altitude and diving Flashcards

1
Q

Acclimatization vs adaptation

A

acclimatization is a subacute to chronic physiologic process that permits more efficient function at altitude that happens to everyone who goes to high altitude. This includes increased ventilation rate, increased EPO, etc. Adaptation is natural selection that occurs over generations

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2
Q
  1. Determine the inspired PO2 (PA02) at various barometric pressures and use this to understand the limitations of human travel at high altitude.
A

Sea level (769 mmHg): 149mmHg PAO2. Denver (630 mmHg): 122 mmHg PAO2. Everest at 27,560 ft (253mmHg) = 35 mmHg PAO2. Arterial O2 saturation on Everest is only 50%

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3
Q

Acute and chronic responses to moderate hypoxia

A

acute: Increased CO, decreased systemic vascular resistance, increased heart rate and increased ventilation. Chronic: increased ventilation, increased hemoglobin concentration, increased CO2 ventilatory response, increased capillary density and myoglobin amount and affinity for O2 in muscles

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4
Q

effects of hypoxia on systemic/brain and pulmonary vascular beds

A

systemic/brain: vasodilation due to decreases SVR. Pulmonary: vasoconstriction

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5
Q

At what alveolar O2 pressure does hyperventilation begin

A

When PAO2 <55mmHg, hyperventilation occurs

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6
Q

Which acute adaptive response to high altitude is most useful

A

Hyperventilation- lasts for days and weeks, plus a small increase in PaO2 can lead to a significant increase in O2 saturation b/c the oxygen dissociation curve is sigmoidal.

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7
Q

Drug used to prevent high altitude illness

A

acetazolamide- a diuretic that cuases metabolic acidosis through renal bicarbonate loss. This acidosis triggers increased ventilation to lower arterial PaCO2, thus PaO2 increases.

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8
Q

Which conditions make traveling to high altitude difficult

A

Conditions that limit the ability to increase ventilation such as pulmonary fibrosis, COPD, obesity, etc. Diseases that cause lower PaO2 at rest such as lung disease (not asthma), CHF, hypoventilation. Existing pulm HTN or Left heart failure also bad

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9
Q

Chronic changes in red cell, Hb %, plasma volume and blood volume at high altitude

A

Hemoglobin and red cell mass are increased, while plasma volume is decreased and overall blood volume increases.

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10
Q

Changes in hemoglobin and oxygen dissociation curve with high altitude (long term)

A

Structural changes in hemoglobin increase its affinity for O2, so there is a leftward shift in the O2-Hb dissociation curve due to respiratory alkalosis. At any PaO2, Hb saturation is increased

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11
Q

Describe ventilatory rates in an acclimatized person vs person just arriving at altitude

A

In persons that have acclimatized to high altitude, the ventilatory responses to both hypoxia and to higher PaCO2 are exaggerated. The acclimatized person’s ventilatory rate will increase when PaO2 falls below 63mmH whereas the un-acclimatized person’s Ve will increased when PaO2 falls below 55mmHg.

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12
Q

A-a gradient and hypoxia

A

In severe hypoxia, the O2 concentration gradient btw pulmonary capillaries and alveoli is small, so the driving force for diffusion is smaller and diffusion may be limited. This is even worse at a higher CO when RBCs travel faster through lung capillaries. During exercise at extreme high altitude, the A-a gradient may be increased even in the abscence of any lung disease

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13
Q

List illnesses associated with exposure to high altitude

A

Acute mountain sickness, high altitude pulmonary edema (HAPE), high altitude cerebral edema (HACE) and chronic mountain sickness

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14
Q

Describe acute mountain sickness manifestations

A

AMS is manifest as headache (near universal), nausea, malaise, insomnia, and anorexia. It is almost universal above 18,000ft.

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15
Q

Acute mountain sickness mechanism

A

Increased brain volume in response to hypoxia, possibly due to cerebral edema and/or increased cerebral blood flow and intravascular volume.

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16
Q

Acute mountain sickness treatment

A

oral dexamethasone (a corticosteroid that blunts hypoxic induction of brain vessel permeability by altering gene expression) OR oral acetazolamide (a diuretic that causes a metabolic acidosis) are best as prevention. Ibuprofen, acclimatization, dexamethasone and acetazolamide may help with treatment

17
Q

High Altitude Cerebral Edema (HACE) manifestation

A

ataxia, confusion/combativeness, hallucinations, and coma

18
Q

HACE treatment

A

Oxygen, descent, mechanical ventilation (for coma), followed by IV dexamethasone

19
Q

High Altitude Pulmonary Edema (HAPE) manifestation

A

Cough, shortness of breath, fatigue. Hypoxia, lung rales and infiltrates on CXR. Pulmonary hypertension (in response to acute hypoxia), increased pulmonary arterial pressure

20
Q

Is HAPE cardiogenic or non?

A

HAPE is a noncardiogenic pulmonary edema (diuretics to decrease intravascular volume won’t help).

21
Q

What does pulmonary hypertension in HAPE lead to

A

Uneven vasoconstriction throughout th elung leading to scattered lung capillary breakdown with blood leakage into alveoli

22
Q

Treatment of HAPE and prevention

A

Immediate descent to lower altitude, oxygen, vasodilators such as nifedipine (lower pulmonary artery pressures). Prevention involves pulmonary vasodilators such as nifedipine and tadalafil, Salmeterol is a bronchodilator that increases clearance of water out of alveoli,

23
Q

Chronic mountain sickness manifestation

A

Polycythemia and pulmonary hypertension, with increased risk of stroke and heart failure. Increases risk of low infant birth weight and preeclampsia

24
Q

Who gets chronic mountain sickness

A

People who live above 10,000 ft who are not as well adapted

25
Q

Physics of diving

A

Atmospheric (or barometric) pressure increases by 1 atmosphere (atm) for every 10 meters of depth in sea water. Holdingour breath prevents airways from being crushed, but the density of gas is increased due t compression. This increases the resistive work of breathing

26
Q

Blood return to lungs while diving

A

Blood return to lungs is increased from squeezed limbs/abdomen and this decreases compliance

27
Q

How does airflow change while diving

A

As the density of gas increases, so does the resistance to flow, so there are decreased flow rates in the lung and the work of breathing increases.

28
Q

Which medical condtions do not tolerate diving well

A

Airflow limiting diseases such as COPD, moderate asthma

29
Q

Lung volumes while diving

A

If pressure increases by factor of 2, volume of gas decreases by half, thus lung volumes decrease.

30
Q

How does diving affect gases in blood and tissues

A

Inert gases like nitrogen can form bubbles because compression increases the dissolved gas in blood

31
Q

Decompression sickness description

A

The bends. With deeper/longer dives, the Partial pressure of inert gases (eg N2) increases in tissues and blood. Supersaturated gases in tissues can form bubbles if a quick decrease in pressure occurs (surfacing). Rapidly ascent: air bubbles ↑ in size and # causing organ damage, limb pain (bends)

32
Q

Prevention/treatment of decompression sickness

A

re-compression, adhere to dive tables, hyperbaric chamber, graded surfacing (professional divers)

33
Q

Nitrogen narcosis

A

Breathing compressed air with 79% N2 at depth leads to increased partial pressure of N2 in tissues (>30 meteres in depth). High N2 in brain causes altered mental states. Helium can be used to decrease this

34
Q

Shallow water blackout

A

Forced hyperventilation decreases chemoreceptor/PaCO2 input to respiratory center so that you can hold your breath for a long time. The brain ranks the PCO2 info over the PaO2 info. If PaO2 goes too low, you become anoxic and drown.

35
Q

Barotrauma

A

Increased pressure in airways can lead to extravasation of air along bronchial tree into interstitium (and so can rapid ascent). This can cause pneumothorax, pneumomediastinum or air embolism