L5- heart failure

NYHA class I

• no limitation of physical activity

• no dyspnea, fatiguem chest pain, or near syncope with exertion

NYHA class II

• slight limitation of physical activity

• no sx at rest, but ordinary physical activity causes dyspnea, fatiguem chest pain, or near syncope

NYHA class III

• marked limitation of physical activity

• no sx at rest, but less than ordinary activity causes dyspnea, fatiguem chest pain, or near syncope

NYHA class IV

• inability to perform any physical activity without sx

• dyspnea, fatigue, chest pain, or near syncope are present at rest and sx worsen with any activity

ACC/AHA heart failure class A

• high ridk for heart failure but no structural heart disease ( htn, cad) and no sx

• at risk of HF

ACC/AHA heart failure class B

• structural heart dz associated with HF and no sx

• pre HF

ACC/AHA heart failure class C

• structural heart disease who have current or prior sx

• symptomatic HF

ACC/AHA heart failure class D

• refractory HF requirign some device or special intervention

• advanced HF

  • monitored by cards

ACAC/AHA vs NYHA

• ACC/AHA describes disease progression (cannot move backwards) and NYHA describes current functional limitation (can move throughout base don sx)

pillars of GDMT fro HF

• evidence based B

• angiotensin receptor- nephrilysin inhib (ARNIs), ACEi/ARBs

• mineralocorticoid receptor antagonist (MRAs)

• sodium glucose co transporter 2 inhib (SGLT2i)

• diuretics (sx releif only- no mortality benefit)

roel of BB in HF

• decrease HR

• decreased conduction

• decrease contractility

role of BB in HF- HR

• decreased

• less oxygen demand, more filling time, better coronary perfusion

role of BB in HF- decreased conduction

• fewer arrhythmias

• more coordinated pumping

role of BB in HF- contractility

• decreased

• protects myocardium from chroni catecholamine toxicity→ reduce remodeling and improving long term func

role of ACEi adn ARBs in HF

• decrease preload

• decrease afterload

• decrease ventricular remodeling

roel of ACEi/ARBs in HF- preload

• decreasd

• less NA.water retention → less congestion and pulm edema

roel of ACEi.ARBs in HF- afterload

• decreased

• vasodilation→ easier for lV to eject blood

role of ACEi/ARBs in HF- ventricualr remodeling

• decreased

• locks angiotensinII- mediated hypertrophy and fibrosis→ sldows HFprogressiona dimproves survival

angiotensin receptor neprilysin inhibitor (ARNI) agent

sacubitril/valsartan

ARNI sight of action

• sacubitril: neprilysin enzyme

• valsartan: angiotensin II receptor

ARNI MOA

• sacubitril: inhibits neprilysin→ increases endogenous nautriuretic peptides (ANP, BNP), bradykinin, and other vasoactive peptides

• blocks angiotensin II receptors→ decreases vasocontricton adn aldosterone release

ARNI net effects

• increase natriuresis

• increase diuresis

• increase vasodilation

• decrease RAAS activation

• decreasse remodeling

ARNI indicaitons

• first line foundational therapy for symptomatic HFrEF

• preferred over ACEi.ARB in appropriate pts with chronic synptomatic HFrEF

• may reduce HF hospitalization and CV mortality

ARNI common ADE

• hypotension

• hyperkalemia

• renal dys

• dizziness

• angioedema (rare but seriosu)

monitor while on ARNI

• BP

• K

• SCr/eGFR

• voluem status

• signs of angioedema

ARNI DDI- ACEi

• increased angioedema

• clinical action: 36hr washout required before starting ARNI to prevent stacking effect

role of MRAs ( aldosterone antagonist)

• contribute to modulation of RAAS system reducing ventricular remodelign in HF adn in post MI pts

• limit K and Mg loss andreduce myocardial fibrosis and hypertrophy

• reduce morbidity adn mortality in appropriate HFrEF pts

sodium glucose cotransporter2 (SGLT2) inihib agents

• dapaglilozin

• empagliflozin

SGLT2i site of action

• proximal convoluted tubule of the kidney

SGLT2i MOA

• reduce glucose reabsorption

• increase urinary glucose exretion

• produce mild antriuresis adn osmotic diuresis

• reduce cardiac preload and afterload

• improve cardiac and renal outcomes through multipek proposed mechanisms

SGLT2i indicaitons

• foundationsal therapy fro HFrEF (with or without diabetes)

• HFpEF

• T2D

• CKD (selected pts)

SGLT2i common ADE

• genital mycotic infections

• uti

• volume depletion

• hypotension

• euglycemic diabetic ketoacidosis (rare)

• aki (rare)

what to monitor fro pts on SGLT2i

• sx of genital infection

• volume status

• BP

• signs of ketoacidosis

• renal function (eGFR)

SGLT2i DDI- loop or thiazide

• increase voluem depletion/hypotension

• monitor BP and volume status

SGLT2i DDI- insulin

• increased hypoglycemia risk (priamrily in diabetics)

• may require insulin dose reduction

SGLT2i DDI- NSAIDs with dehydration

• increased AKI risk

• encourage hydration

• monitor renal fucntion

SGLT2i DDI- keto or prolonged fasting

• increased euglycemic DKA ridk

• hold durign acute illness, surgery, ot prolonged fasting

role of diuretics in HF

• sx relief from fluid removal

• loops: furosemide, torsemide, bumetanide

• ADRs: electrolytes, kidney function

hydralazine- nitrate combo

isosorbide dinitrate/hydralazine (BiDil)

isosorbide dinitrate/hydralazine (BiDil)

• nitrate primarily decreases preload

• hydralazine is na arteriolar dilator that acts directly on smooth muscle of arterioles by incompletetly understood mech and decrease afterload

main roles of isosorbide dinitrate/hydralazine (BiDil)

• in self identified black pts with NYHA III-IV HFrEF recieving optimal GDMT, the fixed dose combination can reduce morbidity and mortality

• may be used when ARNI/ACEi/ARB cannot be used because of intolerance or renal dys

isosorbide dinitrate/hydralazine (BiDil) mechanism

• nitrate primarily reduces preload

• hydralazine primarily reduces afterload

meds to avoid/use cautiously in HFrEF

• NSAIDs adn COX2 inhib

• thiazolidinediones: pioglitazone ,rosiglitazone

• non DHP CCB: verapamil diltiazem

• most class I antiarrhythmias

• dronedarone in sz or recently decompensated HF

• meds with substantial sodium load

• unnecessary neg inotropes

• excessive alcohol

• OTC degcongestants/stimulatns when they increase bP or HR

meds usually acceptable when another indication exists

• amlodapine

• felodipine

• also reinforce:

  • avoid combining ACEi, ARB, adn ARNI therapies

stage B HF tx

• pre HF/structural heart disease

• ACEi or ARB

• evidence based BB

stage C HF tx

• symptomatic HF

• four pillars

  • ARNI (or ACE/ARB)

  • evidence BB

  • MRA

  • SGLT2i

stage D HF tx

• advanced refractory HF

• advanced therapies

• LVAD

• heart transplant

• palliative/supportive care

HF phenotypes- HFrEF

• Ef: ≤40%

• weak squeeze

• high yield tx: four pillars

HF phenotypes- HFmrEF

• EF: 41-49%

• intermediate

• similar to HFrEF but weaker evidence

HF phenotypes- HFpEF

• EF: ≥50%

• stiff ventricle

• treat comorbidities + SGLT2i _ diuretics

HF phenotypes- HFimpEF

• EF: prev ≤40% adn now >40%

• imporved EF

• continue GDMT

stage A HF tx

• treat at risk disease

  • SGLT2i fro pts with diabetes at elevated CV risk

  • GLP1 receptor agonists fro obesity/diabetes

  • BP control, adn lifestyle

can stage A be HFpEF?

NO

• at risk only, no HF

can stage B be HFpEF?

no

• structural heart disease or evidence of eleated filling pressurem but no sx

• may have diastolic dysfunction or LVH, but no HFpEF yet

can stage C be HFpEF?

yes

• sx HF with presereved EF ≥50%

• classic HFpEF

can stage D be HFpEF?

yes

• advanced/refractory HFpEF (less common than advanced HFrEF, but exists)

HFpEF receommended priorities

tx syndrome and comorbidities

• SGLT2i for eligible pts

• diuretic for congestion

• control HTN
  treat afib

• manage CAD, obesity, diabetes, CKD, and sleep apnea

• encourage appropriate physical activity and weight management

sx HF- where GDMT comes into focus; ARNI

• preferred first line RAASi

• start diresctly when appropriate (dont have to “fail” ACE first)

sx HF- where GDMT comes into focus; BB

• best started once the pt is euvolemic and heme stable

sx HF- where GDMT comes into focus; MRA

• easy to add— minimal BP lowering

• monitor K and renal function

sx HF- where GDMT comes into focus; SGLT2i-even with other meds

minimal BP lowering

benefits ppear quickly

• can be started very early