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OEDEMA
M. Budiarto
Pathophysiological mechanism
are traditionally categorized into
two primary cause :
Cardiogenic pulmonary edema
Non cardiogenic pulmonary
edema
Negative Pressure of
Cardiomyopathy LV dysfunction lung inters al
Lympha c Drainage
HT
Pathophysiologic mechanisms :
Imbalance of Starling forces - Ie,
increased pulmonary capillary pressure,
decreased plasma oncotic pressure,
increased negative interstitial pressure
Damage to the alveolar-capillary barrier
Lymphatic obstruction
Idiopathic (unknown) mechanism
CARDIOVASCULAR EMERGENCIES COURSE
Bumi Surabaya Hotel, November 7-8th, 2015
The progression
Elevated LA pressure distension and opening of
small pulmonary vessels
Blood gas exchange does not deteriorate
Alveolar flooding
Abnormalities in gas exchange
Vital capacity and respiratory volumes
Severe hypoxemia EMERGENCIES COURSE
CARDIOVASCULAR
Bumi Surabaya Hotel, November 7-8th, 2015
MECHANISM OF CARDIOGENIC PULMONARY EDEMA
Pneumothorax
Pulmonary embolism
Respiratory failure
Acute Respiratory Distress Syndrome
Asthma
Chronic Obstructive Pulmonary Disease
CARDIOVASCULAR EMERGENCIES COURSE
Bumi Surabaya Hotel, November 7-8th, 2015
INITIAL MANAGEMENT
SaO2 BGA
Early
PO2 , PCO2 O2 mask PO2
State
Hypercapnea (-)
Yes
Yes
O2 Invasif PO2 > 60 continue
Late State PO2 , PCO2 (mechanical
Hypercapnea (+) ventilator) No
PEEP
(5-20 cmH2O)
Reduction of
pulmonary
venous
return
(preload)
Main
Goal Reduction of
Inotropic systemic
support (in vascular
some cases) resistance
(afterload)
Oxygen Furosemide
With caution :
TDS <110 mmHg 35-45
Severe Syldenafil Avoid minutes Natriuresis
Vasoconstriction !!
MS & AS Diuresis
HCM & Obstructive
Nitrat
(vasodilator)
Cardiomyopathy Add Thiazid Diuresis
Lung Congestif
Preload In Patients already taking diuretic, 2.5 times
existing oral dose recommended.
Irrational to use loop diuretic
Good Response on HT, Coronary ischemic, MR in vasoconstriction and renal blood ow &
hypotension blood flow optimization
(vasodilator & inotropic)
Nitroprusside sodium
Vasodilatation & increased inotrophic activity
Dose : 10-15 mcg/min IV, titration until efective dose 30-50
mcg/min ( TDS 90 mmHg)
K/I : hypersensitive, subaortic stenosis, atrophy optic, AF or
flutter
Preload reduction
Vasodilation effect lowers preload reduce
pulmonary congestion
Should be avoided : Systolic blood pressure <110
mmHg
DIURETIC
Intra venous loop diuretic (Furosemide)
Doses: 10-20 mg IV (Ps CHF never use diuretic
40-80 mg IV (Ps had been use diuretic)
80-120 mg IV (Ps no respon in first give)
Interaction : Metformin decreased diuretic in blood
concentration
K/I : hypersensitive, coma hepaticum, anuria, severe
electrolyte depletion
CARDIOVASCULAR EMERGENCIES COURSE
Bumi Surabaya Hotel, November 7-8th, 2015
Diuretics
Morphine 1.
A erload
Anxiety, stress
2.
Preload
1.
Central Sedation O2 demand
2.
Venodilator
CO
Prefer on Renal
Ischemic & Diuresis +
Perfussion
Preload Myocardium SV
Contraindication :
CO Intuba on rate
SBP <80 mmHg K>5
SaO2 Creatinine > 3
ACEi intolerance
ACEI and ARBs Preventing remodeling, reduce
arrhythmias
The Valsartan Heart Failure (Val-HeFT) and
Candesartan in Heart Failure: Assessment in
Reduction of Mortality and Morbidity (CHARM)
ARBs lowers the incidence of atrial fibrillation (AF)
ANALGESIC
Morphine IV
Anxiolytic
Venodilatation decreased preload
Artery dilatation decreased systemic vascular resistance &
increased CO
When :
Reduction in preload and afterload still has not improved
Impaired systolic function
Perfusion disturbances and/or congestion
Used only in heart failure patients with low cardiac index and
stroke volume
0.5-2 g/kg/mnt IV CO
SBP 70-100 mmHg
When :
Remain hypoxic with noninvasive supplemental
oxygenation
Impending respiratory failure
Hemodynamically unstable
Two most common forms of lung oedema are cardiogenic and non-cardiogenic.
Based on history taking, physical examination and medical tests, a clinician can
distinguish between the two causes of acute lung oedema.
Bradicardia Tachycardia
See algorithm See algorithm
Extravasation
SEPSIS (Rich Protein Fluid)
Infection
1 Clinical
Features 2 Laboratory
Studies 3 Electrocardi
ography
Clinical features of Complete blood LA enlargement and
left heart failure count LV hypertrophy
Reflect evidence of Electrolyte Chronic LV
hypoxia and Blood urea nitrogen dysfunction
increased (BUN) and creatinine Tachydysrhythmia or
sympathetic tone Blood gas analysis bradydysrhythmia or
History acute myocardial
to determine the ischemia or
exact cause infarction
Penyebab :
Komplikasi IMA
Tanda-tanda :
TINDAKAN I AF VR cepat
Tensi/shock
Takiaritmia
Freq. nafas
Hipertensi
Sesak
Kx. Katub : MR/MS/AR
Sianosis
Dilated cardiomyopathy
Ronchi -O2 bila perlu intubasi
Hipoksia -Nitroglycerin SL
Sputum berdarah -Furosemide IV 0,5-1 mg/kg TINDAKAN II
-Morphin IV 2-4 mg titrasi Pada Edema Paru Akut
(kecuali pada non cardiac) sebab cardiac
..continue.. COURSE
CARDIOVASCULAR EMERGENCIES
Bumi Surabaya Hotel, November 7-8th, 2015
..lanjutan.. Tindakan II
Pada Edema Paru Akut sebab Kardiak