Acute Effects of AltitudeRapid Ascent (Loss of Cabin Pressure): HypoxiaSleepiness, lazinessFalse sense of well-beingImpaired judgmentBlunted pain perceptionIncreasing errors on simple tasksDecreased visual acuityClumsinessTremors Loss of consciousness or even death

Acute Effects of AltitudeAscent to Moderate Altitude (Acute Mountain Sickness): Hypoxia and Hypocapnia; AlkalosisHeadache, DizzinessBreathlessness at restWeaknessMalaiseNausea, anorexiaSweating, palpitationsDimness of vision, partial deafnessSleeplessnessFluid retentionDyspnea on exertion

( PB - PH O) -

Decreased O2Increased CO2 O2 = 100 torrCO2 = 40 torr HPV HELPS MAINTAIN V / Q..

Hemoglobin saturation, %Partial pressure of oxygen, torr2040608010020406080100120140160P5050% Pco2 , pH temp, BPG

Physiologic Responses to High Altitude Relative to Sea Level Control ValuesIMMEDIATEEARLY ADAPTIVE(72H)LATE ADAPTIVE(2 to 6 WEEKS)Spontaneous Ventilation Minute ventilation Respiratory rate Tidal volume Arterial Po2 Arterial Pco2 Arterial pH Arterial HCO3-

Evaluation of Lung Function Vital capacity Maximum airflow rates Functional residual capacity Ventilatory response to inhaled CO2 Ventilatory response to hypoxia Pulmonary vascular resistance

Variable

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Variable,

Variable,

Physiologic Responses to High Altitude Relative to Sea Level Control ValuesIMMEDIATEEARLY ADAPTIVE(72H)LATE ADAPTIVE(2 to 6 WEEKS)Oxygen Transport Hemoglobin Erythropoietin P50 2,3 - BPG Cardiac output

Central Nervous System Headaches, nausea, insomnia Perception, judgment Spinal fluid pH Spinal fluid HCO3 Cerebral edema

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Arterial Blood Gases and Oxygen Content in Climbers on Mount EverestGrocott, et al., NEJM 360:140-149, 2009

Samples taken at 8440 m (=27,559 ft)From 4 climbers who had reached summitBreathed ambient air for 20 minutes Barometric pressure = 272 mm Hg

Arterial Blood Gases and Oxygen Content in Climbers on Mount Everest (n = 4)Grocott, et al., NEJM 360:140-149, 2009P barom = 272 mm HgPAO2 = 30.0 mm HgPaO2 = 24.6 mm HgSaO2 = 54%[Hb] = 19.3 g/100 ml blood CaO2 = 14.58 ml O2/100 ml bloodpHa = 7.53PaCO2 = 13.3 mm Hg[HCO3-] = 10.8 mmol/liter

Diving PhysiologyPhysiologic StressesThe severity of the stress depends on the depth attained, the length of the dive, whether the breath is held, or breathing apparatus is used.

Major physiologic stresses: Elevated ambient pressure Decreased effect of gravity Altered respiration Hypothermia Sensory impairment

airseawater

DepthGauge PressureAbsolute PressureGas VolumeDensity0 feet0 atm1 atm1 volume1 unit33 feet1 atm2 atm1/2 volume2 units66 feet2 atm3 atm1/3 volume3 units99 feet3 atm4 atm1/4 volume4 units

SubmarineBreath-hold DivingScuba Divingairseawater99 feet1 atm4 atm4 atm

Effects of immersion up to the neckRespiration :Pressure outside chest wall is now positive, averaging about 20 cm H2O. Intrathoracic pressure is less negative at end-expiration. FRC decreases about 50% ERV decreases about 70% VC slight decrease IRV increases Slight decrease in RV, probably due to increased pulmonary blood volume

Result: about 60% increase in the work of breathing

Effects of immersion up to the neckCardiovascular :

Increased venous return due to elevated abdominal pressure and decreased pooling in peripheral veins. (decreased ambient temperature will also lead to venoconstriction).

Increased venous return leads to increased central blood volume (approximately 500 ml). Right atrial pressure increases from about 2 to +16 mmHg.

Cardiac output and stroke volume increase about 30%.

Ventilation perfusion probably better matched.

Effects of immersion up to the neckRenal :

Elevated intrathoracic blood volume immersion diuresis. Urine flow increases 4-5 times but osmolal clearance increases very slightly.

Consistent with ADH suppresion or release of atrial natriuretic hormone.

The Diving Reflex Vagally mediated bradycardia Sympathetically mediated increased systemic vascular resistance, contraction of spleen Same effect as chemoreceptor stimulation without lung inflation reflex Sensors unknown in man

O2CO2RestWork

100Time (sec)Partial Pressure (mmHg)Dive1 Atm00204060O2CO2Descent2 Atm

Gas exchange during a 10 meter, one minute breath-hold dive Usually hyperventilate first Compression during descent, expansion during ascentSurface: PAO2 = 120mmHg PACO2 = 29mmHgPAN2 = 567mmHgPAO2 = 41mmHgPACO2 = 42mmHgPAN2 = 631mmHgPAO2 = 149mmHgPACO2 = 42mmHgPAN2 = 1143mmHg10 meters depth :Before:After:

Therefore, the transfer of O2 from alveolus to blood is undisturbed until ascent. However, the normal transfer of CO2 from blood to alveolus is reversed during descent and results in a significant retention of CO2 in the blood.

Physiologic Problems Encountered in Diving With Underwater Breathing ApparatusIncreased work of breathing not as great a problem since breathing gases at ambient pressure. However, increased gas density leads to increased airway resistance work of breathing. Helium is 1/7 as dense as N2, so at great depths breathe He-O2 mixture.

Respiratory sensitivity to CO2 is decreased at depth because of low breathing rates, high Po2 and increased gas density

Other Hazards at Depth Barotrauma Descent (squeeze): Ears Sinus Dental Pulmonary congestion, edema, hemorrhage Ascent: Ear Sinus Dental Pulmonary Burst Lung pneumothorax, air embolism GI eructation, flatus, abdominal discomfort

Decompression IllnessArterial Gas Embolism and Decompression Sickness

During diving the high ambient pressure PN2. The high PN2 helps dissolve this normally poorly soluble gas in the body tissues, especially fat, which has a relatively high N2 solubility. Therefore, tissues become supersaturated with N2During rapid ascent, the high ambient pressure falls rapidly, and bubbles of N2 form in the blood and body tissues, especially the joints and more dangerously, the CNS.Treatment : Recompression chamberPrevention : Decompression tables : He instead of N2 (He is about as soluble as N2)Can also get if travel in an airplane to soon after a dive

Nitrogen Narcosis high PN2 directly affects CNS at 100 ft.: euphoria, loss of memory, irrational behavior, etc. At greater depths : numbness of limbs, disorientation, motor impairment, loss of consciousness. Mechanism of N2 narcosis is unknown.

Oxygen Toxicity inhalation of 100% O2 at 760 mmHg or lower [O2] at higher pressure can cause both alveolar and CNS damage (convulsions at greater than 2.5Atm.) Mechanism of O2 toxicity is not known.

High Pressure Nervous Syndrome at very great depths divers experience decreased manual dexterity and tremors. Can be prevented by adding very small amounts of N2 to the inspired gas mixture.

**Figure 2-24 Maximal expiratory flow-volume curves representative of obstructive and restrictive diseases