CASE - Barbados Association of Medical Practitioners
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Transcript CASE - Barbados Association of Medical Practitioners
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
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%
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
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
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