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Management of ADHF
Dr.Nishanth
Dr. Srishti
Diagnosing Heart Failure
HISTORY
• Prior HF/myocardial injury
• DOE, orthopnea, PND
• Fatigue
• Edema
• Family history
EXAMINATION
• Congestion
• Perfusion
• Tachy/brady arrhytmias
CXR findings
Lung USG findings
▸ Sliding present
▸ Diffuse B lines
(≥3 in ≥2 zones B/L)
▸ Pleural effusion
Treating Heart failure
GOALS
1. Initial stabilization
2. Relieve symptoms: congestion and low output
3. Identify etiology
4. Identify precipitating factors
5. Minimize side effects
1.Initial Stabilization
• O2 – to prevent hypoxia <90% Spo2 (NOT
routinely)
• NIV indications
Respiratory distress
Respiratory acidosis
Hypoxia despite O2
NIV
Respiratory support
-Increases tidal volume
-Unloads respiratory muscles
-Decreases dead space ventilation
Hemodynamic support
-Alters cardiac transmural pressures
-Decreases preload (venous return) and afterload
-No change in cardiac index
2. Symptoms management
1. Optimize preload - Diuretics
2. Decrease Afterload - Vasodilators
3. Augment contractility – Inotropes and
vasopressors , Mechanical Circulatory support
Overview
Allen LA, O'Connor CM. CMAJ. 2007 Mar 13;176(6):797-805
DIURETICS
• Reduce congestion by increasing excretion of
Na and water
• Preferred - Loop diuretics (Furosemide)
• IV route better
Gut wall edema
Reduced blood flow
VASODILATORS
• Reduce filling pressures
• Reduce afterload
• Commonly used:
NTG
Nitroprusside
NITROGLYCERINE NITROPRUSSIDE
Stimulates guanylate
cyclase
Equipotent venous and
arteriolar dilation
Dose dependent venous
> arteriole dilatation
Useful for HTN, valvular
dysfunction (AR, MR)
Decreases filling pressures Short half life
Headache Methemoglobinaemia
Nitrate tolerance Cyanide toxicity
INOTROPES
• Reserved for low output HF (wet and cold)
• Evidence of hypotension and poor tissue
perfusion despite adequate filling pressures
• Poor response to diuretics with worsening
renal function
• Unresponsive or intolerant to vasodilators
• Short term with lowest dose
Mechanism of action
Pagel, P., & Warltier, D. 2011 (pp. 706-723)
DOBUTAMINE MILRINONE LEVOSIMENDAN
Initial agent in low CO
with maintained BP
Alternative for short
term CO augmentation
Sensitises the cardiac
myocytes to calcium
Add on with Norad in
case of hypotension
Accumulates in renal
failure
Enhance myocardial
contractility at a given
calcium concentration
Increases contractility
and rate
Increases Contractility
and at higher doses HR
Have intrinsic PDE inh
property
Can cause hypotension
and arrhythmia
Can cause hypotension
and arrhythmia
INOTROPES AND HARM
• Increase HR and Arrhythmias
• Increase myocardial oxygen demand
• Direct toxic effect to myocardium: accelerated
apoptosis
VASOPRESSORS
• To increase blood pressure and vital organ
perfusion in cardiogenic shock
• Preferably Noradrenaline
• Monitor ECG and blood pressure
• Intra-arterial blood pressure measurement
may be considered.
MECHANICAL CIRCULATORY DEVICES
Types
IABP
• Inflates in diastole - increases coronary
perfusion
• Deflates in systole - decreases afterload &
increases LV stroke volume
• Trigger
ECG - inflation -middle of T-wave & deflation -
peak of R wave
Pressure - inflation - dicrotic notch and deflates
based on elapsed time
Contraindications
• Uncontrolled bleeding diathesis.
• Moderate to severe aortic regurgitation.
• An aortic aneurysm or aortic dissection.
• Severe peripheral artery disease
Complications
• Limb ischemia - monitor distal pulses
• Positioning- monitor UO , CXR
• Bleeding, hematoma - monitor sheath site,
coagulopathy
VA ECMO
• Deoxygenated venous blood - extracorporeal
centrifugal pump - oxygenated blood to iliac
artery
• Continuous flow via centrifugal pump
Complications
• Haemolysis
• Limb ischemia
• Bleeding
Contrindications
• Severe aortic insufficiency
• Aortic dissection
• Intolerant to systemic anticoagulation
3. Identifying and management of etiology
4. Common precipitating factors
INCREASED METABOLIC
DEMANDS
Fever, anemia, infection,
tachycardia,
hyperthyroidism, pregnancy
INCREASED CIRCULATING
VOLUME
Excessive salt or fluid in diet
Renal failure
INCREASED AFTERLOAD
Hypertension
PE
IMPAIRED CONTRACTILITY
Negative inotropes
Ischemia
Failure to take medications
Management of ADHF.pptx

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Management of ADHF.pptx

  • 2. Diagnosing Heart Failure HISTORY • Prior HF/myocardial injury • DOE, orthopnea, PND • Fatigue • Edema • Family history
  • 5. Lung USG findings ▸ Sliding present ▸ Diffuse B lines (≥3 in ≥2 zones B/L) ▸ Pleural effusion
  • 6.
  • 7. Treating Heart failure GOALS 1. Initial stabilization 2. Relieve symptoms: congestion and low output 3. Identify etiology 4. Identify precipitating factors 5. Minimize side effects
  • 8.
  • 9. 1.Initial Stabilization • O2 – to prevent hypoxia <90% Spo2 (NOT routinely) • NIV indications Respiratory distress Respiratory acidosis Hypoxia despite O2
  • 10. NIV Respiratory support -Increases tidal volume -Unloads respiratory muscles -Decreases dead space ventilation Hemodynamic support -Alters cardiac transmural pressures -Decreases preload (venous return) and afterload -No change in cardiac index
  • 11.
  • 12. 2. Symptoms management 1. Optimize preload - Diuretics 2. Decrease Afterload - Vasodilators 3. Augment contractility – Inotropes and vasopressors , Mechanical Circulatory support
  • 13. Overview Allen LA, O'Connor CM. CMAJ. 2007 Mar 13;176(6):797-805
  • 14. DIURETICS • Reduce congestion by increasing excretion of Na and water • Preferred - Loop diuretics (Furosemide) • IV route better Gut wall edema Reduced blood flow
  • 15.
  • 16. VASODILATORS • Reduce filling pressures • Reduce afterload • Commonly used: NTG Nitroprusside
  • 17. NITROGLYCERINE NITROPRUSSIDE Stimulates guanylate cyclase Equipotent venous and arteriolar dilation Dose dependent venous > arteriole dilatation Useful for HTN, valvular dysfunction (AR, MR) Decreases filling pressures Short half life Headache Methemoglobinaemia Nitrate tolerance Cyanide toxicity
  • 18. INOTROPES • Reserved for low output HF (wet and cold) • Evidence of hypotension and poor tissue perfusion despite adequate filling pressures • Poor response to diuretics with worsening renal function • Unresponsive or intolerant to vasodilators • Short term with lowest dose
  • 19. Mechanism of action Pagel, P., & Warltier, D. 2011 (pp. 706-723)
  • 20.
  • 21. DOBUTAMINE MILRINONE LEVOSIMENDAN Initial agent in low CO with maintained BP Alternative for short term CO augmentation Sensitises the cardiac myocytes to calcium Add on with Norad in case of hypotension Accumulates in renal failure Enhance myocardial contractility at a given calcium concentration Increases contractility and rate Increases Contractility and at higher doses HR Have intrinsic PDE inh property Can cause hypotension and arrhythmia Can cause hypotension and arrhythmia
  • 22. INOTROPES AND HARM • Increase HR and Arrhythmias • Increase myocardial oxygen demand • Direct toxic effect to myocardium: accelerated apoptosis
  • 23. VASOPRESSORS • To increase blood pressure and vital organ perfusion in cardiogenic shock • Preferably Noradrenaline • Monitor ECG and blood pressure • Intra-arterial blood pressure measurement may be considered.
  • 25. Types
  • 26. IABP • Inflates in diastole - increases coronary perfusion • Deflates in systole - decreases afterload & increases LV stroke volume • Trigger ECG - inflation -middle of T-wave & deflation - peak of R wave Pressure - inflation - dicrotic notch and deflates based on elapsed time
  • 27.
  • 28. Contraindications • Uncontrolled bleeding diathesis. • Moderate to severe aortic regurgitation. • An aortic aneurysm or aortic dissection. • Severe peripheral artery disease Complications • Limb ischemia - monitor distal pulses • Positioning- monitor UO , CXR • Bleeding, hematoma - monitor sheath site, coagulopathy
  • 29.
  • 31. • Deoxygenated venous blood - extracorporeal centrifugal pump - oxygenated blood to iliac artery • Continuous flow via centrifugal pump Complications • Haemolysis • Limb ischemia • Bleeding
  • 32. Contrindications • Severe aortic insufficiency • Aortic dissection • Intolerant to systemic anticoagulation
  • 33. 3. Identifying and management of etiology
  • 34. 4. Common precipitating factors INCREASED METABOLIC DEMANDS Fever, anemia, infection, tachycardia, hyperthyroidism, pregnancy INCREASED CIRCULATING VOLUME Excessive salt or fluid in diet Renal failure INCREASED AFTERLOAD Hypertension PE IMPAIRED CONTRACTILITY Negative inotropes Ischemia Failure to take medications