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“When you’re a
nurse
you know that
every day
you will touch a life
or
a life will touch
yours”
PULMONARY EDEMA

Presented By,
Mr. Thomaskutty, RN, MSN,
Accident and Emergency, Fujairah
DEFINITION
Pulmonary edema is a condition
characterized by fluid accumulation in the
lungs caused by extravasations of fluid
from pulmonary vasculature into the
alveoli and interstitial spaces of the lungs
ANATOMY AND PHYSIOLOGY
Lower Respiratory Tract

(Cont.)
Respiratory Bronchioles, Alveolar (Cont.)
Ducts, and Alveoli
• Lungs contain small saccular outpocketings
called alveoli.
• They have a thin wall specialized to promote
diffusion of gases between the alveolus and the
blood in the pulmonary capillaries.
• Gas exchange can take place in the
respiratory bronchioles and alveolar ducts
as well as in the alveoli
• The spongy nature of the lung is due to the
packing of millions of alveoli together.
Surfactant

(Cont.)
Capillary Network

(Cont.)
(Cont.)
Respiratory Membrane
Cells in Alveolus
 Type I cells :
simple squamous cells
forming lining
 Type II cells :
or septal cells secrete
surfactant
 Alveolar macrophages
(Cont.)

Normal Physiology
Hydrostatic pressure increases or
Oncotic pressure decreases

Interstitial Edema
Continues
leak

Lymphatics drain
excess fluid

Alveolar edema
EPIDEMIOLOGY
• Pulmonary edema occurs in about 1% to 2% of
the general population.
• Between the ages of 40 and 75 years, males are
affected more than females.

• After the age of 75 years, males and females are
affected equally.
• The incidence of pulmonary edema increases
with age and may affect about 10% of the
population over the age of 75 years.
CLASSIFICATION
• BASED ON INCITING
MECHANISM
• BASED ON UNDERLINING
CAUSE
A. BASED ON INCITING MECHANISM
1. IMBALANCE OF STARLING FORCE
A. Increased pulmonary capillary pressure
-left ventricular failure
-Volume overload
B. Decreased plasma oncotic pressure
- Hypoalbuminemia due to different cause
C. Increased negativity of interstitial pressure
-Rapid removal of pneumothorax with
large applied negative pressures (unilateral)
Abst
ract

• Study:
Pulmonary edema related to changes in colloid osmotic
and pulmonary artery wedge pressure in patients after
acute myocardial infarction
• Samples:
26 patients with acute myocardial infarction of whom 14
developed pulmonary edema
• Findings:
Both increases in pulmonary capillary pressure and
decreases in colloid osmotic pressure leads to pulmonary
edema
(P L Luz da; H Shubin; M H Weil; E Jacobson)
BASED ON INCITING AGENT…..

2. ALTERED ALVEOLAR-CAPILLARY
MEMBRANE PERMEABILITY
o
o
o
o
o
o
o
o

Infectious pneumonia
Inhaled toxins, Aspiration
Circulating foreign substances
Endogenous vasoactive substances
Disseminated intravascular coagulation
Immunologic—hypersensitivity pneumonitis, drugs
Shock lung in association with non-thoracic trauma
Acute hemorrhagic pancreatitis
BASED ON INCITING AGENT…..

(Cont.)

3. LYMPHATIC INSUFFICIENCY

After lung transplant
Lymphangitic carcinomatosis

Fibrosing lymphangitis
BASED ON INCITING AGENT…..

(Cont.)

4. UNKNOWN OR INCOMPLETELY UNDERSTOOD

High-altitude pulmonary edema
Neurogenic pulmonary edema
Narcotic overdose
Pulmonary embolism
Eclampsia
After anesthesia
After cardiopulmonary bypass
B. BASED ON UNDERLINING CAUSE
Cardiogenic pulmonary edema
Due to increased pressure in the pulmonary
capillaries because of cardiac abnormalities
Increase in pulmonary venous pressure
Non- cardiogenic pulmonary edema
Evidence of alveolar fluid accumulation without
hemodynamic evidence
Hydrostatic pressure is normal
Leakage of protein and other molecule into the
tissue
PATHOGENESIS OF CPE
Congestion &
accumulation of
blood in the
pulmonary area

Decrease
pumping ability
to the systemic
circulation
Left sided
heart failure

Fluid leaks out of the
intravascular space to
the interstitium

Accumulation of
fluid

Pulmonary
edema
STAGING OF PE
Based on the degree of fluid accumulation:
Stage-1
All excess fluid can still be cleared by lymphatic
drainage.
Stage-2
Presence of interstitial edema
Stage-3
Alveolar edema due to altered alveolar- capillary
permeability
(Cont.)
Mild:
Only engorgement of pulmonary vasculature
Moderate:
Extravasations of fluid into the interstitial
space due to changes in oncotic pressure
Severe:
Alveolar filling occurs
Causes of Pulmonary Edema
o Congestive Cardiac Failure
o Over hydration with intravenous Fluids
o Hypoalbuminemia:
Nephrotic Syndrome
Hepatic disease
Nutritional Disorders
oMalignancies of lymph system
Causes of Pulmonary Edema (Cont.)
o Altered Capillary Permeability of Lungs

Inhaled Toxins
Inflammation
Severe Hypoxia
o Respiratory Distress Syndrome
o Unknown Causes

Neurogenic Conditions
Narcotic Overdose
High altitude
Abst
ract

• Study:
Transfusion-related acute lung injury and pulmonary
edema in critically ill patients: a retrospective study
• Samples:
Consecutive patients at four intensive care units (ICUs)
• Findings:
94 required new respiratory support within 6 hours of
transfusion
Among 49 patients with confirmed acute pulmonary
edema, experts identified 7 cases with suspected TRALI
• Conclusion:
In the ICU, pulmonary edema frequently occurs after blood
transfusion
(Rana R, Fernández-Pérez ER, Khan SA, Rana S)
Clinical Manifestations
• Sudden onset of Dyspnea -

Orthopnea, Paroxysmal Nocturnal Dyspnea
• Agitated, Pale and possibly Cyanotic

• Restlessness and Irritability
• Skin- Clammy and Cold
Clinical Manifestations (Cont.)
•
•
•
•

Wheezing and Coughing
Distended Jugular Veins
Noisy wet respiration
On Auscultation- Bubbling Crackles, Wheezes
and Rhonchi
• HR is rapid
• BP- Elevated or Decreased
Differential diagnosis
Pneumothorax
Bronchitis
Cardiac tamponed
COPD
Pericarditis
Pneumonia (bacterial ,viral , PCP)
Pulmonary embolism
Shocks (Cardiogenic ,septic ,anaphylactic)
Venous air embolism
DIAGNOSTIC STUDY
 History and Physical Examination
 Blood studies
Routine; CBC
Liver function tests
Renal Function Tests
Arterial blood gas analysis
Serum cardiac biomarkers
(Cont.)
 Chest X-Ray
 Hemodynamic Monitoring
 Twelve-lead ECG
 Echocardiogram
 Nuclear imaging studies
 Cardiac Catheterization
MEDICAL MANAGEMENT
•
•
•
•
•
•

Improving gas exchange and Oxygenation
Improved cardiac function
Decreased Intravascular Volume
Decreased venous return
Decreased afterload
Reducing Anxiety
DRUG THERAPY
•
•
•
•
•

Morphine
Diuretics
Digitalis
Nitroglycerin
Sodium Nitroprusside
(Cont.)
• Isotropic Therapy
• Digitalis Preparation
• Beta- Adrenergic agonists
• Phosphodiesterase Inhibitor (Milrinone)
• Calcium Sensitizing Agent
(Levosimendan)
• Human B-type natriuretic peptide
• Nesiritide
NURSING DIAGNOSIS
1. Ineffective breathing pattern
related to: fatigue and breathing aids
installation
2. Impaired gas exchange
related to: distention of pulmonary capillaries
NURSING DIAGNOSIS
3. Risk for infection
related to: the invasion of microorganisms area
secondary to endotracheal tube installation

4. Ineffective tissue perfusion
related to: decreased cardiac muscle
contractility
NURSING DIAGNOSIS (CONT.)
5. Risk for Injury / trauma
related to: anxiety secondary to the installation of
breathing aids
6. Anxiety
related to: the threat of biological integrity
secondary to the actual installation of breathing
aids
NURSING DIAGNOSIS (CONT.)
7. Impaired verbal communication
related to: installation of endotracheal tube
COMMON INTERVENTIONS
• Oxygen

• High Fowlers position
• Legs in dependent position
• Activity restrictions
• Emotional rest
• Allay the anxiety
• Monitor ECG,

S. electrolytes
COMMON INTERVENTIONS (CONT.)
• Small meals than larger ones
• Monitor weight daily
• Maintain intake & output chart
• Restrict sodium & fluid intake
• Self care needs
• Increase activity gradually & as tolerated
• Medications

• Watch for complications of treatment such as
electrolyte depletion
COMPLICATION
 Leg swelling(edema)
 Abdominal swelling (ascites)
 Pleural effusion
 Congestion & swelling of liver
 Acute heart attack (myocardial infarction [MI])
 Cardiogenic shock
 Arrhythmias
 Electrolyte disturbances
 Protein enteropathy
 Respiratory arrest
 Death
• Emphasize reporting early signs of fluid overload
• Review all prescribed medications with the
patient and Family
• Discuss ways to observe physical energy
• Teach the patient- How to take slow and deep
breath
• Na restricted dietary pattern
• Need to monitor weight gain
EXPECTED OUTCOMES:
 O2 Sat - >95%
 RR 12 to 20 breaths/min
 Airway Patency
- open, clear tracheobronchial passages
 ABG
• PH 7.35-7.45
• Pa02 80 to 100 mm of Hg
• PaCo2 35 to 45 mm of Hg

 Knowledge: Medications
BIBLIOGRAPHY
Lewis, Heitkemper, Dirksen (2004), MedicalSurgical Nursing, 6th Edition, Mosby,840-853
Manual of Medical & Surgical Nursing Care,
Nursing Intervention and Collaborative
management , 5th Edition, Mosby, 191-195

Lippincott, Manual of Nursing Practice, 8th
Edition, 416-417
(Cont.)
Givertz MM, Colucci WS, Braunwald
E(2005),
Textbook
of
Cardiovascular
Medicine,
7th
ed,
Elsevier
Saunders, Philadelphia,539
Pul edema
Pul edema

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Pul edema

  • 1. “When you’re a nurse you know that every day you will touch a life or a life will touch yours”
  • 2. PULMONARY EDEMA Presented By, Mr. Thomaskutty, RN, MSN, Accident and Emergency, Fujairah
  • 3. DEFINITION Pulmonary edema is a condition characterized by fluid accumulation in the lungs caused by extravasations of fluid from pulmonary vasculature into the alveoli and interstitial spaces of the lungs
  • 6. Respiratory Bronchioles, Alveolar (Cont.) Ducts, and Alveoli • Lungs contain small saccular outpocketings called alveoli. • They have a thin wall specialized to promote diffusion of gases between the alveolus and the blood in the pulmonary capillaries. • Gas exchange can take place in the respiratory bronchioles and alveolar ducts as well as in the alveoli • The spongy nature of the lung is due to the packing of millions of alveoli together.
  • 11. Cells in Alveolus  Type I cells : simple squamous cells forming lining  Type II cells : or septal cells secrete surfactant  Alveolar macrophages
  • 12. (Cont.) Normal Physiology Hydrostatic pressure increases or Oncotic pressure decreases Interstitial Edema Continues leak Lymphatics drain excess fluid Alveolar edema
  • 13. EPIDEMIOLOGY • Pulmonary edema occurs in about 1% to 2% of the general population. • Between the ages of 40 and 75 years, males are affected more than females. • After the age of 75 years, males and females are affected equally. • The incidence of pulmonary edema increases with age and may affect about 10% of the population over the age of 75 years.
  • 14. CLASSIFICATION • BASED ON INCITING MECHANISM • BASED ON UNDERLINING CAUSE
  • 15. A. BASED ON INCITING MECHANISM 1. IMBALANCE OF STARLING FORCE A. Increased pulmonary capillary pressure -left ventricular failure -Volume overload B. Decreased plasma oncotic pressure - Hypoalbuminemia due to different cause C. Increased negativity of interstitial pressure -Rapid removal of pneumothorax with large applied negative pressures (unilateral)
  • 16. Abst ract • Study: Pulmonary edema related to changes in colloid osmotic and pulmonary artery wedge pressure in patients after acute myocardial infarction • Samples: 26 patients with acute myocardial infarction of whom 14 developed pulmonary edema • Findings: Both increases in pulmonary capillary pressure and decreases in colloid osmotic pressure leads to pulmonary edema (P L Luz da; H Shubin; M H Weil; E Jacobson)
  • 17. BASED ON INCITING AGENT….. 2. ALTERED ALVEOLAR-CAPILLARY MEMBRANE PERMEABILITY o o o o o o o o Infectious pneumonia Inhaled toxins, Aspiration Circulating foreign substances Endogenous vasoactive substances Disseminated intravascular coagulation Immunologic—hypersensitivity pneumonitis, drugs Shock lung in association with non-thoracic trauma Acute hemorrhagic pancreatitis
  • 18. BASED ON INCITING AGENT….. (Cont.) 3. LYMPHATIC INSUFFICIENCY After lung transplant Lymphangitic carcinomatosis Fibrosing lymphangitis
  • 19. BASED ON INCITING AGENT….. (Cont.) 4. UNKNOWN OR INCOMPLETELY UNDERSTOOD High-altitude pulmonary edema Neurogenic pulmonary edema Narcotic overdose Pulmonary embolism Eclampsia After anesthesia After cardiopulmonary bypass
  • 20. B. BASED ON UNDERLINING CAUSE Cardiogenic pulmonary edema Due to increased pressure in the pulmonary capillaries because of cardiac abnormalities Increase in pulmonary venous pressure Non- cardiogenic pulmonary edema Evidence of alveolar fluid accumulation without hemodynamic evidence Hydrostatic pressure is normal Leakage of protein and other molecule into the tissue
  • 21. PATHOGENESIS OF CPE Congestion & accumulation of blood in the pulmonary area Decrease pumping ability to the systemic circulation Left sided heart failure Fluid leaks out of the intravascular space to the interstitium Accumulation of fluid Pulmonary edema
  • 22. STAGING OF PE Based on the degree of fluid accumulation: Stage-1 All excess fluid can still be cleared by lymphatic drainage. Stage-2 Presence of interstitial edema Stage-3 Alveolar edema due to altered alveolar- capillary permeability
  • 23. (Cont.) Mild: Only engorgement of pulmonary vasculature Moderate: Extravasations of fluid into the interstitial space due to changes in oncotic pressure Severe: Alveolar filling occurs
  • 24. Causes of Pulmonary Edema o Congestive Cardiac Failure o Over hydration with intravenous Fluids o Hypoalbuminemia: Nephrotic Syndrome Hepatic disease Nutritional Disorders oMalignancies of lymph system
  • 25. Causes of Pulmonary Edema (Cont.) o Altered Capillary Permeability of Lungs Inhaled Toxins Inflammation Severe Hypoxia o Respiratory Distress Syndrome o Unknown Causes Neurogenic Conditions Narcotic Overdose High altitude
  • 26. Abst ract • Study: Transfusion-related acute lung injury and pulmonary edema in critically ill patients: a retrospective study • Samples: Consecutive patients at four intensive care units (ICUs) • Findings: 94 required new respiratory support within 6 hours of transfusion Among 49 patients with confirmed acute pulmonary edema, experts identified 7 cases with suspected TRALI • Conclusion: In the ICU, pulmonary edema frequently occurs after blood transfusion (Rana R, Fernández-Pérez ER, Khan SA, Rana S)
  • 27. Clinical Manifestations • Sudden onset of Dyspnea - Orthopnea, Paroxysmal Nocturnal Dyspnea • Agitated, Pale and possibly Cyanotic • Restlessness and Irritability • Skin- Clammy and Cold
  • 28. Clinical Manifestations (Cont.) • • • • Wheezing and Coughing Distended Jugular Veins Noisy wet respiration On Auscultation- Bubbling Crackles, Wheezes and Rhonchi • HR is rapid • BP- Elevated or Decreased
  • 29. Differential diagnosis Pneumothorax Bronchitis Cardiac tamponed COPD Pericarditis Pneumonia (bacterial ,viral , PCP) Pulmonary embolism Shocks (Cardiogenic ,septic ,anaphylactic) Venous air embolism
  • 30. DIAGNOSTIC STUDY  History and Physical Examination  Blood studies Routine; CBC Liver function tests Renal Function Tests Arterial blood gas analysis Serum cardiac biomarkers
  • 31. (Cont.)  Chest X-Ray  Hemodynamic Monitoring  Twelve-lead ECG  Echocardiogram  Nuclear imaging studies  Cardiac Catheterization
  • 32. MEDICAL MANAGEMENT • • • • • • Improving gas exchange and Oxygenation Improved cardiac function Decreased Intravascular Volume Decreased venous return Decreased afterload Reducing Anxiety
  • 34. (Cont.) • Isotropic Therapy • Digitalis Preparation • Beta- Adrenergic agonists • Phosphodiesterase Inhibitor (Milrinone) • Calcium Sensitizing Agent (Levosimendan) • Human B-type natriuretic peptide • Nesiritide
  • 35. NURSING DIAGNOSIS 1. Ineffective breathing pattern related to: fatigue and breathing aids installation 2. Impaired gas exchange related to: distention of pulmonary capillaries
  • 36. NURSING DIAGNOSIS 3. Risk for infection related to: the invasion of microorganisms area secondary to endotracheal tube installation 4. Ineffective tissue perfusion related to: decreased cardiac muscle contractility
  • 37. NURSING DIAGNOSIS (CONT.) 5. Risk for Injury / trauma related to: anxiety secondary to the installation of breathing aids 6. Anxiety related to: the threat of biological integrity secondary to the actual installation of breathing aids
  • 38. NURSING DIAGNOSIS (CONT.) 7. Impaired verbal communication related to: installation of endotracheal tube
  • 39. COMMON INTERVENTIONS • Oxygen • High Fowlers position • Legs in dependent position • Activity restrictions • Emotional rest • Allay the anxiety • Monitor ECG, S. electrolytes
  • 40. COMMON INTERVENTIONS (CONT.) • Small meals than larger ones • Monitor weight daily • Maintain intake & output chart • Restrict sodium & fluid intake • Self care needs • Increase activity gradually & as tolerated • Medications • Watch for complications of treatment such as electrolyte depletion
  • 41. COMPLICATION  Leg swelling(edema)  Abdominal swelling (ascites)  Pleural effusion  Congestion & swelling of liver  Acute heart attack (myocardial infarction [MI])  Cardiogenic shock  Arrhythmias  Electrolyte disturbances  Protein enteropathy  Respiratory arrest  Death
  • 42. • Emphasize reporting early signs of fluid overload • Review all prescribed medications with the patient and Family • Discuss ways to observe physical energy • Teach the patient- How to take slow and deep breath • Na restricted dietary pattern • Need to monitor weight gain
  • 43. EXPECTED OUTCOMES:  O2 Sat - >95%  RR 12 to 20 breaths/min  Airway Patency - open, clear tracheobronchial passages  ABG • PH 7.35-7.45 • Pa02 80 to 100 mm of Hg • PaCo2 35 to 45 mm of Hg  Knowledge: Medications
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  • 46. BIBLIOGRAPHY Lewis, Heitkemper, Dirksen (2004), MedicalSurgical Nursing, 6th Edition, Mosby,840-853 Manual of Medical & Surgical Nursing Care, Nursing Intervention and Collaborative management , 5th Edition, Mosby, 191-195 Lippincott, Manual of Nursing Practice, 8th Edition, 416-417
  • 47. (Cont.) Givertz MM, Colucci WS, Braunwald E(2005), Textbook of Cardiovascular Medicine, 7th ed, Elsevier Saunders, Philadelphia,539