respiratory physiology at high altitudes

RESPIRATORY PHYSIOLOGY AT HIGH ALTITUDES

DR. DAVIS KURIAN

High altitude = 1,500–3,500 metres (4,900–11,500 ft)

Very high altitude = 3,500–5,500 metres (11,500–18,000 ft)

Extreme altitude = above 5,500 metres (18,000 ft)

The death zone - altitudes above a certain point where the amount of oxygen is insufficient to sustain human life. This point is generally tagged as 8,000 m (26,000 ft) [less than 356 millibars of atmospheric pressure]

Classification of heights

Atmospheric pressure decreases with increase in altitude.

At 5000m it is only half the normal pressure –

½ X 760=380mm Hg. So PO2 of inspired gas

= (380-47)*0.2093 = 70mm Hg

HYPERVENTILATION: Most important mechanism In normal ventilation

PCO2 = 40mm Hg, respiratory exchange ratio = 1, PO2 = 3mm Hg. In hyperventilation – PCO2 = 8mm Hg, alveolar PO2

= 35mm Hg. Mechanism – hypoxic stimulation of peripheral

chemoreceptors – decreased PCO2 and alkalosis – inhibits hyperventilation – inhibition removed by excretion of excess HCO3 by kidneys.

Increased sensitivity of carotid bodies to hypoxia.

ACCLIMATIZATION AT HIGH ALTITUDES

POLYCYTHEMIA Increased RBC concentration – increased Hb

concentration – increases O2 carrying capacity. Mechanism : hypoxemia – stimulates erythropoietin

secretion from kidneys – stimulates bone marrow – polycythemia.

Disadvantage – increases blood viscosity


OTHER CHANGES:

ODC –> right (at moderate heights) –d/t increased 2,3 DPG and respiratory alkalosis – promotes O2 release.

ODC --> left (at very high altitudes) – d/t alkalosis – Increased O2 uptake form pulmonary capillaries.

Number of capillaries per unit volume in peripheral tissues increases and changes occur in the oxidative enzymes in cells.

Increase in maximum breathing capacity because the air is less dense, but O2 uptake declines above 4600m.


Alveolar hypoxia – pulmonary vasoconstriction – increased pulmonary arterial pressure – increased work of right heart – hypertrophy.

Increased pulmonary arterial pressure – pulmonary edema – d/t uneven arteriolar constriction and leakage from unprotected and damaged capillaries. The fluid has increased proteins


Usually above 8,000 feet (2,400 meters) in un-acclimatized climbers.

The faster you climb to a high altitude, the more likelihood of acute mountain sickness.

Symptoms include – nausea, vomiting, headache, fatigue, dizziness, palpitation, loss of apetite and insomnia.

Mechanisms postulated are cerebral edema and alkalosis due to hypoxemia (hypoxemia – arteriolar dilatation – limit of cerebral autoregulatory mechanisms – cerebral edema due to fluid transudition.)

In more severe cases – high altitude pulmonary edema and high altitude cerebral edema develops.

ACUTE MOUNTIAN SICKNESS

Symptoms – reduced by large doses glucocorticoids (decreases cerebral edema) and acetazolamide (decreases alkalosis –by inhibiting carbonic anhydrase).

If not treated – may lead to ataxia, disorientation, coma and finally death – d/t tentorial herniation of brain tissue.

Keys to preventing acute mountain sickness include: Climb the mountain gradually Stop for a day or two of rest for every 2,000 feet (600

meters) above 8,000 feet (2,400 meters) Sleep at a lower altitude when possible Learn how to recognize early symptoms of mountain

sickness

ACUTE MOUNTIAN SICKNESS

HAPE - life-threatening form of non-cardiogenic pulmonary edema due to leaky capillaries.

HAPE - symptoms start gradually within the first 2-4 days at altitude.

Earliest symptoms - shortness of breath with exercise, with decreased exercise performance – may progress to - severe shortness of breath even at rest, a persistent cough sometimes with blood, chest tightness or congestion, and severe weakness.

If untreated - progress to coma and death.

HIGH ALTITUDE PULMONARY EDEMA

The Lake Louise Consensus Definition for High-Altitude Pulmonary Edema has set widely used criteria for defining HAPE symptoms:

Symptoms: at least two of Difficulty in breathing (dyspnea) at rest Cough Weakness or decreased exercise performance Chest tightness or congestion

Signs: at least two of Crackles or wheezing (while breathing) in at least one lung field Central cyanosis (blue skin color) Tachypnea (rapid shallow breathing) Tachycardia (rapid heart rate)

Symptoms worsen at night and tachypnea and tachycardia occurs at rest.


Suggested mechanisms include

Increased pulmonary arterial and capillary pressures (pulmonary hypertension) secondary to hypoxic pulmonary vasoconstriction.

An idiopathic non-inflammatory increase in the permeability of the vascular endothelium.


Treatment includes: Administration of oxygen, and descent to a lower

altitude as soon as possible. Take rest Dexamethasone, CCBs have also been found to be

effective. Phosphodiesterase inhibitors are also effective but can worsen headache


Also called Monge’s disease. Seen in long term residents of high altitude Ill defined syndrome of polycythemia, fatigue,

exercise intolerance and hypoxemia. Treatment is mainly return to lower altitudes

possible.

CHRONIC MOUNTAIN SICKNESS

OXYGEN TOXICITY

Experimental studies in guinea pigs - 100% O2 at atmospheric pressure for 48 hrs produced pulmonary edema.

First change that occurs in oxygen toxicity is in the endothelium of pulmonary capillaries and alveolo-capillary membrane similar to ARDS.

There is evidence of impaired gas exchange after 30hrs of inhalation of 100% O2.

In normal volunteers in experimental study, 100% O2 for 24 hrs produced substernal discomfort which is aggravated by deep breathing and the vital capacity decreased by 500-800ml – probably due to absorption atelectasis.

100% O2 in premature infants – blindness d/t retrolental fibroplasia – d/t local vasoconstriction caused by high PO2 – avoided when arterial PO2 is kept below 140 mm Hg.

Generation of free radicals – superoxide ions, activated hydroxyl ions, singlet O2 and hydrogen peroxide.

Free radicals react with DNA, sulfhydryl proteins and lipids.

Normally protected by SOD, Catalase, antioxidants and free radical scavengers.

PaO2 > 60 mmHg may depress ventilation in some patients with chronic hypercapnia.

FiO2 > 0.5 may cause atelectasis, O2 toxicity & or ciliary or leucocyte depression.

PaO2 > 80 mmHg may cause retinopathy of prematurity in premature infants (arterial O2 tension more important than alveolar O2 tension)

In infants with certain congenital heart ds such as hypoplastic left heart, high PaO2 can compromise balance b/w systemic and pulmonary blood flow and may also cause bronchopulmonary dysplasia.

Patients using 100% O2 for prolonged periods can have tracheobronchitis

Prolonged inhalation of 100% O2 can damage the lung – like absorption atelectasis, depression of mucociliary functions etc.

At high PO2 – CNS damage may result – resulting in seizures – which may be preceded by nausea, ringing in the ears or twitching of the face.

At PO2 of 4 atm – convulsions occur at a frequency of 30 per minute.

Suggested mechanism for CNS action – is the inactivation of certain enzymes esp dehydrogenases containing sulfhydryl groups.

Refers to CNS toxicity of O2 – d/t polymerisation of SH group of enzymes – inactivation – cellular damage – aggravated by stress, cold, fatigue, deficiency of trace elements – Se, Zn (antioxidant elements)

Muscle twitch, spasm, nausea, vomiting, dizziness, vision and hearing difficulty, twitching of facial muscles, irritability, confusion, sense of impending doom, trouble in breathing, in coordination, convulsions.

PAUL BERT EFFECT

Pulmonary toxicity – more than 0.5 ATA – affects pulmonary epithelium and inactivates surfactant – intra-alveolar edema and interstitial thickening – fibrosis and pulmonary atelectasis – resemble paraquat poisoning

Progresses in three phases - Tracheobronchtis ->ARDS - > pulmonary interstitial fibrosis

LORANE SMITH EFFECT

ABSORPTION ATELECTASIS

When 100% O2 is breathed in

Trapped gas in alveoli – 760mm Hg

Sum of partial pressure of gases in venous blood - <760 mm Hg.

Sum of partial pressures in alveoli > venous blood – gas difusion into blood – collapse of alveoli – difficult to reopen d/t surface tension forces

When air is breathed in – the same process happens – but at a slower rate – here the difference being the rate being limited by rate of diffusion of N2 – slow solubility – acts as splint – supports alveoli and delays collapse.

Post op atelectasis is common in patients treated with high oxygen mixtures.

Collapse of alveoli is more common at the base of lung where the parenchyma is less well expanded or the small airways are closed.

ABSORPTION ATELECTASIS

100% - not more than 12hrs 80% - not more than 24hrs 60% - not more than 36hrs

Goal should be to use lowest possible FiO2 compatible with adequate tissue oxygenation

OPTIMUM O2 USE

RESPIRATORY CHANGES IN SPACE FLIGHT

Absence of gravity – more uniform distribution of blood flow and hence small improvement in gas exchange.

Absence of sedimentation – altered deposition of inhaled aerosols.

Thoracic blood volume – initially increases and raises pulmonary capillary blood volume and diffusing capacity.

Postural hypotension occurs on return to earth – cardiovascular deconditioning.

Decalcification of bone and muscle atrophy occurs due to disuse and also a slight reduction in the red cell mass

RESPIRATORY CHANGES

DURING DIVING AND ASCEND

Diving – pressure increases by 1 atmosphere for every 10m (33ft) of descent – a non communicating gas cavity such as lung, middle ear or intracranial sinus – pressure difference causes compression on descent or over expansion on ascent.

Hence scuba divers should exhale as they ascend to prevent over inflation and possible rupture of lungs.

Increased density at depth increases the work of breathing – CO2 retention

Diving – high partial pressure of N2 – forces poorly soluble N2 into tissues (esp fat). The diffusion is slow because of the low solubility of N2 and equilibration takes hours.

Ascend – N2 diffuses out from the tissues. Rapid ascend – bubbles of N2 form – pain at the joints (bends), neurological symptoms – deafness, impaired vision and even paralysis may occur.

DECOMPRESSION SICKNESS

Management

Recompression – reduces volume of bubbles and force them back into circulation.

Reduced incidence with use of He-O2 mixture – helium has one and half times the solubility of N2 – so less dissolved in tissues & 1/7th the molecular wt of N2 – hence diffuses out more rapidly through tissues.

He-O2 mixture has less density hence reduces the work of breathing.

DECOMPRESSION SICKNESS

Mainly used by workers working on under water pipeline systems.

While not in water – they live in high pressure chambers on the supply ship – hence avoiding decompression sickness.

SATURATION DIVING

N2 – inert gas but affects CNS at high pressures.

At a depth of 50m (160ft) – euphoria can occur with increased N2 concentration – further high partial pressures – loss of coordination and coma occurs.

INERT GAS NARCOSIS

HYPERBARIC OXYGEN THERAPY

A mode of medical treatment where the patient breathes 100% oxygen at a pressure greater than one Atmosphere Absolute (1 ATA). Under these conditions, your lungs can gather more oxygen than would be possible breathing pure oxygen at normal air pressure.

The basis is to increase the concentration of dissolved oxygen. This helps fight bacteria and stimulate the release of substances called growth factors and stem cells, which promote healing.

HENRY’S LAW – states that the concentration of any gas in solution is proportional to the partial pressure.

Dissolved O2 in plasma :0.003ml / 100ml of blood / mm PO2

Breathing Air (PaO2 100mm Hg)0.3ml / 100ml of bloodBreathing 100% O2 (PaO2 600mm Hg)1.8ml / 100ml of bloodBreathing 100% O2 at 3 atm (PaO2 2000 mm Hg)6.0ml / 100ml of blood

Bubble reduction (Boyle’s law – P1V1=P2V2) Increasing the oxygen concentration of blood Enhanced host immune function Neovascularization Vasoconstriction

PHYSIOLOGICAL EFFECTS

ACUTE CHRONIC• Decompression sickness Radiation necrosis• Carbon monoxide poisoning Diabetic wounds of

lower limbs• Severe crush injuries Refractory osteomyelitis• Thermal burns• Acute arterial insufficiency• Clostridial gangrene• Necrotizing soft-tissue infection• Ischemic skin graft or flap

INDICATIONS

Temporary nearsightedness (myopia) caused by temporary eye lens changes

Middle ear injuries, including leaking fluid and eardrum rupture, due to increased air pressure

Lung collapse caused by air pressure changes (barotrauma)

Seizures as a result of too much oxygen (oxygen toxicity) in your central nervous system

In certain circumstances, fire — due to the oxygen-rich environment of the treatment chamber

RISKS ASSOCIATED

METHODS OF DELIVERING HBOT

MONOPLACE CHAMBER MULTIPLACE CHAMBER

respiratory physiology at high altitudes

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