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ACUTE HEART
FAILURE
Muhammad Khairulanwar Bin Muhamad Kamal
012012050-144
Emergency Medicine [Y5]
Overview
■ Introduction
■ Pathophysiology
■ Classification
■ Aetiology
■ Diagnosis
■ Management in Emergency (ED)
■ Disposition decision
Introduction
■ A complex clinical syndrome that results from any structural or functional impairment of
ventricular filling or ejection of blood
■ Heart fails to act as a pump
■ Manifested by cardinal symptoms
– Dyspnoea & fatigue  exercise intolerance
– Fluid retention  pulmonary oedema, splanchnic oedema, peripheral oedema
Pathophysiology
Inefficient pump
Responsive adaptations
Maladaptation
Long term disease progressions
Acute
exacerbation
■ “Inefficient pump”  decrease cardiac output (CO)
– Myocardial injury
– Stress
■ “Responsive adaptations”  Neurohormonal mediated cascades
activation
– Renin angiotensin aldosterone system (RAAS)
– Sympathetic nervous system (SNS)
Neurohormonal mediated cascade
RAAS & Sympathetic activation
Na+ and water retention,
increased systemic vascular resistance
Maintain blood pressure and perfusion
*At the cost of increasing myocardial workload, wall
tension and myocardial oxygen demand
Counter regulatory response
■ Atrial natriuretic peptides (Atria)
■ B-type natriuretic peptide (Ventricle)
■ C-type natriuretic peptide (Localized in endothelium)
■ Effects:Vasodilation, natriuresis, decreased levels of endothelin, and inhibition of RAAS
and SNS
■ Importance: (Assays)
– Elevated levels portend a worse prognosis
– Attenuation provides the basis for most chronic therapies proven to delay morbidity and
mortality
Assays for BNP in ED use
N-t pre-pro-BNP
Classification*
Classification
■ Acute vs Chronic
■ Systolic vs Diastolic dysfunction
■ Right sided vs Left sided
■ High output vs Low output
Systolic vs diastolic
Systolic Diastolic
Age All ages Frequently elderly
Sex Often male Frequently female
LV EF Decrease ( <50 ) Normal ( Preserved )
LV cavity size Dilate ( increase intracardiac
volume )
Normal ( often with LVH )
Current categorization
■ Heart failure with a reduced ejection fraction (HFrEF) [SYSTOLIC]
■ Heart failure with preserved ejection fraction (HFpEF) [DIASTOLIC]
Common causes of heart failure
Diagnosis
■ History
■ Clinical examination
■ Fisk factors
■ Precipitating factor
■ Investigations
History – cardinal symptoms
■ Dyspnoea on exertion
■ Orthopnoea
■ Paroxysmal nocturnal dyspnoea
■ Edema
■ Fatigue
History – other symptoms
■ Cough with expectoration
■ CNS : Altered sensorium, confusion, impairment of memory, headache,
insomnia
■ GI : Anorexia, nausea, vomiting, pain abdomen, abdominal fullness
■ GU: Nocturia
Dyspnoea
■ Differential for dyspnoea
– Exacerbation of asthma or COPD
– Pulmonary embolus
– Pneumonia
– Acute coronary syndrome
– Anaphylaxis
Risk factors
■ Male
■ Old ages
■ Hypertension
■ Diabetes mellitus
■ Valvular heart disease
■ obesity
Precipitating factors
General Physical Examination
■ Mild to moderate HF : No distress except when lying flat for more than a
few minutes
■ Severe HF: Must sit upright, labored breathing, unable to finish a
sentence
– Cardiac cachexia
– Cyanosis
– Edema
– Jaundice
Vitals
■ Sinus tachycardia
■ Pulse pressure: ↓
■ SBP: ↓
■ Cold extremities
■ ↑ JVP
– Giant v waves
Examination of JugularVeins
CVS Examination
■ Palpation:Cardiomegaly with hyperdynamic point of maximum impulse
■ Auscultation
– S₃
– PSM
RS Examination
■ Crepitations / Rales
■ Signs of pleural effusion
PA Examination & extremities
■ Hepatomegaly:Tender, pulsatile
■ Ascites
■ Peripheral edema
Investigations
1. Chest X-ray
2. Electrocardiogram
3. Biomarkers
4. Ultrasonography
5. Routine lab tests: CBC, RFT, LFT,TSH, electrolytes
Chest x-ray (upright)
– Pulmonary venous congestion
– Cardiomegaly (80%) or normal (20%)
– Interstitial edema
■ Most specific for a final diagnosis of acute heart failure but the absence
of these does not rule it out
■ CardiomegalyCTR = 18/30 (>50%)
■ Upper zone vessel enlargement (1) – a sign of
pulmonary venous hypertension
■ Septal (Kerley B) lines (2) – a sign of interstitial
oedema – see next picture
■ Airspace shadowing (3) – due to alveolar
oedema – acutely in a peri-hilar (bat's wing)
distribution
■ Blunt costophrenic angles (4) – due to pleural
effusions
Electrocardiogram
■ Not useful for diagnosis
– Early recognition of arrhythmias – atrial fibrillation
– Signs of ischaemia or injury
■ Irregularly irregular rhythm.
■ No P waves.
■ Absence of an isoelectric baseline.
■ Variable ventricular rate.
■ QRS complexes usually < 120 ms
Routine
■ Complete blood count to evaluate anaemia
■ Basic metabolic panel
– Electrolytes
– Renal status
Cardiac biomarkers
■ It is done when cause of
dyspnoea is still unclear
after standard
evaluation
■ This test will detect
ongoing myocyte injury,
which may be clinically
silent
Bedside ultrasound
1. Determine cause of dyspnoea e.g. tamponade
2. Determine LV function and volume status
3. RWMA
4. Valvular abnormality
Focused on
1. Signs of pulmonary congestion
2. Sign of volume overload
3. LV ejection fraction
Signs of pulmonary congestion
■ Sonographic B-lines
– Dx – >2 B-lines in
any sonographic
windows along the
anterior and
posterior chest
Signs of volume overload
■ IVC >2 cm diameter
■ Collapsibility index <50%
– Indicates raised in central venous pressure
Management in ED
Disposition decision
■ Lack of ED-based-risk stratification tool
■ Mainly based on
– Physician judgement
– Physiologic risk assessment
– Assessments of barrier to successful outpatient
High risk physiological marker
1. Renal dysfunction 3. Low serum sodium
2. Low BP 4. Increase natriuretic peptide / cardiac troponin
■ High risk features  admission to ward
■ Patient required invasive monitoring / procedure  ICU
■ Lower risk features  observation unit (12-24h)
References
■ Tintinalli’s Emergency Medicine, 8th edition
■ Rosen’s Emergency Medicine, 8th edition
■ Harrison’s Principle of Internal Medicine, 19th edition
Thank you!

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Acute heart failure [MBBS]

  • 1. ACUTE HEART FAILURE Muhammad Khairulanwar Bin Muhamad Kamal 012012050-144 Emergency Medicine [Y5]
  • 2. Overview ■ Introduction ■ Pathophysiology ■ Classification ■ Aetiology ■ Diagnosis ■ Management in Emergency (ED) ■ Disposition decision
  • 3. Introduction ■ A complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood ■ Heart fails to act as a pump ■ Manifested by cardinal symptoms – Dyspnoea & fatigue  exercise intolerance – Fluid retention  pulmonary oedema, splanchnic oedema, peripheral oedema
  • 5. ■ “Inefficient pump”  decrease cardiac output (CO) – Myocardial injury – Stress ■ “Responsive adaptations”  Neurohormonal mediated cascades activation – Renin angiotensin aldosterone system (RAAS) – Sympathetic nervous system (SNS)
  • 6. Neurohormonal mediated cascade RAAS & Sympathetic activation Na+ and water retention, increased systemic vascular resistance Maintain blood pressure and perfusion *At the cost of increasing myocardial workload, wall tension and myocardial oxygen demand
  • 7.
  • 8. Counter regulatory response ■ Atrial natriuretic peptides (Atria) ■ B-type natriuretic peptide (Ventricle) ■ C-type natriuretic peptide (Localized in endothelium) ■ Effects:Vasodilation, natriuresis, decreased levels of endothelin, and inhibition of RAAS and SNS ■ Importance: (Assays) – Elevated levels portend a worse prognosis – Attenuation provides the basis for most chronic therapies proven to delay morbidity and mortality
  • 9. Assays for BNP in ED use N-t pre-pro-BNP
  • 11. Classification ■ Acute vs Chronic ■ Systolic vs Diastolic dysfunction ■ Right sided vs Left sided ■ High output vs Low output
  • 12. Systolic vs diastolic Systolic Diastolic Age All ages Frequently elderly Sex Often male Frequently female LV EF Decrease ( <50 ) Normal ( Preserved ) LV cavity size Dilate ( increase intracardiac volume ) Normal ( often with LVH )
  • 13. Current categorization ■ Heart failure with a reduced ejection fraction (HFrEF) [SYSTOLIC] ■ Heart failure with preserved ejection fraction (HFpEF) [DIASTOLIC]
  • 14. Common causes of heart failure
  • 15. Diagnosis ■ History ■ Clinical examination ■ Fisk factors ■ Precipitating factor ■ Investigations
  • 16. History – cardinal symptoms ■ Dyspnoea on exertion ■ Orthopnoea ■ Paroxysmal nocturnal dyspnoea ■ Edema ■ Fatigue
  • 17. History – other symptoms ■ Cough with expectoration ■ CNS : Altered sensorium, confusion, impairment of memory, headache, insomnia ■ GI : Anorexia, nausea, vomiting, pain abdomen, abdominal fullness ■ GU: Nocturia
  • 19. ■ Differential for dyspnoea – Exacerbation of asthma or COPD – Pulmonary embolus – Pneumonia – Acute coronary syndrome – Anaphylaxis
  • 20. Risk factors ■ Male ■ Old ages ■ Hypertension ■ Diabetes mellitus ■ Valvular heart disease ■ obesity
  • 22. General Physical Examination ■ Mild to moderate HF : No distress except when lying flat for more than a few minutes ■ Severe HF: Must sit upright, labored breathing, unable to finish a sentence – Cardiac cachexia – Cyanosis – Edema – Jaundice
  • 23. Vitals ■ Sinus tachycardia ■ Pulse pressure: ↓ ■ SBP: ↓ ■ Cold extremities ■ ↑ JVP – Giant v waves
  • 25. CVS Examination ■ Palpation:Cardiomegaly with hyperdynamic point of maximum impulse ■ Auscultation – S₃ – PSM
  • 26. RS Examination ■ Crepitations / Rales ■ Signs of pleural effusion
  • 27. PA Examination & extremities ■ Hepatomegaly:Tender, pulsatile ■ Ascites ■ Peripheral edema
  • 28. Investigations 1. Chest X-ray 2. Electrocardiogram 3. Biomarkers 4. Ultrasonography 5. Routine lab tests: CBC, RFT, LFT,TSH, electrolytes
  • 29. Chest x-ray (upright) – Pulmonary venous congestion – Cardiomegaly (80%) or normal (20%) – Interstitial edema ■ Most specific for a final diagnosis of acute heart failure but the absence of these does not rule it out
  • 30. ■ CardiomegalyCTR = 18/30 (>50%) ■ Upper zone vessel enlargement (1) – a sign of pulmonary venous hypertension ■ Septal (Kerley B) lines (2) – a sign of interstitial oedema – see next picture ■ Airspace shadowing (3) – due to alveolar oedema – acutely in a peri-hilar (bat's wing) distribution ■ Blunt costophrenic angles (4) – due to pleural effusions
  • 31.
  • 32. Electrocardiogram ■ Not useful for diagnosis – Early recognition of arrhythmias – atrial fibrillation – Signs of ischaemia or injury
  • 33. ■ Irregularly irregular rhythm. ■ No P waves. ■ Absence of an isoelectric baseline. ■ Variable ventricular rate. ■ QRS complexes usually < 120 ms
  • 34. Routine ■ Complete blood count to evaluate anaemia ■ Basic metabolic panel – Electrolytes – Renal status
  • 35. Cardiac biomarkers ■ It is done when cause of dyspnoea is still unclear after standard evaluation ■ This test will detect ongoing myocyte injury, which may be clinically silent
  • 36. Bedside ultrasound 1. Determine cause of dyspnoea e.g. tamponade 2. Determine LV function and volume status 3. RWMA 4. Valvular abnormality Focused on 1. Signs of pulmonary congestion 2. Sign of volume overload 3. LV ejection fraction
  • 37. Signs of pulmonary congestion ■ Sonographic B-lines – Dx – >2 B-lines in any sonographic windows along the anterior and posterior chest
  • 38. Signs of volume overload ■ IVC >2 cm diameter ■ Collapsibility index <50% – Indicates raised in central venous pressure
  • 39.
  • 41.
  • 42. Disposition decision ■ Lack of ED-based-risk stratification tool ■ Mainly based on – Physician judgement – Physiologic risk assessment – Assessments of barrier to successful outpatient High risk physiological marker 1. Renal dysfunction 3. Low serum sodium 2. Low BP 4. Increase natriuretic peptide / cardiac troponin
  • 43.
  • 44. ■ High risk features  admission to ward ■ Patient required invasive monitoring / procedure  ICU ■ Lower risk features  observation unit (12-24h)
  • 45.
  • 46. References ■ Tintinalli’s Emergency Medicine, 8th edition ■ Rosen’s Emergency Medicine, 8th edition ■ Harrison’s Principle of Internal Medicine, 19th edition Thank you!

Editor's Notes

  1. AHF : AMI, CHF : Dilated cardiomyopathy SD : impairment of contractility, with stroke output reduced and forward flow compromised, DD : primary problem with ability of the ventricles to relax and fill normally
  2. Cyanosis due to excessive adrenergic activity Edema: B/L pedal. Presacral, scrotal in bedridden
  3. Diminished PP due to reduced stroke volume Cold extremities due to peripheral vasoconstriction V waves -TR
  4. Creps/rales – pulmo edmea
  5. May pulsate during systole if TR is present Ascites and jaundice are late signs Increased pressure in the hepatic veins and the veins draining the peritoneum Impairment of hepatic function secondary to hepatic congestion and hepatocellular hypoxemia -- Jaundice
  6. If CXR and ECG are normal = decrease likelihood of heart failure
  7. Airspace shadowing is due to alveolar oedema caused by fluid filling the alveoli and small airways Bat's wing or butterfly pulmonary opacities refer to a pattern of bilateral perihilar shadowing
  8. caused by thickening of the interlobular septa which separate the secondary lobules at the periphery of the lungs
  9. Ashman’s Phenomenon
  10. Anemia may be the cause of S.O.B or exacerbate it
  11. B lines representing thickened inter-alveolar/interlobular septa
  12. Collapse during respiration highly correlated with pulmonary capillary wedge pressure and are specific for acute heart failure Measurement of IVC diameter in different phases of respiration differentiates normal subjects from patients with elevated right atrial pressure, cyclic variations in pleural pressure, which are transmitted to the right atrium, produce cyclic variations in venous return, which is increased by inspiration, leading to an inspiratory reduction of about 50% in IVC diameter
  13. 12-24h – complete symptoms resolution with standard theraphy