copyright © 2006 by mosby, inc. slide 1 part iv pulmonary vascular diseases

Copyright © 2006 by Mosby, Inc.Slide 1

PART IVPART IV

Pulmonary Vascular DiseasesPulmonary Vascular Diseases


Chapter 19Chapter 19Pulmonary EdemaPulmonary Edema

Figure 19-1. Pulmonary edema. Cross-sectional view of alveoli and alveolar duct in pulmonary edema. Figure 19-1. Pulmonary edema. Cross-sectional view of alveoli and alveolar duct in pulmonary edema. FWS,FWS, Frothy white secretions; Frothy white secretions; IE,IE, interstitial edema; interstitial edema; RBC,RBC, red blood cell. red blood cell. Inset,Inset, Atelectasis, a common Atelectasis, a common

secondary anatomic alteration of the lungs. secondary anatomic alteration of the lungs.

FWS

IE

RBC


Anatomic Alterations of the LungsAnatomic Alterations of the Lungs

Interstitial edema, including fluid engorgement of Interstitial edema, including fluid engorgement of the perivascular and peribronchial spaces and the the perivascular and peribronchial spaces and the alveolar wall interstitiumalveolar wall interstitium

Alveolar floodingAlveolar flooding

Increased surface tension of pulmonary surfactantIncreased surface tension of pulmonary surfactant

Alveolar shrinkage and atelectasisAlveolar shrinkage and atelectasis

Frothy white (or pink) secretions throughout the Frothy white (or pink) secretions throughout the tracheobronchial treetracheobronchial tree


EtiologyEtiology

Cardiogenic pulmonary edemaCardiogenic pulmonary edema Congestive heart failureCongestive heart failure


EtiologyEtiology

Movement of fluid in and out of the capillaries is Movement of fluid in and out of the capillaries is expressed by Starling’s equation:expressed by Starling’s equation:

J = K (Pc – Pi) – (J = K (Pc – Pi) – (c – c – i)i)

where J is the net fluid movement out of the where J is the net fluid movement out of the capillary, K is the capillary permeability factor, capillary, K is the capillary permeability factor, Pc and Pi are the hydrostatic pressures in the Pc and Pi are the hydrostatic pressures in the capillary and interstitial space, and capillary and interstitial space, and c and c and i i are the oncotic pressures in the capillary and are the oncotic pressures in the capillary and interstitial spaceinterstitial space


EtiologyEtiology

Noncardiogenic pulmonary edemaNoncardiogenic pulmonary edema

Increased capillary permeabilityIncreased capillary permeability Alveolar hypoxiaAlveolar hypoxia

Acute respiratory distress syndromeAcute respiratory distress syndrome

Inhalation of toxic agentsInhalation of toxic agents

Pulmonary infectionsPulmonary infections

Therapeutic radiation of the lungsTherapeutic radiation of the lungs

Head injuryHead injury


EtiologyEtiology

Lymphatic insufficiencyLymphatic insufficiency

Decreased intrapleural pressureDecreased intrapleural pressure

Decreased oncotic pressureDecreased oncotic pressure OvertransfusionOvertransfusion

UremiaUremia

HypoproteinemiaHypoproteinemia

Acute nephritisAcute nephritis

Polyarteritis nodosaPolyarteritis nodosa


Overview of the Cardiopulmonary Overview of the Cardiopulmonary Clinical Manifestations Associated Clinical Manifestations Associated

with PULMONARY EDEMAwith PULMONARY EDEMA

The following clinical manifestations result from The following clinical manifestations result from the pathophysiologic mechanisms caused (or the pathophysiologic mechanisms caused (or activated) by activated) by AtelectasisAtelectasis (see Figure 9-7) (see Figure 9-7), , Increased Alveolar-Capillary Membrane Increased Alveolar-Capillary Membrane Thickness Thickness (see Figure 9-9) and, in severe cases, (see Figure 9-9) and, in severe cases, Excessive Bronchial SecretionsExcessive Bronchial Secretions (see Figure 9- (see Figure 9-11)—the major anatomic alterations of the lungs 11)—the major anatomic alterations of the lungs associated with pulmonary edema (see Figure associated with pulmonary edema (see Figure 19-1)19-1)


Figure 9-7. Atelectasis clinical scenario.Figure 9-7. Atelectasis clinical scenario.


Figure 9-9. Increased alveolar-capillary membrane thickness clinical scenario.Figure 9-9. Increased alveolar-capillary membrane thickness clinical scenario.


Figure 9-11. Excessive bronchial secretions clinical scenario.Figure 9-11. Excessive bronchial secretions clinical scenario.


Clinical Data Obtained at the Clinical Data Obtained at the Patient’s BedsidePatient’s Bedside

Vital signsVital signs

Increased respiratory rateIncreased respiratory rate

Increased heart rate, cardiac output, Increased heart rate, cardiac output, blood pressureblood pressure


Clinical Data Obtained at the Clinical Data Obtained at the Patient’s BedsidePatient’s Bedside

Cheyne-Stokes respirationCheyne-Stokes respiration

Paroxysmal nocturnal dyspnea (PND) and Paroxysmal nocturnal dyspnea (PND) and orthopneaorthopnea

CyanosisCyanosis

Cough and sputum (frothy and pink)Cough and sputum (frothy and pink)

Chest assessment findingsChest assessment findings Increased tactile and vocal fremitusIncreased tactile and vocal fremitus

Crackles, rhonchi, and wheezingCrackles, rhonchi, and wheezing


Clinical Data Obtained from Clinical Data Obtained from Laboratory Tests andLaboratory Tests andSpecial ProceduresSpecial Procedures


Pulmonary Function Study: Pulmonary Function Study: Expiratory Maneuver FindingsExpiratory Maneuver Findings

FVC FEVT FEF25%-75% FEF200-1200

N or N or N

PEFR MVV FEF50% FEV1%

N N or N N or

FVC FEVT FEF25%-75% FEF200-1200

N or N or N

PEFR MVV FEF50% FEV1%

N N or N N or


Pulmonary Function Study: Pulmonary Function Study: Lung Volume and Capacity Findings Lung Volume and Capacity Findings

VT RV FRC TLC

N or

VC IC ERV RV/TLC%

N

VT RV FRC TLC

N or

VC IC ERV RV/TLC%

N


Arterial Blood GasesArterial Blood Gases

Mild to Moderate Pulmonary EdemaMild to Moderate Pulmonary Edema

Acute alveolar hyperventilation with Acute alveolar hyperventilation with hypoxemiahypoxemia

pH PaCO2 HCO3- PaO2

(Slightly)

pH PaCO2 HCO3- PaO2

(Slightly)


Time and Progression of Disease Time and Progression of Disease

100100

5050

3030

8080

00

PaCO2

1010

2020

4040

Alveolar HyperventilationAlveolar Hyperventilation

6060

7070

9090 Point at which PaO2 declines enough to stimulate peripheral oxygen receptors

Point at which PaO2 declines enough to stimulate peripheral oxygen receptors

PaO2

Disease OnsetDisease OnsetP

aO2

or

PaC

O2

PaO

2 o

r P

aCO

2

Figure 4-2. PaO2 and PaCO2 trends during acute alveolar hyperventilation.


Arterial Blood GasesArterial Blood Gases

Severe Pulmonary EdemaSevere Pulmonary Edema

Acute ventilatory failure with hypoxemiaAcute ventilatory failure with hypoxemia

pH PaCO2 HCO3- PaO2

(slightly)

pH PaCO2 HCO3- PaO2

(slightly)


Time and Progression of DiseaseTime and Progression of Disease

100100

5050

3030

80

0

PaO2

1010

2020

4040

Alveolar HyperventilationAlveolar Hyperventilation

6060

7070

9090Point at which PaO2 declines enough to stimulate peripheral oxygen receptors

Point at which PaO2 declines enough to stimulate peripheral oxygen receptors

PaCO 2

Acute Ventilatory Failure Acute Ventilatory FailureDisease OnsetDisease Onset

Point at which disease becomes severe and patient begins to become fatigued

Point at which disease becomes severe and patient begins to become fatigued

Pa0

2 o

r P

aC0 2

Pa0

2 o

r P

aC0 2

Figure 4-7. PaO2 and PaCO2 trends during acute ventilatory failure.


Oxygenation IndicesOxygenation Indices

QS/QT DO2 VO2 C(a-v)O2

Normal Normal

O2ER SvO2

QS/QT DO2 VO2 C(a-v)O2

Normal Normal

O2ER SvO2


Hemodynamic Indices Hemodynamic Indices (Cardiogenic Pulmonary Edema)(Cardiogenic Pulmonary Edema)

CVP RAP PA PCWP

CO SV SVI CI

RVSWI LVSWI PVR SVR

CVP RAP PA PCWP

CO SV SVI CI

RVSWI LVSWI PVR SVR


Abnormal Laboratory Tests and Abnormal Laboratory Tests and ProceduresProcedures

Serum potassium: lowSerum potassium: low

Serum sodium: lowSerum sodium: low

Hypokalemia and hyponatremia are often Hypokalemia and hyponatremia are often seen in patients with left-sided heart failure seen in patients with left-sided heart failure and may result from diuretic therapy or and may result from diuretic therapy or excessive fluid retentionexcessive fluid retention


Radiologic FindingsRadiologic Findings

Chest radiographChest radiograph

Fluffy opacitiesFluffy opacities

Left ventricular hypertrophyLeft ventricular hypertrophy

Kerley A and B linesKerley A and B lines

Pleural effusionPleural effusion


Figure 19-2. Cardiomegaly (Figure 19-2. Cardiomegaly (arrowarrow) and pulmonary edema in congestive heart failure.) and pulmonary edema in congestive heart failure.


General Management of General Management of Pulmonary EdemaPulmonary Edema

Respiratory care treatment protocolsRespiratory care treatment protocols

Oxygen therapy protocolOxygen therapy protocol

Bronchopulmonary hygiene therapy protocolBronchopulmonary hygiene therapy protocol

Hyperinflation therapy protocolHyperinflation therapy protocol

Aerosolized medication protocolAerosolized medication protocol



Medications and procedures commonlyMedications and procedures commonlyprescribed by the physicianprescribed by the physician

Positive inotropic agentsPositive inotropic agents

Afterload reduction agentsAfterload reduction agents

Morphine sulfateMorphine sulfate

Diuretic agentsDiuretic agents



Medications and procedures commonlyMedications and procedures commonlyprescribed by the physicianprescribed by the physician

Albumin and mannitolAlbumin and mannitol

Alcohol (ethanol, ethyl alcohol)Alcohol (ethanol, ethyl alcohol)

Decreasing hydrostatic pressureDecreasing hydrostatic pressure Positioning the patient in Fowler’s positionPositioning the patient in Fowler’s position

Rotating tourniquets (rarely used)Rotating tourniquets (rarely used)

Phlebotomy (rarely used)Phlebotomy (rarely used)


Classroom DiscussionClassroom DiscussionCase Study: Case Study:

Pulmonary EdemaPulmonary Edema

copyright © 2006 by mosby, inc. slide 1 part iv pulmonary vascular diseases

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