1. Chapter 7 Pulmonary Edema

2. Topics Pulmonary edema Stages of Pulmonary edema
Causes of Pulmonary edema
Hypoxia caused by shunt
Shunt measurement

3. Case Study #7: George 55 yr old Stock Broker Well until 3 yrs ago
Central chest discomfort during exertion
Severe central chest pain on admission
Crushing pain which radiated to L shoulder
Very short of breath, coughed up frothy, clear fluid
1 pack a day for 35 yrs
Father died at 60 of Heart attack

4. Physical exam #7: George
Anxious and SOB
Coughed up pink frothy fluid
BP 110/65, pulse 100 bpm
No neck vein engorgement
Rales upon ausculatation
No dependent edema
No edema

5. Investigations ECG: recent L anterior wall infarct
Blotchy bilateral opacities in lungs
Po2= 59; Pco2= 35 mmHg; pH=7.35
Lung scan (radioactive albumin): absent blood flow
Pulmonary edema and MI
Treatment: bed rest, morphine, diuretics and oxygen therapy
Pulm edema resolved quickly (2 days); sever obstruction of LAD CA; CABG performed

6. Pathophysiology L.V. failure and pulmonary edema
Probably had CAD for several years
Pain on exertion was angina
The pain he felt on admission was from a myocardial infarction
When LV cannot function properly
Pressure builds up in the LA and also the Pulm. Veins
This increases Pulm capillary pressure, causes stress failure and alveolar flooding

7. Pathophysiology: Pulm Edema
Capillary endothelium is permeable to water and some solutes
Alveolar epithelium:
Much less permeable
Water actually travels in the other direction
Actively pumped from alveolus to interstitium (Na+-K+ ATP pump)
Hydrostatic forces: move fluid out of capillary
Osmotic forces: tend to oppose this

8. Physiology and Pathophysiology of the lung
Starling equation
Q=K[Pc-Pi)-σ(πc-πi)]
Q=net flow out of the capillary
K=filtration coefficient
Pc=cap hydrostatic pressure
Pi=interstitial pressure
πc=colloid osmotic press; cap
πi=colloid osmotic press; interstitium

9. Physiology and Pathophysiology of the lung
The values are not exactly know for most of the variables in the Starling eq
However, net flow out of cap at arterial end (higher Pcap)
Net inward flow and venular end; osmotic effect
Any excess outward fluid is collected in lymphatic vessels and returned to central circulation (empty into L subclavian v.)

10. Physiology and Pathophysiology of the lung
Note that in normal circumstances
Very little fluid build-up around either the vasculature or the bronchial tree
This increases in interstitial edema and reaches a critical stage in alveolar edema
Two factors limit the outward flow of fluid from caps
Colloid osmotic pressure is higher in the vasculature (and gets greater as mostly water is leaking out of caps)
Rise in hydrostatic pressure of interstitium as fluid passes out of caps

11. Interstitial and pulmonary edema
Interstitial edema
Engorgement of perivascular and peribronchial spaces (“cuffing”)
Pulm function minimally affected
Alveolar edema
Fluid in alveoli
Alveoli shrink (due to surface tension)
Ventilation is impaired
hypoxemia

12. Causes of pulmonary edema
Increased cap hydrostatic pressure
Recognized by measuring capillary “wedge” pressure (~pulm venous press.)
Increased cap permeability
Also inc. cap hydrostatic pressure
Reduced lymph drainage
Heart failure exacrebates this as central venous pressure rises
Decreased interstitial pressure
rare
Decreased colloid osmotic pressure
Uncertain etiology
Heroin overdose

13. Features of pulm edema Dyspnea Rapid, shallow breathing
Stim of J receptors
Orthopnea
Paroxysmal nocturnal dyspnea
Periodic breathing
Cough
Pink, frothy discharge
Rales (crackles)
Rhonchi: musical sounds (severe edema)
Septal lines

14. Pulmonary function Not normally done Patients are pretty sick
Gas exchange
Impaired (particularly in alveolar edema)
Shunt
Blood that bypasses the gas exchange portion of lung; normally accounts for ~5mmHg A-a diff

15. Shunt Shunt eq. QT x CaO2 must equal QS X CvO2 (shunt) and
(QT-QS) x CcapO2
Rearranged as on Fig 7-6
End result?
CaO2 is lower than optimal
Normally 1-2%

16. Shunt II 100% does not correct hypoxemia due to shunt
Shunted blood never exposed to 100% O2
This is actually HOW best to measure shunt
This is why O2concentration and Po2 are not raised very much by breathing 100% O2
Actually rise in Cao2 is ml/dl/mmHg Po2
So, 600 x = 1.8 so CaO2 rises only a small amount
Due to the flatness of the upper portion of the O2 dissociation curve

17. Hypoxemia Pco2 does not rise with shunt; why? Chemoreceptors
J receptors (George)
Hypoxemia (stim breathing)
Low VA/Q also contributes to hypoxemia
Obstructed airways are not ventilated
Low cardiac output also contributes to hypoxemia
In George; the CHF
Mixed venous Po2 falls due to increased O2 extraction by tissues

18. Pulmonary mechanics Reduced distansibility of the lung
Reduces compliance
Airway resistance in increased
Some reflex VC
Some due to cuffing
Reduces the radial traction effect of increasing lung volume

19. Surface tension Pressure is determined by the law of Laplace P=4T/r
Thus, Pressure will fall as the radius of the sphere increases
Thus, a smaller sphere should empty into a larger sphere

20. Surface tension Note that air inflation curve is right shifted
Reduced compliance
Due to surface tension
Surfactant
Reduces surface tension
Produced by type II alveolar cells
Contains a phospholipid; dipalmitoyl phosphatidylcholine (DPPC)
May be important contributor to respiratory distress syndrome in newborns

21. Surface tension Main points Water has very high surface tension
Placing detergent in water reduces surface tension
Lung extracts have variable surface tension
How/Why does surfactant work?
DPPC molecules are hydrophobic at one end and hydrophilic at the other; thus the individual molecules tend to repel each other, an effect that gets stronger as they get closer

22. Physiological advantages of surfactant
Low surface tension increases compliance
Stability of alveoli is improved (remember the tendency of small bubbles to empty into larger ones)
Surfactant reduces surface tension more in smaller bubbles
Keeps alveoli dry; elevated surface tension tends to suck fluids out of the low pressure caps

23. Other physiological changes with Pulmonary Embolism
Gas Exchange
Reduced Po2
Atelectatic areas act as shunt
Pulmonary edema
Lung mechanics
Post-embolism areas receive no blood flow
Causes bronchoconstriction (reason why X-ray showed no ventilation in the region distal to emboli); short-lived usu.

24. Chapter 8: PneumoconiosisOr
Pneumonoultramicroscopicsilicovolcanoconiosis

25. Black lung disease: Harry
60 yr old retired coal miner
SOB
Fatigue
Productive cough
Started working in mines at 17
SOB started ~12 yrs ago
Smoked 1-2 packs a day since 15

26. Harry Physical exam Only positive findings Chest slightly overinflated
Rhonchi heard on auscultation

27. Investigations Blood work normal
X-ray showed fine particulate matter in lungs
Slightly elevated lung volumes
Slight obstruction and flow limitation
Slight hypoxemia

28. Pathogenesis Types of pollutants Carbon monoxide Largest pollutant
Nitrogen oxides
Produced from burning of fossil fuels, like coal and oil (forms smog)
Sulfur oxides
Gases that come from burning sulfur containing fuels (power stations)
Hydrocarbons
Normally found in air; in combo with sunlight can cause Photochemical oxidants

29. Pathogenesis Particulate matter Wide variety of particles; soot
Power stations and industrial plants
Photochemical oxidants
Ozone, peroxy-nitrates
Formed from the action of sunlight on hydrocarbons and nitrogen oxides
Cigarette smoke
~4% CO
Nicotine
Hydrocarbons (tar); causes bronchial carcinoma

30. Deposition of aerosols in the lung
Aerosol: particles that remain airborne for a substantial period of time
Impaction:
Largest particles fail to turn corners
Lodge in nasopharynx
Nose filters large particles well 5-20 μ are almost completely filtered

31. Deposition of aerosols in the lung
Sedimentation
Gradual settling of particles because of their weight
Medium sized particles
1-5 μ; in small airways
Diffusion
Random movement of gases
Only in smallest particles; <0.1 μ
Many particles are exhaled; to small to sediment, to large to diffuse into blood

32. Clearance of deposited particles
Mucociliary clearance
Mucus: bronchial seromucus glands
Goblet cells
Film is 5-10 μ thick
Sol and gel layer
Gel: superficial, viscous; traps deposited particles
Sol: less viscous; allows beating of cilia

33. Clearance of deposited particles
Mucus Contains IgA
Important in defense against foreign particles, bacteria and viruses
Cilia: 5-7 μ long, beat times/min
Propel gel layer forward
Moves at 1mm-2cm/min dependent upon the diameter of the airway
Eventually swallowed or “gobbed” up
Normal mucociliary clearance is impaired
Pollution
Toxic gases
Tobacco smoke

34. Alveolar macrophages No mucociliary apparatus in alveoli Macrophages
Engulf foreign particles via amoeboid motion
Phagocytose these particles (kill through lysozomal activity)
Can migrate to small airways and climb The mucociliary ladder
Leave blood in lymphatics (or blood)
Activity of macrophages is impaired by
Cigarette smoke, ozone, hypoxia, radiation, corticosteroids and alcohol

35. Other pneumoconioses Coal worker’s lung Massive fibrosis Silicosis
Inhalation of silica
Quarrying, mining or snadblasting
These are toxic particles
Provoke severe fibrosis
Asbestos-related disease
Commonly used in insulation, brake linings, roofing materials (anything that must resist heat
Diffuse interstitial pulm fibrosis (Chpt 5)
Bronchial carcinoma; aggravated by smoking
Pleural disease; malignant mesothelioma (sometimes up to 40 yrs after exposure)
Byssinosis
Cotton dust
Histamine reaction
Obstructive disease pattern
Occupational asthma
Allergenic organic dusts
Flour; wheat weevil
Gum acacia
Polyurethane; Toluene diisocyanate