The Respiratory System Under Stress
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Transcript of 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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