Acute Heart Failure - Pharmacotherapy

1. Acute decompensated HF

2. Definition
O rapid onset of new or worsening signs and
symptoms of HF, as a result of volume
overload and/or low cardiac output .It is
often a potentially life-threatening
condition.
O Generally requires hospitalization,
intensive therapy, IV meds, intensive
monitoring.

3. Etiology and Pathophysiology
1. Large MI -> left ventricular dysfunction
2. sudden elevation in blood pressure.
3. refractory to oral therapies
4. decompensate after mild insult (eg, dietary
indiscretion, nonsteroidal anti-inflammatory drug
use)
5. medication nonadherence,
6. concurrent noncardiac illness (eg, infection).
7. New or worsening cardiac processes, such as
MI, atrial or ventricular arrhythmias, hypertensive
crises, myocarditis, or acute valvular
insufficiency,

4. Prognostic factors:
O BUN ≥43mg/dl
O SBP ≤ 115mmHg
O SrCr ≥2.75 mg/dl
O Hyponatremia
O troponin I
O Ischemic etiology
O Poor functional capacity

5. Clinical presentation
O Hx & physical examination
Hx include: precipitating factors, onset,
duration, severity of s/s and PMH.
O Determine hemodynamic status to guide
therapy.

6. Subsets of Acute HF

7. Monitoring Pulmonary artery
catheter:
O Invasive hemodynamic monitoring helps
evaluate volume and perfusion status but
NOT REQUIRED
O Pulmonary artery catheter (PAC)
placement:
O PCWP > 18mmHg -> overload
O CI <2.2 l/min/m2 -> cold

8. Signs & symptoms:
O Wt gain of atleast 5kg, AMS, dyspnea,
HoTN, worsening of renal fcn, polmunary
or systemic congestion, arrhythmias
O Labs: BNP, BUN, Scr, electrolytes (K),
troponins., thyroid, LFT
O Cardiac enzymes to exclude myocardial
ischemia.

9. Goals of therapy:
O Correct underlying factors and prevent
further episodes
O Relieve symptoms
O Improve hemodynamic measures
O Optimize chronic PO therapy before D/C
O Educate pt about compliance w/ meds
and lifestyle changes

10. General approach to treatment
O B-blockers should be continues unless C/I
O May need to hold other agents (ACEi,
sprionolactone) as needed.
O Continue digoxin in most pts unless toxic.
O Treat using simple clinical parameters
(s/s, BP, renal fcn) or invasive
hemodynamic monitoring.
O Strict monitor of I/O, vital S/S, &
electrolytes

11. Subset I (Warm and dry)
O No signs and symptoms of volume overload
or hypoperfusion
O values within ranges(CI >2.2 and PCWP < 18
)
O normal compensatory mechanisms in Patient
significant left ventricular dysfunction or drug.
O lowest risk of mortality
O do not require immediate intervention just
optimization PO drugs for HF

12. Subset II (Warm & Wet)
O Well perfused, with congestion
O CI >2.2 but a PCWP greater than 18 mm
Hg.
O Management
- relieve symptoms of congestion by
lowering PCWP
- without reducing CO, increasing heart
rate, provoking neurohormonal
activation(SVR) .

13. Subset III Cold & Dry
O Hypoperfusion w/o congestion.
O CI of less than 2.2 L/min/m2 but normal
range of PCWP <18.
O The mortality is higher
O Treatment focuses on increasing CO w/
positive inotropes, very cautious fluid
replacement and vasodilators.

14. Subset IV Cold & wet
O Volume overload & peripheral
hypoperfusion
O Worst prognosis (end stage HF)
O CI <2.2 L/min/m2, PCWP >18 mm Hg
O If patient compromise MAP :combined
inotrope and vasopressor therapy (eg,
dobutamine plus norepinephrine) or an
inotrope with vasopressor activity (eg,
dopamine) to rise MAP

16. Diuretics:
O Loop diuretics are 1st line in ADHF w/ o/l
O Furosemide, Torsemide, Bumetanide.
O Reduce preload, PCWP but no effect on
CO
O Reduce pulmonary congestion and
dyspnea
O IV bolus or continuous infusion
• 2 mechanisms: Reduces preload within
5 to 15 min by venodilation
• within 20 min by sodium and water
excretion
• Reduce pulmonary congestion
O Titrate to U/O, PCWP, congestion, BP

17. Vasodilators:
O NTG, nitroprusside, nesiritide
O Arteriodilators reduce SVR, afterload,
increase CO
O Venodilators (NTG, nesitiride) relieve s/s
of congestion via reducing preload and
PCWP
O Nitroprusside is mixed vasodilator

18. Nitroglycerin
O Venodilation is predominant effect, also has
mild arteriodilation at higher doses
(200mcg/min)
O Causes coronary dilation, ideal in HF pt w/
CAD and myocardial ischemia
O Continuous infusion (short half-life 1-3mins)
O Reduce preload and PCWP
O Tachyphylaxis develops w/in 72h (resistance)
O Initial dose 5-10 mcg/min increased every 5-
10 mins
O Maintenance dose: 35-200mcg/min
O S.E: HoTN, excessive decrease in PCWP

19. Nesiritide
O Recombinant Human BNP
O Causes vensous & arterial dilation and
natriuresis
O Reduces PCWP, preload, afterload, SVR,
BP, increases CO, no effect on HR
O No tolerance build up
O Longer half life than NTG and
Nitroprusside
O Use in cardiac ischemic
O S.E: worsening of renal fcn

20. Sodium nitroprusside
O Source of nitric oxide in vascular smooth
muscle
O Given as continuous IV infusion
O Venodilation & arteriodilation at any dose
O Decrease preload, congestion, PCWP, SVR,
BP,
O Increase CO
O More potent in lowering BP than NTG
O Can worsen myocardial ischemia
O Cyanide and/or thiocyanate toxicity w/ liver or
renal insuffeciency

21. Vasopressin antagonists
O Tolvaptan & conivaptan: inhibit AVP
receptors.

22. Ultrafiltration:
O Renal impairment
O rapid fluid removal
O salt and water may be eliminated at rates
of up to 500 mL/h
O reduces PCWP and increases diuresis.
O Potential candidates for : diuretic
resistance, renal impairment following
diuretic administration, or continued renal
impairment despite inotropic therapy

23. Inotropes:
O Dobutamine, Milrinone
O Increase intracellular cAMP -> increase
contractility
O Help perfuse vital organs
O May increase workload/ischemia
O All are associated w/ risk for arrhythmias
O Improve diuresis

24. Dobutamine
O synthetic catecholamine, β1- and β2-receptor
agonist with some α1-agonist effects.
O Improve contractility and CO w/ minimal
change in HR and MAP.
O Increase CO-> decrease SVR
O Reduce PCWP (useful in congestion)
O Causes increase in myocardial oxygen
consumption
O Avoid use if pts is on B-blocker
O S.E tachycardia & arrhythmia

25. Milrinone
O Phosphodiesterase inhibitors
O Positive inotrope, vasodilator
O Causes increase in SV, CO, reduce
PCWP with minimal change on HR &
MAP
O Useful for congestion and low CO
O Ideal for use in pts on B blockers
O IV administration
O S.E arrhythmia, HoTN, thrombocytopenia

26. Dopamine (inotropic &
vasopressor activity)
O At lower doses (3-10mcg/kg/min)
activates B1, B2, D1 receptors increasing
inotropy, SV, HR, CO.
O At higher doses (>10mcg/kg/min) activate
a1 & increase chronotropy & arrhythmia
O increase BP ,CO,PCWP, coronary
ischemia
Highly proarrhythmic, should be reserved for
pts w/ HoTN and near cardiogenic shock.

27. Monitoring parameters:
O Fluid I/O
O Vital signs
O Daily body wt
O Daily serum electrolytes, BUN, Cr
O Clinical s/s perfusion & congestion