Pulmonary Edema
Abnormal accumulation of fluid from pulmonary vascular system into lung parenchyma
Anatomical Changes of Pulmonary Edema
Interstitial Edema
Alveolar Flooding
Increased Surface Tension of Alveolar Fluids
Alveolar Shrinkage and Atelectasis
Frothy White/Pink Secretions
Cardiogenic Pulmonary Edema
Occurs when left ventricle is unable to pump out sufficient amount of blood during ventricular contraction
Noncardiogenic Pulmonary Edema
Develops due to damage to the lungs
What causes cardiogenic pulmonary edema?
CHF and Other Heart Diseases
Congenital Heart Defects
Excessive Fluid Administration
Pulmonary Emboli
Renal Failure
How do you diagnose cardiogenic pulmonary edema?
Echocardiogram
LVEF = < 40% may confirm heart failure
What are possible causes of noncardiogenic pulmonary edema?
Increased Capillary Permeability
Lymphatic Insufficiency
Decreased Intrapleural Pressure
High-Altitude
Decreased Oncotic Pressure
Examples of Decreased Oncotic Pressure
Severe Malnutrition
Over Transfusion of Hypotonic IV Fluids
Abnormal Labs Found with Pulmonary Edema
Low Potassium
Low Sodium
Low Chloride
Elevated BNP ——> Cardiac Indicator
X-Rays Findings of Cardiogenic Pulmonary Edema
Enlarged Heart - Cardiomegaly
‘Bat’s Wing’ or ‘Butterfly’ Patterns
Pleural Effusion
Kerley A and B Lines
X-Ray Findings of Noncardiogenic Pulmonary Edema
Granular / Ground Glass Appearance
Reticulograndular or Honeycombing
Bilateral Fluffy Opacities with a Predominantly Central Position in the Chest
Management of Cardiogenic Pulmonary Edema
Initial Management
Therapeutic Intervention
Preload Reduction
Afterload Reduction
Treatment of Reduced Cardiac Contractility
Other Agents
Management of Noncardiogenic Pulmonary Edema
Largely Supportive (i.e. adequate oxygenation and ventilation)
No Specific Treatment, except for Specific Infections or High Altitude
Pleural Effusion
Fluid that accumulates in pleural space
Restrictive Disorder
Shunt
Empyema
When fluid in the pleural space is infected
Hydrostatic Pressure
Mainly a function of the arterial circulation
Creates the ‘push’ pressure on the walls of the vessels
Oncotic Pressure
Reflects largely the protein concentration in the blood and lymphatic vessels
Creates the ‘pull’ pressure to pull fluid into the vessels
Transudative Pleural Effusions
Develops when fluid from the pulmonary capillaries moves into pleural space
Thin
Watery
Contains Few Blood Cells
Contains Little Protein
High Hydrostatic Pressure
Exudative Pleural Effusions
Develops when pleural surfaces are diseases
High Protein Content
High Cellular Debris
Lymphatic System is Not Working Properly
Usually Caused by Infection or Cancer
High Oncotic Pressure
Causes of Transudative Pleural Effusions
CHF - Most Commom
Pulmonary Embolism
Peritoneal Dialysis
Nephrotic Syndrome
Hepatic Hydrothorax
Causes of Exudative Pleural Effusions
Empyema
Fungal Diseases
TB
Pneumonia
Cancer
Signs and Symptoms of Pleural Effusions
Tachypnea, Tachycardia, Increased BP, Chest Pain, Dry Nonproductive Cough, Dyspnea, Decreased Chest Expansion, Cyanosis, Chest Pressure when Effusions is about 500-1500mL, Tracheal Shift Away from Affected Side, Dull Percussion Note, Pleural Friction Rub (Occasionally), Decreased Tactile and Vocal Fremitus
ABG’s of Mild Pleural Effusion
High pH
Low PaCO2
Low PaO2
Normal HCO3
ABG’s of Moderate/Severe Pleural Effusion
Low pH
High PaCO2
Low PaO2
Normal HCO3
General Treatment of Pleural Effusions
Best Way to Resolve Pleural Effusion is to Treat Underlying Cause.
Thoracentesis
Appropriate Antibiotic
Chest Tube in Severe Cases
Specific Treatment for Transudative Pleural Effusion
Lower BP
Diuretics
Give Proteins
Specific Treatment for Exudative Pleural Effusion
Test for Bacteria and Give Antibiotics
Cytologic Exam to Identify Cancer
2 Disorders of COPD
Emphysema
Chronic Bronchitis
Chronic Bronchitis
Chronic Productive Cough for 3 Months in each of 2 Successive Years in a Patient in Whom Other Causes of Productive Chronic Cough Have Been Excluded
Emphysema
The Presence of Permanent Enlargement of the Air Spaces Distal to the Terminal Bronchioles, Accompanied by Destruction of Bronchiole Walls and Without Obvious Fibrosis
Structures Affected by Chronic Bronchitis
Conducting Airways Especially the Bronchi
Structures Affected by Emphysema
Alveoli
Dysfunction Caused by Chronic Bronchitis
Smooth Muscle Constriction
Mucus Plugging
Hyperinflated Alveoli
Enlarged Submucosal Glands
Mucus Accumulation
Epithelial Inflammation
Why are Patients Who Have Chronic Bronchitis Called Blue Bloaters?
Cyanosis
Overweight
Fluid Retention
Why are Patients Who Have Emphysema Called Pick Puffers?
Flushed Skin
‘Puffing’ from Pursed-Lip Breathing
2 Types of Emphsema
Panacinar (Panlobular)
Centriacinar (Centrilobular)
Panacinar (Panlobular) Emphysema
Abnormal Weakening and Enlargement of ALL Alveoli Distal to the Terminal Bronchioles
Centriacinar (Centrilobular) Emphysema
Involves the Respiratory Bronchioles Proximal (Central) Portion of the Acinus
Most Common Form of Emphysema
Acinus
A region of the lung supplied with air from one of the terminal bronchioles
Emphysema Percussion Sound
Hperresonnant due to Air Trapping
Polycythemia
High Levels of RBCs
Common in Patients with Chronic Bronchitis
Genetic Disorder that Causes Early Onset of Emphysema/COPD
Alpha-1 Antitrypsin Deficiency (ATT1)
Alpha-1 Antitrypsin Deficiency (AAT1)
Protease Inhibitor
Without it Patient Experiences Damaged Airways
Normal Range: 150 - 350mg
Spirometry Test for Diagnosing COPD
Post-Bronchodilator FEV1/FVC
For Diagnosis Patient must Score Less than 70%
Normal Range is Greater Than or Equal to 70%
Score on mMRC to be Considered High-Risk for Severe COPD Exacerbations
Score > 2 is High-Risk
Score on CAT to be Considered High-Risk for Severe COPD Exacerbations
Score > 10 is High Risk
SpO2 Goals for COPD Patients
Target is 88% - 92%
Symptoms of Cor Pulmonale
Enlarged Heart
Right-Sided Heart Failure
Swollen Ankles and Legs
Distended Neck Veins
Gold 1 Standard for COPD - Mild
FEV1 ≥ 80% Predicted
Gold 2 Standard for COPD - Moderate
50% ≤ FEV1 < 80% Predicted
Gold 3 Standard for COPD - Severe
30% ≤ FEV1 < 50% Predicted
Gold 4 Standard for COPD - Very Severe
FEV1 < 30% Predicted
Cystic Fibrosis
Progressive Genetic Disease that can Affect Lungs, Pancreas, Liver, and Sweat Glands
What Causes CF?
Mutations of the CFTR Gene Causes to Become Dysfunctional
Creates an Inability to Transport Sodium and Chloride Across Epithelial Surfaces
Most Common Defect of CF
ΔF508
Gating Defect (Class III) of CF
Channel Doesn’t Open
Conductance Defect (Class IV) of CF
Channel is Open, but Chloride Doesn’t Move Effectively
Common Gram Negative Bacteria Found in CF Patients
Pseudomonas Aeruginosa
Burkholderia Cepacia Complex (Most Dangerous)
Common Gram Positive Bacteria Found in CF Patients
Staphylococcus Aureus
Immunoreactive Trypsin (IRT)
Test Performed on All Newborns on Birth
Detection of Atleast 1 CF Mutation is Considered a Positive Screen for CF
Most Reliable Test in Diagnosing CF?
Sweat Chloride Test
x > 60 mmol/L
Nonallergic / Nonatopic / Intrinsic Asthma
Onset Seen in Adults After Age 40
Not Related to Hypersensitivity to Antigens
Does Not Respond Well to ICS Therapy
Causes / Irritants of Intrinsic Asthma
Cold Air
Infections
Emotional Stress
Exercise
Dust
Drugs
Smoke
Allergic / Atopic / Extrinsic Asthma
Typically Appears in Childhood
Sputum Contains Eosinophils
Is Considered Type 1 (Immediate Hypersensitivity Reaction)
Elevated IgE Levels
Common Vital Signs of Asthma Exacerbation
Tachypnea
Tachycardia
Hypertension
Pulsus Paradoxus
Bronchial Provocation Test
Most Often Using Inhaled Methacholine to Provoke Bronchospasm in a Controlled Environment
Atopy
Genetic Disposition to Develop Allergic Diseases
Associated with Overproduction of IgE to Specific Antigen
FeNO
Fractional Concentration of Nitric Oxide
Increased Levels are Caused by Airway Inflammation
Normal Range:
Adult: < 25 ppb
Children = < 20ppb
What is Prescribed for High FeNO Levels?
Inhaled Corticosteroids (ICS)