Acute Decompensated Heart Failure management

1. Acute Decompensated
Heart Failure
By:
Dr. Ammar Sabir Siddiqui
Senior Resident
Department of Medicine, KGMU

2. WHAT IS HEART FAILURE?
• AHA guidelines define HF as a complex clinical syndrome that results
from structural or functional impairment of ventricular filling(diastolic
dysfunction) or ejection of blood(systolic dysfunction)

3. ETIOLOGY

4. CLASSIFICATION
• LVEF is used to subdivide HF patients into groups for therapeutic and
prognostic purposes. These groups are:
1. EF<40%: HF with reduced EF(HFrEF)
2. EF 40-50%: HF with borderline EF
3. EF>50% : HF with preserved EF(HFpEF)

5. NYHA CLASSIFICATION-Based on Symptom Status

6. PATHOPHYSIOLOGY
• Activation of neurohormonal pathways which are activated as a
compensatory mechanism. These include:
1. Renin Angiotensin Aldosterone System
2. Adrenergic nervous system
Sustained activation of these systems leads to secondary end-organ
damage within the ventricle, with worsening left ventricular remodeling
and subsequent cardiac decompensation
Hence pharmacotherapy of HF is based on RAAS and β- adrenergic
blockade and on the use of vasoldilators and diuretics if there is
pulmonary congestion

7. HOW TO IDENTIFY HEART FAILURE?
• The cardinal symptoms of HF are fatigue and shortness of breath
• Exercise intolerance
• Orthopnea- Usually associated with nocturnal cough
• Paroxysmal Nocturnal Dyspnea- severe shortness of breath and coughing that
generally occur at night and awakens the patient from sleep, usually 1–3 h
after the patient retires.
• Cheyne Stokes Respiration- Also referred to as periodic respiration or cyclic
respiration-present in 40% of patients with advanced HF
• Anorexia, nausea, and early satiety associated with abdominal pain
• Right upper quadrant pain- as a result of congestive hepatomegaly
• Nocturia is common in HF

8. PHYSICAL EXAMINATION
INSPECTION:
• General Appearance: Patient presents to you with a predilection to sit
upright, with labored breathing, inability to finish a sentence because of
shortness of breath
• Elevated JVP- Suggestive of overt HF
PALPATION
• Hepatojugular reflux- Suggestive of incipient RVF
• Apical impulse- Displaced down and lateral- Sustained in nature- LVH
• Sustained and prolonged left parasternal impulse extending throughout
systole-RVH

9. • Hepatomegaly
• Pulsatile liver (pulsations felt during systole)
Auscultation-
Pulmonary crackles (rales or crepitations) bilaterally
May be accompanied by expiratory wheezing (cardiac asthma)
• S3- suggestive of LVF- heard at the Apex

10. INVESTIGATIONS
1. Routine blood investigations
2. Cardiac biomarkers- Both BNP and NT-pro BNP are elevated. Levels
>400 pg/ml is consistent with HF. Levels <100 pg/ml has a good
NPV to exclude HF in patients presenting with dyspnea
BNP levels may increase in patients taking ARNIs. Levels can be falsely
low in obese patients
Age specific cut points :
AGE BNP LEVELS( in pg/ml)
<50 450
50-75 900
>75 1800

11. 2. ECG-An ECG should be performed to look for
- evidence of ischemia (ST-T wave abnormalities)
- hypertrophy (increased voltage)
- infiltration (reduced voltage)
- previous myocardial infarction (MI) (Q waves)
- conduction block (PR interval)
- interventricular conduction delays (QRS)
- arrhythmias (supraventricular and ventricular).
3. CXR-PA- Cephalization and interstitial edema are highly specific
• Cardiomegaly may be present

13. 4. Echocardiography- An echocardiogram should be performed to
assess right ventricular (RV) and LV systolic and diastolic function,
valvular structure and function, and chamber size and to exclude
cardiac tamponade.
5. Cardiac MRI: Useful in assessing ventricular function and evaluating
the presence of intracardiac shunting, valvular heart disease, infiltrative
cardiomyopathy, myocarditis, and previous MI.

14. ACUTE DECOMPENSATED HEART FAILURE
• ADHF is a heterogeneous clinical syndrome most often resulting in
need for hospitalization due to confluence of interrelated
abnormalities of decreased cardiac performance, renal dysfunction,
and alterations in vascular compliance
• The management of these patients has remained difficult and
principally revolves around volume control and decrease of vascular
impedance while maintaining attention to end-organ perfusion
(coronary and renal)

15. TREATMENT
• Placing the patient in a sitting position improves pulmonary function.
• Bed rest, pain control, and relief of anxiety can decrease cardiac workload.
• Supplemental oxygen should be administered initially to raise the arterial
oxygen tension to >60 mm Hg.
• Mechanical ventilation is indicated if oxygenation is inadequate or
hypercapnia occurs.
• Noninvasive positive-pressure ventilation is preferred and may have
particularly favorable effects in the setting of pulmonary edema
• Precipitating factors should be identified and corrected, because resolution
of pulmonary edema can often be accomplished with correction of the
underlying process.

16. • The most common precipitants are:
1. Severe hypertension
2. MI or myocardial ischemia (particularly if associated with MR)
3. Acute valvular regurgitation
4. New-onset tachyarrhythmias or bradyarrhythmias
5. Volume overload in the setting of severe LV dysfunction

17. VOLUME MANAGEMENT
• First line of therapy in volume overload with congestion; may use
bolus or continuous dosing; initial low dose (1 × home dose) or high
dose (2.5 × home dose) equally effective with higher risk of renal
worsening with higher dose
• Intravenous diuretics: Loop diuretics( Furosemide, Torsemide) are the
preferred agents
-When high doses of diuretic agents are required or when the effect is
suboptimal, a continuous infusion may be needed to reduce toxicity
and maintain stable serum drug levels

18. • Addition of a thiazide diuretic eg. Metolazone provides a synergistic
effect and is often required in patients receiving long-term therapy
with loop diuretic agents
• Spironolactone is useful in presence of severe hypokalemia and
normal renal function
• Acetazolamide is useful in presence of alkalosis

19. VASODILATORS- REDUCE VASCULAR IMPEDANCE
• Vasodilators are used in presence of pulmonary congestion for rapid
relief of dyspnea, in presence of a preserved blood pressure

20. • Other agents that have been tried but not proven effective in trials
are:
1. Recombinant human relaxin-2, or serelaxin- A peptide upregulated
in pregnancy
2. Urodilatin- A natriuretic peptide

21. INOTROPIC THERAPY
-Used in hypotension, end-organ hypoperfusion, or shock states

22. • Levosimendan is a calcium sensitizer that provides inotropic activity,
but also possesses phosphodiesterase-3 inhibition properties that are
vasodilators in action
• Omecamtiv mecarbil is a selective myosin activator, prolongs the
ejection period and increases fractional shortening

26. TREATMENT PRINCIPLES IN HFrEF
• The initial clinical strategy should be to use a two-drug combination
first (ACEI and beta blocker; if beta blocker intolerant, then ACEI and
ARB; if ACEI intolerant, then ARB and beta blocker)
• In symptomatic patients (NYHA class II–IV), an aldosterone antagonist
should be strongly considered, but four-drug therapy should be
avoided.
• Combination of hydralazine and nitrates has been demonstrated to
improve survival in HFrEF.
• Digoxin should be considered for patients who remain symptomatic
when taking diuretics and ACE inhibitors as well as for patients with
heart failure who are in atrial fibrillation and require rate control

27. • No role of statins has been demonstrated in HFrEF
• HFrEF is accompanied by a hypercoagulable stateAnticoagulation is
recommended primarily in patients who are in atrial fibrillation, who
have had thromboemboli, or who have had a large recent anterior
myocardial infarction- these patients should receive warfarin for 3
months following the myocardial infarction.
• Current guidelines support the use of aspirin in patients with ischemic
cardiomyopathy
• Treatment with long-chain omega-3 polyunsaturated fatty acids (ω-3
PUFAs) has been shown to be associated with modestly improved
clinical outcomes in patients with HFrEF

28. • Reversible heart failure has been described as a consequence of
severe thiamine and selenium deficiency. Small exploratory
randomized studies have suggested a benefit of supplementation of
thiamine in HFrEF
• Rhythm Control- Antiarrhythmic drug therapy should be restricted to
amiodarone and dofetilide
• The drug empagloflozin was tested in the EMPA-REG study and
demonstrated a decrease in cardiovascular mortality as well as
hospitalizations for heart failure- SGLT-2 inhibitors represent a viable
therapeutic avenue in diabetics with heart failure.

29. DRUGS TO BE AVOIDED IN HFrEF
• Thiazoladinediones (glitazones) that cause worsening heart failure
• Calcium channel blockers (with the exception of amlodipine and
felodipine)
• Nonsteroidal anti-inflammatory medications, and cyclooxygenase-2
inhibitors that cause sodium and water retention and renal
impairment
• The combination of an ACE inhibitor, ARB, and aldosterone blocker
that increases the risk of hyperkalemia