ANDREA JOHNSON
P.C.
 60 year old female
 Hypertensive – non-compliant X 1year
PRESENTING COMPLAINT
 SEVERE SOB
 Began while “swearing & getting on bad”
 Drank 1 bottle extra strength Codeine
 Then 20mls rum cream
 GOT WORSE !!!!
DENIED
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Chest, abdominal or back pain
Palpation
Nausea or vomiting
Diaphoresis
Cough
fever
Previous episodes of SOB
History of immobilization
PMH
 NO previous admission to QEH
 No Diabetes Mellitus/heart disease
 Admission to Psyche hospital for “social reasons ?!!” -
? # times
 On no medication
 Given Natrilix on 1 occasion ~ 1year previously
EXAMINATION
 Obvious CP distress
 Mm pink, hydration adequate
 No pedal oedema
 Temperature 36o C axillary
RESPIRATORY SYSTEM
 OXYGEN SAT (room air)- 78%
 RR 40/min, use of accessory muscles
 BS vesicular
 Creps – laterally + posteriorly
 Wheeze – throughout posteriorly
CARDIOVASCULAR SYS
 Distal pulses palpable + = bilaterally
 JVP not elevated
 PULSE 107/min, regular, synchronous
 BP 260 / 145 mmHg
 Normal heart sounds
 No murmurs
ABDOMEN
 Soft, non-tender
 No masses or organomegaly
 Normal BS
MUSCULOSKELETAL
 No calf swelling or tenderness
DIASCAN
 22.3 MMOL / L
ASSESSMENT
 1. ACUTE PULMONARY OEDEMA

r/o Acute Myocardial Infarction
 2. Uncontrolled HTN – 2o non-compliance
 3. ? Newly Diagnosed Diabetic
PLAN
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Oxygen 15 L / min- nonbreather face mask
GTN 2 puffs – X 2
Nitroglygerin infusion @ 1mcg/kg/min (100mcg/min)
Enalapril 1.25mg IV
Lasix 60mg IV
Aspirin 300mg stat
Soluble insulin 10u IV
PLAN
 ECG (RT sided leads subsequently)
ABG
 Cardiac enzymes
 FBC
PT PTT n/a
. Urea and electrolytes
CXR
Urethral catheter + urinalysis
RESULTS
 ECG: sinus, regular



LVH with Strain
ST depression II, aVF
? ST elevation vs high J point V1-V3
 Right sided leads - NAD
RESULTS
 CXR- fluffy opacity throughout
 ABG – 15 L O2
 O2 sat 93.2%
 pO2 - 74.3
 pCO2 – 39.6
 HCO3 – 18.1
RESULTS
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Hb 15.1
WBC 19.8
PLT 332
Sodium 137
Potassium 3.6
Chloride 101
Urea 9.9
Creatinine 125
CK 120
CKMB 41
Troponin I 0.22
FURTHER MX
 Referred To Med on Call
 1 hour after seen significant improvement
 RR 32/ min, BP 195 / 109, pulse 85/min
 2 hours later
 1000 mls urine emptied
 Admitted to MED
ON WARD
 Treated for UTI
 Day 4 aggressive, speaking loudly
 Seen by psyche
 Diagnosis ? Paranoid Schizophrenia vs


Delusional disorder
? Hypomanic symptoms
DISCHARGE
 DAY 7
 F/U: MOPD + Psyche Hospital
 TTH: Lasix 40mg od

Norvasc

Tritace

ASA

Lipitor

Diamicron MR 30mg od

Complete Septrin
ACUTE CARDIOGENIC PULMONARY
OEDEMA

ANDREA JOHNSON
DEFINITION
 Leakage of fluid from the pulmonary capillaries and
venules into the alveolar space as a result of increased
hydrostatic pressure
 Inability of left ventricle to effectively handle its
pulmonary venous return

MATTU ET AL
PATHOPHYSIOLOGY
Angiotensinogen
Angiotensin I
(LIVER)
RENIN
ACE
Angiotensin II
ALDOSTERONE
VASOCONSTRICTION
PATHOPHYSIOLOGY
↓ CARDIAC
OUTPUT
INCREASED PCWP
SYMTOMATIC
DECOMPENSATION
ACTIVATION
OF RENIN ANGIOTENSIN
SYSTEM
ACTIVATION OF S/S SYSTEM
CARDIAC ISCHAEMIA
↓
LEFT VENTRICULAR
FUNCTION
INCREASED HEART RATE
INCREASED SYSTEMIC VASCULAR RESISTANCE
INCREASED PRELOAD
PRECIPITATING FACTORS
 Myocardial ischaemia or infarction
 Arrhythmias
 Uncontrolled HTN/HTN crisis
 Medication Non-compliance
 Thyrotoxicosis
 Fluid overload
 Anaemia
 Pulmonary & other infections
 Inappropriate medications- -ve inotropes, NSAIDS
CLINICAL FEATURES
 SOB
 Orthopnoea - sensitivity 5%

- specificity 77%
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PND
Tachycardia
BP
Wheezing – sensitivity 22%
- specificity 58%
Crepitations - sensitivity 6%
- specificity 78%
EMERGENCY MEDICINE PRACTICE DEC 2006
DIFFERENTIAL DIAGNOSIS
 Physicians only 80% accurate at differentiating Acute
Heart Failure from other disease processes
DIFFERENTIAL DIAGNOSIS
 ASTHMA
 COPD
 PULMONARY EMBOLISM
 PNEUMONIA
INVESTIGATIONS
 1. Blood
 2. Electrocardiography
 3. Radiologic
BLOOD INVESTIGATIONS
 ABG
 FBC – anaemia, infection
 U & Es
 CARDIAC MARKERS
CARDIAC MARKERS
 CARDIAC ENZYMES
 OTHER CARDIAC MARKERS
OTHER CARDIAC MARKERS
 B – NATRIURETIC PEPTIDE (BNP)
 N-TERMINAL PRO BNP
PRE-PRO BNP
BNP + NT PRO-BNP
B – NATRIURETIC PEPTIDE (BNP)
 EFFECTS
 1.Vasodilation
 2. Diuresis
 3. Natriuresis
 4. Suppression of Renin Angiotensin Sys
IMPORTANCE OF BNP IN HF
 1. Useful in Diagnosis
 2. Assessing Severity
 3. Predicting short & long-term CVS mortality
WHAT LEVELS ?
 NO HEART FAILURE
 BNP < 100pg / dl
 NT PRO-BNP < 300pg / dl
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
HEART FAILURE
BNP >500pg / dl
NT PRO-BNP > 1000pg / dl
80% Sensitivity for heart failure
PROBLEMS !!!
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GRAY AREA: 100pg/dl – 500pg/dl
BNP 
in non-cardiac conditions
Renal disease

Age
Pulmonary Embolism
Cor pulmonale
BNP 
in CCF
OBESITY: BMI inversely related to BNP
USEFULNESS OF BNP
 Does not add much when diagnosis certain from
clinical presentation
 Uncertain diagnosis when BNP < 100pg/dl
 Known baseline in certain conditions
 20% obese patients with acute heart failure have values
< 100pg/dl
ELECTROCARDIOGRAM
 Ischaemia / infarction
 Arrhythmia – A fib
 LVH
 Prolonged QRS
CHEST RADIOGRAPH
 FINDINGS IN HEART FAILURE
 Cardiomegaly – 74% sensitive, 78% specific
 Vascular redistribution
 Interstitial oedema
 Pleural effusions (right sided/bilateral)
CXR – BUT !!
 20% patients with Acute heart failure have none of the
“typical features”
 No longstanding HF- Normal size heart
 Longstanding CCF – lymphatics
 COPD – minimal findings
Other investigation
 Echocardiography
 1.Identify reversible cause eg tamponade
 2.Distinguish between systolic and diastolic
dysfunction
TREATMENT
 AIMS
 ABCs
 Decrease Preload (right-sided filling)
 Increase left-sided emptying
↓ Afterload, 
Cardiac output
 ± improve LV contractility – inotropes
 Overall aim- Redistribute fluid out of lungs!

AVAILABLE TREATMENT
 OXYGEN
 PHARMACOTHERAPY

INOTROPIC RX
 NONINVASIVE POSITIVE PRESSURE
VENTILATION
PHARMACOTHERAPY
 AVAILABLE
 1. NITRATES
 2. DIURETICS
 3. ACE INHIBITORS
 4. MORPHINE
 5. NATRIURETIC PEPTIDES
NITRATES

NITROGLYCERIN
 MECHANISM OF ACTION
 Venodilation (low dose)↓ PRELOAD
 Arteriolar dilatation (higher dose)
 ↓ AFTERLOAD
 ↓pulmonary hydrostatic pressure

NITROGLYCERIN
 DOSE
 SL: 0.4mg q 5-10 min
 IV: titrate up to 3 – 5mcg /kg /min
 Topical: may be unreliable in poor perfusion
 Effect seen within minutes !!!
NITROPRUSSIDE
 ↓ Afterload
 Useful in
 Pulmonary oedema unresponsive to standard therapy
 Severe HTN
 Severe mitral/aortic regurge
NITROGLYCERIN
 Excellent single agent for acute pulmonary oedema !!
ACE INHIBITORS
 MECHANISM OF ACTION
 Sublingual or IV
 ↓ Afterload
 ↓ Preload
 ↓ Pulmonary Capillary Wedge Pressure
 Down-regulate renin-angiotensin system
ACE INHIBITORS
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Sublingual
12.5mg Captopril Sys BP < 110
25mg Captopril Sys BP >110
Intravenous
Enalapril - 0.004mg/kg bolus
- 1mg infusion over 2 hrs
- 1.25 mg bolus
Effect seen within 10 minutes!!!!
CARE with ACE INHIB
 NOT easily titratable
 Long duration of action
 ↓↓ BP
DIURETICS
 MOA - Furosemide
 EARLY – 1st 30 min
 Activate renin angiotensin system
 Activate S/S nervous system (Release of
Norepinephrine)

SVR (afterload), 
HR, BP

↓CO
MOA - Furosemide
cont’d
 LATER (30 – 120 min)
 Decrease Preload
 A. Diuresis
 B. Direct venodilator effect
RECOMMENDATION
 Give Nitrates PRIOR to Furosemide
 High dose Nitrate + low dose Diuretic 

more consistent improvement
EVEN BETTER !??
 Premedication with Nitrates + ACE Inhibitors 
Immediate and sustained ↓ PCWP by Furosemide
MORPHINE
 ↓ Preload
 Anxiolysis
 BUT
 Nitrate provide better preload reduction
 Histamine release
NATRIURETIC PEPTIDES
 NESERITIDE
 Recombinant form of BNP
 FDA approved
NESERITIDE
PROS
 More effective than Nitrates at
 1. improving haemodynamic function
 2. self reported symptoms
NESERITIDE
CONS
 EXPENSE: 40 x > NTG
 Bolus (2mcg/kg) followed by 24 - 48 hour infusion
(0.01mcg/kg/min)
OTHER NATRIURETIC PEPTIDES
 Undergoing research
 Carperitide – atrial natriuretic peptide
 Ularitide – renal natriuretic peptide
NIPPV
 Continuous positive airway pressure (CPAP)
 Bi-level positive airway pressure (BIPAP)
NIPPV MOA
 Decrease work of breathing
 Decrease preload & afterload
 Improve Cardiac output
 Must be used early to maximize effect !!
?  MI with BIPAP
INOTROPIC SUPPORT
 CARDIOGENIC SHOCK
 SYS BP < 80mmHg
 PCWP >18mmHg
 Cardiac Index < 1.8L/min/m2 (normal 2.5 4.0
L/min/m2 )
INOTROPIC SUPPORT
 1. Catecholamines
 2. Phosphodiesterase inhibitors
 3. Calcium sensitizers (undergoing research)
 3. Intra-aortic balloon pump
Catecholamines
 Dopamine
 Dobutamine (less arrhythmogenic)
 Cons
 Increase myocardial oxygen demand
 Tolerance may develop requiring higher doses
Phosphodiesterase inhibitors
 PREFERRED !!
 Work independent of adrenoreceptor activity and
plasma catecholamine levels
 No tolerance
 Decrease preload and afterload !
 MILRINONE !
DISPOSAL
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ALMOST ALL PATIENTS SHOULD BE ADMITTED !!
Discharge only if
Mild failure
No increased oxygen requirement
Cause: non-compliance
Ischaemia ruled out
No arrhythmia
Normal labs
Normal mental status
Good follow-up
SUMMARY
 ABC
 REDISTRIBUTE FLUID OUT OF LUNGS!
 1ST Line: Nitrates
 2 ND Line: ACE Inhibitors
 3RD Line: Diuretics
 NIPPV – use early !
 Milrinone – preferred inotrope
THANK YOU
REFERENCES
 1.
Mattu A. Management of Acute pulmonary
edema-Pearls and Pitfalls
2. Kosowsky J, et al. Acutely decompensated heart
failure:
diagnostic and therapeutic Strategies.
Emergency Medicine Practice Dec
2006;8(12)
 3. Mattu A, et al. Pulmonary edema,
cardiogenic. Emedicine