prazosin)
- decr SVR/afterload
- incr CO, incr BP!
HFrEF tx:
ACEI and ARBs
ACEI (ACE inhibitors)
- decr: Ang II, aldosterone
- incr: bradykinins
- limit maladaptive remodeling
- improve survival
ARBs (Ang II receptor blocker)
- total inhibition of Ang II, no effect on bradykinins
- similar efficacy and survival benefit as ACEI
hydralazine/nitrates
- alternative if intolerant to ACEI, ARB
HFrEF tx:
inotropes
inotropes
beta-agonists: dobutamine, dopamine
PDE inhibitor: milrinone
- no oral form!
- long term use is ltd by tolerance
digoxin
- IV or oral
- blunts SNS drive, slows AVN conduction
- inhibits Na/K ATPase → incr intracellular Ca
- improves sx, reduces hospitalizations
- no effect on survival
HFrEF tx:
aldosterone antagonists
spironolactone and eplerenone
- blunt cardiac fibrosis and remodeling
- incremental survival venefit as add-on treatment
need to moitor K level, side effects
HFpEF
no real treatment options
general recs:
- volume control
- bp control
- rate/rhythm control
- revascularization if needed
- address comorbidities
R sided HF keys
usually due to LV failure → use HF tx
if due to cor pulmonale → address pulmonary issues
avoid overdiuresis, might drop preload
last resort: inotropes
acute decompensated HF
look at:
- congestion at rest
- low perfusion at rest
acute decompensated HF
wet and warm
- makes up majority of patients
- DIURESE THEM
- if they fail to response do diuretics: increase dose, Na and fluid restriction, add another diuretic
- if no hypotension, can use IV vasodilators!
- keep on beta blockers and other home meds
acute decompensated HF
wet and cold
- IV inotropes if..
- low EF and low CO syndrome with
- marginal bp less than 90mm Hg
- unresponsive to vasodil
- poor response to diuretics
- worsening renal fx
- low EF and low CO syndrome with
acute decompensated HF
dry and cold
- usually don’t get admitted unless they’re at end-stage
- make sure they’re not too dry
- vasodilators if BP is ok
- inotropes if BP is low
acute decompensated HF
dry and warm
- stable chronic HF
- want to double check to make sure they are not wet
- if theyre actually dry, then their sx are from something else
acute decomp heart failure keys
treatmend depends on hemodynamic status
- mainstay: IV diuretics
- if low output: vasodilators and inotropes
- address precipitating factors, optimize meds once stable
