© 2007 McGraw-Hill Higher Education. All rights reserved. Chapter 3 Chronic Obstructive Pulmonary...

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

Chapter 3Chronic Obstructive Pulmonary Disease


Topics

• Emphysema• Chronic Bronchitis• Pressure-volume curve• Dynamic airway compression• Ventilation-perfusion inequality


Case Study #3: Chuck• Used car salesman• SOB over the last 3 years

– Chronic cough for 15 yrs• Yellow, purulent

sputum• 45 yr smoking history• 2 packs a day• Intermittent swelling of

the ankles• Respiratory infection

history• No family history of

lung disease


Case Study #3: Chuck

• Dyspneic• Florid appearance• Cyanotic• BP: 150/80• Barrel shaped

chest• Ankle edema• Whistling lung

sounds


Chuck• Hb: 17 g/dl• X-ray

– Showed over inflation• Ppa: 30 mmHg• Vo2 max: 1.2 L/min• Treatment

– Bed rest, oxygen therapy, bronchodilators, diuretics

– Advised to stop smoking– COPD rehab program


Chuck

• 6 mo later– Admitted with acute

chest infection– Marked dyspnea– Purulent sputum– Cyanosis– Rales– Obvious ankle

edema– PaO2: 42 mmHg– PaCO2: 55 mmHg– pH 7.30– died


• Autopsy– Lungs voluminous and lacked elastic recoil, some bronchi

filled with mucus secretions, much destruction, with alveolar destruction prominent

– Definite Chronic Bronchitis (blue bloaters) and emphysema (pink puffers), which caused respiratory failure

Chronic Bronchitis


Pathology• Structure

– Alveolar destruction

– Enlarged airspaces

– Emphysema:– From the latin to

inflate– Characterized by

enlargement of the air spaces distal to the terminal bronchioles w/ destruction of the alveolar walls


COPD and lung function• Chronic bronchitis

– Marked by hypertrophied mucus glands

– Inflammatory response due to irritants in smoke

– Airways are swollen and blocked by mucus

– Increased sputum production


• Increasing SOB– Thickened bronchial walls– Obstruction– Poorly supported airways– Airway collapse– Florid with central

cyanosis• Elevated Hb• Low SaO2

• Low Po2

–Release of EPO

Physiology & pathophysiology


• Overinflation: inc. lung volume• Whistling sounds caused by

increased turbulence• Neck vein engorgement, ankle

edema and enlarged liver consistent with pulm hypertension– Right axis deviation is

consistent with hypertrophy of the RV

Physiology & pathophysiology


Pulmonary function tests


• Gives you the compliance curve– Gives information about the elasticity of the lung– Pleural pressure is the negative pressure created by

the outward pull of the ribcage and the inward pull of the lung

– The lung will inflate as this pressure becomes more negative

– Hysteresis– Transpulmonary pressure: pressure differential

across the lung• Diff betw intrapulmonary and intrapleural

pressures

Pressure volume curve


• Volume change per unit pressure change (ΔV/ΔP)• Lung very compliant in the middle of the curve; very

stiff on the ends• Emphysema Increases the compliance and reduces

the elasticity of the lung

Compliance


Regional differences in Ventilation• Uneven

– Higher in lower lung units, lowest in upper• Posture dependent• Laying supine

–Highest in posterior lung


• Why?• Intrapleural pressure

less negative at base– Due to the weight

of the lung– Upper lobes are

already somewhat distended

– Lower lobes thus fill more (larger unit change in volume)

Regional differences in Ventilation•At low lung volumesNow intrapleural pressures are uniformly less negative (lung is smaller); base is now being compressed and ventilation is impossible; so apex is now better ventilated; typically apex is better ventilated


Airway closure

• Compressred regions do not have all the air squeezed out– Small airways close first – Traps gas– Usu. Occurs only at low lung volumes– In aging the volume this occurs at rises; why?

• Dependent regions of the lung are poorly ventilated


Forced expiration

• Measured with spirometer

– FEV1.0

– FVC– Measured after breath to TLC

– FEF25-75% Measure of elasticity of lung


• Descending limb is invariant because it is “effort independent”

• What limits flow?• Only at high volumes does increased

effort result in increased flow

Dynamic compression of Airways


• Airways are compressed as intrathoracic pressure increases

• A: opening pressure of 5 cmH2O

• B: Opening pressure of 6 cmH2O

• C: Opening pressure of 8

• D: Closing pressure of 11 cmH2O

• Thus, maximal flow decreases with lung volume

• Lung volume changes here are entirely due to elastic recoil

• Worse in emphysematous lungs as elastic recoil is reduced

Dynamic airway compression


• PaO2 declines somewhat with age

• Cause:

– VA/Q mismatch

– Po2 is determined by the ratio of ventilation to blood flow

Blood gases


Ventilation-perfusion inequality

– A: normal VA/Q

– B: No ventilation; so VA/Q of 0

– C: No blood flow: VA/Q of ∞

– Note how VA/Q is different betw apex and base of lung


• Areas with very high VA/Q add very little to oxygen to blood; thus PaO2 is dominated by areas of low VA/Q

• Also shape of O2-Hb dissociation curve dictates that areas of very high VA/Q cannot increase the oxygenation of the blood very much, while areas of low VA/Q can lower Po2 considerably

Ventilation-perfusion


• Normal lung, A-aDO2 is about 4 mmHg due to VA/Q mismatching

• Disease can increase this by quite a bit

• MIGET– Inert gases with

range of solubilities infused intravenously

– Measure concentrations in arterial blood and expired air

– No blood flow to unventilated areas (no shunt)

Ventilation-perfusion


• Alveolar-arterial Po2 difference

– PAO2 = PIO2 – [PACO2/R]

– Chuck:– 149-[49/0.8] = 88 mmHg

– PaO2 = 58

– AaDO2= 30

• PaCO2

– Chuck: 49 mmHg

• VA/Q mismatch

• Hypoventilation: Pco2 = [Vco2/VA]*K

• pH: falls due to elevated Pco2 (respiratory acidosis)

Measurement of ventilation-perfusion inequality


Acclimatization and High-altitude diseases

• Hyperventilation– Hypoxemia stimulates peripheral chemoreceptors; blows off

Co2, raises PAO2

– PB 250 mmHg do calculation– Renal compensation reduces HCO3

-

• Polycythemia– Increased Hct and [Hb]– Increases O2 carrying capacity: draw eq.– EPO form kidney

• Other features– Rightward shift in O2-Hb dissociation curve (Leftward at

extreme altitude)• Improves off-loading of O2 at the tissues• Caused by ↑2,3 DPG at altitude• Increased capillary-to-fiber volume ratio

– Muscle mass drops at altitude


• Acute mountain sickness– Headache, dizziness, palpitations, insomnia, loss of appetite

and nausea• Hypoxemia and resp. alkalosis

• Chronic mountain sickness– Cyanosis, fatigue, severe hypoxemia, marked polycythemia

• High altitude pulmonary edema– Severe dyspnea, orthopnea, cough, cyanosis, crackles and

pink, frothy sputum– Life threatening– Associated with elevated Ppa (hypoxic pulm

vasoconstriction)• High altitude cerebral edema

– Confusion, ataxia, irrationality, hallucinations, loss of consciousness and death

– Fluid leakage into brain

Acclimatization and High-altitude diseases

© 2007 McGraw-Hill Higher Education. All rights reserved. Chapter 3 Chronic Obstructive Pulmonary...

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