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PART IV
Pulmonary Vascular Diseases
Slide 1
Copyright © 2006 by Mosby, Inc.
Chapter 19
Pulmonary Edema
RBC
IE
FWS
Figure 19-1. Pulmonary edema. Cross-sectional view of alveoli and alveolar duct in pulmonary edema.
FWS, Frothy white secretions; IE, interstitial edema; RBC, red blood cell. Inset, Atelectasis, a common
secondary anatomic alteration of the lungs.
Slide 2
Copyright © 2006 by Mosby, Inc.
Anatomic Alterations of the Lungs
Slide 3

Interstitial edema, including fluid engorgement of
the perivascular and peribronchial spaces and the
alveolar wall interstitium

Alveolar flooding

Increased surface tension of pulmonary surfactant

Alveolar shrinkage and atelectasis

Frothy white (or pink) secretions throughout the
tracheobronchial tree
Copyright © 2006 by Mosby, Inc.
Etiology

Cardiogenic pulmonary edema

Slide 4
Congestive heart failure
Copyright © 2006 by Mosby, Inc.
Etiology
Movement of fluid in and out of the capillaries is
expressed by Starling’s equation:
J = K (Pc – Pi) – (c – i)
where J is the net fluid movement out of the
capillary, K is the capillary permeability factor,
Pc and Pi are the hydrostatic pressures in the
capillary and interstitial space, and c and i
are the oncotic pressures in the capillary and
interstitial space
Slide 5
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Slide 6
Copyright © 2006 by Mosby, Inc.
Slide 7
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Slide 8
Copyright © 2006 by Mosby, Inc.
Etiology
Noncardiogenic pulmonary edema

Slide 9
Increased capillary permeability

Alveolar hypoxia

Acute respiratory distress syndrome

Inhalation of toxic agents

Pulmonary infections

Therapeutic radiation of the lungs

Head injury
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Etiology
Slide 10

Lymphatic insufficiency

Decreased intrapleural pressure

Decreased oncotic pressure

Overtransfusion

Uremia

Hypoproteinemia

Acute nephritis

Polyarteritis nodosa
Copyright © 2006 by Mosby, Inc.
Slide 11
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Slide 12
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Overview of the Cardiopulmonary
Clinical Manifestations Associated
with PULMONARY EDEMA
The following clinical manifestations result from
the pathophysiologic mechanisms caused (or
activated) by Atelectasis (see Figure 9-7),
Increased Alveolar-Capillary Membrane
Thickness (see Figure 9-9) and, in severe
cases, Excessive Bronchial Secretions (see
Figure 9-11)—the major anatomic alterations of
the lungs associated with pulmonary edema
(see Figure 19-1)
Slide 13
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Figure 9-7. Atelectasis clinical scenario.
Slide 14
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Figure 9-9. Increased alveolar-capillary membrane thickness clinical scenario.
Slide 15
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Figure 9-11. Excessive bronchial secretions clinical scenario.
Slide 16
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Clinical Data Obtained at the
Patient’s Bedside
Vital signs
Slide 17

Increased respiratory rate

Increased heart rate, cardiac output,
blood pressure
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Clinical Data Obtained at the
Patient’s Bedside
Slide 18

Cheyne-Stokes respiration

Paroxysmal nocturnal dyspnea (PND) and
orthopnea

Cyanosis

Cough and sputum (frothy and pink)

Chest assessment findings

Increased tactile and vocal fremitus

Crackles, rhonchi, and wheezing
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Clinical Data Obtained from
Laboratory Tests and
Special Procedures
Slide 19
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Pulmonary Function Study:
Expiratory Maneuver Findings
FVC

FEVT
N or 
FEF25%-75%
N or 
FEF200-1200
N
PEFR
MVV
FEF50%
FEV1%
N
Slide 20
N or 
N
N or 
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Pulmonary Function Study:
Lung Volume and Capacity Findings
VT
Slide 21
RV
FRC
TLC
N or 



VC

IC

ERV

RV/TLC%
N
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Arterial Blood Gases
Mild to Moderate Pulmonary Edema

pH

Slide 22
Acute alveolar hyperventilation with
hypoxemia
PaCO2

HCO3 (Slightly)
PaO2

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Time and Progression of Disease
Disease Onset
Alveolar Hyperventilation
100
90
PaO2 or PaCO2
80
Point at which PaO2
declines enough to
stimulate peripheral
oxygen receptors
70
60
PaO2
50
40
30
20
10
0
Figure 4-2. PaO2 and PaCO2 trends during acute alveolar hyperventilation.
Slide 23
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Arterial Blood Gases
Severe Pulmonary Edema

Acute ventilatory failure with hypoxemia
pH

Slide 24
PaCO2

HCO3 (slightly)
PaO2

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Time and Progression of Disease
Disease Onset
Alveolar Hyperventilation
Acute Ventilatory Failure
100
90
Pa02 or PaC02
80
70
Point at which PaO2
declines enough to
stimulate peripheral
oxygen receptors
Point at which disease
becomes severe and patient
begins to become fatigued
60
50
40
30
20
10
0
Figure 4-7. PaO2 and PaCO2 trends during acute ventilatory failure.
Slide 25
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Oxygenation Indices
QS/QT
DO2
VO2


Normal
O2ER

Slide 26
C(a-v)O2
Normal
SvO2

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Hemodynamic Indices
(Cardiogenic Pulmonary Edema)
Slide 27
CVP
RAP
PA
PCWP




CO
SV
SVI
CI




RVSWI
LVSWI
PVR
SVR




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Abnormal Laboratory Tests and
Procedures
Slide 28

Serum potassium: low

Serum sodium: low

Hypokalemia and hyponatremia are often
seen in patients with left-sided heart failure
and may result from diuretic therapy or
excessive fluid retention
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Radiologic Findings
Chest radiograph
Slide 29

Fluffy opacities

Left ventricular hypertrophy

Kerley A and B lines

Pleural effusion
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Figure 19-2. Cardiomegaly (arrow) and pulmonary edema in congestive heart failure.
Slide 30
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General Management of
Pulmonary Edema
Respiratory care treatment protocols
Slide 31

Oxygen therapy protocol

Bronchopulmonary hygiene therapy protocol

Hyperinflation therapy protocol

Aerosolized medication protocol
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General Management of
Pulmonary Edema
Medications and procedures commonly
prescribed by the physician
Slide 32

Positive inotropic agents

Afterload reduction agents

Morphine sulfate

Diuretic agents
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General Management of
Pulmonary Edema
Medications and procedures commonly
prescribed by the physician
Slide 33

Albumin and mannitol

Alcohol (ethanol, ethyl alcohol)

Decreasing hydrostatic pressure

Positioning the patient in Fowler’s position

Rotating tourniquets (rarely used)

Phlebotomy (rarely used)
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Classroom Discussion
Case Study:
Pulmonary Edema
Slide 34
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