IN THE NAME OF GOD

CARDIOGENIC PULMONARY
EDEMA
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Cardiogenic pulmonary
edema
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CPE
CPE due to:
increased capillary hydrostatic pressure
secondary to elevated pulmonary venous
pressure

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following major 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
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Mechanism of CPE

alveolar-capillary membrane
Increase of net flux of fluid from the
vasculature into the interstitial space
Net flow of fluid across a membrane is
determined by applying the following
equation:
Q = K(Pcap - Pis) - l(Pcap - Pis)

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Lymphatics
10-20 mL/h
acute rise in pulmonary arterial capillary
pressure (ie, to >18 mm Hg)
chronically elevated LA pressure, the rate
of lymphatic removal can be as high as
200 mL/h
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Stages
Stage 1
elevated LA pressure distention and
opening of small pulmonary vessels
blood gas exchange does not deteriorate
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Stage 2
fluid and colloid shift into the lung
interstitium from the pulmonary
capillariesbut an initial increase in
lymphatic outflow efficiently removes the
fluid
may overpower the drainage capacity of
the lymphatics
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Stage 2
mild hypoxemia
Tachypneastimulation of
juxtapulmonary capillary (J-type)

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Stage 3
alveolar flooding
abnormalities in gas exchange
vital capacity and other respiratory
volumes are substantially reduced
hypoxemia becomes more severe
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Cardiac disorders manifesting
as CPE
Atrial outflow obstruction
LV systolic dysfunction
LV diastolic dysfunction
Dysrhythmias
LV hypertrophy and cardiomyopathies
LV volume overload
Myocardial infarction
LV outflow obstruction
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Presentation
History

Physical Examination
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History

Symptoms
Sudden (acute)
Long-term (chronic)
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Sudden (acute)
Extreme shortness of breath or difficulty
breathing (dyspnea) that worsens when lying
down
A feeling of suffocating or drowning
Wheezing or gasping for breath
Anxiety, restlessness or a sense of apprehension
A cough that produces frothy sputum that may
be tinged with blood


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Sudden (acute)
Excessive sweating
Pale skin
Chest pain, if pulmonary edema is caused
by heart disease
A rapid, irregular heartbeat (palpitations)

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Long-term (chronic)

Having more shortness of breath than normal
when you're physically active
Difficulty breathing with exertion, often when
you're lying flat as opposed to sitting up
Wheezing
Awakening at night with a breathless feeling
that may be relieved by sitting up
Rapid weight gain
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Long-term (chronic)
Swelling in your legs and ankles
Loss of appetite
Fatigue
Ortner sign?

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Physical Examination
Tachypnea
Tachycardia
sitting uprightair hunger
Confuse
agitate
anxious
diaphoretic
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Hypertension
Hypotension indicates severe LV systolic
dysfunction and the possibility of
cardiogenic shock
Cool extremities may indicate low
cardiac output and poor perfusion.
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Auscultation
fine, crepitant rales
rhonchi or wheezes may also be present
Cardiovascular findingsS3,accentuation
of the pulmonic component of S2, jugular
venous distention
Auscultation of murmursacute valvular
disorders
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Auscultation
Aortic stenosis harsh crescendo-
decrescendo systolic murmur, which is heard
best at the upper sternal border and radiating to
the carotid arteries
acute aortic regurgitationshort, soft diastolic
murmur
Acute mitral regurgitation produces a loud
systolic murmur heard best at the apex or lower
sternal border

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Mitral stenosis typically produces a loud
S1, opening snap, and diastolic rumble at
the cardiac apex
skin pallor or mottlingperipheral
vasoconstriction, low cardiac output

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Severe CPEmental statushypoxia or
hypercapnia
hypercapnia with respiratory acidosis may be seen
in patients with severe CPE or underlying
chronic obstructive pulmonary disease (COPD).
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Diagnostic Considerations
Cardiogenic pulmonary edema (CPE) should be
differentiated from pulmonary edema associated
with injury to the alveolar-capillary membrane,
caused by diverse etiologies.
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DDx
Acute Respiratory Distress Syndrome
Asthma
Cardiogenic Shock
Chronic Obstructive Pulmonary Disease
Emphysema
Goodpasture Syndrome
Myocardial Infarction
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DDx
Pneumothorax
High-altitude pulmonary edema
Neurogenic pulmonary edema
Pulmonary embolism
Respiratory failure
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DDx
Pneumocystis (carinii) jiroveci
Pneumonia
Pneumonia, Bacterial
Pneumonia, Viral
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differentiate CPE from NCPE
In CPE, a history of an acute cardiac
event is usually present
low-flow state
S3 gallop
jugular venous distention
crackles on auscultation
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differentiate CPE from NCPE
Patients with NCPE have a warm periphery, a
bounding pulse, and no S3 gallop or jugular
venous distention
Definite differentiation is based on pulmonary
capillary wedge pressure (PCWP) measurements.
The PCWP is generally >18 mm Hg in CPE and <
18 mm Hg in NCPE, but superimposition of chronic
pulmonary vascular disease can make this
distinction difficult to assess.
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Workup
Lab studies
Complete blood count
Serum electrolyte measurements
Blood urea nitrogen (BUN) and creatinine
Pulse oximetry
Arterial blood gas analysis
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Electrocardiography
LA enlargement
LV hypertrophy
acute tachydysrhythmia
bradydysrhythmia
acute myocardial ischemia or infarction
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BNP
EFFECTS
1.Vasodilation
2. Diuresis
3. Natriuresis
4. Suppression of Renin Angiotensin Sys

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BNP testing
high negative predictive value; that is, in
patients with BNP value of under 100 pg/mL,
heart failure is unlikely

Values of 100-400 pg/mL may be related to
various pulmonary conditions, such as cor
pulmonale, COPD, and pulmonary embolism.
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Radiography
Chest radiography is helpful in distinguishing CPE from other
pulmonary causes of severe dyspnea.
Features that suggest CPE rather than NCPE and other lung
pathologies include the following:
Enlarged heart
Inverted blood flow
Kerley lines
Basilar edema (vs diffuse edema)
Absence of air bronchograms
Presence of pleural effusion (particularly bilateral and
symmetrical pleural effusions)

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Echocardiography
important diagnostic tool in determining the etiology of
pulmonary edema
helpful in identifying a mechanical etiology for pulmonary
edema, such as the following:
Acute papillary muscle rupture
Acute ventricular septal defect
Cardiac tamponade
Contained LV rupture
Valvular vegetation with resulting acute severe
mitral, aortic regurgitation
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Pulmonary Arterial Catheter
PCWP can be measured with a pulmonary arterial catheter
(Swan-Ganz catheter)
This method helps in differentiating CPE from NCPE
A PCWP exceeding 18 mm Hg in a patient not known to
have chronically elevated LA pressure indicates CPE.
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Treatment
Following initial management, medical treatment of CPE
focuses on 3 main goals
(1) reduction of pulmonary venous return (preload
reduction)
(2) reduction of systemic vascular resistance (afterload
reduction)
(3) inotropic support
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Treatment
Patients with severe LV dysfunction or acute valvular
disorders may present with hypotension. These patients
may not tolerate medications to reduce their preload and
afterload. Therefore, inotropic support is necessary in
this subset of patients to maintain adequate blood
pressure.
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Ventilatory Support
Noninvasive pressure-support ventilation

Mechanical ventilation

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Preload Reduction
Nitroglycerin
Diuretics
Morphine sulfate
Nesiritide
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Afterload Reduction
ACE inhibitors
Angiotensin II receptor blockers
Nitroprusside
Phosphodiesterase inhibitors
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Inotropic support
Dobutamine
Dopamine
Norepinephrine
Phosphodiesterase inhibitors
Calcium sensitizers
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SUMMARY
ABC
REDISTRIBUTE FLUID OUT OF LUNGS!
1
ST
Line: Nitrates
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ND
Line: ACE Inhibitors
3
RD
Line: Diuretics
NIPPV use early !
Milrinone preferred inotrope
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