Acute Decompensated Heart Failure
(ADHF)- Management
• Acute Heart failure ( Acute HF syndromes or
ADHF) is rapid occurrence of symptoms and
signs of HF, or the deterioration of stable HF,
leading the requirement of hospitalisztion and
/ or intensive therapy.
• 65% to 85% of admissions are due to
worsening of existing HF.
• In hospital mortality is 3-4%
• Aim of management
• 1. Immediate Assessment
• 2. Relief of symptoms by intensive monitored care
• 3 .Identification of precipitating causes
• 4. Stabilisation of the patient
• 5. Review of the old therapy
• 6. Modification of therapy
• 7. Patient education.
• 8. Plan for interventions
• 9. Plan for discharge.
Assessment
• Symptoms
» Fatigue
» Indigestion
» Insomnia
» PND
» Light headedness
» Palpitations
» Nocturnal cough
» Right hypochondrial pain
» Wt gain / wt loss
• Signs
Appearence
Pulse - regularity, volume, alternans, paradoxes
BP disparity in BP between limbs
Respiration
Cyanosis
JVP
Edema
Signs of renal failure
Signs of hepatic failure
• Initial investigations
• 12 lead ECG
• BS / BUN / Creatinine
• ECHO
• CXR
• Others
• Cardiac enzymes
• Electrolytes
• BNP
Low-Intermediate clinical suspicion of ADHF
BNP (A)
BNP > 500pg/ml
ADHF more likely
BNP < 50-100pg/ml
ADHF less likely
BNP 100-500pg/ml
Likely, but
consider other causes
• What are the things to be monitored?
• 1. SpO2
• 2.BP
• 3. respiratory rate
• 4. urine output
• 5. response to treatment
• 6. filling pressures
• 7. Invasive monitoring
• A word about filling pressures.
– 1. pts with DCM have elevated RV filling pressure-
30mmHg.
– Can be brought down to 15-16mmHg to improve the CO
by reducing the RV size, reducing the severity of MR
• But in Ischemic heart disease
– The filling pressure needs to be little high as the compliance is
reduced.
Differential Diagnosis
 Pneumonia
 Reactive airway disease
 Pulmonary embolus
• Treatment:
» 1. propped up position
» 2. removal of iatrogenic cause
» 3. oxygen in adequate dose
» 4. Hemodynamic monitoring . ( Invasive and Noninvasive)
» 4. Intravenous diuretics
» 5.Intravenous vasodilators
» 6. inotrops
» 7.management of precipitating cause
• Ischemia, arrythmia, renal failure ,
COPD,DM, infections.
• Profile A:
– Warm and Dry
– That means they are not congested and they are adequately
perfused.
• Profile B:
– Warm and wet .
– That means they are adequately perfused but congested.
– The most common presentation
– Management
• Reduction of filling pressures by veno
dilators and diuretics
• Reduction of afterload
• Positive pressure ventilation.
• Profile C:
– Cold and wet
– that means under perfused but congested.
– True cardiogenic shock
– Needs rapidly escalating support ( like early interventions
– Needs vasoactive drugs-
• Vasodilators to reduce SVR which is invariably
high
• Choice - dobutamine
• Profile D: NO NO
– Profile L
• Dry and Cold
» Means that there is under perfusion and no congestion
» Rare situation
» Look for filling pressures
» Stop diuretics
» Try to replace volume by careful monitoring
» If heart rate is high reduce by BB
» Inotrops - ? value
(D) Unresolved hypoperfusion
Transient use of Vasopressor therapy
Epinephrine
0.05-0.5 ug/kg/min inf. Norepinephrine 0.2-1ug/kg/min
+/- dobutamine
0.05-0.5 ug/kg/min inf.
Use of invasive
hemodynamic monitoring C
Non-pharmacologic Management
• Daily weight
• Strict I’s and O’s
• Low sodium diet (<2g daily)
• Fluid restriction
– Typically only for patients with hyponatremia
Treatment: Diuretics
• Recommend to give intravenously initially
• Typically at least twice a day
• Agents
– Furosemide
• Can give home dose as IV (2:1 po to IV ratio)
• Titrate up based on response (goal net negative
1.5-2L daily on average)
– Bumetanide
• Alternative to Furosemide in tolerant patients
• 40 mg IV Lasix = 1 mg IV Bumetanide = 1mg po
Bumetanide
Treatment: Diuretics
• If not responding to initial diuretic dose:
– Can titrate dose up further
– Older patients, underlying renal dysfunction may require
higher doses
• Can consider adding Metolazone for additional effect
– Thiazide diuretic
• Monitoring of electrolytes closely
– Check potassium and magnesium at least daily
– If aggressive diuresis, check at least twice daily
Treatment: Beta blockers
• Typically not initiated during acute exacerbation
• Continue if already on
– Stopping can worsen RAAS activation
– If SYMPTOMATIC hypotension, can decrease the
dose
• Options
– Carvedilol: lowest dose 3.125mg BID
– Metoprolol XL: lowest dose 25mg daily
– Titrate to goal HR of 60 bpm
• Or as much as BP can tolerate
Summary
• Identify clinical signs and symptoms of ADHF
• Pertinent labs
– Sodium, creatinine, troponin, BNP
• Relevant imaging
– EKG, CXR, echocardiography
• Treatment
– Diuresis, BB, ACEI/ARB, Spironolactone, Digoxin,
Isosorbide dinitrate/Hydralazine
• Transition to outpatient
– Strict instructions, close-follow-up
• Thanking You All
Acute decompensated heart failure
Acute decompensated heart failure
Acute decompensated heart failure
Acute decompensated heart failure
Acute decompensated heart failure
Acute decompensated heart failure
Acute decompensated heart failure

Acute decompensated heart failure

  • 1.
    Acute Decompensated HeartFailure (ADHF)- Management
  • 2.
    • Acute Heartfailure ( Acute HF syndromes or ADHF) is rapid occurrence of symptoms and signs of HF, or the deterioration of stable HF, leading the requirement of hospitalisztion and / or intensive therapy.
  • 3.
    • 65% to85% of admissions are due to worsening of existing HF. • In hospital mortality is 3-4%
  • 7.
    • Aim ofmanagement • 1. Immediate Assessment • 2. Relief of symptoms by intensive monitored care • 3 .Identification of precipitating causes • 4. Stabilisation of the patient • 5. Review of the old therapy • 6. Modification of therapy • 7. Patient education. • 8. Plan for interventions • 9. Plan for discharge.
  • 8.
    Assessment • Symptoms » Fatigue »Indigestion » Insomnia » PND » Light headedness » Palpitations » Nocturnal cough » Right hypochondrial pain » Wt gain / wt loss
  • 9.
    • Signs Appearence Pulse -regularity, volume, alternans, paradoxes BP disparity in BP between limbs Respiration Cyanosis JVP Edema Signs of renal failure Signs of hepatic failure
  • 11.
    • Initial investigations •12 lead ECG • BS / BUN / Creatinine • ECHO • CXR • Others • Cardiac enzymes • Electrolytes • BNP
  • 12.
    Low-Intermediate clinical suspicionof ADHF BNP (A) BNP > 500pg/ml ADHF more likely BNP < 50-100pg/ml ADHF less likely BNP 100-500pg/ml Likely, but consider other causes
  • 13.
    • What arethe things to be monitored? • 1. SpO2 • 2.BP • 3. respiratory rate • 4. urine output • 5. response to treatment • 6. filling pressures • 7. Invasive monitoring
  • 15.
    • A wordabout filling pressures. – 1. pts with DCM have elevated RV filling pressure- 30mmHg. – Can be brought down to 15-16mmHg to improve the CO by reducing the RV size, reducing the severity of MR
  • 17.
    • But inIschemic heart disease – The filling pressure needs to be little high as the compliance is reduced.
  • 21.
    Differential Diagnosis  Pneumonia Reactive airway disease  Pulmonary embolus
  • 22.
    • Treatment: » 1.propped up position » 2. removal of iatrogenic cause » 3. oxygen in adequate dose » 4. Hemodynamic monitoring . ( Invasive and Noninvasive) » 4. Intravenous diuretics » 5.Intravenous vasodilators » 6. inotrops » 7.management of precipitating cause • Ischemia, arrythmia, renal failure , COPD,DM, infections.
  • 24.
    • Profile A: –Warm and Dry – That means they are not congested and they are adequately perfused.
  • 25.
    • Profile B: –Warm and wet . – That means they are adequately perfused but congested. – The most common presentation – Management • Reduction of filling pressures by veno dilators and diuretics • Reduction of afterload • Positive pressure ventilation.
  • 26.
    • Profile C: –Cold and wet – that means under perfused but congested. – True cardiogenic shock – Needs rapidly escalating support ( like early interventions – Needs vasoactive drugs- • Vasodilators to reduce SVR which is invariably high • Choice - dobutamine
  • 27.
    • Profile D:NO NO – Profile L • Dry and Cold » Means that there is under perfusion and no congestion » Rare situation » Look for filling pressures » Stop diuretics » Try to replace volume by careful monitoring » If heart rate is high reduce by BB » Inotrops - ? value
  • 31.
    (D) Unresolved hypoperfusion Transientuse of Vasopressor therapy Epinephrine 0.05-0.5 ug/kg/min inf. Norepinephrine 0.2-1ug/kg/min +/- dobutamine 0.05-0.5 ug/kg/min inf. Use of invasive hemodynamic monitoring C
  • 32.
    Non-pharmacologic Management • Dailyweight • Strict I’s and O’s • Low sodium diet (<2g daily) • Fluid restriction – Typically only for patients with hyponatremia
  • 33.
    Treatment: Diuretics • Recommendto give intravenously initially • Typically at least twice a day • Agents – Furosemide • Can give home dose as IV (2:1 po to IV ratio) • Titrate up based on response (goal net negative 1.5-2L daily on average) – Bumetanide • Alternative to Furosemide in tolerant patients • 40 mg IV Lasix = 1 mg IV Bumetanide = 1mg po Bumetanide
  • 34.
    Treatment: Diuretics • Ifnot responding to initial diuretic dose: – Can titrate dose up further – Older patients, underlying renal dysfunction may require higher doses • Can consider adding Metolazone for additional effect – Thiazide diuretic • Monitoring of electrolytes closely – Check potassium and magnesium at least daily – If aggressive diuresis, check at least twice daily
  • 35.
    Treatment: Beta blockers •Typically not initiated during acute exacerbation • Continue if already on – Stopping can worsen RAAS activation – If SYMPTOMATIC hypotension, can decrease the dose • Options – Carvedilol: lowest dose 3.125mg BID – Metoprolol XL: lowest dose 25mg daily – Titrate to goal HR of 60 bpm • Or as much as BP can tolerate
  • 37.
    Summary • Identify clinicalsigns and symptoms of ADHF • Pertinent labs – Sodium, creatinine, troponin, BNP • Relevant imaging – EKG, CXR, echocardiography • Treatment – Diuresis, BB, ACEI/ARB, Spironolactone, Digoxin, Isosorbide dinitrate/Hydralazine • Transition to outpatient – Strict instructions, close-follow-up
  • 38.