Acute decompensated heart failure

1. Acute Decompensated Heart
Failure

2. Definition
• 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.
• Generally requires hospitalization, intensive
therapy, IV meds, intensive monitoring.

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

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

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

6. The Heart Failure Society of American guidelines
recommend the following treatment goals for patients
admitted for ADHF
• Improve symptoms, especially congestion and low-output
symptoms
• Restore normal oxygenation
• Optimize volume status
• Identify etiology
• Identify and address precipitating factors
• Optimize chronic oral therapy
• Minimize side effects
• Identify patients who might benefit from revascularization.
• Identify patients who might benefit from device therapy
(LVAD)
• Identify risk of thromboembolism and need for anticoagulant
therapy
• Educate patients concerning medications and self-
management of HF

7. Subsets of Acute HF (systolic)

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

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

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

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

13. Monitoring Pulmonary Artery Catheter:
• Invasive hemodynamic monitoring helps
evaluate volume and perfusion status
• Pulmonary artery catheter (PAC) placement:
• PCWP > 18mmHg -> overload
• CI <2.2 l/min/m2 -> cold
• BUT IT IS NOT ALWAYS REQUIRED

14. • Uses pulmonary artery (PA)
- refractory to initial therapy
- whose volume status is unclear,
- with clinically significant hypotension (ie, systolic
blood pressure <80 mm Hg)
- or worsening renal function despite standard
therapy.
- patients being evaluated for mechanical circulatory
support (MCS) or cardiac transplantation.

15. Systolic Versus Diastolic Dysfunction
• In the acute setting, however, some of the initial therapies are
similar in systolic and diastolic HF, including the following:
• Diuresis
• Supplemental oxygen and assisted ventilation, if necessary
• Vasodilator therapy in selected patients
• in systolic dysfunction, some medications should not be
initiated or should be used with caution in the acute setting
(eg, angiotensin converting enzyme inhibitors and beta
blockers).
• In diastolic dysfunction, treatment of hypertension and
tachycardia is particularly important.
• Inotropic agents are not indicated in patients with diastolic
dysfunction with preserved systolic function.

16. Diuretics:
• Loop diuretics are 1st line in ADHF
• Furosemide, Torsemide, Bumetanide.
• Reduce preload, PCWP but no effect on CO
• Reduce pulmonary congestion and dyspnea
• 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
• Titrate to U/O, PCWP, congestion, BP

17. • To overcome diuretic resistance:
• increase dose, frequency, switch to continuous
infusion
• Add thiazide like diuretic e.g metolazone
• IV vasodilator, inotropes, ultrafiltration or
vasopressin antagonist.
• Non-pharm strategy: limit Na and water intake.

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

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

20. Nesiritide
• Recombinant Human BNP
• Causes vensous & arterial dilation and
natriuresis
• Reduces PCWP, preload, afterload, SVR, BP,
increases CO, no effect on HR
• No tolerance build up
• Longer half life than NTG and Nitroprusside
• Use in cardiac ischemic
• S.E: worsening of renal fcn
• Natriuresis ( loss of Na & water)
• Difficult to titrate due to longer half life

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

22. • Rapid onset of action but effects last less than 10
mins
• initiated at low doses (0.1-0.2
mcg/kg/min) increments (0.1-0.2 mcg/kg/min)
every 5 to 10 minutes to avoid hypotension.
• Effective doses :from 0.5 to 3 mcg/kg/min
• Avoid in increase ICP pts may worsen cerebral
edema

23. Vasopressin antagonists
• Tolvaptan & conivaptan: inhibit AVP
receptors.

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

25. • Complications of ultrafiltration:
• central venous access (infection)
• rapid volume removal
• intravascular depletion
• electrolyte depletion

26. Inotropes:
• Dobutamine, Milrinone
• Increase intracellular cAMP -> increase
contractility
• Help perfuse vital organs
• May increase workload/ischemia
• All are associated w/ risk for arrhythmias
• Improve diuresis
• Give to patient with cardiogenic shock,
depressed CO and low SBP

27. Dobutamine
• synthetic catecholamine, β1- and β2-receptor agonist
with some α1-agonist effects.
• Improve contractility and CO w/ minimal change in HR
and MAP.
• Increase CO-> decrease SVR
• Reduce PCWP (useful in congestion)
• Causes increase in myocardial oxygen consumption
• Avoid use if pts is on B-blocker
• Effect is observed w/in 10 mins elimination half life 2
mins
• Initial dose 2.5-5 mcg/kg/min may be increase to
20mcg/kg/min
• S.E tachycardia & arrhythmia

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

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

30. Arrhythmia Management
• Both supraventricular and ventricular
arrhythmias can occur in association with
pulmonary edema , all may associate to ADHF

31. Atrial Fibrillation
• there are several possible relationships:
• Acute HF can precipitate AF due to increases in
left atrial pressure and wall stress.
• AF can cause acute HF, particularly if the
ventricular response is rapid.
• AF may be chronic and not directly related to the
acute HF decompensation.

32. • In some patients with AF and ADHF, effective
treatment of pulmonary edema results in
slowing of the ventricular rate or spontaneous
reversion of the arrhythmia.
• If AF persists, it is treated in the same fashion as
AF in other situations , rate control are preferred

33. • Restoration of sinus rhythm should be considered in
the following settings (DC Shock):
• If AF is associated with hypotension or evidence of
cardiogenic shock
• If AF is clearly the cause for pulmonary edema
• If AF is associated with new or increased ischemia
• If the response to effective therapy of pulmonary
edema is slow or suboptimal
• Heparin should be started prior to cardioversion if
possible

34. Ventricular Arrhythmia
• Ventricular tachycardia during pulmonary
edema is usually life-threatening.
• As a result, prompt electrical cardioversion or
defibrillation is required.
• If the arrhythmia recurs after reversion,
antiarrhythmic therapy, particularly
with amiodarone, may be effective.

35. Renovascular Hypertension
• Recurrent unexplained heart failure (HF)
decompensation and/or flash (sudden-onset)
pulmonary edema occurs in some patients with
renovascular hypertension.
• often with preserved (normal or near normal) left
ventricular systolic function.
• Flash pulmonary edema appears to be more
common in patients with bilateral renal artery
stenosis as compared to those with unilateral
disease.

36. • The combination of bilateral renal artery stenosis
and flash pulmonary edema has been named the
Pickering syndrome.
• Acute treatment of acute decompensate HF in
patients with this syndrome includes blood pressure
control , diuresis.
• In patients who are euvolemic or dehydrated,
diuresis should be avoided, as it may lead to renal
insufficiency, and preload reduction with nitrates is
preferable.

37. Monitoring
• daily monitoring of vital signs (including orthostatic
blood pressure) and at least daily monitoring of
weight, fluid intake and output, symptoms and signs
of congestion, serum electrolytes, blood urea
nitrogen, serum creatinine, and oxygen saturation
until stable Serum potassium and magnesium levels
should be monitored at least daily, and more
frequent monitoring may be required when diuresis
is rapid.
• Routine tests include blood glucose, troponin,
complete blood count, and the International
Normalized Ratio if warfarin is used.

38. • Evaluation of liver function tests, and urinalysis
is frequently indicated and arterial blood gas
testing is occasionally indicated (eg, to detect
carbon dioxide retention).
• Measurement of brain natriuretic peptide (BNP)
or N-terminal pro BNP can be of value in
clarifying the cardiac basis of respiratory
distress and/or guiding therapy.

39. Summary And Recommendations
• Hospital admission is recommended for patients with acute
decompensated heart failure (ADHF) with evidence of severe
decompensation (including hypotension, worsening renal function,
or altered mentation), dyspnea at rest, hemodynamically significant
arrhythmia including new onset atrial fibrillation, or acute coronary
syndrome.
• Hospitalization should be considered for other patients with ADHF,
including those with signs or symptoms of pulmonary or systemic
congestion (with or without weight gain), major electrolyte
disturbance, or associated comorbid conditions.
• High hospital readmission rates are partly due to ineffective fluid
removal. Daily assessment of patient weight may be the most
effective method for documenting effective diuresis. For accurate
comparisons, daily measurements should use the same scale and
should be performed at the same time each day, usually in the
morning, prior to eating and after voiding.

40. • Treatment goals for patients admitted with ADHF include
improving symptoms, optimizing volume status, identifying
etiology and precipitating factors (particularly ischemia),
initiating and optimizing oral therapy, minimizing side
effects, educating patients, and considering a disease
management program.
• The following initial therapies are similar in systolic and
diastolic HF: diuresis, supplemental oxygen and assisted
ventilation, and vasodilator therapy in selected patients.
• Some medications should be avoided or used with caution in
the acute setting (eg, angiotensin converting enzyme [ACE]
inhibitors and beta-blockers) in patients with systolic
dysfunction. In patients on ACE inhibitors and beta blockers,
the medications can be continued if the patient is relatively
stable (eg, just needs diuresis). Inotropic agents are not
indicated in patients with diastolic dysfunction with preserved
systolic function.

41. • Atrial fibrillation can precipitate ADHF and ADHF
can promote atrial fibrillation (AF).
• An initial strategy of rate control is reasonable if AF
does not appear to be the precipitant of ADHF.
• Restoration of sinus rhythm should be considered if
AF is associated with hypotension or cardiogenic
shock, if AF is the cause for pulmonary edema, or if
the response to therapy of pulmonary edema is
suboptimal.

42. • Ventricular tachycardia during pulmonary
edema generally requires prompt electrical
cardioversion or defibrillation.
• Careful discharge planning and transition to
outpatient care is indicated to reduce the risk of
post-discharge mortality and readmission