MANAGEMENT OF

PULMONARY OEDEM

Sri Sulistyowati
Wisnu Prabowo
Wisnu Prabowo
FETOMATERNAL DIVISION
OBSTETRICS AND GYNECOLOGY DEPARTMENT
SEBELAS MARET UNIVERSITY/DR MOEWARDI HOSPITAL
SURAKARTA
 Acute Pulmonary Oedema
Characterised
dyspnea & hypoxia secondary to
fluid accumulation in the lungs which Mortality rate + 40%.
impairs gas exchange and lung
compliance

Medical Emergecies
which requires immediate
management

The goals of Treatment

Causes
myocardial ischemia,
arrhythmias (e.g. atrial fibrillation),
acute valvular dysfunction and fluid
overload, pulmonary embolus,
anemia renal artery stenosis.
to provide symptomatic relief,
improve oxygenation, maintain
cardiac output & perfusion of vital
organs, and reduce excess
extracellular fluid. Any underlying
cause should be identified when
starting treatment
Pathophysiology

Causes
(starling
equation)

•Caused by a variety of perturbations of any one of the key determinants of

cardiovascular function and fluid flow into the pulmonary interstitium.

•Reduction in colloid osmotic pressure (or in colloid osmotic

pressure/ pulmonary capillary wedge pressure gradient
•Increased capillary permeabillity
•Increased Intravascular hydrostatic pressure

 Will lead extravasation of fluid from the vasculature and predispose to

the development of PO
 Establishing Diagnosis
Worsening dyspnea and orthopnea

Respiratory compromise (tachypnea, crackles, rales, hypoxemia

Arterial blood gas and chext X-Ray

Electrocardiography, echocardiography

Spiral CT Imaging

Ventilation/ perfusion scan

Pulmonary arteriography

Pulmonary embolism
To Exclude cardiopulmonary pneumonia
compromise

cardiomyopathy
Arterial Blood Gas Values in Nonpregnant
and Pregnant Women
 Nitrate
Smooth Muscle Increased
Improve
relaxation coronary blood
oxygenation
flow

Reduce
Coronary
Venodilation workload of
arteries
heart

Preload Reduced
Given
reduction at low afterload &
sublingually
dose Blood pressure

Speed onset on
Arteriolar
Higher dose IV line & ability
dilatation
titrate dose
 Nitrate
Associated
hypotension

Associated
tachyphylaxis within BP maintain >
16-24hrs continous 90mmHg
administration

Contraindicated
Adverse effect:
phosphodiesteras
paradoxical
e invibitor
bradicardia
(sildenafil)

Adverse Adverse
effect : effect :
tachycardia headache
Coons JC, McGraw M, Murali S. 2011
 Diuretics

•Lack of studies benefit to PO •Indicated to fluid overload

•Loop diuretic (furosemide) •Used in patients intravascular

reduce preload volume depletion
 Diuretics
• IV line preferred. Urine catheter for monitoring urine output
administered

• Furosemide 40-80mg

• Higher doses used in patient already oral diuretic or Chronic

Kidney Disease

• IV bolus slowly & repeated 20min if required, after bolus give

infusion rate 5-10mg/hrs

• A small RCT did not find difference outcome between bolus and
continous infusion

• Higher Dose improve dyspnea, but associated worsening renal

function, admitted ICU, reflect more severe disease.
Baird A., 2010; Colucci WS., 2017
 Morphine

• Adverse effect: respiratory & CNS Depression, reduce cardiac

output and hypotension

• Associated with adverse events: increased rates of

mech.ventilation, ICU Admission and mortality

• No Longer recommended routine use for acute PO. Beneficial

if there is ongoing chest pain resistant to nitrates

• Low dose (1 –2,5 mg) useful to facilitate tolerance non-invasive

ventilation but need to monitored for sedation
 Inotropes
• IV inotropic drugs: hypotension • Limited critically ill patients 
and evidence of reduced longer length of hospital stay
organ perfusion and increased mortality.

• Dobutamine: peripheral
• Impaired left ventricular
vasodilatory effects 
function and hypotension  IV
worsening hypotension 
infusion of dobutamine.
vasopressor.

• Dobutamine: cause
arrhythmias and
contraindicated if patient has
ventricular arrhythmias or rapid
atrial fibrillation.
• Another inotrope that may increase cardiac output and
improve peripheral perfusion is milrinone

• It used for the short-term management of severe

heart failure that not responded to others

• Milrinone may increase mortality in acute

exacerbations of chronic heart failure. It can be
considered in patients with chronic beta blockade
 Anatomical Effects Functional Effects
Functional effects
Increased respiratory
drive
Airway edema
friability Minimal change in TLC
Increased Minute
ventilation
Widened AP and Reduced FRC
Transverse diameter

Increased cardiac output

Elevated
Diaphragm
Normal diaphramatic Fxn
Widened Subcostal
angle

Enlarging uterus
Increased O2
consumption
and CO2 production

.w medtau.org
 PRE-ECLAMPSIA

VASCULAR BLOOD
LEAKAGE PRESSURE

DIRECT IMPACT ON
PULMONAL CAPILLARY
VESSELS

PLEURAL
LUNG EDEMA
EFFUSION

LOW VENTILATOR
SATURATION
MAGNESIUM INTUBATION INDIRECT
SIDE EFFECT IMPACT
CONVULSION 
UNCONCIOUSC VAP
 PATHOGENESIS
OF PULMONARY EDEMA IN
PREECLAMPSIA
 PATHOGENESIS
OF PULMONARY EDEMA
IN PREECLAMPSIA

Oxidative
Stres

VENTRICULAR DYSFUNCTION –
LVH (HIGH PERIPHERAL
RESISTANCE + INCREASING
PLASMA LEVELS
 Pathogenesis Pulmonary Oedema in
Preeclampsia
• Increase plasma blood
volume, cardiac output,
HR, capillary
permeability, decrease
colloid osmotic pressure

• Maternal changes • These Changes

during pregnancy exaggerated in
predispose preeclampsia

•Pulmonary
Oedema
 Pathogenesis Pulmonary Oedema in
Preeclampsia

• Normal: plasma • 18mmHg at • Reduction

colloid osmotic term to colloid osmotic
decrease 22mmHg 14mmHg after delivery
at term to 15 mmHg postpartum in from excessive
after delivery Preeclampsia blood loss

• These changes
• Fluid shift secondary to
explain at least 70-
increased capillary permeability
80% PO in
(esp in Preeclampsia) or
Preeclampsia develop
excessive crystalloid infusion
after delivery
 Management of acute pulmonary
edema-- LMNOP

• Lasix (furosemide)
• Morphine sulfate 2 to5 mg in an attempt to reduce the
adrenergic vasoconstrictor stimuli to the pulmonary arteriolar
and venous beds
• Na+ and water restriction
• Oxygen supplementation and capillary leak syndrome has
been breathed by mechanical ventilation and PEEP 5-15
cmH2O
• Positioning (elevation) by reducing pulmonary capillary
wedge pressure
 THE ART OF FUROSEMIDE USAGE IN PE
COMPLICATED BY LUNG EDEMA

• Lasix (furosemide) administered intravenously as a single

dose of 20 to 40 mg over 2 minutes to promote diuresis.
• If an adequate response is not seen within 30 to 50 minutes,
the dose should be increased to 40 to 60 mg
• Administered by slow intravenous injection to a maximum of
120 mg in 1 hour.
• Electrolytes (especially potassium) should be supplemented
as needed.
According to
ACOG, severe preeclampsia with pulmonary CVP INSERTION IS
edema is one of the indications for invasive MANDATORY!
pulmonary artery catheterization,
 INDIRECT IMPACT – IATHROGENIC –
MAGNESIUM TOXICITY

Effects of Increasing Plasma Magnesium Levels

• MgSO4 in excess of therapeutic range

– Skeletal muscle weakness
– Respiratory depression
– Cardiac arrest (Ca++ can counter-act this)
– MgSO4 potentiates NMB and sedative effects of opiods

Observed Condition mEq/L

Normal Plasma level 1.5-2.0
Therapeutic Range 4.0-8.0
ECG Changes (Prolonged P-Q, widened QRS) 5.0-10
Loss of deep tendon reflexes 10
SA and AV node block 15
Respiratory Paralysis 15
Cardiac Arrest 25

CA GLUCONATE 10% 1v. –saline diluted 1 gr/100cc Piggy bag 20dpm

Megan Purvey, George Allen, 2017
 Summary

•Acute PO has hight mortality. Require emergency

management in hospital

•Goals: improve Oxygenation, maintain adequate blood

pressure for perfusions vital organs & reduce excess
extracellular fluid. Underlying causes must be addressed

•Lack of high-quality evidence to guide treatment of acute

PO. Strongest evidences are nitrates and non-invasive
ventilators
 Summary
•Diuretics indicated for fluid overload patients.
Furosemide should be given IV injection slowly

•Routine use of Morphine not recommended because

the adverse effect. Oxygen given in hypoxemia
condition

•Inotropic drugs started in hypotension & evidence of

reduced organ perfusion. Dobutamine as first-line
treatment
Terima Kasih
 FOLLOW UP

The underlying cause of PO should be treated.

This includes reviewing their medicines to see if any drugs,

such as NSAIDs, verapamil or diltiazem, could have
contributed to the problem

Additional monitoring: daily weights, measurements of serum

electrolytes and renal function
 Follow Up

Cardiogenic with acute PO has been stabilized, the goal of therapy is

to improve long-term outcomes

Echocardiogram shows a preserved left ventricular ejection fraction,

the focus is to treat any associated conditions  hypertension with
antihypertensive, reduction of pulmonary congestion and peripheral
oedema with diuretics, and rate control for atrial fibrillation

Reduced ejection fraction and chronic heart failure  ACE inhibitor,

beta blocker and mineralocorticoid receptor antagonist
 FOLLOW UP
ACE inhibitors best at 24-48hrs after admitted, given if
hemodinamically stable

Caution in hypotension or renal impairment, stricly monitored on

blood pressure and renal function

Beta blockers (bisoprolol) given at low dose if euvolemic condition

before discharge from hospital

Mineralocorticoid receptor antagonist (spironolactone) best started

soon after discharge with monitoring on blood pressure, potassium
level and renal function
 VAP
• Pneumonia that develops in someone who has been
intubated
• Typically in studies, patients are only included if intubated
greater than 48 hours
• Early onset= less than 4 days
• Late onset= greater than 4 days
• Endotracheal intubation increases risk of developing
pneumonia by 6 to 21 fold
• Accounts for 90% of infections in mechanically ventilated
patients

American Thoracic Society, Infectious Diseases Society of America.

Guidelines for the management of adults with hospital-acquired, ventilator-associated,
and healthcare-associated pneumonia.
 THE BUGS

•Figure 1 from Park

Park DR. The microbiology of ventilator-associated pneumonia.

 Treatment- Early onset VAP with no risk factors,
any disease severity

American Thoracic Society, Infectious Diseases Society of America. Guidelines for

the management of adults with hospital-acquired, ventilator-associated, and
healthcare-associated pneumonia.
 Treatment- Late Onset or Risk Factors for MDR
or All Disease Severity

American Thoracic Society, Infectious Diseases Society of America. Guidelines for

the management of adults with hospital-acquired, ventilator-associated, and
healthcare-associated pneumonia.
American Thoracic Society, Infectious Diseases Society of America. Guidelines for
the management of adults with hospital-acquired, ventilator-associated, and
healthcare-associated pneumonia.
 Treatment

American Thoracic Society, Infectious Diseases Society of America. Guidelines for the
management of adults with hospital-acquired, ventilator-associated, and healthcare-
associated pneumonia.
 Treatment

”Delivery of the fetus and plac

management of severe preeclampsia. Once severe
disease has been established and is progressing,
delivery of the fetus and placenta must be accomplished
to limit maternal risk.