copyright © 2006 by mosby, inc. slide 1 part iv pulmonary vascular diseases
TRANSCRIPT
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PART IVPART IV
Pulmonary Vascular DiseasesPulmonary Vascular Diseases
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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
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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
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EtiologyEtiology
Cardiogenic pulmonary edemaCardiogenic pulmonary edema Congestive heart failureCongestive heart failure
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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
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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
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EtiologyEtiology
Lymphatic insufficiencyLymphatic insufficiency
Decreased intrapleural pressureDecreased intrapleural pressure
Decreased oncotic pressureDecreased oncotic pressure OvertransfusionOvertransfusion
UremiaUremia
HypoproteinemiaHypoproteinemia
Acute nephritisAcute nephritis
Polyarteritis nodosaPolyarteritis nodosa
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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)
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Figure 9-7. Atelectasis clinical scenario.Figure 9-7. Atelectasis clinical scenario.
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Figure 9-9. Increased alveolar-capillary membrane thickness clinical scenario.Figure 9-9. Increased alveolar-capillary membrane thickness clinical scenario.
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Figure 9-11. Excessive bronchial secretions clinical scenario.Figure 9-11. Excessive bronchial secretions clinical scenario.
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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
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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
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Clinical Data Obtained from Clinical Data Obtained from Laboratory Tests andLaboratory Tests andSpecial ProceduresSpecial Procedures
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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
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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
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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)
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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.
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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)
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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.
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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
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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
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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
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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
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Figure 19-2. Cardiomegaly (Figure 19-2. Cardiomegaly (arrowarrow) and pulmonary edema in congestive heart failure.) and pulmonary edema in congestive heart failure.
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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
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General Management of General Management of Pulmonary EdemaPulmonary Edema
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
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General Management of General Management of Pulmonary EdemaPulmonary Edema
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)
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Classroom DiscussionClassroom DiscussionCase Study: Case Study:
Pulmonary EdemaPulmonary Edema