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DIAGNOSIS AND EARLY
HOSPITAL MANAGEMENT OF
ACUTE HEART FAILURE
dr. I Wayan Gunawan
Program Studi Spesialis Jantung dan Pembuluh Darah FK Unud – Provita Hospital
Why is it important...?
ADHF ACS
Hospitalizations/year 1,000,000 1,000,000
Inpatient Mortality 3-4% 3-4%
30-days Readmission 10-15% 6-8%
Guidelines for :
Risk Stratification Yes Yes
Therapy Sort of
(Lack in HFpEF)
Yes
Largest RCT 7,141 58,050
J Am Coll Cardiol 2009;54:386
1. National Cancer Institute. Cancer stat fact sheets. Available at: http://seer.cancer.gov/statfacts. Accessed 31 May 2016;
2. Roger et al. JAMA 2004;292:344–50
0
10
20
30
40
50
Breast cancer Hodgkin's
lymphoma
Non-Hodgkin's
lymphoma
Colon and
rectum cancer
Leukemia Heart failure
5-YEAR DEATH RATES
Percentage
10%1
14%1
29%1
34%1
40%1
48%2
HF is Deadlier than Many Cancers
So….. Will Chronic HF always be STABLE?
• We always think that our job is done.
• Stable CHF sometimes has several pitfalls
at the back side, leads to decompensate
the stable state
 only good at front
CHF is Progressive Condition With High Mortality
and High Risk of Re-hospitalization
Stage A
•At high risk for HF but
without structural heart
disease or HF symptoms
Stage B
•Structural heart disease
but without sign or
symptoms of HF
Stage C
•Structural heart disease
with prior or current
symptoms of HF
Stage D
•Refractory HF recruiting
specialized HF
intervention
Disease Risk Asymptomatic Disease Symptomatic Disease
Yancy et al. JACC Vol. 62, No. 16, 2013; Graphic is downloaded from http://heartfailure.onlinejacc.org/content/5/12/948/F1. LV: left ventricular
Gheorghiade et al. Am J Cardiol 2005;96:11G–17G; Gheorghiade & Pang. J Am Coll Cardiol 2009;53:557–73
Chronic decline
Mortality
Acute episodes
Disease progression
Function
& quality of
life (QoL)
• Increasing frequency of acute events with disease progression leads to high rates of hospitalization
and increased risk of mortality
• With each acute event, myocardial injury may contribute to progressive LV dysfunction
Definition of Heart Failure
• A complex clinical syndrome that results from any structural
or functional impairment of ventricular filling or ejection of
blood¹
• A clinical syndrome characterized by typical symptoms that
may be accompanied by signs caused by a structural and/or
functional cardiac abnormality, resulting in a reduced
cardiac output and/or elevated intracardiac pressures at
rest or during stress²
1. 2013 ACCF/AHA Guideline for the Management of Heart Failure
2. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
Simultaneous Inhibition of Neprilysin and Suppression of The
RAAS With Sacubitril/Valsartan has Complementary Effects
SNS
RAAS
Vasoconstriction
Blood pressure
Sympathetic tone
Aldosterone
Hypertrophy
Fibrosis
Ang II AT1R
HFrEF
Symptoms
& Progression
INACTIVE
FRAGMENTS
NP system
Vasodilation
Blood pressure
Sympathetic tone
Natriuresis/diuresis
Vasopressin
Aldosterone
Fibrosis
Hypertrophy
NPRs NPs
Epinephrine
Norepinephrine
α1, β1, β2
receptors
Vasoconstriction
RAAS activity
Vasopressin
Heart rate
Contractility
Neprilysin
inhibitors
RAAS inhibitors
(ACEI, ARB, MRA)
β-blockers
Sacubitril/Valsartan
 Sacubitril/Valsartan: enhancement of natriuretic and other vasoactive peptides, with simultaneous RAAS suppression
1. McMurray et al. Eur J Heart Fail 2013;15:1062–73; Levin et al. N Engl J Med 1998;339:321–8; Nathisuwan & Talbert. Pharmacotherapy 2002;22:27–42; Kemp & Conte. Cardiovascular Pathology
2012;365–371; Schrier & Abraham N Engl J Med 2009;341:577–85
Valsartan
Sacubitril
Clinical Course of Heart Failure
Hollenberg et al. Heart Failure Hospitalization Pathway. https://doi.org/10.1016/j.jacc.2019.08.001
AHF refers to Rapid Onset or Worsening of
Symptoms and/or Signs of HF
• De novo vs Acute Decompensation of Chronic HF
• Primary cardiac dysfunction
• Acute myocardial dysfunction (ischaemic, inflammatory or toxic)
• Acute valve insufficiency or pericardial tamponade
• (and/or) with/without known precipitant factors
• AHF might have a ‘time to therapy’ concept  ‘pre-hospital’
management is considered a critical component of care.
Mebazaa A, et al. European Heart J (2015) 17, 544-588.
Factors
Triggering of
Acute Heart
Failure
Pulmonary Edema
Acutely
Decompensated
Chronic HF
Cardiogenic
shock
Right HF
ACS &
HF
Hypertensive AHF
Clinical Presentation of Acute HF
More
Frequent
Dickstein K, et al. Eur Heart J (2008) 29, 2388-2442. doi:10.1093/eurheartj/ehn309
HFrEF is Characterized By Frequent Hospitalization
and Linked to Higher Mortality1–5
5
Year
1
Year
60
Days
~40–50%
Mortality rate
after 5 years4,5
~20–30%
Mortality rate
after 1 year3,4
30–50%
Mortality or
hospitalization rate
60 days after
admission2
4%
Mortality rate
in hospital1*
~50% of heart failure deaths occur suddenly6
*Study data based on 105.388 US patients, hospitalized between 1997 and 2004 because of heart failure in the Acute Decompensated Heart Failure National Registry
HFrEF=heart failure with reduced ejection fraction
1. Adams et al. Am Heart J 2005;149:209–16; 2. Dickstein et al. Eur Heart J 2008;29:2388–42; 3. Chen et al. JAMA 2011;306:1669–78;
4. Loehr et al. Am J Cardiol 2008;101:1016–22; 5. Roger et al. Circulation 2012;125:e2–220; 6. McMurray et al.. Eur Heart J 2012;33:1787–847
Guideline Recommended Treatment Goals In Heart
Failure1,2
Improve
symptoms1,2 Prevent
hospitalization1,2
Reduce
mortality1,2
1. Ponikowski et al. Eur Heart J 2016;37:2129–200; 2. Yancy et al. Circulation 2016;134:e282–93
The goals of treatment in patients with HF are to:1
• improve clinical status, functional capacity and quality of life
• prevention of recurrent hospitalizations due to worsening HF
• reduce mortality
Haemodynamic Profile of Acute HF
(Forrester Classification)
Most Common
presentation
SHOCK
CARDIOGENIC
Pre-hospital and Early
Management Strategies
in Acute Heart Failure
Pre-Hospital Setting
•pulse oximetry, blood pressure, respiratory rate, and a
continuous ECG, instituted within minutes of patient
contact and in the ambulance if possible.
Non-invasive
monitoring
•based on clinical judgment unless SaO2 <90% in which
case oxygen therapy should be routinely administered.
Oxygen therapy
• in patients with respiratory distress.
Non-invasive
ventilation
•initiated based on blood pressure and/or the degree of
congestion using vasodilators and/or diuretics (i.e.
furosemide
Medical treatment
•to the nearest hospital, preferably to a site with a
cardiology department and/or CCU/ICU
Rapid transfer
Mebazaa A, et al. European Heart J (2015) 17, 544-588.
Step 1:
Initial Management of Patient
With Acute Heart Failure in Hospital
Urgent Management of “CHAMP”
“CHAMP” Management
Acute Coronary syndrome
PCI ˂2 hours from hospital admission, irrespective of ECG or biomarkers
findings
Hypertensive emergency
i.v. vasodilator and i.v. loop diuretic
Reduce BP 25% in the first few hours
Arrhythmia
Electrical cardioversion for atrial or ventricular tachyarrhythmias with
hemodynamic instability
Temporary pacing for severe bradycardia
Acute Mechanical cause Surgical or percutaneous intervention
Pulmonary embolism
Thrombolysis
Embolectomy (surgical or catheter-based)
STEP 2:
(Diagnosis of AHF)
“Rule-in” or “Rule-out” AHF in Patients
Presenting with Congestion and/or
Hypoperfusion
Symptoms and Signs
• Fluid overload (pulmonary congestion and/or
peripheral edema)
• Hypoperfusion due to low cardiac output
THE SENSITIVITY AND SPECIFICITY OF SYMPTOMS AND SIGNS
ARE OFTEN NOT SATISFACTORY
NEED ADDITIONAL INVESTIGATION
STEP 3:
Management of AHF Based on Symptoms
and Signs of Fluid Congestion and
Hypoperfusion
Intravenous Diuretic and Ultrafiltration
• Loop diuretics are recommended for all patients with congestion to
improve symptoms.
• Combination with either oral thiazide diuretic or spironolactone may
be considered in the presence of resistant edema or insufficient
symptom response
• Initial dose is 20-40 mg
• May be given as intermittent boluses or continuous infusion
• Regularly monitor renal function and electrolytes
• Ultrafiltration should be considered in patients with refractory
volume overload and acute kidney injury and may be considered in
patients with refractory congestion who fail to respond to diuretic-
based therapy
Diuretic sites of action
Mebazaa et al. EJHF (2015) 17, 544-558
Dose Recommendation For Diuretic Therapy
Intravenous Vasodilators
Vasodilators Dose Main side effects Other
Nitroglycerine
Start with 10–20 μg/min,
increase up to 200 μg/min
Hypotension,
headache
Tolerance on
continuous use
Isosorbide
dinitrate
Start with 1 mg/h, increase
up to 10 mg/h
Hypotension,
headache
Tolerance on
continuous use
Nitroprusside
Start with 0.3 μg/kg/min
and increase up to 5
μg/kg/min
Hypotension,
isocyanate toxicity
Light sensitive
Ponikowski P, et al. Eur Heart J doi:10.1093/eurheartj/ehw128
Action of nitrates on circulation
Ponikowski P, et al. Eur Heart J doi:10.1093/eurheartj/ehw128
Intravenous Inotropes and Vasopressors
Inotropes/Vasopresso
rs
Bolus Infusion rate
Dobutamine No 2-20 μg/kg/min
Dopamine No
3-5 μg/kg/min (inotrope)
> 5 μg/kg/min (vasopressor)
Norepinephrine No 0.2-1 μg/kg/min
Epinephrine
1 mg can be given i.v
during resuscitation,
repeated every 3-5
minutes
0.05-0.5 μg/kg/min
Ponikowski P, et al. Eur Heart J doi:10.1093/eurheartj/ehw128
Ponikowski P, et al. Eur Heart J doi:10.1093/eurheartj/ehw128
Target Hemodynamic : Warm Dry
FLUID RESCUCITATION
INOTROPES
DIURETICS
VASODILATORS
VASOPRESSOR
Management of Oral Therapy in Acute HF
Mebazaa A, et al. European Heart J (2015) 17, 544-588.
SPENDING TIME…
Traditional HF Treatment Approach :
Concentrate on Optimizing 1 or 2 Meds Before Go To The Next Steps
Can All 4 pillars drugs be started at the same time ?
WHAT DO EXPERT
SAY ?
• Ensure All 4 drugs are
started
• Minimize the possibility
of clinical inertia
Tolerability :
• 2 of 4 can affect BP
• Starting MRA and ARNI
can increase hyper K
• Difficult to sort out an
AE
Greene SJ, et al.JAMA.2021
Criteria for Discharge
• Clinical response to initial treatment is an important indicator of likely
disposition
• Indicators of good response to initial therapy that might be considered in
discharge include :
• 1. Patient-reported subjective improvement
• 2. Resting HR < 100 bpm
• 3. No hypotension when standing up
• 4. Adequate urine output
• 5. Oxygen saturation > 95% in room air
• 6. No or moderate worsening of renal function (chronic renal disease might
be present)
Mebazaa A, et al. European Heart J (2015) 17, 544-588.
Criteria for Discharge
• Haemodynamically stable, euvolemic, established on evidence-based
oral medication and with stable renal function for at least 24 h before
discharge
• Once provided with tailored education and advice about self-care
• Patients should be:
• enrolled in a disease management program
• seen by their general practitioner within 1 week of discharge, by the
hospital cardiology team within 2 weeks of discharge
Summary
• AHF is a life-threatening medical condition requiring
evaluation and treatment
• Classification based on patients clinical profile
• Urgent evaluation and early diagnosis is important for
guiding the appropriate management
• Perform all ‘Steps’ simultaneously and urgently
Tentiran GP Provita Acute Heart Failure (2).pptx

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Tentiran GP Provita Acute Heart Failure (2).pptx

  • 1. DIAGNOSIS AND EARLY HOSPITAL MANAGEMENT OF ACUTE HEART FAILURE dr. I Wayan Gunawan Program Studi Spesialis Jantung dan Pembuluh Darah FK Unud – Provita Hospital
  • 2.
  • 3. Why is it important...? ADHF ACS Hospitalizations/year 1,000,000 1,000,000 Inpatient Mortality 3-4% 3-4% 30-days Readmission 10-15% 6-8% Guidelines for : Risk Stratification Yes Yes Therapy Sort of (Lack in HFpEF) Yes Largest RCT 7,141 58,050 J Am Coll Cardiol 2009;54:386
  • 4. 1. National Cancer Institute. Cancer stat fact sheets. Available at: http://seer.cancer.gov/statfacts. Accessed 31 May 2016; 2. Roger et al. JAMA 2004;292:344–50 0 10 20 30 40 50 Breast cancer Hodgkin's lymphoma Non-Hodgkin's lymphoma Colon and rectum cancer Leukemia Heart failure 5-YEAR DEATH RATES Percentage 10%1 14%1 29%1 34%1 40%1 48%2 HF is Deadlier than Many Cancers
  • 5. So….. Will Chronic HF always be STABLE? • We always think that our job is done. • Stable CHF sometimes has several pitfalls at the back side, leads to decompensate the stable state  only good at front
  • 6. CHF is Progressive Condition With High Mortality and High Risk of Re-hospitalization Stage A •At high risk for HF but without structural heart disease or HF symptoms Stage B •Structural heart disease but without sign or symptoms of HF Stage C •Structural heart disease with prior or current symptoms of HF Stage D •Refractory HF recruiting specialized HF intervention Disease Risk Asymptomatic Disease Symptomatic Disease Yancy et al. JACC Vol. 62, No. 16, 2013; Graphic is downloaded from http://heartfailure.onlinejacc.org/content/5/12/948/F1. LV: left ventricular Gheorghiade et al. Am J Cardiol 2005;96:11G–17G; Gheorghiade & Pang. J Am Coll Cardiol 2009;53:557–73 Chronic decline Mortality Acute episodes Disease progression Function & quality of life (QoL) • Increasing frequency of acute events with disease progression leads to high rates of hospitalization and increased risk of mortality • With each acute event, myocardial injury may contribute to progressive LV dysfunction
  • 7. Definition of Heart Failure • A complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood¹ • A clinical syndrome characterized by typical symptoms that may be accompanied by signs caused by a structural and/or functional cardiac abnormality, resulting in a reduced cardiac output and/or elevated intracardiac pressures at rest or during stress² 1. 2013 ACCF/AHA Guideline for the Management of Heart Failure 2. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
  • 8. Simultaneous Inhibition of Neprilysin and Suppression of The RAAS With Sacubitril/Valsartan has Complementary Effects SNS RAAS Vasoconstriction Blood pressure Sympathetic tone Aldosterone Hypertrophy Fibrosis Ang II AT1R HFrEF Symptoms & Progression INACTIVE FRAGMENTS NP system Vasodilation Blood pressure Sympathetic tone Natriuresis/diuresis Vasopressin Aldosterone Fibrosis Hypertrophy NPRs NPs Epinephrine Norepinephrine α1, β1, β2 receptors Vasoconstriction RAAS activity Vasopressin Heart rate Contractility Neprilysin inhibitors RAAS inhibitors (ACEI, ARB, MRA) β-blockers Sacubitril/Valsartan  Sacubitril/Valsartan: enhancement of natriuretic and other vasoactive peptides, with simultaneous RAAS suppression 1. McMurray et al. Eur J Heart Fail 2013;15:1062–73; Levin et al. N Engl J Med 1998;339:321–8; Nathisuwan & Talbert. Pharmacotherapy 2002;22:27–42; Kemp & Conte. Cardiovascular Pathology 2012;365–371; Schrier & Abraham N Engl J Med 2009;341:577–85 Valsartan Sacubitril
  • 9. Clinical Course of Heart Failure Hollenberg et al. Heart Failure Hospitalization Pathway. https://doi.org/10.1016/j.jacc.2019.08.001
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  • 12. AHF refers to Rapid Onset or Worsening of Symptoms and/or Signs of HF • De novo vs Acute Decompensation of Chronic HF • Primary cardiac dysfunction • Acute myocardial dysfunction (ischaemic, inflammatory or toxic) • Acute valve insufficiency or pericardial tamponade • (and/or) with/without known precipitant factors • AHF might have a ‘time to therapy’ concept  ‘pre-hospital’ management is considered a critical component of care. Mebazaa A, et al. European Heart J (2015) 17, 544-588.
  • 14. Pulmonary Edema Acutely Decompensated Chronic HF Cardiogenic shock Right HF ACS & HF Hypertensive AHF Clinical Presentation of Acute HF More Frequent Dickstein K, et al. Eur Heart J (2008) 29, 2388-2442. doi:10.1093/eurheartj/ehn309
  • 15. HFrEF is Characterized By Frequent Hospitalization and Linked to Higher Mortality1–5 5 Year 1 Year 60 Days ~40–50% Mortality rate after 5 years4,5 ~20–30% Mortality rate after 1 year3,4 30–50% Mortality or hospitalization rate 60 days after admission2 4% Mortality rate in hospital1* ~50% of heart failure deaths occur suddenly6 *Study data based on 105.388 US patients, hospitalized between 1997 and 2004 because of heart failure in the Acute Decompensated Heart Failure National Registry HFrEF=heart failure with reduced ejection fraction 1. Adams et al. Am Heart J 2005;149:209–16; 2. Dickstein et al. Eur Heart J 2008;29:2388–42; 3. Chen et al. JAMA 2011;306:1669–78; 4. Loehr et al. Am J Cardiol 2008;101:1016–22; 5. Roger et al. Circulation 2012;125:e2–220; 6. McMurray et al.. Eur Heart J 2012;33:1787–847
  • 16. Guideline Recommended Treatment Goals In Heart Failure1,2 Improve symptoms1,2 Prevent hospitalization1,2 Reduce mortality1,2 1. Ponikowski et al. Eur Heart J 2016;37:2129–200; 2. Yancy et al. Circulation 2016;134:e282–93 The goals of treatment in patients with HF are to:1 • improve clinical status, functional capacity and quality of life • prevention of recurrent hospitalizations due to worsening HF • reduce mortality
  • 17. Haemodynamic Profile of Acute HF (Forrester Classification) Most Common presentation SHOCK CARDIOGENIC
  • 18. Pre-hospital and Early Management Strategies in Acute Heart Failure
  • 19. Pre-Hospital Setting •pulse oximetry, blood pressure, respiratory rate, and a continuous ECG, instituted within minutes of patient contact and in the ambulance if possible. Non-invasive monitoring •based on clinical judgment unless SaO2 <90% in which case oxygen therapy should be routinely administered. Oxygen therapy • in patients with respiratory distress. Non-invasive ventilation •initiated based on blood pressure and/or the degree of congestion using vasodilators and/or diuretics (i.e. furosemide Medical treatment •to the nearest hospital, preferably to a site with a cardiology department and/or CCU/ICU Rapid transfer Mebazaa A, et al. European Heart J (2015) 17, 544-588.
  • 20. Step 1: Initial Management of Patient With Acute Heart Failure in Hospital
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  • 31. Urgent Management of “CHAMP” “CHAMP” Management Acute Coronary syndrome PCI ˂2 hours from hospital admission, irrespective of ECG or biomarkers findings Hypertensive emergency i.v. vasodilator and i.v. loop diuretic Reduce BP 25% in the first few hours Arrhythmia Electrical cardioversion for atrial or ventricular tachyarrhythmias with hemodynamic instability Temporary pacing for severe bradycardia Acute Mechanical cause Surgical or percutaneous intervention Pulmonary embolism Thrombolysis Embolectomy (surgical or catheter-based)
  • 32. STEP 2: (Diagnosis of AHF) “Rule-in” or “Rule-out” AHF in Patients Presenting with Congestion and/or Hypoperfusion
  • 33. Symptoms and Signs • Fluid overload (pulmonary congestion and/or peripheral edema) • Hypoperfusion due to low cardiac output THE SENSITIVITY AND SPECIFICITY OF SYMPTOMS AND SIGNS ARE OFTEN NOT SATISFACTORY NEED ADDITIONAL INVESTIGATION
  • 34.
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  • 38. STEP 3: Management of AHF Based on Symptoms and Signs of Fluid Congestion and Hypoperfusion
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  • 40.
  • 41. Intravenous Diuretic and Ultrafiltration • Loop diuretics are recommended for all patients with congestion to improve symptoms. • Combination with either oral thiazide diuretic or spironolactone may be considered in the presence of resistant edema or insufficient symptom response • Initial dose is 20-40 mg • May be given as intermittent boluses or continuous infusion • Regularly monitor renal function and electrolytes • Ultrafiltration should be considered in patients with refractory volume overload and acute kidney injury and may be considered in patients with refractory congestion who fail to respond to diuretic- based therapy
  • 43.
  • 44. Mebazaa et al. EJHF (2015) 17, 544-558 Dose Recommendation For Diuretic Therapy
  • 45.
  • 46.
  • 47. Intravenous Vasodilators Vasodilators Dose Main side effects Other Nitroglycerine Start with 10–20 μg/min, increase up to 200 μg/min Hypotension, headache Tolerance on continuous use Isosorbide dinitrate Start with 1 mg/h, increase up to 10 mg/h Hypotension, headache Tolerance on continuous use Nitroprusside Start with 0.3 μg/kg/min and increase up to 5 μg/kg/min Hypotension, isocyanate toxicity Light sensitive Ponikowski P, et al. Eur Heart J doi:10.1093/eurheartj/ehw128
  • 48. Action of nitrates on circulation
  • 49. Ponikowski P, et al. Eur Heart J doi:10.1093/eurheartj/ehw128
  • 50. Intravenous Inotropes and Vasopressors Inotropes/Vasopresso rs Bolus Infusion rate Dobutamine No 2-20 μg/kg/min Dopamine No 3-5 μg/kg/min (inotrope) > 5 μg/kg/min (vasopressor) Norepinephrine No 0.2-1 μg/kg/min Epinephrine 1 mg can be given i.v during resuscitation, repeated every 3-5 minutes 0.05-0.5 μg/kg/min Ponikowski P, et al. Eur Heart J doi:10.1093/eurheartj/ehw128
  • 51. Ponikowski P, et al. Eur Heart J doi:10.1093/eurheartj/ehw128
  • 52. Target Hemodynamic : Warm Dry FLUID RESCUCITATION INOTROPES DIURETICS VASODILATORS VASOPRESSOR
  • 53. Management of Oral Therapy in Acute HF Mebazaa A, et al. European Heart J (2015) 17, 544-588.
  • 54. SPENDING TIME… Traditional HF Treatment Approach : Concentrate on Optimizing 1 or 2 Meds Before Go To The Next Steps
  • 55. Can All 4 pillars drugs be started at the same time ? WHAT DO EXPERT SAY ? • Ensure All 4 drugs are started • Minimize the possibility of clinical inertia Tolerability : • 2 of 4 can affect BP • Starting MRA and ARNI can increase hyper K • Difficult to sort out an AE Greene SJ, et al.JAMA.2021
  • 56. Criteria for Discharge • Clinical response to initial treatment is an important indicator of likely disposition • Indicators of good response to initial therapy that might be considered in discharge include : • 1. Patient-reported subjective improvement • 2. Resting HR < 100 bpm • 3. No hypotension when standing up • 4. Adequate urine output • 5. Oxygen saturation > 95% in room air • 6. No or moderate worsening of renal function (chronic renal disease might be present) Mebazaa A, et al. European Heart J (2015) 17, 544-588.
  • 57. Criteria for Discharge • Haemodynamically stable, euvolemic, established on evidence-based oral medication and with stable renal function for at least 24 h before discharge • Once provided with tailored education and advice about self-care • Patients should be: • enrolled in a disease management program • seen by their general practitioner within 1 week of discharge, by the hospital cardiology team within 2 weeks of discharge
  • 58. Summary • AHF is a life-threatening medical condition requiring evaluation and treatment • Classification based on patients clinical profile • Urgent evaluation and early diagnosis is important for guiding the appropriate management • Perform all ‘Steps’ simultaneously and urgently

Editor's Notes

  1. ACC/AHA 2013 = HF is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. The cardinal manifestations of HF are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary and/or splanchnic congestion and/or peripheral edema. Some patients have exercise intolerance but little evidence of fluid retention, whereas others complain primarily of edema, dyspnea, or fatigue. Because some patients present without signs or symptoms of volume overload, the term “heart failure” is preferred over “congestive heart failure. ESC 2016 = HF is a clinical syndrome characterized by typical symptoms (e.g. breathlessness, ankle swelling and fatigue) that may be accompanied by signs (e.g. elevated jugular venous pressure, pulmonary crackles and peripheral oedema) caused by a structural and/or functional cardiac abnormality, resulting in a reduced cardiac output and/or elevated intracardiac pressures at rest or during stress. WHO = Impaired physical exercise as a result of proven impairment of cardiac function From The haemodynamic/metabolic stand point = pathophysiological state where impaired cardiac function is responsible for the inability of the heart to pump the quantity of blood that matches the requirements of metabolising tissue and/or can only meet these requirements through an abnormal increase in filling pressure From the neurohumoral standpoint = HF is a state of neurohumoral imbalance where the harmful neurohormones (angiotensin II, catecholamines) predominate over favourable neurohormones (ANP, BNP) Recent data show that, much like acute coronary syndrome, AHF might have a “time to therapy” concept. Accordingly, “prehospital” management is considered a critical component of care.
  2. Neprilysin metabolizes Ang I and Ang II via several pathways1,2 Inhibition of neprilysin alone is insufficient as it associated with an increase in Ang II levels, counteracting the potential benefits of neprilysin inhibition2 Neprilysin inhibition must be accompanied by simultaneous RAAS blockade (e.g. AT1 receptor blockade)2
  3. Graphic depiction of course of heart failure admission, showing the degree of focus on clinical decompensation (red), discharge coordination (blue), ongoing coordination of outpatient care (light blue), and optimization of guideline-directed medical therapy (green), with ongoing assessment of the clinical course (circle with arrows), and key time point for review and revision of the long-term disease trajectory for the HF journey (compass signs).
  4. Acute HF : - Rapid onset of or change in the sign and symptoms of heart failure - Arises as a result of deterioration in patients previously diagnosed with HF or may also be the first presentation of HF (De Novo) - Cardiac dysfunction may be related to ischemia, arrhythmia, valvular abnormalities, pericardial disease, increased filling pressure or elevated systemic resistance - Characterized by pulmonary congestion, decreased cardiac output & tissue hypoperfusion; most Acute HF patients present with normal or high BP & sign &/or symptoms of congestion instead of low cardiac output - Life-treathening condition that needs immediate medical attention - May be transient & reversible with resolution of the acute syndrome or may induce permanent damage leading to chronic HF Recent data show that, much like acute coronary syndrome, AHF might have a “time to therapy” concept. Accordingly, “prehospital” management is considered a critical component of care.
  5. efisiensi
  6. if feasible atients with chronic heart failure should be followed up within a multi-professional heart failure service