High Altitude/Diving Adaptations Flashcards Preview

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Flashcards in High Altitude/Diving Adaptations Deck (23)
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Method of calculation of inspired O2, PAO2, and the A-a gradient

  • PAO2 = (Pb – PH20) x FiO2 – (PaCO2 / R)
    • Pb = barometric pressure
    • R=~0.8 (generally)

  • barometric pressure decreases (at high altitude) ==> PaO2 decreases ==> ventilation increases (PaCO2 decreases) to compensate 

  • A-a = PAO2 - PaO2 
    • PaO2 = arterial O2 content


Acute cardiac adaptations to high altitude

  • 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


Acute ventilatory adaptations to high altitude

  • Increased minute ventilation (VE)
    • hypoxemia ==> hyperventilate ==> increased PaO2 (& decreased in PaCO2) & increased Hb saturation
    • can last days-weeks & is most useful short-term adaptation


Acetazolamide characteristics/fxn

  • Oral diuretic 

  • acetazolamide causes a metabolic acidosis through renal bicarbonate loss 

  • acidosis triggers a reflexive increase in VE to lower PaCO2 and thus incrase pH back toward normal and via the law of partial pressures a parallel increase in PaO2 follows 


Chronic adaptations to high altitude (general)

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


Hb adaptations to high altitude

  • 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 





Ventilator response adaptation to high altitude

  • 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 




Major illnesses associated w/high altitude exposure

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


Characteristics of AMS

  • 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”)


AMS tx and prevention

  • 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


HACE sx & tx

  • 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


HAPE sx, signs, mechanism

  • 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 


HAPE tx & prevention

  • 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) 


Chronic mountain sickness characteristics

  • 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 


General characteristics of breathing at depth (underwater)

  • 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 


Major clinical syndromes associated w/diving

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


Characteristisc of pulmonary barotrauma

  • 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  




Characteristics of decompression sickness ("the bends")

  •  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 


Characteristics of nitrogen narcosis

  • 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 




Characteristics of shallow water blackout

  • 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 


Conditions exacerbated/@ risk at altitude

  • 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 


Conditions exacerbated/@ risk while diving 

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