Pathophys 1 Exam 3 ( PULMONARY EDEMA)

Alveoli

◦Primary gas-exchange units

◦Pores of Kohn

◦Permit air to pass through the septa from alveolus to alveolus

◦Collateral ventilation and even air distribution

Lungs contain approximately 25 million alveoli at birth and 300 million by adulthood

Pulmonary and Bronchial Circulation

Alveolocapillary membrane

◦Formed by shared alveolar and capillary walls

◦Thin membrane of alveolar epithelium, the alveolar basement membrane, interstitial space, the capillary basement membrane, and the capillary endothelium

Requirements for Ventilation, Perfusion, and Diffusion

Adequate inspired O2 - (FiO2)

Ventilation and perfusion of alveoli

A permeable alveolocapillary membrane

Adequate blood flow

Ability to transport O2 and CO2

Ability of cell to use O2 and eliminate CO2

Surface Tension of Water

Tendency of water molecules to contract to the smallest possible surface area (bead) with exposure to air

Increased surface tension = increased work of breathing

Laplace's Law

The smaller a sphere's radius (alveoli) the greater the surface tension and the more difficult (work) to expand the alveoli

Surfactant reduces fluid surface tension lining the alveoli and decreases tendency to collapse, preventing atelectasis

Gas Transport

Four steps

◦Ventilation of the lungs

◦Diffusion of oxygen from the alveoli into the capillary blood

◦Perfusion of systemic capillaries with oxygenated blood

◦Diffusion of oxygen from systemic capillaries into the cells

Diffusion of CO2 occurs in reverse order

Introduction to Pulmonary Edema

Accumulation of fluid in lung interstitium and alveoli

Impaired gas exchange → hypoxia

Common cause of respiratory distress

Normal Pulmonary Fluid Balance

Maintained by Starling forces

Low pulmonary capillary hydrostatic pressure

Effective lymphatic drainage

Starling Equation

Fluid movement = Kf [(Pc - Pi) - σ(πc - πi)]

Kf = filtration coefficient

Pc = capillary hydrostatic pressure

πc = capillary oncotic pressure

Mechanisms of Pulmonary Edema

1. Increased hydrostatic pressure

2. Decreased oncotic pressure

3. Increased capillary permeability

4. Lymphatic obstruction

Lymphatic Role in Pulmonary Edema

Drain excess fluid from interstitium

Obstruction or overload can exacerbate edema

Chronic edema may impair lymphatic clearance

Gas Exchange Impairment

Fluid in alveoli blocks oxygen diffusion

V/Q mismatch and shunt physiology

Hypoxia and dyspnea result

Clinical Features

Dyspnea, orthopnea, crackles on auscultation

Pink frothy sputum (severe cases)

Tachypnea, hypoxia, cyanosis

Radiologic Findings

Cardiogenic: Kerley B lines, perihilar infiltrates, cardiomegaly

Non-cardiogenic: bilateral infiltrates, normal heart size

CT may show ground-glass opacities

Cardiogenic Pulmonary Edema

Due to elevated left atrial pressure

Common causes: LV failure, mitral stenosis

↑ Pulmonary capillary hydrostatic pressure

Hemodynamic Changes in Cardiogenic Edema

Backward transmission of pressure

Fluid leaks into interstitium → alveoli

Often seen in congestive heart failure

Non-Cardiogenic Pulmonary Edema

Normal cardiac pressures

Caused by increased capillary permeability

Etiologies: ARDS, sepsis, aspiration, trauma

Capillary Leak Syndrome

Endothelial damage → protein-rich fluid

Inflammatory cytokines: TNF-α, IL-1

Seen in ARDS and infections

Acute Respiratory Distress Syndrome (ARDS)

Severe form of non-cardiogenic edema

Diffuse alveolar damage and inflammation

Leads to hypoxemia and stiff lungs

High Altitude Pulmonary Edema (HAPE)

Non-cardiogenic: triggered by hypoxia

Vasoconstriction → elevated pulmonary pressures

Capillary stress failure and leakage

Neurogenic Pulmonary Edema

Occurs after CNS insult (e.g., head trauma)

Sympathetic surge causes vasoconstriction

↑ Hydrostatic pressure in pulmonary circulation

Pulmonary Edema in Renal Failure

Fluid overload and hypoalbuminemia

↓ Oncotic pressure → fluid transudation

Often mixed mechanism with cardiac involvement

Summary of pulmonary Edema

Pulmonary edema arises from various pathophysiological pathways

Cardiogenic vs. non-cardiogenic classification aids management

Understanding mechanisms is key to diagnosis and treatment

Chest X-rays

X-rays are emitted by an X-ray machine (stationary or portable), traverse the patient, and are picked up by a receptor on the other side of the patient (film or digital) creating an image. Tissues absorb the x-rays differently, and this differential absorption results in an image on a spectrum from black to white.

Black - air

Dark gray - fat

Light gray - soft tissue

Off white - bone

White - metal

Chest X-rays Density

Bone

Air

Fat

Soft Tissue

lung

blood

muscle

liver

Metal

System: DRSABCDE

D - Details

R - RIPE

S - Soft tissues and bones

A - Airways

B - Breathing

C - Circulation

D - Diaphragm

E - Extras

Details

Is this my patient's X-ray done today?

Patient's information.

Type of film. PA, AP, lat, erect/supine, L/R

Date and time of X-ray.

RIPE

R - Rotation. Look at clavicles.

I - Inspiration. 5-6 anterior ribs/8-10 posterior ribs in MCL

P - Picture. All of lung fields included. Angulation.

E - Exposure aka Penetration. Look at spinous processes, diaphragm.

Soft tissues and bones

Shoulders, clavicles, ribs, sternum, spine

Soft tissue symmetry, swelling, subcutaneous air, masses

Breasts

Calcifications - especially in vessels

Airways and mediastinum

Trachea midline

Mediastinal masses

Carina and main stem bronchi

Aortic knob

Hilum

Vessels

Breathing

Pneumothorax. Look at apices.

Lung fields.

Vascularity.

Lesions, masses, air-fluid levels

Pleura

Circulation

Heart position

Heart size

Heart borders

Heart shape

Aortic stripe

Diaphragm

Diaphragm shape

Hemidiaphragms

Costophrenic angles

Gastric bubble

Pneumoperitoneum

Extras

Tubes and lines- ETT, NGT, central lines, chest tube, PICC lines

Wires - Pacemaker, AICD, EKG electrodes

Metal -bone fixators, bullets, buck shot, coins