HFPEF

new universal definition of heart failure

clinical syndrome characterized by symptoms and/or signs of HF caused by a structural and/or functional cardiac abnormality and corroborated by at least one of the following:

elevated natriuretic peptide levels

or objective evidence of cardiogenic pulmonary or systemic congestion

HFrEF results from _________ dysfunction

systolic

HfPEF results from ______ dysfunction

diastolic

preload

pressure exerted on the walls of the heart at maximal filling

determined by the amnt of blood sitting in the ventricle at the end of diastole/filling

estimated by measuring pulmonary capillary wedge pressure- catheter passed thru RA into pulm artery and wedged into an end artery- gives an approx value of L atrial pressure

starling’s law of the heart (preload)

normal heart: increased pre load with increase CO (up to a limit)
HF: increased preload doesn’t increase CO and will actually decrease CO by overwhelming the pumping capacity of the heart

increase in preload causes HF but also happens as a result of HF - compensation for decreased CO- increased volume of blood presented to the heart

afterload

the resistance or force against which the ventricle must work to eject blood

estimated clinically by measuring systemic vascular resistance (BP=CO x SVR)

starlings law of heart (afterload)

normal heart: increased afterload doesnt change CO much

HF: increased afterload makes the already weakened heart work harder and will actually decrease CO

stroke volume + what is it affected by

stroke volume is the amount of blood ejected from the ventricle during systole

affected by:

• preload: more blood=more stretch= more power (to a point) - doesnt work in HF heart

• afterload

• myocardial contractility

what is cardiac output

the volume of blood pumped per min by each ventricle

the product of HR and SV

what is ejection fraction

the proportion of blood pumped out of the LV after systole (emptying), compared to how much was in the ventricle at the end of diastole (filling)

measured by echocardiogram

normal EF = 60-70%

Left ventricular dysfunction is considered when values fall <40% (HFrEF)

primary cardiac etiology of HF

• cardiomyopathy

• MI

• Arrythymia (a fib) - loss of atrial kick which contributes to CO

• valvular dysfunction (contraction is normal but regurgitiation of blood decreases CO)

list 5 main etiology of HF

1. primary cardiac

2. pressure overload

3. volume overload

4. high output (CO normal but increased body demand means tissues are underperfused)

5. other (meds, inflammation or infection, substance abuse)

volume overload etiology of HF

sodium and volume overload

poor compliance with diuretics

renal or hepatic dysfunction

high output etiology of HF

shunt, severe anemia, sepsis, thyrotoxicosis

medication etiology of HF

may be directly cardiotoxic, exhibt negative inotropy, lusitropy or chronotropy, exacerbate HTN, deliver a high sodium load or interact with HF meds to limit their effects

B blocker, CCB, antiarrythmics

NSAIDs, COX2i

thiazolinediones

doxorubicin

ephedra like products, Vit E supplementation >400IU/d + some also interact with CV meds used in HF

symptoms of HF

cardinal triad of Sx: fatigue, edema and dyspnea

typically FED ± orthopnea, paroxysmal nocturnal dyspnea, exercise intolerance, cough, weight gain, abdominal distention

atypical presentations may occur esp in women, obese pts and elderly (cognitive impairment, nausea, abdominal discomofrt, anorexia, cyanosis, oliguria)

S3/S4 heart sounds may be present

left sided s/sx

dyspnea at rest or on exertion

cough

paroxysaml nocturnal dyspnea

orthopnea

rales

right sided s/sx

weight gain

peripheral edma (ankle or pedal edema, or sacral if lying)

nausea, abdominal pain

elevated jugulovenous pressure

hepatomegaly

lab test findings in HF

B type naturetic peptide (BNP) >400pg/mL= HF likely (possible at 100-400)

NT pro BNP >300pg/mL - HF possible (increased likelihood with higher levels, cut offs vary depending on age)

SCr may be increased due to renal hypoperfusion (diversion of blood to essential organs in decrease CO)

sodium <130mmol/L is associated with reduced survival, may indicate worsening volume overload and/or disease progression

chest x ray: may show pulmonary edema, pleural effusions and/or cardiac enlargement

NYHA class I HF

no symptoms or symptoms only at higher than ordinary activity

NYHA class II HF

symptoms with ordinary activity

ex: climbing stairs, walking (longer distances)

NYHA class III HF

symptoms with minimal activity

ex: dressing, walking 20-100m

NYHA class IIIa HF

no dyspnea at rest

NYHA class IIIb HF

recent dyspnea at rest

NYHA class IV HF

symptoms at rest, mainly in chair, bedriddin

5 year HF survival rate

40%

cause of death in pts with HF

usually due to worsening HF (organ shutdown) or sudden cardiac death (arrythmias)

warm and wet meaning

congestion present but maintaining perfusion

cold and wet meaning

poor perfusion, end stage HF

chronic HF

refers to persistent and progressive nature of the disease

acute HF

defined as a gradual or rapid change in HF signs and symptoms resulting in need for urgent therapy

advanced HF

generally refers to patients who continue to exhibit progressive/persistent NYHA III or IV symptoms with additional poor prognostic indicators

HFrEF physiologic features

large left ventricle

thin left ventricle wall

HFpEF physiologic features

small left ventricle

thick left ventricle wall

common risk factors/comorbidities of HFrEF

male

obesity

htn

diabetes

kidney disease

volume overload

myocarditis

MI

common risk factors/comorbidities of HFpEF

female

older age

obesity

htn

IHD

diabetes

kidney disease

COPD

anemia

inflammation

liver disease

sleep apnea

gout

cancer

afib

HFmrEF ejection fraction

LVEF 41-49%

HFpEF ejection fraction

LVEF >/= 50%

what is the only drug to clearly reduce HF hospitilizations (but not all cause mortality) in HFpEF

only SGLT2i

what drugs reduce HF hospitalizations in HFmrEF

SGLT2i (definently), MRAs (likely), ARBs (inconsistently)

beta blocker recommendation HFpEF

no recommendation

ARB recommendation HFpEF (canadian, european, american guidelines)

weakly recommended per canadian and american guidelines

no recommendation for european guidelines

MRA recommendation HFpEF (canadian, american, european guidelines)

weakly recommended per canadian and american guidelines

no recommendation for european guidelines

ARNI (instead of ARB) recommendation HFpEF per canadian/european/american guidelines

no recommendation for canadian and european guidelines

recommended weakly per american guidelines

loop diuretics recommendation HFpEF

canadian, european and american guidelines recommend loop diuretics to treat congestion and htn

beta blocker recommendation HFmrEF (canadian, american, european guidelines)

no recommendation canadian guidelines

weakly recommended european/american guidelines

ARB recommendation HFmrEF (canadian, american, european guidelines)

no recommendation canadian guidelines

weakly recommended per european and american

MRA recommendation HFmrEF (Canadian, european, american guidelines)

canadian guidelines no recommendations (they have no rec for anything for MR)

weakly recommended european and american

ARNI (instead of ARB) recommendation HFmrEF (canadian, american, european guidelines)

no recommendation canadian guidelines

weakly recommended european anfd american

loop diuretic recommendation HFmREF

all guidelines recommend loop diuretics to treat congestion and htn

beta blockers evidence + benefits in HFpEF

reduction in mortality -low certianty evidence

no significant differences in HF hospitilizations

if there is mortality benefit, it depends on LVEF (mostly for HFrEF and some for HFmrEF) and rhythm (ex; for afib)

ACEI evidence/benefits in HFpEF

no significant difference in QoL, morbidity, death, or HF hospitilizations

ARB evidence/benefits in HFpEF

no significant difference in death or HF hospitilizations

heart failure hospitlizations: no sig diff (2017 CCS HF guidelines recommend ARBs based on CHARM-PRESERVED trial based on reduction in HFH HR 0.84 0.70-1 - weak recommendation for candesarten)

**therefore MAY reduce HFH but not sig

ARNI evidence/benefits in HFpEF

no significant difference in death or HF hospitlizations

signal that ARNi had similar reductions in HFH to ARB, mostly with men with EF <55% and in women

sprinolactone benefit/evidence in HFpEF (TOPCAT)

TOPCAT trial (contreversial trial)

no significant difference in death

HFH: RR 0.82 (0.69-0.98)

benefit is better as EF decreases (more so for mrEF than pEF)

SGLT2i benefit/evidence in HFpEF

reduce CV death in HF with LVEF >40%

QoL improvement NNT 20-34 (good)

which drugs show reduction in HF hosp/CV death in HFpEF

SGLT2i

which drugs show reduction in HF hosp/CV death in HFpEF

only SGLt2 clearly

ACC guidelines loop diuretics recommendation + class of evidence

fluid retention, NYHA class II-IV (class 1 evidence)

ACS guidelines for MRA recommendation + class of evidence

women of all EFs, men with EF <55-60%, those with fluid retention (class 2b)

ACS guidelines for ARNI recommendation + class of evidence

for women (all EFs), men with LVEF <55-60% (class 2b)

ACS guidelines for ARB recommendations + class of evidence

for ARNI elgible individuals who cannot take due to cost or intolerance (class 2b)

AHA guideline recommendations for improved LVEF - who previously had HFrEF and now have LVEF >40%

continue HFrEF treatment

when should MRAs be considered in HFmrEF (K, eGFR)

if pts K <5 and GFR >30

why should ARBs be considered in HFmrEF (candesartan)

potentially to decrease HF hospitlizations

H2FPEF score criteria

H2- heavy (2), Htn

F- AF diagnosis (3)
P-PAH
E-Elderly

F-filling pressure

H2FPEF score 0 meaning

HFpEF unlikely

HF2FPEF score 1-5 meaning

low to intermediate likelihood of HFpEF; further testing required

H2FPEF score 6-9 meaning

HFpEF highly likely; further testing not required