Presented by Mohammed Elias

Pulmonary
INTRODUCTION
Pulmonary oedema is a condition that results from the
accumulation of fluid in the lung interstitium and
alveoli.
Fluid congestion decreases gas exchange across the
alveoli, resulting in decreased oxygenation of the blood
and, in some cases, accumulation of carbon dioxide
(CO2).
Pathophysiology
The pathophysiology of pulmonary
oedema can be thought of in terms of
three factors:

Flow Fluid Filter

Flow
The ability of the heart to eject the blood
delivered to it depends on three factors:
1. The amount of blood returning to the heart (preload)
2. The co-ordinated contraction of the myocardium
3. The resistance against which it pumps (afterload).

Preload Contractility Afterload

Fluid
Over- Heart
retention Hypertensio Atherosclero Aortic valve
infusion of IV muscle
(Renal n sis stenosis
fluid damage
failure)
LeftSOsidedWHAT Blood
HAPPENSbacking up in WHEN Pulmonary
THE HEART IS NOT
heart the pulmonary veins capillary
ABLE TO EJECT THE BLOOD SUFFICIENTLY Pulmonary
?edema
problems left atrial pressure and hydrostatic
Such as LV pulmonary venous pressure pressure
infarction, LV rise because of accumulating increases
failure, or mitral blood
stenosis.
Fluid
The blood passing through the lungs must have
enough oncotic pressure to hold on to the
fluid portion as it passes through the
pulmonary capillaries.
As albumin is a key determinant of oncotic
pressure, low albumin states lead to pulmonary
oedema, e.g. burns, liver failure, nephrotic
syndrome.
Filter
The capillaries through which the fluid
passes may increase in permeability, e.g.,
acute lung injury (as in smoke inhalation),
pneumonia or drowning.
Classification
Cardiogenic (or hydrostatic) pulmonary oedema
caused by an elevated pulmonary capillary pressure
from left-sided heart failure
Non-cardiogenic pulmonary oedema

Flow Fluid Filter

PHYSICAL FINDINGS & CLINICAL
PRESENTATION
Dyspnea with rapid, shallow breathing
Diaphoresis, perioral and peripheral cyanosis
Pink, frothy sputum
Moist, bilateral pulmonary rales
Increased pulmonary second sound, S3 gallop
Hypertension (unless in cardiogenic shock and hypotensive)
Tachycardia
Bulging neck veins
LABORATORY TESTS
Arterial blood gases (ABGs)
Measurement of plasma brain natriuretic peptide
(elevated).
Cardiac biomarkers: evaluate for possible acute
myocardial infarction.
Basic chemistries: hyponatremia is common in chronic
heart failure; evaluate renal function.
IMAGING STUDIES
ECG:
May have evidence of ischemia,
arrhythmias, or LV hypertrophy (often
seen in diastolic dysfunction)
IMAGING STUDIES
Chest x-ray
Pulmonary congestion with Kerley B lines; fluffy perihilar
infiltrates in the early stages; bilateral interstitial alveolar
infiltrates
Pleural effusions
Enlarged cardiac silhouette
Upper zone vessel enlargement (1) a sign of pulmonary venous hypertension
Septal (Kerley B) lines (2) a sign of interstitial oedema
Airspace shadowing (3) due to alveolar oedema acutely in a peri-hilar (bat's
wing) distribution angles (4) due to pleural effusions
Blunt costophrenic
IMAGING STUDIES
Echocardiogram:
Useful to evaluate valvular abnormalities, diastolic
versus systolic dysfunction
Can help differentiate cardiogenic versus
noncardiogenic pulmonary edema
Can also estimate pulmonary capillary wedge
pressure and rule out presence of myxoma or atrial
thrombus
RIGHT HEART
CATHETERIZATION
A pulmonary artery catheter (Swan-Ganz) is inserted into the
large veins of the chest or the neck and advanced through
the right-sided chambers of the heart and lodged into the
pulmonary artery.
This device has the capability of directly measuring the
pressure in the pulmonary vessels, called the pulmonary
artery wedge pressure.
A wedge pressure of 18 mmHg or higher is consistent
withcardiogenic pulmonary edema.
whereas a wedge pressure of less than 18 mmHg usually favors
anon-cardiogenic cause of pulmonary edema.
MANAGEMENT
Immediate, aggressive therapy is
mandatory for survival. The following
measures should be instituted as
simultaneously as possible for
cardiogenic pulmonary edema:
1. SUPPORT OF OXYGENATION AND
VENTILATION
Administer 100% O2by mask to achieve
PaO2>60 mmHg; if inadequate, use positive-
pressure ventilation by face or nasal mask, and
if necessary, proceed to endotracheal
intubation.
2. REDUCE PRELOAD:
Seat pt upright to reduce venous return, if not hypotensive.

Intravenous loop diuretic (e.g.,furosemide, initially 0.51.0 mg/kg); use lower dose if pt
does not take diuretics chronically.

Nitroglycerin (sublingual 0.4 mg 3 q5min) followed by 520 g/ min IV if needed.

Morphine24 mg IV; assess frequently for hypotension or respiratory depression;

naloxoneshould be available to reverse effects ofmorphineif necessary.

Consider ACE inhibitor if pt is hypertensive, or in setting of acute MI with heart failure.

Consider nesiritide (2-g/kg bolus IV followed by 0.01 g/kg per min) for refractory
symptomsdo not use in acute MI or cardiogenic shock.
3. INOTROPIC AGENTS
Inotropic agents are indicated in cardiogenic
pulmonary edema and severe LV dysfunction:
dopamine,dobutamine,milrinone
4. TREAT THE CAUSE
The precipitating cause of cardiogenic pulmonary
should be sought and treated, particularly acute
arrhythmias or infection.
For refractory pulmonary edema associated with
persistent cardiac ischemia, early coronary
revascularization may be life-saving.

For noncardiac pulmonary edema, identify and treat/remove

cause.
ULTRAFILTRATION
Venovenous isolated ultrafiltration is sometimes used
to remove fluid in patients with heart failure, although
it is usually reserved for those unresponsive or
resistant to diuretics.
STIMULATION OF ALVEOLAR FLUID
CLEARANCE
Recent mechanistic studies on alveolar epithelial ion
transport have defined a variety of ways to upregulate
the clearance of solute and water from the alveolar
space.
In patients with acute lung injury (noncardiogenic
pulmonaryedema), IV -adrenergic agonist
treatment decreases extravascular lung water, but the
outcome benefit is uncertain.
Unusual Types of Edema
Specific etiologies of pulmonaryedema may require particular therapy.

Reexpansion pulmonary edema can develop after removal of air or fluid that has been

in the pleural space for some time. These patients may develop hypotension oroliguria

resulting from rapid fluid shifts into the lung. Diuretics and preload reduction are

contraindicated, and intravascular volume repletion often is needed while supporting

oxygenation and gas exchange.

High-altitude pulmonaryedema often can be prevented by use ofdexamethasone,

calcium channel-blocking drugs, or long-acting inhaled 2-adrenergic agonists. Treatment

includes descent from altitude, bed rest,oxygen, and, if feasible, inhalednitric

oxide;nifedipine may also be effective.

Take-home points:
1. Elevation of pulmonary wedge pressures helps to differentiate cardiogenic
from non-cardiogenic causes of pulmonary edema.
2. CXR, ECG, and ABG are indicated in most patients. History and physical
exam can help differentiate causes.
3. For treatment think: UNLOAD ME
1. Upright position
2. Nitrates
3. Lasix
4. Oxygen
5. Ace inhibitors, albuterol
6. Dopamine
7. Morphine
8. Electricity
Thank you!
References:
1 ABC of heart failure. London: BMJ Books, 2002.
2 Ferris Clinical Advisor 2015 5 Books in 1, Expert
Consult
3 Davidsons Principles and Practice of Medicine, 22nd
Edition
4 The Johns Hopkins Internal Medicine Board Review, 4th
Edition