(4/9) Dwyer Lecture: Acute Decompensated Heart Failure and Transitions of Care Acute Decompensated Heart Failure (ADHF)

- Exacerbations of heart failure are associated with increased risk of readmission and mortality. It is most frequently a result of: Ischemia/ACS, Uncontrolled HT, nonadherence to meds, worsening renal function, respiratory infection. ADHF will present as-

- Either: • Rapidly developing symptoms of new-onset heart failure (massive MI, damage) • Gradual worsening of chronic heart failure (this is the majority of patients seen)

- S/Sx: ADHF, depending on its cause, can present as either Wet or Cold Wet: Volume Overload

• This presentation is the result of S/Sx: ÝBNP, Pulmonary/peripheral edema, JVD + HJR, weight gain, cough, worsening orthopnea, PND, anorexia

Cold: Low Cardiac Output • This presentation is the result of low/poor forward flow S/Sx: Tachycardia, cold/clammy extremities, ÝBUN/SCr, decreased urine output, worsening DOE or dyspnea at rest, fatigue, altered mental status

- Dx: Forrester Hemodynamic Subsets of ADHF o The Forrester classifications consider the patient’s fluid status and

cardiac output. The typical patient presenting with ADHF will have class II or IV, both are associated with an increased mortality.

o Class IV: Cardiogenic shock – very concerning diagnosis Once a patient is identified as ADHF, we should establish our goals of treatment

- Initiate/Optimize Guideline-directed medical therapy (GDMT): This goal is most applicable to the pharmacist. ~ensure the patient has their ACE-I/ARB + BB optimized

Guideline-Directed Medical Therapy (GDMT) Continue chronic therapy

- 2013 AHA/ACCF: In the absence of hemodynamic instability or contraX, continue GDMT (Evidence: B) - 2010 HFSA: In ADHF, continue the current BB therapy. D/c is associated with poor outcomes (Evidence: C)

Administered Parenteral Therapy - Loops, Inotropes, Vasodilators

Loop Diuretics (Furosemide, Bumetanide, Torsemide) -THE BACKBONE OF ADHF- - Patients with normal heart function exhibit a proportional increase in stroke volume (SV) with an increased

preload. In HF patients, the ability to compensate for increased preload is lessened, leading to backflow and symptoms of volume overload (‘wet’), such as pulmonary congestion and lower extremity swelling.

- Purpose: Loops are used to decrease preload in patients experiencing volume overload. This is the backbone of ADHF therapy since most patients are ‘wet’. Loops should be initiated EARLY

- IV Dosing (furosemide equivalents) Naïve: 20-80mg q8-12º Chronic: Initial IV dose = Total at-home dose Max 200-250mg/dose

- Monitoring o Urine Output: Should be 250-500mL within the first 2 hours of dosing. (Goal: Net diuresis of -1.5-2L) o Cryptic Response: Everyone responds differently to loops. HF patients tend to be ‘down and to the right’

§ à Right: HF pts will require higher diuretic doses to achieve similar response as healthy pt § ßDown: HF pt also have lower ceilings! - Hence, this is why monitoring urine output is critical

o Intensification: If patient does not respond to the initial diuretic regimen… § Step 1: Double the dose If they still don’t respond… § Step 2: Make it a continuous infusion, and add another agent

• Options: Thiazide (IV Chlorthiazide, PO Metolazone), or Spironolactone § Step 3: If previous steps fail, consider ultrafiltration (It is like dialysis, but if pulls fluid off)

Vasodilators (Nitroglycerin, Nitroprusside, Nesiritide) -THE MAYBE RESCUE THERAPY, but never monotherapy- - As of late, IV vasodilators have fallen out of favor in clinical practice. Though, there are still niche situations

where we need them. They function to dilate blood vessels, both arterial and venous o Vasodilators are not associated with a reduction in re-hospitalization or mortality

- Function: Increase cardiac output via arterial and venous dilation o Venous Dilation: ßCongestion, ßPreload, ßMAP, Improves cardiac output o Arterial: ßAfterload (and there ÝSV), ßMAP, Improves cardiac output

- Place in Therapy (2013 AHA/ACC): In absence of symptomatic hypotension, IV vasodilators may be used as an adjuvant to diuretic therapy for relief of dyspnea in patients with ADHF (Evidence: A) Symptomatic therapy

o Indications: Acute pulmonary edema ± HT, need rapid improvement of sx, pulmonary congestion refractory to IV diuresis. (Yo yo,.. quick secret… IV Vasodilators… NEVER monotherapy! J )

- Nitroglycerin: NO donor, T1/2= 4m, Duration: 5-15m. Dosed by time (Continual infusion) o Metabolized by the Liver, NTG dilates both vessels, but predominately the venous end o Preferred in patients with coronary ischemia. Yo watch out, 20% of pt get that tachyphylaxis shit

- Nitroprusside: NO donor, T1/2= 4m, Duration: 1-4m. Dosed by weight + time (Continual infusion) o Eliminated by both the kidney and liver, prusside evenly affects the vessels, and has a pronounced BPß o Potential for cyanide/thiocyanate toxicity with longer infusion. Minimize use in renal impaired pt

- Nesiritide: Potent BNP, T1/2= 18m, Duration: 1-3h. Dosed by weight + time (Bolus + Infusion) o Very potent drug with a notably longer half-life. As a result, give a bolus o Sounds great, right? Dwyer says it is kind-of a wild-card. It is not used often.

Inotropes (Dobutamine, Milrinone) - Purpose: Increase forward flow. This is done by dropping the afterload and increasing the contractility, thereby

increasing the SV. Paired with increasing the HR, ÝSV*ÝHR=ÝCO o Inotrope MoA: Increase [cAMP] either directly or indirectly, which promotes: positive chronotropy,

positive inotrope, and vasodilation. (Dobutamine = Direct, Milrinone = Indirect) - Place in Therapy (2013 AHA/ACC): Patients presenting with low blood pressure, significantly depressed cardiac

output, and perhaps documented history of severe systolic dysfunction are candidates for short-term continuous IV inotropic support in order to maintain systemic perfusion and end-organ performance (Evidence: B)

o Indication: Simply put, Class IV patients with systolic dysfunction related to poor forward flow (HF-rEF) • Diminished peripheral perfusion or end-organ dysfunction • Palliative therapy for Stage D pt • Marginal systolic BP (< 90mmHg) • Symptomatic Hypotension à Excellent option for patients in cardiogenic shock or diuretic resistance

- Benefits and Risks • Cons: Tachycardia, tachyarrhythmia, Ý myocardia O2 demand (ischemia), hypotension • Pros: Ý Contractility, ßafterload, ÝCO, improved end-organ perfusion and diuresis

o Avoid Long-term use: Long-term use and/or intermittent use without proper indications may be associated with increased mortality.

- Dobutamine: A direct b-agonist that predominately targets b1 receptors [+inotrope, +chronotrope, Ývasodilation] o Metabolism: Hepatic, T1/2= 2 minutes. Dosing: 2-20mcg/kg/min o AE: Proarrhythmia, tachycardia, tachyphylaxis, hypotension (at high doses)

- Milrinone: A PDE-3-inhibitor that induces smooth muscle relaxation [+inotrope, +chronotrope, ÝÝÝvasodilation] o Metabolism: 90% renal, T1/2= 2.4h Dosing: 0.1-1.0mcg/kg/min o AE: Proarrhythmia, hypotension

Patient Presents – Time to administer pharmacologic treatment

- Class II Picture: No Shock, simply congested o à Slam the IV diuretics o Acute pulmonary picture? à Add the Vasodilators

- Class IV Picture: Cardiogenic Shock, poorly perfused and congested o à Slam the IV Inotropes + Diuretics ASAP

VTE Prophylaxis: All patients that get admitted will require VTE prophylaxis - Administer: UFH, LMWH, Fonda - ContraX: Already receiving anticoagulation therapies, concurrent bleed

o If contraX to VTE prophylactic therapy, use IPC (intermittent pneumatic compression) devices, or compression stockings

Specific Monitoring Parameters: Shown on the table top right, all patients admitted will require at least once daily monitoring for multiple parameters. Particularly, our Ins-and-Outs. Some patients require additional monitoring

- Continuous Telemetry: For patients with arrhythmias, or receiving IV vasoactive therapy - Invasive Hemodynamic Monitoring: Specifically for those in shock, with hypotension, or Forrester Class IV

Transitions of Care: Before the patient is out the door and on their way, we want to make certain that all discharge criteria are followed: The patient should transition from an IVàPO diuretic and have a 24-hour trial on their PO diuretic to assess efficacy and safety. Before leaving, they should have optimal fluid status. Educate both the patient and the patient’s family. Document LV EF, and optimize GDMT

- Follow-up clinic visit in 7-10 days - The discharge regimen should be better than the admission regimen.

Best of luck to everyone! Remember, this should only act as a supplement! You learn best using your own methods first