(5) Acute decompensated Heart Failure

Acute decompensated Heart failure

• worsening of baseline symptoms (or new diagnosis) usually caused by volume overload and/or hypoperfusion

• precipitating events:

  • dietary indiscretion, noncompliance, infection/other non-cardiac illness, low-output syndrome, new cardiac event, medications

• patients may become refractory to oral diuretic therapy and decompensate following relatively mild insult

Common reasons for hospital admissions

• inevitable disease progression

• increasing incidence of HF

• incomplete diuresis in hospital

• failure to utilize HF guideline recommendations

• noncompliance with diet and drugs

Goals of therapy

• relieve congestive symptoms

• optimize volume status

  • improve hemodynamics

    • decrease PCWP and/or increase CO

• treat symptoms of low cardiac output if present

Pulmonary artery or Swan-Ganz catheter

• used to estimate pulmonary capillary wedge pressure (or LVEDP)

• Cardiac: 2.5-3.5 L/Min/M²

  • less than 2.2 is forward failure and cardiogenic shock

• PCWP: 5-12 mm/Hg

  • greater than 18 is pulmonary congestion

• SVR: 800-1200 dyne.sec/cm⁵

  • greater than 1400 is associated with systolic failure

Clinical presentation: Dry

• no pulmonary congestion

• no systemic congestion

Clinical presentation: Wet

• fluid overload

• pulmonary congestion

• systemic congestion

Clinical presentation: cold

• low cardiac output

• extreme fatigue

• inadequate perfusion of vital organs

Clinical presentation: warm

• adequate cardiac output

• good organ and tissue perfusion

Hemodynamic Classification: Subset I

• Dry and warm (normal/ not ADHF)

• presentation

  • CI> 2.2

  • PCWP: 15-18

• Goals

  • maximize oral therapy and monitor

• Treatment

  • no immediate intervention required

Hemodynamic Classification: Subset II

• wet and warm (pulmonary congestion)

• presentation

  • PCWP > 18

  • CI > 2.2

• Goals

  • decreased preload PCWP 15-18

• Treatment

  • diuretics

  • ± venodilators

Hemodynamic Classification: Subset III

• dry and cold (hypoperfusion)

• clinical presentation:

  • CL < 2.2

  • PCWP < 18

• goals:

  • increase CI and perfusion to essential organs

• treatment:

  • PCWP < 15 → give fluids (NS, LR)

  • PCWP 15-18 and adequate arterial pressure → iv inotropes

  • PCWP 15-18 and low arterial pressure → dopamine

Hemodynamic Classification: Subset IV

• wet and cold (pulmonary congestion and hypoperfusion)

• clinical presentation:

  • CI < 2.2

  • PCWP > 18

• goals:

  • increase CI > 2.2

  • Decrease PCWP to 15-18

  • maintain adequate MAP

• treatment:

  • iv inotropes

  • mechanical support

Diuretic IV options

• furosemid

• bumetanide

• torsemide

Diuretics Hemodynamic effects

• decreased PCWP (improves symptoms of congestion)

• no change or decrease in MAP

Diuretic resistance: treatment options

• larger IV bolus dose of diuretics (don’t go lower in doses)

• use an alternative diuretic

• continuous IV infusion

• combination therapy:

  • LOOp + thiazide diuretic for syngergistic effect

  • remember to give PO metolazone 30 min prior or at the same time of loop

IV vasodilators: Arterial dilators

• reduce afterload

• reflex increase in cardiac output

IV vasodilators: Venodilators

• reduce preload

• increase venous capacitance

Nitroprusside

• mixed arterial/veno dilator

• hemodynamic effects

  • decrease SVR and PCWP

  • increase CO

  • no change/decrease in MAP

  • no change/increase in HR

Nitroprusside dosing

• initiate at 0.1-0.2 mcg/kg.min

• titrate upwards

• rebound phenomenon → taper doses

Nitroprusside adverse effects

• hypotension

• tachycardia

• coronary steal

• cyanide and thiocyanate toxicity

  • lactic acidosis; nausea, disorientation, confusion, psychosis, weakness, muscle spasm, convulsions

• must be in ICU with arterial line for monitoring

Nitroglycerin

• preferred for preload reduction

• hemodynamic effects

  • decreases PCWP

  • no change/decrease SVR, MAP

  • No changes/increase HR, CO

Nitroglycerin Dosing

• initiate at 5-10 mcg/min

• maintenance: 35-200 mg/min

• tolerance may occur over 12-72 hours

nitroglycerin adverse effects

• headache

• hypotension

• excessive decrease in preload (PCWP)

• may worsen cerebral edema

Positive Inotropic agents

• enhance contractility by increasing rate and extent of calcium influx during diastole

• most common: dobutamine and milrinone

Dobutamine

• B-agonist

• MOA: B1 and B2 agonist with some A1 agonist effects

• activate adenylate cyclase: ATP → cAMP

• more pronounced increase in HR

• B2 vasodilation may offset a1 vasoconstriction

Dobutamine dosing

• 2.5-5 mcg/kg/min up to 20 mcg/kg/min

• very short half-life

• may titrate easily

dobutamine major adverse effects

• increase in oxygen consumption

• tachycardia (less increase in HR compared to dopamine)

• proarrhythmic (primarily tacharrhythmias)

Milrinone

• phosphodiesterase inhibitor

• reduce the degradation of cAMP by inhibiting PDE3

• Inodilator

  • positive inotropic effects

  • arterial and venous vasodilator

• could lead to decrease in BP (and reflex tachycardia) but also could produce little change in MAP increase in SV → increase in CO

  • use caution in patients with hypotension

milrinone dosing

• 0.2 mcg/kg/min (up to 0.75 mcg/kg.min) (omit loading dose due to risk of hypotension)

• renally eliminated therefore decrease infusion rate by 50-75%

• long half life: 2-4 hours (up to 7 hours in renal dysfunction)

Milrinone Adverse effects

• arrhythmias

• hypotension

• thrombocytopenia

Dopamine

• combined inotropic and vasopressor activity

  • a1, B1, B2, and D1 effects

• Role in HF (could be combined with traditional inotropes if hypotension precludes use by itself)

  • marked systemic hypotension or cardiogenic shock with elevated (or at least adequate) ventricular filling pressure

Dopamine dosing

• dose-dependent hemodynamic effects

• titratable: short half-life, may increase dose and see effects quickly

dopamine dosing: 0.5-3 mcg/kg/min

• dopaminergic effects

• increase renal blood flow

Dopamine dosing: 3-10 mcg/kg/min

• primarily B stimulation

• increases CO and HR

Dopamine dosing: > 10 mcg/kg/min

• a1 receptor mediated vasoconstriction

• increases BP, SVR, and PCWP

Dopamine major adverse effects

• increase in oxygen consumption

• tachycardia

• proarrhythmic

OPTIME-CHF trial

• purpose: benefit of inotropic agents in ADHF and systolic dysfunction without low output syndrome

• results

  • long-term use of either continuous or intermittent infusions of inotropes may be harmful and are not recommended, except as palliation in end-stage disease

  • use of parental inotropic agents in hospitalized patients without severe systolic dysfunction, low BP, or impaired perfusion and significantly depressed CO is potentially harmful due to arrhythmias and increased mortality

OPTIMIZE-CHF trial

• purpose

  • continue or withdrawl beta blockers in ADHF with systolic heart failure

• Results

  • patients continued on beta blockers had

    • shorter hospital stays

    • lower post-discharge mortality rates

    • associated with lower risk of combined mortality/rehospitalization

B-CONVINCED TRIAL

• purpose

  • should beta blockers be stopped in ADHF with systolic heart failure

• Results

  • no difference in dyspnea and general wellbeing at days 3 and 8

  • higher rate of beta blocker therapy at 3 months

• Although continuing beta blockers seems counterintuitive they should be continued unless signs/symptoms of cardiogenic shock or hemodynamic instability

Nonpharmacologic therapy

• ultrafiltration: removal of fluid

• wireless implantable hemodynamic monitoring

• temporary mechanical support

  • intra-aortic balloon pump

  • ventricular assist device

• cardiac transplantation

ICD (implantable cardiac defibrilator)

• recommended for

  • primary prevention EF < 35% for NYHA II and III

  • secondary prevention reduced EF and history of sudden cardiac death or hemodynamically unstable VT

CRT (cardiac resychronization therapy= biventricular pacemaker)

• recommended for EF < 35%, NSR but QRS >120 msec

Negative inotropic drugs that may precipiate ADHF event

• antiarrhytmics

• beta blockers

• Non-dhp calcium channel blockers

• itraconazole

Cardiotoxic drugs that may precipiate ADHF event

• doxorubicin

• daunomycin

• cyclophosphamide

drugs that may precipiate ADHF event: Na/H2O retention

• NSAIDs

• COX-2 inhibitors

• Thiazolidinediones

• glucocorticoids

• androgens

• salicylates

• sodium containing drugs

Treatment strategies

• all patients- think core 4

• fluid retention- add diuretic

• persistent fluid retention- aggresive diuretic therapy

• Sympotmatic or hypertension- add hydralazine/nitrate

• elevated HR- optimized on BB?- if so add ivabradine

• black?- add hydralazine/nitrate

• Angina? consider nitrates, amlodipine/felodipine