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Lung in-extreme-environments

This document examines the effects of extreme environments on lung physiology, covering underwater diving, high altitude, and space conditions. It discusses the challenges of gas pressures, decompression stress, and the associated risks like pulmonary barotrauma and decompression sickness. Additionally, it highlights respiratory adaptations to these environments and recommendations for prevention and management of related health issues.

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Lung in extreme environments Dr. Karan Madan Senior resident Deptt. Of Pulmonary Medicine
Introduction Lung - First barrier between the body and its surrounding atmosphere. Various activities expose humans to different environments in which the stresses are beyond our physiologic capabilities. Extreme environments & the lung U d t Underwater High altitude Space Extreme cold
History of Diving – Apnoea diving SCUBA Costeau & Gagnan 1943 French navy
Lung p y g physiology in diving gy g Diving - Exposure to higher than normal ambient pressure. Compression, isobaric, and decompression phases. One atmosphere - 760 mm Hg or 101.3 kPa. One bar corresponds to a pressure of 750 mm Hg, 100 kPa, or 10 msw (Metres of sea water). Depth of 30 msw - pressure of 4 bars 100 msw - pressure equivalent of 11 bars. 4 bars / 30 msw, the fractional concentration of oxygen is still 0.21 but the partial pressure is 84 kPa.
Hyperoxia - > 50 kPa , reduction in VC dependent on pressure and exposure time. p Unit pulmonary toxic dose (UPTD) - toxic effect equivalent to the exposure t oxygen at 101 kP f 1 minute. to t kPa for i t Symptoms of nonproductive coughing and a retrosternal burning sensation before a reduction in VC takes place. The recovery of VC reductions as large as 20%–30% is usually complete within 1 or 2 weeks. Toxic effects of oxygen are mediated by reactive oxygen species, and inflammatory changes in the lung parenchyma are induced.
Gas density and respiratory mechanical loading Density increases p p y proportionately with pressure. y p Airway resistance is proportional to density with turbulent flow characteristics Maximal expiratory flow Ma imal e pirator flo rate is in ersel proportional to the sq are inversely square root gas density. When breathing air at a pressure of 4 bars, gas density is 4 times normal and maximum voluntary volume (MVV) and FEV1 are reduced by 50% of normal. normal To reduce the internal resistance of breathing gas mixtures, helium is usually used instead of air when diving deeper The helium and oxygen mixture breathed in deep experimental dives to pressures (500–700 msw) has a fractional concentration of oxygen of less than 2%, with the rest being helium and, sometimes, some nitrogen. it
Respiratory heat and water loss Gas mixtures used for diving are dry so as to prevent icing in the gas supply lines. l li Specific heat capacity for helium is five times greater than for nitrogen but density is only 0.18 g/L for helium and 1.25 g/L for nitrogen. Therefore, respiratory heat loss when diving with air remains higher compared with diving with helium-oxygen mixtures, g p g yg , because it is the product of density and specific heat capacity that determines heat loss. Respiratory heat loss when diving is always larger than at normal atmospheric pressure whatever the gas mixture is.
Decompression stress and venous gas microembolism Supersaturated fluids - Inherently unstable and there is a y risk of free gas evolving in gas bubbles. Gas bubbles - Interstitially in the tissues / more commonly commonly, intravascularly in venous blood. Large shower of venous gas microemboli (VGM) → large increase in pulmonary arterial pressure - spillover of gas bubbles to the pulmonary veins. veins Reductions in DlCO and maximal oxygen uptake correlating with the cumulative load of VGM have been demonstrated.
Pulmonary barotrauma (PBT) Exposure to ab upt p essu e changes. posu e abrupt pressure c a ges Individuals at risk of PBT - Astronauts, aviators, compressed air workers, and divers. Diving related PBT – Second among all causes of SCUBA diving fatalities. PBT during descent of apnoea dive - Lung g g squeeze PBT during ascent
PBT during ascent Boyle’s law – Relevance oy e s a e e a ce Rate of ascent vs rate of elimination. Overdistention – May lead to lung rupture Precipitating factors – Breath holding , airway obstruction. Transpulmonary pressure rather than absolute p intratracheal pressure is the critical factor.
Rupture P Peribronchial space P Pulmonary interstitial emphysema P Pneumomediastinum Pneumothorax /Pneumoperitoneum P Rupture into PA / Dissection into Pulmonary veins AGE (Arterial gas embolism) ( g ) P Head position, buoyancy of the gas bubbles, and blood p , y y g , flow dynamics – Gas bubbles (Brain) – Critical injury Fatal cases of PBT - Obstruction of the heart (pneumocardium) and central circulation after massive AGE Misapprehension that diving accidents do not occur in shallow water – Max risk just below surface
Symptoms appear on or shortly after surfacing , 5 mins (90 % cases) Without AGE ,only pulmonary symptoms may be present. Hoarseness /strange voice with mild chest pain after scuba dives – Think of PBT Risk factors for PBT - Technique of ascent - Intrapulmonary air trapping – Bullae/cysts p y pp g y No convincing data indicating PFT’s to be predictive for g g p detecting those divers who are at risk of PBT.
Decompression illness AGE as a result o PBT G esu t of DCS – Decompression sickness - Multiorgan system disorder - micro or macroscopic nitrogen bubble formation on surfacing. Pathogenesis – On ascent , dissolved inert gas in the tissue and blood forms a free gas phase to equalize the pressures Reaches lungs by venous return – Intravascular gas b bbl may be seen in absence of bubbles b i b f symptoms (Silent bubbles)
Clinical features of DCS Musculoskeletal/ Cutaneous – Type 1 DCS – “the bends” Cutis marmorata (Cutaneous manifestation) Most cases responsive to immediate recompression. More severe DCS T M DCS- Type II- N II Neurologic, audiovestibular, or l i di tib l respiratory manifestations. Nitrogen saturation and elimination kinetics of neural tissues / Minimal ischemia tolerance. Marked interindividual variation – Sensory symptoms predominate – Risk of DCS negligible at 0 – 10 msw
Risk factors for DCS Exposure to cold – unclear mechanisms posu e co d u c ea ec a s s Predive exercise – Beneficial effects Obesity may be contributory Exposure to high altitude post diving - a minimum interval of 24 hours is recommended before flying breathing at depth – Even longer Respiratory DCI – “the chokes” y Rare Clinical symptoms tachypnoea, cough, cyanosis, y p yp , g , y , and thoracic discomfort or pain.
Management of DCI Delay - inversely related to outcome. y y Postpone time-consuming diagnostic procedures. CXR – Pneumothorax – Treat before recompression. Fast elimination of the gas phase and the correction of tissue hypoxia. H b i th lt i P O Hyperbaric oxygen therapy – R Results in PaO2 > 2000 mm Hg Most commonly used Algorithm - US Navy Table 6 Oxygen breathing at 18 msw for approximately 75 minutes and at 9 msw for approximately 3 hours, with air pauses in between to minimize adverse oxygen effects
Management of DCI If hyperbaric oxygen therapy not immediately available yp yg py y (eg, at remote locations) early administration of 100% oxygen Elevated serum creatine kinase level has been shown to be related to the size and severity of AGE Paradoxic gas embolism – PFO / Pulmonary capillaries / Intra or extrapulmonary right to left shunts Studies – 2.6 fold increase in the risk of DCI with PFO , but absolute increased risk relatively small.
Pulmonary edema Only recently been recognized as a diving-related y y g g clinical problem No evidence of a single common risk factor. Subjects affected once are at risk of further incidents. Dyspnea , cough, hemoptyses, hypoxemia, tachypnoea Radiographic findings usually normalize within 48 hours. Removal from water and with supportive treatment pp Subjects should be advised not to dive again. Nifedipine (5 mg) before the dive may prevent recurrence
Apnoea diving Hae Nyo Sponge divers Pearl divers Competitive freediving
Growing popularity of Apnoea diving Constant weight diving Free immersion Variable weight diving Static apnoea Dynamic apnoea D i No limit freediving – Most dangerous Not N t approved as sport d t Exhibition sport for diving extremists
Theoretical limits of diving depth g p Descent – Decrease in lung volume ( Boyle’s law) esce t ec ease u g ou e oy e s a ) Decrease below RV – Lung squeeze – harmful TLC/RV ratio – Determinant of diving depth Ex. TLC – 6L RV – 1.5 L so TLC/RV – 4 atm = 30 ( p ) msw (Concept till 1970) Bob croft – Father of american freediving 73 msw - Had exceptionally high TLC
Redistribution during apnoea dives – 1 to 1.5 L Therefore now TLC – 9.6 L (Pipin ferreiras WR ) RV– 2.2 L so TLC/RV = 4.4 Atm or 34 msw Redistribution 1.5 L – RV 0.7 L so TLC/RV = 127 msw Side effects – may lead to Alv. Hemorrhage / hemoptysis Also may occur due to STRUGGLE PHASE
Lung packing / Buccal pumping – They Will do any thing to dive deeper !!!! Can increase TLC by 30 50 % 30-50 (Average 1.5-3 L) Applying to Pipin Ferreiras TLC – 9.6 + 2 = 11.6 TLC / RV = 11.6 / 0.7 = 156 msw No reports of PBT associated with buccal pumping
Change in partial pressures of breathing gases Critical hypoxia - E Cii lh i Extended di i d d diving duration at significant depth. Loss of motor control and consciousness in most cases appears immediately pp y before or shortly after surfacing. Elite apnea divers are able to tolerate a lower Pao2 and oxygen saturation than controls and are more tolerant to carbon dioxide
Excessive hyperventilation yp PaCO2 decreased – Prolongs breaking point of approx. 55 to 60 mm Hg. Pure oxygen also prolongs the apnea time substantially. substantially Prolonged oxygen uptake during apnea - decreased PaO2. While ascending, rapid decompression of the lungs marked fall of PaO2. ( Sigmoid curve) More dangerous if divers engaged in strenous exhertion before diving SAMBA – Shallow water blackout (Fatal accidents)
Nitrogen narcosis & Decompression sickness “Rapture of the depth” “taravana” (Neurologic DCS) Nitrogen elimination slower than uptake Risk increases with repititve dives
Cardiovascular effects of Diving g DIVING REFLEX – Diving related bradycardia , usually g y y associated with peripheral vasoconstriction Breath-holding Breath holding at elevated lung volume and stimulation of facial trunks of the trigeminal nerve by water The lower the water temperature, the more pronounced the bradycardia. Normally the initial fall in heart rate - approx 60% to 70% of Normally, approx. the predive level. Rates as low as 10 to 15 beats per minute, however, are reported. In contrast to diving animals, in humans the diving reflex animals humans, usually is not associated with a fall in cardiac output
May lead to cardiac dysrhythmias with increasing incidence of supraventricular extrasystoles, particularly at the end of the dives – p y ,p y Sec. to cardiac dilatation Diving Di i response is acknowledged as an oxygen-conserving reflex i k l d d i fl in diving species that maintains perfusion to the brain, reduces cardiac work and blood flow to viscera and muscle and, thus, limits overall oxygen consumption In humans – Less eff. Reduction in CO – Increased BP – Increased eff Metabolic rate Splenic contraction – Increased PCV – Prolongs apnoea times.
High altitude related pulmonary disease Marco polo 1272 – “ the headache mountains” Spectrum of High altitude pulmonary p g p y illness 1. AMS , HACE 2. HAPE 3. PH from chronic hypoxia 4. CMS
Pulmonary physiology at height Ventilatory adaptation - Hypoxic ventilatory response (HVR) y y y ( ) – Measurable Minute ventilation is plotted against the PaO2 or arterial oxygen saturation. Acute response in ventilation to hypoxia is blunted by repository alkalosis, but the carotid body continues to undergo adaptation. adaptation Net result - ↑ Ventilation at any PaO2. Related to climbers’ success at climbing to extreme altitudes
Greater heights come for a greater price Increased work of breathing for any given level of work , greater the ascent t
Acute mountain sickness (AMS) Cause – Hypobaric hypoxia Incidence – 25 % of sojourners at 8000ft (2440 m) I id f j t ) At 2400 3100 m , SpO2 – 92-93 % 2400-3100 92 93 %. At 3660 m , SpO2 – low 80’s Sleeping at high altitudes – Nocturnal periodic breathing – 5-8 % decline in saturation Fact known to mountaineers – “ climb high sleep low” At himalayan trekking altitudes, (3000-4500m) Incidence of AMS approx. 50 %
Features of AMS Onset within 24 hours , usually first few hours. Hallmark symptoms – Neurologic Lake louise scoring system Headache and at least one of – GI complaints (anorexia ,nausea & vomitings) , lightheadedness, insomnia, and malaise. Pathogenesis – Cerebral edema appears to be the cardinal event HACE – Severest form of AMS Reascent AMS & Reascent HACE occur – Acclimatization is not permanent (Hypoxia induced gene expression)
Management of AMS Most patients - Mild to moderate symptoms that abate in 2–3 days without specific treatment. Mild to moderate AMS - Several therapies are efficacious in hastening recovery (acetazolamide, dexamethasone, oxygen, and descent) Severe symptoms/HACE - Transport to lower altitudes. Those who develop AMS - susceptible and usually have a recurrence with f future ascents unless they take preventative measures. AMS rarely results in death, unless evacuation of rare patients who have HACE to lower altitude is not possible.
HAPE (High altitude pulmonary edema) Symptoms at least 2 of 4: Dyspnea at rest, cough, weakness y y g or decreased exercise performance, and chest congestion or tightness. Diagnosis of HAPE - At least 2 of 4criteria: (1) crackles or wheezing, (2) central cyanosis, (3) tachypnea, and (4) tachycardia. The incidence of HAPE (0 1 – 1 %) is lower than that of AMS (0.1 AMS. HAPE usually occurs within the first 5 days (Not on the first day)
Pathogenesis Most compelling theory - PAH with uneven hypoxic vasoconstriction leading to focal areas of pressure and flowrelated vascular shear and overperfusion. Endothelial failure, capillary leak, and eventual noncardiogenic pulmonary edema . Acute PAH is a central feature of HAPE and resolves with oxygen and descent. HAPE easily can result in death if descent and adequate oxygen cannot be provided. Effective preventive treatments available – Oral Nifedipine & Inhaled Salmeterol
Chronic mountain sickness CMS has a more important human impact worldwide than AMS and HAPE. d HAPE Sequelae of polycythemia fatigue and right heart failure from polycythemia, fatigue, pulmonary hypertension in adulthood after decades of life in a hypoxic environment. High-altitude dwellers sustain distinct illnesses related to chronic hypoxia, such as having low birthweight children. yp , g g After a period at low altitude, some high altitude residents also experience more severe PH, even the development of HAPE, on i PH th d l t f HAPE returning to their usual high-altitude residence. Acclimatization is not permanent.
Lung in Space
Making measurements in Microgravity Parabolic flight in aircraft Adv. – Accesible / Inexpensive Disadv. – Short periods of p microgravity interspersed with hypergravity Motion sickness
Space shuttle & ISS US led ISS – Research friendly environment Spacelab / Spacehab Problems – Small study population Limited time for experiments Absence of experimenter High maintainence g requirements Studies require design so viable results with n= 4 or 3 Subjects serve as their own controls Analogs of microgravity – HDT , Thermoneutral water immersion Do not adequately simulate microgravity
Lung volumes & Chest wall mechanics in space – Vital Capacity Changes likely due to changes in intrathoracic blood l bl d volume
FRC µg reduces FRC by approx. 10 %. Mainly d t M i l due to cranial shift of diaphragm & abdominal contents when i l hift f di h bd i l t t h gravity removed. RV In sustained µg , RV shown to ↓ by app. 18 %. Plausible cause - Large apicobasal gradients in regional lung volume present in 1 G, are abolished in µg.
Reduction in MEFR & PEFR ‘s Lack of a firm platform to push against during the maneuver , p p g g recovery later - may be the result of improved subject performance as they adapted to µg Shape & movement of the chest wall Inward displacement of the abdominal wall seen in µg causing a reduction in lung volume Increase in abdominal wall compliance increase in the abdominal contribution to TV from 33% in 1 G to 51% in µg. µg Diffusing capacity Substantial ↑ by 28% on exposure , remained elevated over the course of 9-day flight. Due to parallel increase in pulmonary capillary blood volume (Vc) & membrane-diffusing capacity (Dm). Attributed to transition of the lung from its zone 1, 2, 3 configuration to an entirely zone 2 or zone 3 – more uniform filling.
Pulmonary perfusion No direct measurements of the distribution of pulmonary blood flow during space flight. Radioactively labeled microaggregated albumen- some increase in apical blood flow compared with the upright position in 1 G. Carbon dioxide expirogram - Cardiogenic oscillations & terminal fall in CO2 – Indicators of inhomogenity of perfusion
The ventilatory response to exercise largely is unaffected by μG. Cardiac output increase with increasing VO2 is substantially lower that that measured upright or supine on the ground preflight. Ventilatory control - Substantial changes in the ventilatory response to hypoxia (Nearly halving of hypoxic drive) Ventilatory response to carbon dioxide essentially unchanged Given the magnitude of the reduction in hypoxic response in mG and sup e, it is interesting to specu ate o t e poss b e role t s a d supine, t s te est g speculate on the possible o e this may have in some hypoventilation syndromes and their postural components.
Increased BP at the level of the carotid bodies bodies. In the upright position in 1 G, BP at the carotid bodies is lower than at heart level because of the hydrostatic p y pressure difference. Difference is abolished in the supine position and in μG. i iti di G In dogs, it is established that stimulation of the carotic baroreceptors results in an inhibition of the carotid chemoreceptor output
Sleep in space Significant ↓ in AHI and time spent snoring Demonstration of gravitatinal component of OSA Marked reduction in Respiratory related arousals Conclusion – Poor sleep in space flight not related to respiratory system
Extravehicular activity (EVA) Space Shuttle and the ISS - 760 mm Hg breathing air environment environment. Need for mobility - Space suits operate at a much lower pressure y p p p with a 100% oxygen environment . Denitrogenation procedure must be performed before an EVA (220 D it ti d tb f db f mm Hg United States space suit). A direct transition from cabin pressure to suit pressure would result in decompression sickness (DCS). To date, no astronaut formally has reported DCS during EVA Presence of VGM - More than 50% of the participants had detectable bubbles, as indicated by Doppler ultrasound.
Lung p y g physiology in Antarctica gy
Observations made at the Soviet antarctic station, Vostok. Tachypnea and considerable hyperventitation during the first days after arrival. With acclimatization, the frequency of respiration normal, depth of resp. increased. Pulmonary ventilation decreased, lowest level during the polar night period (Still 1 1/2 times greater than the normal value). Every individual had Cheyne-Stokes respiration, especially during sleep. The blood oxygenation during quiet respiration was 80–87%, increasing with voluntary hyperventilation to 85–94%. Hypoxemia rose considerably with voluntary breath holding and physical strain accomp. with dyspnoea
Healthy tropical Indian men (n= 10). Baseline recordings at Delhi. Delhi Initial decrease in VC, FVC, FEV1, PEFR and MVV VC FVC FEV1 on acute exposure to cold stress Gradual recovery during acclimatisation for 4 weeks and a further significant improvement after 9 weeks of stay at the arctic region. On return to India all the parameters reached near baseline values except for MVV which remained slightly elevated. Respiratory responses during acute cold exposure are similar to those of initial altitude responses. responses
Summary Humans are exposed to a number of extreme environmental stresses and lung is a major organ i t l t dl i j affected. Understanding of physiological response of the respiratory system to these stresses is important important. It can help in prevention and timely treatment of illnesses resulting due to exposure to extreme environmental stresses.

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Lung in-extreme-environments

  • 1.
    Lung in extremeenvironments Dr. Karan Madan Senior resident Deptt. Of Pulmonary Medicine
  • 2.
    Introduction Lung - Firstbarrier between the body and its surrounding atmosphere. Various activities expose humans to different environments in which the stresses are beyond our physiologic capabilities. Extreme environments & the lung U d t Underwater High altitude Space Extreme cold
  • 3.
    History of Diving– Apnoea diving SCUBA Costeau & Gagnan 1943 French navy
  • 4.
    Lung p y gphysiology in diving gy g Diving - Exposure to higher than normal ambient pressure. Compression, isobaric, and decompression phases. One atmosphere - 760 mm Hg or 101.3 kPa. One bar corresponds to a pressure of 750 mm Hg, 100 kPa, or 10 msw (Metres of sea water). Depth of 30 msw - pressure of 4 bars 100 msw - pressure equivalent of 11 bars. 4 bars / 30 msw, the fractional concentration of oxygen is still 0.21 but the partial pressure is 84 kPa.
  • 5.
    Hyperoxia - >50 kPa , reduction in VC dependent on pressure and exposure time. p Unit pulmonary toxic dose (UPTD) - toxic effect equivalent to the exposure t oxygen at 101 kP f 1 minute. to t kPa for i t Symptoms of nonproductive coughing and a retrosternal burning sensation before a reduction in VC takes place. The recovery of VC reductions as large as 20%–30% is usually complete within 1 or 2 weeks. Toxic effects of oxygen are mediated by reactive oxygen species, and inflammatory changes in the lung parenchyma are induced.
  • 6.
    Gas density andrespiratory mechanical loading Density increases p p y proportionately with pressure. y p Airway resistance is proportional to density with turbulent flow characteristics Maximal expiratory flow Ma imal e pirator flo rate is in ersel proportional to the sq are inversely square root gas density. When breathing air at a pressure of 4 bars, gas density is 4 times normal and maximum voluntary volume (MVV) and FEV1 are reduced by 50% of normal. normal To reduce the internal resistance of breathing gas mixtures, helium is usually used instead of air when diving deeper The helium and oxygen mixture breathed in deep experimental dives to pressures (500–700 msw) has a fractional concentration of oxygen of less than 2%, with the rest being helium and, sometimes, some nitrogen. it
  • 7.
    Respiratory heat andwater loss Gas mixtures used for diving are dry so as to prevent icing in the gas supply lines. l li Specific heat capacity for helium is five times greater than for nitrogen but density is only 0.18 g/L for helium and 1.25 g/L for nitrogen. Therefore, respiratory heat loss when diving with air remains higher compared with diving with helium-oxygen mixtures, g p g yg , because it is the product of density and specific heat capacity that determines heat loss. Respiratory heat loss when diving is always larger than at normal atmospheric pressure whatever the gas mixture is.
  • 8.
    Decompression stress andvenous gas microembolism Supersaturated fluids - Inherently unstable and there is a y risk of free gas evolving in gas bubbles. Gas bubbles - Interstitially in the tissues / more commonly commonly, intravascularly in venous blood. Large shower of venous gas microemboli (VGM) → large increase in pulmonary arterial pressure - spillover of gas bubbles to the pulmonary veins. veins Reductions in DlCO and maximal oxygen uptake correlating with the cumulative load of VGM have been demonstrated.
  • 9.
    Pulmonary barotrauma (PBT) Exposureto ab upt p essu e changes. posu e abrupt pressure c a ges Individuals at risk of PBT - Astronauts, aviators, compressed air workers, and divers. Diving related PBT – Second among all causes of SCUBA diving fatalities. PBT during descent of apnoea dive - Lung g g squeeze PBT during ascent
  • 10.
    PBT during ascent Boyle’slaw – Relevance oy e s a e e a ce Rate of ascent vs rate of elimination. Overdistention – May lead to lung rupture Precipitating factors – Breath holding , airway obstruction. Transpulmonary pressure rather than absolute p intratracheal pressure is the critical factor.
  • 11.
    Rupture P Peribronchialspace P Pulmonary interstitial emphysema P Pneumomediastinum Pneumothorax /Pneumoperitoneum P Rupture into PA / Dissection into Pulmonary veins AGE (Arterial gas embolism) ( g ) P Head position, buoyancy of the gas bubbles, and blood p , y y g , flow dynamics – Gas bubbles (Brain) – Critical injury Fatal cases of PBT - Obstruction of the heart (pneumocardium) and central circulation after massive AGE Misapprehension that diving accidents do not occur in shallow water – Max risk just below surface
  • 12.
    Symptoms appear onor shortly after surfacing , 5 mins (90 % cases) Without AGE ,only pulmonary symptoms may be present. Hoarseness /strange voice with mild chest pain after scuba dives – Think of PBT Risk factors for PBT - Technique of ascent - Intrapulmonary air trapping – Bullae/cysts p y pp g y No convincing data indicating PFT’s to be predictive for g g p detecting those divers who are at risk of PBT.
  • 13.
    Decompression illness AGE asa result o PBT G esu t of DCS – Decompression sickness - Multiorgan system disorder - micro or macroscopic nitrogen bubble formation on surfacing. Pathogenesis – On ascent , dissolved inert gas in the tissue and blood forms a free gas phase to equalize the pressures Reaches lungs by venous return – Intravascular gas b bbl may be seen in absence of bubbles b i b f symptoms (Silent bubbles)
  • 14.
    Clinical features ofDCS Musculoskeletal/ Cutaneous – Type 1 DCS – “the bends” Cutis marmorata (Cutaneous manifestation) Most cases responsive to immediate recompression. More severe DCS T M DCS- Type II- N II Neurologic, audiovestibular, or l i di tib l respiratory manifestations. Nitrogen saturation and elimination kinetics of neural tissues / Minimal ischemia tolerance. Marked interindividual variation – Sensory symptoms predominate – Risk of DCS negligible at 0 – 10 msw
  • 15.
    Risk factors forDCS Exposure to cold – unclear mechanisms posu e co d u c ea ec a s s Predive exercise – Beneficial effects Obesity may be contributory Exposure to high altitude post diving - a minimum interval of 24 hours is recommended before flying breathing at depth – Even longer Respiratory DCI – “the chokes” y Rare Clinical symptoms tachypnoea, cough, cyanosis, y p yp , g , y , and thoracic discomfort or pain.
  • 16.
    Management of DCI Delay- inversely related to outcome. y y Postpone time-consuming diagnostic procedures. CXR – Pneumothorax – Treat before recompression. Fast elimination of the gas phase and the correction of tissue hypoxia. H b i th lt i P O Hyperbaric oxygen therapy – R Results in PaO2 > 2000 mm Hg Most commonly used Algorithm - US Navy Table 6 Oxygen breathing at 18 msw for approximately 75 minutes and at 9 msw for approximately 3 hours, with air pauses in between to minimize adverse oxygen effects
  • 17.
    Management of DCI Ifhyperbaric oxygen therapy not immediately available yp yg py y (eg, at remote locations) early administration of 100% oxygen Elevated serum creatine kinase level has been shown to be related to the size and severity of AGE Paradoxic gas embolism – PFO / Pulmonary capillaries / Intra or extrapulmonary right to left shunts Studies – 2.6 fold increase in the risk of DCI with PFO , but absolute increased risk relatively small.
  • 18.
    Pulmonary edema Only recentlybeen recognized as a diving-related y y g g clinical problem No evidence of a single common risk factor. Subjects affected once are at risk of further incidents. Dyspnea , cough, hemoptyses, hypoxemia, tachypnoea Radiographic findings usually normalize within 48 hours. Removal from water and with supportive treatment pp Subjects should be advised not to dive again. Nifedipine (5 mg) before the dive may prevent recurrence
  • 19.
    Apnoea diving Hae Nyo Spongedivers Pearl divers Competitive freediving
  • 20.
    Growing popularity ofApnoea diving Constant weight diving Free immersion Variable weight diving Static apnoea Dynamic apnoea D i No limit freediving – Most dangerous Not N t approved as sport d t Exhibition sport for diving extremists
  • 21.
    Theoretical limits ofdiving depth g p Descent – Decrease in lung volume ( Boyle’s law) esce t ec ease u g ou e oy e s a ) Decrease below RV – Lung squeeze – harmful TLC/RV ratio – Determinant of diving depth Ex. TLC – 6L RV – 1.5 L so TLC/RV – 4 atm = 30 ( p ) msw (Concept till 1970) Bob croft – Father of american freediving 73 msw - Had exceptionally high TLC
  • 22.
    Redistribution during apnoeadives – 1 to 1.5 L Therefore now TLC – 9.6 L (Pipin ferreiras WR ) RV– 2.2 L so TLC/RV = 4.4 Atm or 34 msw Redistribution 1.5 L – RV 0.7 L so TLC/RV = 127 msw Side effects – may lead to Alv. Hemorrhage / hemoptysis Also may occur due to STRUGGLE PHASE
  • 23.
    Lung packing /Buccal pumping – They Will do any thing to dive deeper !!!! Can increase TLC by 30 50 % 30-50 (Average 1.5-3 L) Applying to Pipin Ferreiras TLC – 9.6 + 2 = 11.6 TLC / RV = 11.6 / 0.7 = 156 msw No reports of PBT associated with buccal pumping
  • 24.
    Change in partialpressures of breathing gases Critical hypoxia - E Cii lh i Extended di i d d diving duration at significant depth. Loss of motor control and consciousness in most cases appears immediately pp y before or shortly after surfacing. Elite apnea divers are able to tolerate a lower Pao2 and oxygen saturation than controls and are more tolerant to carbon dioxide
  • 25.
    Excessive hyperventilation yp PaCO2 decreased– Prolongs breaking point of approx. 55 to 60 mm Hg. Pure oxygen also prolongs the apnea time substantially. substantially Prolonged oxygen uptake during apnea - decreased PaO2. While ascending, rapid decompression of the lungs marked fall of PaO2. ( Sigmoid curve) More dangerous if divers engaged in strenous exhertion before diving SAMBA – Shallow water blackout (Fatal accidents)
  • 26.
    Nitrogen narcosis &Decompression sickness “Rapture of the depth” “taravana” (Neurologic DCS) Nitrogen elimination slower than uptake Risk increases with repititve dives
  • 27.
    Cardiovascular effects ofDiving g DIVING REFLEX – Diving related bradycardia , usually g y y associated with peripheral vasoconstriction Breath-holding Breath holding at elevated lung volume and stimulation of facial trunks of the trigeminal nerve by water The lower the water temperature, the more pronounced the bradycardia. Normally the initial fall in heart rate - approx 60% to 70% of Normally, approx. the predive level. Rates as low as 10 to 15 beats per minute, however, are reported. In contrast to diving animals, in humans the diving reflex animals humans, usually is not associated with a fall in cardiac output
  • 28.
    May lead tocardiac dysrhythmias with increasing incidence of supraventricular extrasystoles, particularly at the end of the dives – p y ,p y Sec. to cardiac dilatation Diving Di i response is acknowledged as an oxygen-conserving reflex i k l d d i fl in diving species that maintains perfusion to the brain, reduces cardiac work and blood flow to viscera and muscle and, thus, limits overall oxygen consumption In humans – Less eff. Reduction in CO – Increased BP – Increased eff Metabolic rate Splenic contraction – Increased PCV – Prolongs apnoea times.
  • 29.
    High altitude relatedpulmonary disease Marco polo 1272 – “ the headache mountains” Spectrum of High altitude pulmonary p g p y illness 1. AMS , HACE 2. HAPE 3. PH from chronic hypoxia 4. CMS
  • 30.
    Pulmonary physiology atheight Ventilatory adaptation - Hypoxic ventilatory response (HVR) y y y ( ) – Measurable Minute ventilation is plotted against the PaO2 or arterial oxygen saturation. Acute response in ventilation to hypoxia is blunted by repository alkalosis, but the carotid body continues to undergo adaptation. adaptation Net result - ↑ Ventilation at any PaO2. Related to climbers’ success at climbing to extreme altitudes
  • 31.
    Greater heights comefor a greater price Increased work of breathing for any given level of work , greater the ascent t
  • 32.
    Acute mountain sickness(AMS) Cause – Hypobaric hypoxia Incidence – 25 % of sojourners at 8000ft (2440 m) I id f j t ) At 2400 3100 m , SpO2 – 92-93 % 2400-3100 92 93 %. At 3660 m , SpO2 – low 80’s Sleeping at high altitudes – Nocturnal periodic breathing – 5-8 % decline in saturation Fact known to mountaineers – “ climb high sleep low” At himalayan trekking altitudes, (3000-4500m) Incidence of AMS approx. 50 %
  • 33.
    Features of AMS Onsetwithin 24 hours , usually first few hours. Hallmark symptoms – Neurologic Lake louise scoring system Headache and at least one of – GI complaints (anorexia ,nausea & vomitings) , lightheadedness, insomnia, and malaise. Pathogenesis – Cerebral edema appears to be the cardinal event HACE – Severest form of AMS Reascent AMS & Reascent HACE occur – Acclimatization is not permanent (Hypoxia induced gene expression)
  • 34.
    Management of AMS Mostpatients - Mild to moderate symptoms that abate in 2–3 days without specific treatment. Mild to moderate AMS - Several therapies are efficacious in hastening recovery (acetazolamide, dexamethasone, oxygen, and descent) Severe symptoms/HACE - Transport to lower altitudes. Those who develop AMS - susceptible and usually have a recurrence with f future ascents unless they take preventative measures. AMS rarely results in death, unless evacuation of rare patients who have HACE to lower altitude is not possible.
  • 35.
    HAPE (High altitudepulmonary edema) Symptoms at least 2 of 4: Dyspnea at rest, cough, weakness y y g or decreased exercise performance, and chest congestion or tightness. Diagnosis of HAPE - At least 2 of 4criteria: (1) crackles or wheezing, (2) central cyanosis, (3) tachypnea, and (4) tachycardia. The incidence of HAPE (0 1 – 1 %) is lower than that of AMS (0.1 AMS. HAPE usually occurs within the first 5 days (Not on the first day)
  • 36.
    Pathogenesis Most compelling theory- PAH with uneven hypoxic vasoconstriction leading to focal areas of pressure and flowrelated vascular shear and overperfusion. Endothelial failure, capillary leak, and eventual noncardiogenic pulmonary edema . Acute PAH is a central feature of HAPE and resolves with oxygen and descent. HAPE easily can result in death if descent and adequate oxygen cannot be provided. Effective preventive treatments available – Oral Nifedipine & Inhaled Salmeterol
  • 37.
    Chronic mountain sickness CMShas a more important human impact worldwide than AMS and HAPE. d HAPE Sequelae of polycythemia fatigue and right heart failure from polycythemia, fatigue, pulmonary hypertension in adulthood after decades of life in a hypoxic environment. High-altitude dwellers sustain distinct illnesses related to chronic hypoxia, such as having low birthweight children. yp , g g After a period at low altitude, some high altitude residents also experience more severe PH, even the development of HAPE, on i PH th d l t f HAPE returning to their usual high-altitude residence. Acclimatization is not permanent.
  • 38.
  • 39.
    Making measurements inMicrogravity Parabolic flight in aircraft Adv. – Accesible / Inexpensive Disadv. – Short periods of p microgravity interspersed with hypergravity Motion sickness
  • 40.
    Space shuttle &ISS US led ISS – Research friendly environment Spacelab / Spacehab Problems – Small study population Limited time for experiments Absence of experimenter High maintainence g requirements Studies require design so viable results with n= 4 or 3 Subjects serve as their own controls Analogs of microgravity – HDT , Thermoneutral water immersion Do not adequately simulate microgravity
  • 41.
    Lung volumes &Chest wall mechanics in space – Vital Capacity Changes likely due to changes in intrathoracic blood l bl d volume
  • 42.
    FRC µg reduces FRCby approx. 10 %. Mainly d t M i l due to cranial shift of diaphragm & abdominal contents when i l hift f di h bd i l t t h gravity removed. RV In sustained µg , RV shown to ↓ by app. 18 %. Plausible cause - Large apicobasal gradients in regional lung volume present in 1 G, are abolished in µg.
  • 43.
    Reduction in MEFR& PEFR ‘s Lack of a firm platform to push against during the maneuver , p p g g recovery later - may be the result of improved subject performance as they adapted to µg Shape & movement of the chest wall Inward displacement of the abdominal wall seen in µg causing a reduction in lung volume Increase in abdominal wall compliance increase in the abdominal contribution to TV from 33% in 1 G to 51% in µg. µg Diffusing capacity Substantial ↑ by 28% on exposure , remained elevated over the course of 9-day flight. Due to parallel increase in pulmonary capillary blood volume (Vc) & membrane-diffusing capacity (Dm). Attributed to transition of the lung from its zone 1, 2, 3 configuration to an entirely zone 2 or zone 3 – more uniform filling.
  • 44.
    Pulmonary perfusion No directmeasurements of the distribution of pulmonary blood flow during space flight. Radioactively labeled microaggregated albumen- some increase in apical blood flow compared with the upright position in 1 G. Carbon dioxide expirogram - Cardiogenic oscillations & terminal fall in CO2 – Indicators of inhomogenity of perfusion
  • 45.
    The ventilatory responseto exercise largely is unaffected by μG. Cardiac output increase with increasing VO2 is substantially lower that that measured upright or supine on the ground preflight. Ventilatory control - Substantial changes in the ventilatory response to hypoxia (Nearly halving of hypoxic drive) Ventilatory response to carbon dioxide essentially unchanged Given the magnitude of the reduction in hypoxic response in mG and sup e, it is interesting to specu ate o t e poss b e role t s a d supine, t s te est g speculate on the possible o e this may have in some hypoventilation syndromes and their postural components.
  • 46.
    Increased BP atthe level of the carotid bodies bodies. In the upright position in 1 G, BP at the carotid bodies is lower than at heart level because of the hydrostatic p y pressure difference. Difference is abolished in the supine position and in μG. i iti di G In dogs, it is established that stimulation of the carotic baroreceptors results in an inhibition of the carotid chemoreceptor output
  • 47.
    Sleep in space Significant↓ in AHI and time spent snoring Demonstration of gravitatinal component of OSA Marked reduction in Respiratory related arousals Conclusion – Poor sleep in space flight not related to respiratory system
  • 48.
    Extravehicular activity (EVA) SpaceShuttle and the ISS - 760 mm Hg breathing air environment environment. Need for mobility - Space suits operate at a much lower pressure y p p p with a 100% oxygen environment . Denitrogenation procedure must be performed before an EVA (220 D it ti d tb f db f mm Hg United States space suit). A direct transition from cabin pressure to suit pressure would result in decompression sickness (DCS). To date, no astronaut formally has reported DCS during EVA Presence of VGM - More than 50% of the participants had detectable bubbles, as indicated by Doppler ultrasound.
  • 49.
    Lung p y gphysiology in Antarctica gy
  • 50.
    Observations made atthe Soviet antarctic station, Vostok. Tachypnea and considerable hyperventitation during the first days after arrival. With acclimatization, the frequency of respiration normal, depth of resp. increased. Pulmonary ventilation decreased, lowest level during the polar night period (Still 1 1/2 times greater than the normal value). Every individual had Cheyne-Stokes respiration, especially during sleep. The blood oxygenation during quiet respiration was 80–87%, increasing with voluntary hyperventilation to 85–94%. Hypoxemia rose considerably with voluntary breath holding and physical strain accomp. with dyspnoea
  • 52.
    Healthy tropical Indianmen (n= 10). Baseline recordings at Delhi. Delhi Initial decrease in VC, FVC, FEV1, PEFR and MVV VC FVC FEV1 on acute exposure to cold stress Gradual recovery during acclimatisation for 4 weeks and a further significant improvement after 9 weeks of stay at the arctic region. On return to India all the parameters reached near baseline values except for MVV which remained slightly elevated. Respiratory responses during acute cold exposure are similar to those of initial altitude responses. responses
  • 53.
    Summary Humans are exposedto a number of extreme environmental stresses and lung is a major organ i t l t dl i j affected. Understanding of physiological response of the respiratory system to these stresses is important important. It can help in prevention and timely treatment of illnesses resulting due to exposure to extreme environmental stresses.