the respiratory system under stress

The respiratory system under stress

FromRespiratory Physiology – The Essentials

ByJ.B. West

“The human urge to climb higher and dive deeper puts the respiratory system under great stress, although these situations are minor insults compared with the process of being

born!”

Topics

• Exercise

• High Altitude– Hyperventilation– Polycythemia– Other Physiological Changes at High– Altitude

• O2 Toxicity– Absorption Atelectasis

Topics

• Increased Pressure– Decompression Sickness– Inert Gas Narcosis

• Perinatal Respiration– Placental Gas Exchange– The First Breath– Circulatory Changes

Exercise

O2 Consumption @Rest 300 mL/min

CO2 output @Rest 240 mL/min

Exercise3000 mL/min

Exercise

• Body burns more CHO than fat

• R @ rest 0.8• R even higher with anaerobic glycolysis

• ↑ H+

R during exercise1.0

↑ Ventilation

Exercise ~ Oxygen consumption

Changes with exercise-1

Diffusing capacity of the lung increases

Recruitment and distension of pulmonary capillaries↑Volume of blood in the pulmonary capillaries, Vc

↑ Diffusing capacity of the membrane, DM

Changes with exercise-2

Fick equations

VO2 = Q(CaO2 − CVO2 ) VO2 = VE(FIO2 - FEO2 )

Cardiac output increases, PVR fallsIncrease in CO – 1 x Increase in Ventilation - 4 x

Exercise↑ Heart rate ↑ Stroke volume

Changes with exercise-3• Oxygen dissociation curve

moves to the right in exercising muscles…

• … and to the left when blood returns to lungs

• Additional capillaries open up• Peripheral vascular resistance

falls• Dynamic exercise – BP

remains at or slightly above baseline

• Static exercise – BP increases• pH, PCO2 and PO2 little affected

High Altitude

High Altitude

• Hyperventilation– Alveolar gas equation: • PAO2 = [ FiO2 * (Patmos - PH2O)] - (PaCO2 / RQ)

• If PACO2 remained at normal values then on Mt Everest, PAO2 = 43 – 40 = 3 mm Hg

• But when ventilation increases five-fold and PACO2 ↓ to 8 mm Hg, then PAO2 = 35 mm Hg

– Hypoxic stimulation of the peripheral chemoreceptors

Exposure to low PO2

• Hypoxic stimulation of arterial chemoreceptors (1.65 X) immediately– decreased CO2 limits

• After several days ventilation 5X as inhibition fades– HCO3 pH + chemosensitive area of

brainstem

Mechanism of Hyperventilation

Hypoxia

Stimulation of Peripheral

Chemoreceptors

Hyperventilation

Hypocapnoea and Alkalosis

Inhibition of respiratory drive

CSF HCO3 moves outCSF pH normalizesRenal elimination of HCO3

Acclimatization• Great in pulmonary ventilation• RBC (Hct)• diffusing capacity of the lungs• tissue vascularity ( capillary density)• ability of tissues to use O2

– slight cell mitochondria (animals)– slight cellular oxidative systems (animals)

• Moderate altitudes– Increased synthesis of 2,3-DPG– Shifts oxy-hemoglobin dissoc. curve to right

• Advantage-tissue

• Higher altitudes– Respiratory alkalosis– Shifts oxy-hemoglobin dissoc. curve to left

• Advantage - lung

Chronic Mountain Sickness

• Red cell mass (Hct) and Hypoxia• pulmonary arterial BP• Enlarged right ventricle• total peripheral resistance• congestive heart failure• Death if person is not removed to lower

altitude

Acute effects of ascending to great heights

• Unacclimatized person suffers deterioration of nervous system function

• effects due primarily to hypoxia– sleepiness, false sense of well being, impaired

judgment , clumsiness, blunted pain perception, visual acuity, tremors, twitching, seizures

• Acute mountain sickness (onset hours - 2 d)– cerebral edema hypoxia + local vasodilatation – pulmonary edema hypoxia + local vasoconstriction

Natural Acclimatization• Humans living at altitudes > 13,000 ft in the

Andes & Himalayas• Acclimatization begins in infancy– chest to body ratio

• high ratio of ventilatory capacity to body mass• increased size of right ventricle• shift in oxy-hemoglobin dissociation curve

– PO2 of 40 have greater O2 in blood than lowlanders at 95

• Work capacity greater than even well acclimatized lowlanders at high altitudes (17,000 ft) (87% vs. 68%)

Hyperbaric conditions

• As people descend beneath the sea, the pressure increases tremendously which can have a profound impact on the respiratory system.

• To keep the lungs from collapsing air must be supplied at high pressures which exposes pulmonary capillary blood to extremely high alveolar gas pressures hyperbarism

• These high pressures can be lethal

Relationship of pressure to sea depth

Depth

Sea level

33 feet (10.1 m)

66 feet (20.1 m)

100 feet (30.5 m)

133 feet (40.5 m)

166 feet (50.6 m)

233 feet (71.1 m)

300 feet (91.4 m)

400 feet (121.9 m)

500 feet (152.4 m)

Atmospheres/vol of gas

1 1 liter of gas

2 ½ liter of gas

3

4 ¼ liter of gas

5

6

8 1/8 liter of gas

10

13

16

Effect of High Partial Pressures• High PN2

– Causes narcosis in about an hour of being submerged• 120 feet- joviality, carefree• 150-200- drowsyness• 200-250- weakness• Beyond 250- unable to function

– Similar to alcohol intoxication• “raptures of the deep”• Mechanism similar to gas anesthetics

– Dissolves in neuronal membranes altering ionic conductance

Effect of High Partial Pressures• High PO2

– Oxygen toxicity• Seizures followed by coma within 30-60 minutes

– Likely lethal to divers

• Above a critical alveolar PO2 (> 2 atmospheres PO2) – Free radical damage can occur

» Damage to cell membranes, cellular enzymes, » Nervous tissue highly suscpectable resulting in brain

dysfunction• Oxygen toxicity is preventable if one never exceeds the

established maximum depth of a given breathing gas. – For deep dives - generally past 180 feet (55 m), divers use

"hypoxic blends" containing a lower % of O2 than atmospheric air

Absorption Atelectasis

Decompression• When a person breaths air under high pressure

for an extended period of time the amount of N2 in the body fluids increases as higher N2

levels equilibrate with levels in tissues.• N2 is not metabolized by the body– It remains dissolved in the tissues until N2 pressure

in the lungs decreases as the person ascends back to sea level.

• Several hours are required for gas pressures of N2 in all body tissues to equilibrate with alveolar PN2

Decompression (cont.)• Blood does not flow rapidly enough & N2

doesn’t diffuse rapidly enough to cause instantaneous equilibration

• N2 dissolved in H2O equilibrates in < 1 hour

• N2 dissolved in fat equilibrates in several hours

• Potential problem if person is submerged at a deep level for several hours

Volume of N2 dissolved in body

Feet below

O

33

100

200

300

liters

1

2

4

7

10

Decompression sickness “Bends”

• Nitrogen bubbles out of fluids after sudden decompression– Bubbles block many blood vessels– First smaller blood vessels, then as bubbles

coalesce larger vessels are blocked– S/S

• Pain in joints, muscles of arms/legs (85-90%)• Nervous system symptoms (5-10%)

– Dizziness, paralysis, unconsciousness• Pulmonary capillaries blockes “the chokes” (2%)

Preventing Decompression sickness• Decompression tables (U.S. Navy) link• A diver who has been breathing air and has been on

the sea bottom at a depth of 190 feet for 60 minutes is decompressed as follows:– 10 minutes at 50 foot depth– 17 minutes at 40 foot depth– 19 minutes at 30 foot depth (total decompression – 50 minutes at 20 foot depth time = 3 hours)– 84 minutes at 10 foot depth

• Heliox– Less diffusion into tissues, faster diffusion out– Low density reduces WOB

Respiratory adjustments at birth• Most important adjustment is to breathing• Normally occurs within seconds• Stimulated by:– Hypoxemia– Slightly asphyxiated state (elevated CO2)– Cooling of skin– Increased sensitivity of chemoreceptors

• 40-60 cm H20 of negative pleural P necessary to open alveoli on first breath

• Surfactant

Circulatory changes at birth

• Placenta disconnects• TPR increases• Pulmonic resistance decreases (elimination of

hypoxia)• Closure of foramen ovale (atria)• Closure of ductus arteriosis (great vessels)• Closure of ductus venosus (bypass liver)

The End

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