High Altitude/Diving Adaptations

Question 1

Method of calculation of inspired O₂, P_AO2, and the A-a gradient

Answer 1

• P_AO2 = (P_b – P_H20) x FiO2 – (P_aCO2 / R)
  
  • P_b = barometric pressure
  • R=~0.8 (generally)
• barometric pressure decreases (at high altitude) ==> PaO2 decreases ==> ventilation increases (PaCO2 decreases) to compensate
• A-a = P_AO2 - P_aO2
  
  • P_aO2 = arterial O₂ content

Question 2

Acute cardiac adaptations to high altitude

Answer 2

• Increased CO
• HR increases within minutes of hypoxia exposure (sympathetic response)

SV increases as a result of systemic vasodilation, which decreases afterload

• Acute adaptive response only – returns to normal within days

Question 3

Acute ventilatory adaptations to high altitude

Answer 3

• Increased minute ventilation (VE)
  
  • hypoxemia ==> hyperventilate ==> increased P_aO2 (& decreased in P_aCO2) & increased Hb saturation
  • can last days-weeks & is most useful short-term adaptation

Question 4

Acetazolamide characteristics/fxn

Answer 4

• Oral diuretic
• acetazolamide causes a metabolic acidosis through renal bicarbonate loss
• acidosis triggers a reflexive increase in VE to lower P_aCO2 and thus incrase pH back toward normal and via the law of partial pressures a parallel increase in P_aO2 follows

Question 5

Chronic adaptations to high altitude (general)

Answer 5

• increased Hb content & saturation
• exaggerated ventilator response
• skelatal muscle adaptations
• vascular adaptations

Question 6

Hb adaptations to high altitude

Answer 6

• Increased Hb content
  
  • Via EPO secreted from the kidneys – occurs over weeks
  • Overall effect is to increase Hb and red cell mass
  • Increased hematocrit with decreased plasma volume
• Increased Hb saturation
  
  • Structural changes in Hb that alter its affinity for O2
  • A “left shift” in the O2-Hb curve occurs due to respiratory alkalosis (hyperventilation/decreased PaCO2) which increases O2 saturation of Hb at any given PaO2

Question 7

Ventilator response adaptation to high altitude

Answer 7

• Acclimatized individuals have increased VE at a given PAO2 compared to the VE of a person just arrived at the same altitude; this decreases PACO2 and allows PaO2 levels to remain up
• Hypoxic ventilator responses are triggered at higher PaO2 (63 mmHg) in acclimatized individuals vs. in un-acclimatized (55mmHg)
• Due to altered gene expression/altered “set points” for PaCO2 and PaO2

Question 8

Major illnesses associated w/high altitude exposure

Answer 8

• Acute mountain sickness (AMS)
• High altitude cerebral edema (HACE)
• High altitude pulmonary edema (HAPE)
• Chronic mountain sickness

Question 9

Characteristics of AMS

Answer 9

• Mildest but most common form of acute altitude illness
• Headache, nausea, malaise, insomnia, anorexia
• rare < 6,000 ft but increases to 25% at altitudes 9-10,000 ft
• Symptoms start after 6 hours at altitude and peak by 1 day
• Quick ascent increases AMS risk
• Mechanism: increase in brain volume in response to hypoxia, caused by vasogenic cerebral edema and/or increased cerebral blood flow (“tight box”)

Question 10

AMS tx and prevention

Answer 10

• Treatment: Sx usually resolve without treatment
  
  • treatment with oral dexamethasone (corticosteroid) [blunts hypoxic induction of brain vessel permeability-inducing proteins] OR
  • oral acetazolamide (diuretic causing metabolic acidosis and compensatory hyperventilation) will hasten resolution of AMS symptoms
• Prevention:
  
  • either dexamethasone or acetazolamide may be used to prevent
  • ibuprofen to prevent headache

Question 11

HACE sx & tx

Answer 11

• HACE = extreme form of AMS – medical emergency!
• Mechanism: same as AMS but more severe
• Early symptoms are similar to AMS but progressively worsen to include confusion, hallucinations, and coma
• Treatment is supportive (oxygen, descent) followed by IV dexamethasone

Question 12

HAPE sx, signs, mechanism

Answer 12

• onset is usually on the 2nd day
• Sx: cough (occasionally pink frothy sputum), SOB, fatigue +/- signs and symptoms of AMS
• Signs: hypoxia, lung rales, infiltrates on CXR
• Mechanism: non-cardiogenic pulmonary edema (LA pressures normal, diuretics don’t help) associated with pulmonary hypertension in response to acute hypoxia
  
  • Occurs in people who are more prone to accentuated hypoxic PHTN

Question 13

HAPE tx & prevention

Answer 13

• Treatment: descent, supplemental oxygen, vasodilator medications to lower pulmonary artery pressure (Nifedipine [CCB])
• Prevention:
  
  • Pulmonary vasodilators (Nifedipine)
  • Dexamethasone
  • Salmeterol (a long acting beta-agonist bronchodilator that increases the clearance rate of water out of alveoli by increasing activity of Na-K ATPase)

Question 14

Chronic mountain sickness characteristics

Answer 14

• Occurs in people who live at high mountain altitudes > 10,000 ft but are not genetically adapted (i.e. Han Chinese living in Tibet
• Polycythemia and PHTN = Chronic Mountain Sickness (CMS)
  
  • Increased risk of stroke and heart failure
• Treatment: move to lower altitude, supplemental O2, phlebotomy
• w/severe hypoxia, the concentration gradient for oxygen (the difference in PO2 between mixed venous blood and alveolar PO2) is lessened, leading to diffusion limitation for oxygen

Question 15

General characteristics of breathing at depth (underwater)

Answer 15

• increased barometric pressure below sea level ==> exerts pressure on airways/organs
• increased airway pressure ==> increased density of air gas ==> increased resistive work of breathing
• “squeeze” ==> decreased lung volumes
  
  • divers breathing pressurized gas avoid this problem
  • increased venous return ==> increased CO & central filling pressure

Question 16

Major clinical syndromes associated w/diving

Answer 16

• pulmonary barotrauma
• decompression sickness
• nitgrogen nacosis
• shallow water blackout

Question 17

Characteristisc of pulmonary barotrauma

Answer 17

• Increased pressure ==> gas is pushed into the interstitium from the alveolar spaces, and then migrates along the airways to the mediastinum causing
  
  • ​Pneumothorax
  • Pneumomediastinum
  • Air embolism (air bubbles in blood)
• Usually seen in breath-holding free divers without SCUBA gear as air in lung expands with ascent

Question 18

Characteristics of decompression sickness (“the bends”)

Answer 18

• inert gases (i.e. Nitrogen and helium) form supersaturated bubbles in blood and tissues increases
  
  • bubbles expand in the tissues, diffuse into the blood, travel to the heart, and can cause air embolism with end organ dysfunction
• Clinical features: confusion, MSK pain, dyspnea, stroke, coma, seizures, paralysis, death
• Treatment: recompression (hyperbaric chamber) drives gases back into the dissolved state

Question 19

Characteristics of nitrogen narcosis

Answer 19

• Occurs when a diver breathes compressed air (75% nitrogen) at depths > 100 ft
• High nitrogen in brain tissues causes altered mental status
  
  • helium is used at dives > 100 ft
• Clinical features: Clumsiness, bizarre behavior, euphoria, unconsciousness

Question 20

Characteristics of shallow water blackout

Answer 20

• During apneic swims or dives, subjects hyperventilate to increase PaO2 before submerging;
• as the PaO2 falls, hypoxemia can cause unconsciousness before PaCO2 rises enough to stimulate breathing
• Recall that brain prioritizes CO2 signaling over hypoxic O2 signaling from the carotid body

Question 21

Conditions exacerbated/@ risk at altitude

Answer 21

• Conditions that lower PaO2 at rest
  
  • Lung disease, congestive heart failure, hypoventilation
• Conditions that limit the patient’s ability to increase VE
  
  • Pulmonary fibrosis, COPD, obesity hypoventilation

Question 22

Conditions exacerbated/@ risk while diving

Answer 22

• Conditions that limit airflow (COPD, asthma)
• Due to increased resistive work of breathing at depth