Chapter 7 Pulmonary Edema

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Chapter 7Pulmonary Edema


Topics

• Pulmonary edema• Stages of Pulmonary

edema• Causes of

Pulmonary edema• Hypoxia caused by

shunt• Shunt measurement


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


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


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


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


• 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

Pathophysiology: Pulm Edema


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



• 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.)



• 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


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


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– rare

• Uncertain etiology– Heroin overdose


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


• 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

Pulmonary function


• 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%

Shunt


• 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 0.003 ml/dl/mmHg Po2

• So, 600 x 0.003 = 1.8 so CaO2 rises only a small amount

• Due to the flatness of the upper portion of the O2 dissociation curve

Shunt II


• 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

Hypoxemia


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


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


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


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


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


• 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.

Other physiological changes with Pulmonary Embolism


Chapter 8: Pneumoconiosis

• Or• Pneumonoultramicroscopicsilicovolcanoconiosis


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


Harry• Physical exam

– Only positive findings• Chest slightly

overinflated• Rhonchi

heard on auscultation


Investigations

• Blood work normal• X-ray showed fine

particulate matter in lungs

• Slightly elevated lung volumes

• Slight obstruction and flow limitation

• Slight hypoxemia


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


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


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


• 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

Deposition of aerosols in the lung


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


Clearance of deposited particles• Mucus Contains IgA

– Important in defense against foreign particles, bacteria and viruses

• Cilia: 5-7 μ long, beat 1000-1500 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


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


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

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Chapter 7 Pulmonary Edema