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
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
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
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 ACTIVATION
DECOMPENSATION 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%

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

HEART FAILURE
BNP >500pg / dl
NT PRO-BNP > 1000pg / dl
80% Sensitivity for heart failure
PROBLEMS !!!
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
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
contd
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
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