Lecture 7 - Barometric Pressure.pptx

THE RESPIRATORY SYSTEM
LECTURE 7:
EFFECTS OF BAROMETRIC PRESSURE
Dr. Eamonn O’Connor
Human Form & Function
Adaptation to Altitude: Hyperventilation
1
 
Cause: ↓ PaO2 acting on carotid body peripheral chemoreceptors
(ie: hypoxic ventilatory drive)
 
 
 
CO2 clearance increases
Blood pH increases
Respiratory alkalosis (reduces ventilation)
To prevent alkalosis:
 
Kidney excrete bicarbonate ions
 
More acid remains in the blood
 
Alkalosis is reversed
 
pH normal within 2-3 days
 
Ventilation then increases again
 
 
Reason for maintained ventilation is unknown
Likely increased sensitivity to PaO2
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Adaptation to Altitude: Polycythaemia
2
 
Increases in:
  RBC
concentration in blood
  Hb content in blood
 
↓ PaO2 (hypoxemia) stimulate erythropoietin (EPO)
after ~3 h (peak 24-48 h)
  From
kidney
  Acts on bone marrow
  Stimulates
  Reticulocyte
maturation and release
  Synthesis (erythropoiesis)
The Respiratory System - Lecture 7
Adaptation to Altitude: Polycythaemia
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 
↓ Despite
PaO2
  ↓ Hb saturation via O2-Hb dissociation curve
  ↓
 
Total O2 content may be normal or elevated
  eg:
Peruvian Andes residents (4,572 m)
  PaO2
= 45mmHg; Hb saturation = 81%
  [Hb] increased from 15 to 19.8 g.100ml-1
  Arterial
 
O2 content = 22.4 ml.100ml-1
Elevated blood viscosity
  ↑
cardiac work (hypertrophy)
  Uneven blood flow distribution
The Respiratory System - Lecture 7
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Other Adaptations to Altitude
4
 
Right shifted O2-Hb dissociation curve (moderate
altitudes)
  Better
unloading at tissue level (possible loading limitation)
  Caused by alkalosis induced ↑ [2,3-BPG]
 
Left shifted O2-Hb dissociation curve (high altitudes)
  Better
loading at the pulmonary capillaries
  Caused by respiratory alkalosis
 
Improved diffusion capacity via:
  Expanded
surface area via greater lung volume on inflation
  Increased tissue capillarisation (angiogenesis) (days)
The Respiratory System - Lecture 7
Acute Mountain Sickness
5
 
Symptoms:
  Headaches,
Loss of appetite & Insomnia, Nausea, Vomiting,
Dyspnea (difficult breathing)
  Begin from 6 to 48 h after arrival to altitude (most severe
days 2 and 3)
 
Incidence varies with altitude, rate of ascent &
individual’s susceptibility
  Elevations
2,500–3,500 m: incidence ~15% (higher in
women)
  Maybe linked to low ventilatory response to hypoxia
  Physical conditioning little protection against effect of
hypoxia
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High-Altitude Pulmonary Oedema
6
 
Linked to pulmonary vasoconstriction (hypoxia): high
[protein] oedema fluid from damaged capillaries.
  Fluid
accumulation leads to persistent cough, shortness
of breath, cyanosis of lips & fingernails & loss of
consciousness
  Could lead to high altitude cerebral ooedema
 
Treatment:
  Descending
to lower altitude & supplemental oxygen
The Respiratory System - Lecture 7
Inspired Pressures
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Gas Measurements at Altitude
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The Respiratory System - Lecture 7
Respiration at Depth
 
Total pressure increases
 
1 atmosphere
 
 
Therefore,
 
 
every 10m (33 feet)
Gas partial pressures also
increase when under water
Problems
 
Gas cavities (lung, middle
ear)
 
 
 
Compression with descent
Over-expansion with ascent
Behavior of Gases
 
Gas solubility ∝ partial
pressure
The Respiratory System - Lecture 7
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Nitrogen Narcosis
10
 
At Sea Level
  N2
is poorly soluble
  Low [N2] dissolved - no adverse effects
 
At Depth
  ↑
N2 partial pressures → ↑ N2 solubility
[N2] dissolved in blood, and
  High
  Fatty
substances (membranes)
ion regulation and therefore excitable cells
  Influences
 
  ↑
 
 
e.g. neurons
Depth, ↑ [N2] dissolved
↑ N2 solubility → Reduced neuron excitability
→nitrogen narcosis
The Respiratory System - Lecture 7
Nitrogen Narcosis
11
 
50m (150 ft)
  “Cocktail”
 
effect (euphoria and drowsiness)
50-90m (150 - 300 ft)
  Fatigued
and weak
  Loss of coordination
  Clumsiness
 
100-120m (350 - 400 ft)
  Lose
 
consciousness
Prevention
  Use
N2 free gas
  Helium substitution (Solubility ½ that of N2)
  100% O2 not appropriate (O2 toxicity)
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Decompression Sickness
12
 
During rapid ascent &↓pressure
 
N2 less soluble, N2 comes out of solution
 
 
Bubble formation - “Champagne Cork Effect”
Effects depend on size and location of bubbles:
 
Gas embolus in circulation → tissue ischaemia
May be critical in Brain, Coronary or Pulmonary circulations
Avascular necrosis common in head of femur
  Bubble formation in the myelin sheath
  Compromise nerve conduction (dizziness, paralysis)
 
 
 
Bubble/Gas expansion
Muscle and joints (The Bends): severely painful
Ear: vestibular disturbances, deafness
  Lung: tissue rupture (airway bursting)
 
 
 
 
increased bubble dispersal and multiple emboli
catastrophic if not fatal
The Respiratory System - Lecture 7
Decompression Sickness
13
 
Prevention
 
Slow ascent - according to prescribed tables
 
Depends on
 
 
 
 
 
N2 gas replacement
(Helium)
 
 
 
 
Depth
Time
N2 wash-in & wash-out times
Tissue types
Half Solubility of N2
↓ MW → faster diffusion
(and thus washout)
Exhale during ascent
Treatment
 
Recompression
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