acute lung edema - r. mohammad budiarto, md, fiha.pdf

8/18/2019 Acute Lung Edema - R. Mohammad Budiarto, MD, FIHA.pdf

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CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8 th , 2015

M. Budiarto

ACUTE LUNGOEDEMA


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Acute Lung edema :

Condition characterized by fluid accumulation in lungs caused byextravasation of fluid from pulmonary vasculature into the

inerstitium and alveoli of the lungs.

INTRODUCTION

ALO is a severe respiratory distress,tachypnea, orthopnea and rales onall lung field verified by chest X-rayand/or with arterial oxygensaturation


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Pathophysiological mechanism

are traditionally categorized into

two primary cause :Cardiogenic pulmonary edema

Non cardiogenic pulmonary

edema

ETIOLOGY


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CARDIOGENIC PULMONARY

EDEMA

Defined as pulmonary edema due to increasedcapillary hydrostatic pressure secondary toelevated pulmonary venous pressure

McMurray JJ, 2012


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CARDIOGENIC LUNG OEDEMA

CAD

Myocarditis

Cardiomyopathy

HT

CHD

LV dysfunction

LA pressure ↑ > 25 mmHg(18-25 mmHg normal)

Lung Capillary Pressure ↑

Decreased OncoticPlasma Pressure

Negative Pressure of lung inters al ↑

Lympha c Drainage ↓

Hydrosta c pressure ↑

Oedema Fluid ThroughLung Epitelium

Alveoli drowned by lowprotein fluid

Lung Oedema


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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

PATHOPHYSIOLOGY


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Elevated LA pressure distension and opening of

small pulmonary vesselsBlood gas exchange does not deteriorate

Elevated LA pressure distension and opening of

small pulmonary vesselsBlood gas exchange does not deteriorate

The progression

Fluid and colloid shift into the lung interstitium

Lymphatic outflow removes the fluid

Fluid and colloid shift into the lung interstitium

Lymphatic outflow removes the fluid

Alveolar floodingAbnormalities in gas exchange

↓ Vital capacity and respiratory volumesSevere hypoxemia

Filling interstitial space (can contain up to 500mL)Filling interstitial space (can contain up to 500mL)


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Increased Pressure in Pulmonary Vascular Bed Increased Permeability of Alveolar-Capillary Walls

MECHANISM OF CARDIOGENIC PULMONARY EDEMA


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HOW TO MAKE THE DIAGNOSIS


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Breathlessness developssuddenly

Anxious

Feeling of drowning

Coughs

Expectorates pink, frothyliquid

Sitting bolt upright or maystand

S3 gallop

Raised jugular venouspressure

Peripheral edema

History past illness :cardiomypathy, valvulerheart disease,hypertension, MI,

congenital heart disease

CLINICAL MANIFESTATION


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Complete blood count

Electrolyte

Blood urea nitrogen (BUN) andcreatinine serum

Blood gas analysis

LABORATORIUM STUDIES


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Brain-type natriureticpeptide (BNP)

High negative predictive value

Cutoff value : 100 pg/mL

BNP value of under 100pg/mL heart failure isunlikely

The level of BNP increase:age, renal dysfunction

LABORATORIUM STUDIES

N -terminal pro BNP(NT-pro BNP)

Well correlated with BNP

levels

NT-proBNP > 450 pg/mL (inpatients 100 pg/mL


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Sign of hypertrophy, enlargement cardiac chronic LV

dysfunction

Sign ischemia or infarction

conduction disturbance tachydysrhytmia or bradysrhytmia

ELECTROCARDIOGRAPHY


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X RAY


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Establish the etiology of pulmonary edema

Evaluate LV systolic and diastolic function,

valvular function, and pericardial disease.

Non-invasive hemodynamic parametersappropriate therapy

ECHOCARDIOGRAPHY


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Helps in differentiating CPE from Non Cardiogenic PulmonaryEdema (NCPE).

A PCWP exceeding 18 mm Hg indicates CPE

Monitor hemodynamic condition

Pulmonary Arterial Catheter


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Conditions to consider in the differential diagnosis of CPEinclude the following :

Pneumothorax

Pulmonary embolismRespiratory failure

Acute Respiratory Distress Syndrome

Asthma

Chronic Obstructive Pulmonary Disease

DIFFERENT DIAGNOSIS


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• Airway, breathing and circulation

• Oxygen should be administered to all patients to keep oxyge

saturation > 90 %

• Method oxygen delivery include : face mask, non invasive

pressure support ventilation (CPAP and BiPAP and mechanic

ventilation.

INITIAL MANAGEMENT


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Oxygen

↓ SaO 2 BGA

O2 mask PO2 ↑PO2 ↓, PCO2 ↓Hypercapnea (-)

EarlyState

Late State PO2 ↓ ↓, PCO2 ↑Hypercapnea (+)

O2 Invasif (mechanicalventilator)

PO2 > 60 continueYesYes

PO2 > 60YesYes

NoNo

continue

NIV(Non Invasif Ventilator)

NoNo

PEEP(5-20 cmH 2O)


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OXYGEN

• Oxygen mask• Oxygen flow 100 %, monitor with oxcimetry

(oxygen saturation)

• If still hypoxia; NPPV (Noninvasive Pressure PositiveVentilation) , intubation


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MEDICAL MANAGEMENT

MainGoal

Reduction of pulmonary

venousreturn

(preload)

Reduction of systemicvascular

resistance

(afterload)

Inotropicsupport (in

some cases)


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• Many drug are now used in the hospital treatment of acute lungoedema. These include :

Oxygen

Nitrat

Furosemide

ACEi ARB

Inotropic CPAP IABPOpiate

Management of ALO(focus on Cardiogenic Lung oedema)


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Nitrat

CLOAdrenergik ↑, Aldosteron ↑, RAS ↑

SevereVasoconstriction

Nitrat(vasodilator)

Preload ↓Lung Congestif

↓

Good Response on HT, Coronary ischemic, MR

With caution :• TDS


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NITRAT

Nitroprusside sodium

Vasodilatation & increased inotrophic activity

Dose : 10-15 mcg/min IV, titration until efective dose 30-50mcg/min ( TDS ≥ 90 mmHg)

K/I : hypersensitive, subaortic stenosis, atrophy optic, AF orflutter


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Vasodilators ( Nitroglycerin )

•Preload reduction•Vasodilation effect lowers preload reduce

pulmonary congestion•Should be avoided : Systolic blood pressure


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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 bloodconcentration

K/I : hypersensitive, coma hepaticum, anuria, severeelectrolyte depletion


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Diuretics

•Loop diuretics : Furosemide

•Affect the ascending loop of Henle

Diminished renal perfusionDelay the onset of effects of loop diuretics

•Long-term use electrolyte disturbances,

hypotension and worsening renal function


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Opiate

Morphine

Central Sedation

Venodilator

1.

2.

Anxiety, stress ↓

O2 demand ↓

Prefer onIschemic

MyocardiumPreload ↓

CO ↑

ACEi

↓ ↓ A erload

↓ Preload

CO ↑

SV ↑

&&

1.

2.

RenalPerfussion ↑ Diuresis +

Contraindication :• SBP 3

• K > 5• K > 5Intuba on rate ↑ ↑SaO2 ↓ ↓


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ACE inhibitor (ACEi)•Hemodynamic effects of ACEI :

Reduce afterload, improving stroke volume andcardiac output, and slightly reduce preload

improve renal perfusion diuresis

•Caution in patients with : – Hypotension (systolic 3 mg / dl) – Bilateral renal artery stenosis

– Increased blood potassium levels (> 5 mEq / L)


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Angiotensin II receptor blockers (ARBs)

•ACEi intolerance•ACEI and ARBs Preventing remodeling, reducearrhythmias

•The Valsartan Heart Failure (Val-HeFT) andCandesartan in Heart Failure: Assessment inReduction of Mortality and Morbidity (CHARM)

– ARBs lowers the incidence of atrial fibrillation (AF)


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ANALGESIC

Morphine IVAnxiolytic

Venodilatation decreased preload

Artery dilatation decreased systemic vascular resistance &increased CO

Dose: 2-5 mg IV, every 10-15 minute ( if RR


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Opiates

•Reduce the anxiety associated with dyspnea•Venodilators reduce preload

•Reduce sympathetic drive•Depress respiratory drive

Increasing the need for invasive ventilation


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ACE INHIBITOR

• Decreased vascular sistemic resistance, ????????• Menurunkan tahanan sistemik vaskuler, memperbaiki tekanan

pasak paru, isi sekuncup, curah jantung dan memperbaiki mitral

regurgitasi, tanpa mempengaruhi denyut jantung maupun MAP• Captopril 25-50mg, bila tidak hipotensi• Enalapril 10-20mg• Efek perbaikan dispnea dalam 6-12 menit


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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 andstroke volume

INOTROPES


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Inotropic

Dobutamine

Dopamine

Norepinephrine

CO ↑, SVR ↓

SBP 70-100 mmHg

Shock ( - )

CO

CO ↑, SVR ↑

SVR ↑ ↑

SBP 70-100 mmHg

Shock ( + )

2-20 μg/kg/mnt IV

0.5-2 μg/kg/mnt IV

5-10μg/kg/mnt IV

>10μg/kg/mnt IV

0.5-30 μg/mnt IVSBP


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INOTROPIC

Dopamin, dobutamin, milrinone

Hypotension with CHF : dopamin & dobutamin

Milrinone: inhibits fosfodiesterase ↑ cAMP & change incalsium transport ↑ heart contractility & ↓ vascular tonus(vasodilatation)


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INOTROPIC : DOPAMIN

Adrenergic and dopaminergic receptor stimulation

Hemodynamic effect ‘dose dependent ’

Dose: 5 mcg/kg/min IV, titrationInteracts : phenytoin, α & β adrenergic blockers, generalanesthesia, MAO inhibitor (anti depressant) ↑ &prolonged dopamin effect

K/I: hypersensitive, pheochromocytoma, VF


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Useful in patients with renal dysfunction and diuretic resistance

ULTRAFILTRATION


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Reducing aortic impedance and systolic pressure

In cardiogenic shock :

decreases LV filling pressures by 20-25%

improves cardiac output by 20%

Provide hemodynamic support in perioperative andpostoperative period in high-risk patients

severe coronary disease, severe LV dysfunction, or recentMI

IABP


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Ultrafiltration should be considered in acute heart failure with volume overload whodo not respond to high doses of diuretics or in patients with impaired renal function


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Intra-Aortic Balloon Pumping ( IABP )

•Reducing aortic impedance and systolic pressure•In cardiogenic shock :

– decreases LV filling pressures by 20-25% – improves cardiac output by 20%

•Provide hemodynamic support in perioperativeand postoperative period in high-risk patients

– severe coronary disease, severe LV dysfunction, orrecent MI


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Ventilatory Support


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Noninvasive pressure-support ventilation (NPSV)

•Consider in severe CPE•Two types :

– CPAP and BiPAP

•Improves air exchange•Increases intrathoracic pressure reductionpreload & afterload

•Several studies : – Decreased length of stay in the ICU – Decreased need for mechanical ventilation


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Mechanical ventilation

•When : – Remain hypoxic with noninvasive supplemental

oxygenation

– Impending respiratory failure

– Hemodynamically unstable

•Maximizes myocardial oxygen delivery andventilation

•Increase alveolar patency


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INOTROPIC : DOBUTAMIN

Vasodilatation & ↑ inotropic

Dose: 2.5 mcg/kg/min IV

Interacts: β adrenergic blockers antagonism todobutamin effect

K/I: hipersensitifity, idiopathic subaortic stenosis, AF orflutter


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Dopamine1 Dobutamine2 Norepinephrine3Cardiogenic shock Low dosedopaminergicreceptorsincreasing diuresisModerate doseβ

-receptors↑ Cardiaccontractility andHeart rateHigh doseα -receptorsVasoconstriction(increased afterload),↑Blood pressure

Hypotension due todecreasedcontractilityPositive chronotropic& inotropicModerate or severe

hypotensionshould be avoided

α -receptorsvasoconstrictionUse in severehypotensionCombination withdobutamine

improvehemodynamic


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Phosphodiesterase inhibitors ( milrinone )

•Increase the level of intracellular cyclic adenosinemonophosphate (cAMP)

– Positive inotropic effect on the myocardium – Peripheral vasodilation (decreased afterload)

– Reduction in pulmonary vascular resistance(decreased preload)

•Improvements in stroke volume, cardiac output,

PCWP (preload), and peripheral vascularresistance (afterload)

•increased incidence of arrhythmias


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Calcium sensitizers ( Levosimendan )

•Inotropic, metabolic, and vasodilatory effects•Binding to troponin C•Not increase myocardial oxygen demand

•Not a proarrhythmogenic agent•Effective and safe alternative to dobutamine


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Acute lung oedema is a life threatening condition and needmanagement immediately.

Hospital mortality of ALO are 15-20% mortality of ALO wasreported are 15-20% and it depends on severity when it comesto ED/ first medical contact.

Infark myocard acute and hypotension will increase mortality

PROGNOSIS


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CASE(1) A man 42 years old, chest pain, dyspnea (+), rales (+),wheezing(-),BP 70/50, CRT >2 s, SaO 2 89%. CKMB 200, Troponin 5, ECGSinus rhythm 130x, AMI Inferior-RV-Post. Onset chest pain 4h.What should we do ?

O 2 SaO 2 >94%, double IV line, Catheter urine

NE 0.5-30 μg/mnt IV, SaO 2 >94% anxious ↑↑Morphine

TDS ≥ 100 Furosemide

PCI


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CASE(2) A man 55 years old, dyspnea (+), rales (+),wheezing(+), BP190/120, CRT 94%, double IV line, Catheter urine

FurosemideNitrate 1 mg/h IV, SaO 2 >94% anxious ↑↑ Morphine

Observation Dyspnea (+), rales ( ↓ ),wheezing(-), BP 80/60,

CRT


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Acute lung oedema is a severe respiratory distress, tachypnea, orthopnea andrales on all lung fields verified by chest x-ray and/or with arterial oxygen

saturation


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Clinical signs: Shock, hypoperfusion,Congestive heart failure, acute pulmonary edema

Most likely problem ?

Acute pulmonary edema Volume problem Pump problem Rate problem

TachycardiaSee algorithm

BradicardiaSee algorithm

Blood

Pressure ?

1st – Acute pu lmonary ed ema• Furosemide iv 0.5 – 1.0 mg/kg• Morphine iv 2 – 4 mg• Nitroglycerin SL•Oxygen /intubation as needed

Administer :• Fluids • Blood transfusions • Cause-specific interventions Consider vasopressors


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Systolic BP> 100 mmHg

Systolic BP70 to 100 mmHg

No sign/symptomsof shock

Systolic BP70 to 100 mmHg

Signs/symptomsof shock

Systolic BP< 70 mmHg

Signs/symptomsof shock

Systolic BPBP defines 2 nd

Line of action(see below)

• Norepinephrine iv0.5 – 30 mcg/min

• Dopamine iv5 – 15 mcg/kg/min

• Dobutamine iv2 – 20 mcg/kg/min

•Nitroglycerin iv10– 20 mcg/minConsider

•Nitroprusside iv0.1-5 mcg/kg/min

2nd - Acute pulmonary edema• Nitroglycerin / nitroprussideif BP > 100mmHg• Dopamineif BP 70 – 100 mmHg, signs/symptoms of shock• Dobutamineif BP > 100 mmHg, no signs/symptoms of shock

Further diagnostic / therapeutic consideration• Pulmonary artery catheter • Intra-aortic balloon pump• Angiography for AMI / ischemia• Additional diagnostic studies

Further diagnostic / therapeutic consideration• Pulmonary artery catheter • Intra-aortic balloon pump• Angiography for AMI / ischemia• Additional diagnostic studies


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Hemodynamic subsets in

acute

heart failure

NormalNormal

Pulmonary

edema2.2

2.0

1.5

1.0

0.5

0

normal blood pressure

5 10 15 18 20 25 30 35 40Pulmonary Wedge Pressure

Forrester Α et al: Am J Cardiol 1977; 39:137

reduced blood pressure

high blood pressure

Cardiogenicshock

Hypovolaemicshock

Mor:2.2% Mor:10.1%

Mor:22.4%

Mor:55.5%


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SummaryCommon cause of acute heart failure, life-threatening and require

immediate actionDefined as pulmonary edema due to increased capillary hydrostaticpressure secondary to pulmonary venous pressure

High mortality rate

Acute myocardial infarction, hypotension and a history of frequentacute attacks increase the risk of mortality

BNP and echocardiography Important diagnostic tools

Therapeutic goal :

Improve the patient's symptoms

Improves fluid status

Identification of causal factors


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The pathogenesis of hydrostatic that accompaniesvarious disorders of the left side of the heart (coronaryartery disease, myocardiomyopathies, aortic or mitralvalve abnormalities).

Fluid extravasation attributable to an increasedhydrostatic or reduced oncotic pressure gradient acrossthe intake alveolo-capillary barrier.

Furthermore, capacity of the lymphatic system toremove fluid from the interstitial space and to drain intothe systemic veins is dependent on systemic venous

pressure and the intergrity of the lymphatics.

Cardiogenic LO


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Cardiogenic pulmonary oedemaOccurs when cardiac output drops despite an increasedsystemic resistance, so that blood returning to the leftatrium exceeds that leaving the left ventricle (LV)

As a result, pulmonary venous pressure increases,

causing the capillary hydrostatic pressure in the lung toexceed the oncotic pressure of the blood, leading to anet filtration of protein poor fluid out of the capillaries


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LV BACKWARD EFFECTSPengosongan ventrikel kiri

Peningkatan volume & tekanan end-diastolic ventrikel kiri

Peningkatan volume (tekanan ) pada atrium kiri

Peningkatan volume pada vena pulmonalis


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Peningkatan volume pulmonary capillarybed = peningkatan tekanan hidrostatik

Transudasi cairan dari kapiler ke alveoli

Pengisian cepat rongga alveolar

Edema Paru

LV BACKWARD EFFECTS lanjutan


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NON CARDIOGENIC LUNG OEDEMA

SEPSIS

Infection

Trauma

Coagulationimpaired

etc

Lung Endotelpermeability ↑ ↑

Extravasation(Rich Protein Fluid)

Fill Interstitial Space& Alveolar

Alveoli drowned byRich protein fluid

Lung Oedema

Algorithm for the Clinical Differentation between Cardiogenic and


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Algorithm for the Clinical Differentation between Cardiogenic andNoncardiogenic


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HOW TO MAKE DIAGNOSIS

ClinicalFeatures1 LaboratoryStudies2

Electrocardiography3

Clinical features of left heart failureReflect evidence of

hypoxia andincreasedsympathetic toneHistoryto determine theexact cause

Complete bloodcountElectrolyte

Blood urea nitrogen(BUN) and creatinineBlood gas analysis

LA enlargement andLV hypertrophyChronic LV

dysfunctionTachydysrhythmia orbradydysrhythmia oracute myocardialischemia orinfarction


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Brain-type

natriuretic peptide(BNP)4

High negative predictivevalueCutoff value : 100 pg/mLBNP value of under 100pg/mL heart failure isunlikelyThe level of BNP increase:age, renal dysfunction

N -terminal pro BNP(NT-pro BNP)5 Well correlated with BNP

levelsNT-proBNP > 450 pg/mL

(in patients 100 pg/mL


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EDEMA PARU AKUT

KARDIAK NON KARDIAK

TINDAKAN I

Penyebab : Komplikasi IMA

AF VR cepat TakiaritmiaHipertensiKx. Katub : MR/MS/AR Dilated cardiomyopathy

Tanda-tanda :

Tensi↑/shock Freq. nafas ↑Sesak SianosisRonchiHipoksiaSputum berdarah

-O2 bila perlu intubasi-Nitroglycerin SL-Furosemide IV 0,5-1 mg/kg-Morphin IV 2-4 mg titrasi(kecuali pada non cardiac)

TINDAKAN IIPada Edema Paru Akut

sebab cardiac

..continue..


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..lanjutan..

TDS > 100 mmHg Nitroglycerin 10-20 µ /mnt IV Nitropruside 0,1-5 µ /kg/mnt IV

TDS 70-100 mmHg Gejala shock +

Dopamin 5-15 µ /kg/mnt IV

TDS 70-100 mmHg Gejala shock – Dobutamin 2-20 µ /kg/mnt IV

Selanjutnya Dx. dan Tx. : 1. Identifikasi penyebab yang reversible2. Kateterisasi A. Pulmonal3. IABP4. Angiografi & PCI5. Surgical interventions6. Tambahan pemeriksaan untuk Dx7. Tambahan terapi

Tindakan IIPada Edema Paru Akut sebab Kardiak


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Hemodynamic subsets in “acute ” heart failure

NormalNormal

Pulmonaryedema2.2

2.0

1.5

1.0

0.5

0

normal blood pressure

5 10 15 18 20 25 30 35 40Pulmonary Wedge Pressure

Forrester Α et al: Am J Cardiol 1977; 39:137

reduced blood pressure

high blood pressure

Cardiogenicshock

Hypovolaemicshock

Mor:2.2% Mor:10.1%

Mor:22.4%

Mor:55.5%


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CARDIOVASCULAR EMERGENCIES COURSE

MAIN GOALS OF TREATMENT1.Reducing pulmonary venous return

(pre-load reduction)

2.Reducing systemic vascular resistance

(after-load reduction)3.Maintaining adequate blood pressure by

inotropic support

4.Preventing and treating respiratory

distress with ventilatory support

acute lung edema - r. mohammad budiarto, md, fiha.pdf

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