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© 2007 McGraw-Hill Higher Education. All rights reserved. Chapter 7 Pulmonary Edema.

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1 © 2007 McGraw-Hill Higher Education. All rights reserved. Chapter 7 Pulmonary Edema

2 © 2007 McGraw-Hill Higher Education. All rights reserved. Topics Pulmonary edema Stages of Pulmonary edema Causes of Pulmonary edema Hypoxia caused by shunt Shunt measurement

3 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. Investigations ECG: recent L anterior wall infarct Blotchy bilateral opacities in lungs Po 2 = 59; Pco 2 = 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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

8 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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

13 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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

15 © 2007 McGraw-Hill Higher Education. All rights reserved. Shunt eq. –Q T x CaO 2 must equal –Q S X CvO 2 (shunt) and –(Q T -Q S ) x CcapO 2 Rearranged as on Fig 7-6 End result? –CaO 2 is lower than optimal –Normally 1-2% Shunt

16 © 2007 McGraw-Hill Higher Education. All rights reserved. 100% does not correct hypoxemia due to shunt –Shunted blood never exposed to 100% O 2 –This is actually HOW best to measure shunt –This is why O 2 concentration and Po 2 are not raised very much by breathing 100% O 2 –Actually rise in Cao 2 is ml/dl/mmHg Po 2 So, 600 x = 1.8 so CaO 2 rises only a small amount Due to the flatness of the upper portion of the O 2 dissociation curve Shunt II

17 © 2007 McGraw-Hill Higher Education. All rights reserved. Pco 2 does not rise with shunt; why? Chemoreceptors J receptors (George) Hypoxemia (stim breathing) Low V A /Q also contributes to hypoxemia –Obstructed airways are not ventilated Low cardiac output also contributes to hypoxemia –In George; the CHF –Mixed venous Po 2 falls due to increased O 2 extraction by tissues Hypoxemia

18 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. Gas Exchange –Reduced Po 2 Atelectatic areas act as shunt Pulmonary edema Lung mechanics –Post-embolism areas receive no blood flow Causes bronchoconstricti on (reason why X-ray showed no ventilation in the region distal to emboli); short- lived usu. Other physiological changes with Pulmonary Embolism

24 © 2007 McGraw-Hill Higher Education. All rights reserved. Chapter 8: Pneumoconiosis Or Pneumonoultramicroscopicsilicovolcanoconiosis

25 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. Harry Physical exam –Only positive findings Chest slightly overinflated Rhonchi heard on auscultation

27 © 2007 McGraw-Hill Higher Education. All rights reserved. Investigations Blood work normal X-ray showed fine particulate matter in lungs Slightly elevated lung volumes Slight obstruction and flow limitation Slight hypoxemia

28 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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

32 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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 © 2007 McGraw-Hill Higher Education. All rights reserved. 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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