GNG Hyperbaric physiology and medicine 1.pptx

hyperbaric physiology

1. HYPERBARIC PHYSIOLOGY AND MEDICINE MODERATOR : DR.B.SYAMASUNDARA RAO PROF, DEPT. OF ANAESTHESIOLOGY, CAIMS PRESENTER : DR.G.NAGARAJ PG Ist YEAR

2. HISTORY OF HYPERBARIC MEDICINE Hyperbaric means "relating to or occurring at pressures higher than normal atmospheric pressure .” Hyperbaric medicine began in the 19th century, when clinical improvement was observed after recompression of divers and compressed air workers with decompression sickness. It was subsequently used for a variety of diseases, including tuberculosis, heart failure, emphysema, bronchitis, asthma, croup, whooping cough, anemia, anorexia, dyspepsia, leukorrhea , menorrhagia , neuralgic pain, and depression, without any scientific basis.

3. Henshaw : 1662 Using organ bellows he adjusted the pressure inside a sealed chamber ( domicilium ) Acute conditions responded to increased pressure Chronic conditions required decreased pressure. Junod : 1834 Stated that hyperbaric pressure of 2-4 ATA “increased the circulation to the internal organs, improved the cerebral blood flow, and produced a feeling of well being.”

4. Fontaine: 1879 mobile hyperbaric chamber for anesthesia and surgery. Compressed to 1.25 to 1.33 atmospheres absolute (ATA), a nitrous oxide/oxygen mixture was provided to the patient . Breathing air in Fontaine's chamber would have provided an inspired P o 2 equivalent to 26% to 28% O 2 at 1 ATA. This was probably the first use of an elevated P o 2 during anesthesia and certainly the first administration of hyperbaric nitrous oxide. No accepted standards.

5. Cunningham, 1920 Kansas City Initially used to treat victims of the Spanish Influenza Later treated many maladies including hypertension, diabetes, syphilis and cancer In Cleveland in 1928, Cunningham built the largest hyperbaric chamber in history 5 stories tall 64 feet in diameter

6. HYPERBARIC PHYSIOLOGY The compression or decompression of a given amount of gas basically does three things. 1) it changes volume 2) it changes density 3) it changes the partial pressure of the constituent gases. These changes are better explained by various gas laws as follows..

7. Gas laws All the gases obey’s certain laws k/a gas laws. Boyle’s Law, Dalton’s Law, Henry’s Law and Graham’s Law.

8. 1. Boyle’s Law “At a constant temperature, the volume of a gas is inversely proportional to the pressure.” p ∞ 1 /v i.e., as the pressure increases, the volume of a gas decreases and vice versa. Density = mass / volume. (d=m/v) , i.e., d ∞ 1/v hence, d ∞ p.

9. i.e., As the pressure ↑ the volume of the space containing the gas molecules ↓ , but it still contains the same number of gas molecules. The molecules become more tightly packed as the volume ↓ . The molecules are denser, more concentrated in a smaller area. Consequence: The volume of the alveolus ↓ as the pressure ↑ around it. The oxygen molecules in the alveolus become more concentrated or denser which presents more oxygen molecules to be transferred to the blood by diffusion.

10. Dalton’s Law “ The total pressure exerted by a mixture of gases is equal to the sum of the pressure of each individual gas in the mixture.” i.e., P = p1+ p2 + p3 +…………..+ p n To determine the pressure that each gas in a mixture exerts we can multiply the % of the gas in the mixture times the total pressure of the mixture.

11. The air we breath is a mixture of gases: 21% oxygen 78% nitrogen 1% other gases a. At sea level the atmospheric pressure is 760 mmHg. Therefore, P o 2 = 760 mmHg x .21 (21%) = 159.6 mmHg P N 2 = 760 mmHg x .79 (79%) = 600.4 mmHg b. I f we breath a gas that is 100% oxygen instead of 21% oxygen at sea level. P o 2 = 760 mmHg x 1.0 (100%) = 760 mmHg O2 The pressure of oxygen we breath in this case is now 4 times higher than if we were breathing air at sea level, 760 mmHg vs. 159.6 mmHg.

12. If we increase the pressure at which we breath a gas or mixture of gases (increase the total pressure) to some pressure other than sea level (760 mmHg), the pressure of each component gas in line ↑ with their percent of the whole. Ex: At 2 atmospheres (2 ATA) of pressure (33 ft. under sea water) P air =760 mmHg (1 ATA) x 2 = 1520 mmHg I f we breath normal air, then P O2 = 1520 mmHg x .21 (21%) = 319.2 mmHg ( twice as much O2 than breathing air at sea level) I f we breath a gas that is 100% oxygen at this level, P O2 = 1520 mmHg x 1.0 (100%) = 1520 mmHg ( 9.5 times more O2 than breathing air at sea level) .

13. Graham’s Law Graham’s law states that “oxygen and carbon dioxide (and other gases) move independently, at different rates, from an area of high pressure to an area of lower pressure.” As we inhale atmospheric air it mixes with air coming from the alveoli of the lung which is low in O2 and high in CO2 . This mixing causes a dilution of the oxygen in the new inspired air. Therefore, the actual O2 conc. in the alveolus will be less than the O2 conc. breathed in with each breath.

14. In a patient with normal respiratory function & breathing air at sea level, the alveolar O2 pressure is approximately 100-115 mmHg which is 44-59 mmHg less than the oxygen pressure in the atmospheric air. The effect of breathing 100% oxygen at sea level (760 mmHg) on the oxygen pressure in the alveolus would be to increase the concentration, but the dilution with air coming from the alveolus would again reduce the final oxygen concentration delivered to the alveolus. Therefore, with 100% Oxygen, PO2= 760 mmHg x 1.0 = 760 mm 0f Hg.

15. In the alveolus the final concentration would be Approximately 678 mmHg, 82 mmHg less. If we increase the concentration of oxygen in the alveolus, we will cause even more oxygen to move into the blood. Molecules of gas are very active. As we increase the concentration we increase the number of molecules hitting the semi-permeable membrane. This will increase the number that diffuse across. The same law of diffusion apply at the tissue level. As the tissues use oxygen, the concentration becomes lower in the tissue than the concentration in the blood, so more oxygen diffuses from the blood to the tissues.

16. Henry’s Law Henry’s Law states that the solubility of a gas in a liquid is directly proportional to the pressure of the gas in contact with the liquid. In the case of the body the liquid is the blood. The pressure is the concentration of oxygen as it diffuses from the alveolus to the blood. Consequence: By ↑ the conc. Of Oxygen in the blood, the amount of soluble O2 can be ↑.

17. If the patient is breathing air at sea level most of the oxygen in the blood is combined with hemoglobin . In general, 100 ml of blood carries approximately 20.4 ml of oxygen. A very small amount of oxygen, not combined with hb , is dissolved in the plasma . Approximately 100 ml of blood has only 0.31 ml of dissolved oxygen in it at sea level. For each 100 mmHg increase in the oxygen pressure in the alveolus another 0.31 ml of oxygen can be dissolved in the plasma. We can increase the dissolved oxygen up to 15 times normal by the use of hyperbaric therapy.

18. summary

19. Physiological response to hyperbaric environment Physiologic responses and problems due to exposure to a hyperbaric environment may be categorized and differentiated into complications due to a) direct physical effect of pressure b) secondary complications due to abnormal, high volume of respiratory gases dissolved in blood and tissues. When man is placed in a compressed air environment, two things are considered a) both the soft tissues b) air cavities of the body.

20. An inc. in environmental pressure is accompanied by significant adiabatic heat production, whereas decompression generates cooling. This results in an inc. in chamber temp. during compression and in cooling and precipitation of water droplets during decompression. CO dec ., SVR inc. and PVR dec . Additionally, pockets of trapped gas within the body will contract and expand on compression and decompression. Such pockets include gas in the middle ear, and paranasal sinuses, intestinal gas, pneumothorax , and gas pockets within monitoring and life-support systems.

21. Increased Inert Gas Partial Pressure Elevation of the partial pressure of the inert gas (usually nitrogen) present in a breathing mixture is associated with a narcotic effect, Based on its solubility in olive oil, N 2 has 0.03 to 0.05 times the narcotic potency of nitrous oxide. At 3 ATA (breathing air) - mild euphoria. At 6 ATA - memory loss and poor judgment. At 10 ATA- some individuals lapse into unconsciousness. thought to be d/t activation of GABA A receptors of dopaminergic neurons in the nigrostriatal pathway, leading to a decrease in dopamine release. Argon and, to a lesser degree, hydrogen are narcotic, whereas helium has minimal if any narcotic effect.

22. Elevation of Absolute Pressure High pressure induces a constellation of symptoms consisting of tremor, ataxia, nausea, and vomiting, known as the high-pressure nervous syndrome (HPNS). It occurs at an ambient pressure greater than 15 to 20 ATA and was first described during the compression phase of deep dives with a helium-oxygen atmosphere. HPNS is ameliorated by slow compression and addition of a narcotic gas (e.g., nitrogen) to the breathing mix. Its pathogenesis may be related to an increase in striatal dopamine.

23. Barotrauma : As the ambient pressure is altered, the pressure within gas-containing spaces in the body must equilibrate with the ambient pressure or undergo a change in volume. Volume change can easily occur in compliant compartments such as the gastrointestinal tract, but if there is obstruction to free flow of gas into and out of containing spaces surrounded by a rigid shell, such as the lung, paranasal sinuses, and middle ear, then tissue disruption and hemorrhage can occur. Indeed, the m.c . side effect of hyperbaric chamber use is the difficulty with middle ear pressure equilibration.

24. In awake pt.s , equilibration may be accomplished using several techniques, such as performing intermittent Valsalva maneuvers , swallowing while the nose is pinched, thrusting the jaw forward, or simply swallowing intermittently during compression. Pt.s with prior irradiation of the head and neck and acute respiratory tract infections are at particular risk. Equilibration may be facilitated by application of a topical nasal vasoconstrictor e.g., oxymetazoline , 0.05% . For patients who cannot equalize despite these measures, or for obtunded or intubated patients, myringotomy or tympanostomy tubes may be required. Theoretically, HBO exposure in a patient with obstructed eustachian tubes could cause labyrinthine window rupture, but this has not been reported during HBO treatment.

25. Pulmonary barotrauma is most likely during decompression. Areas of regional hypoventilation could lead to pulmonary overpressurization and alveolar rupture, causing pneumothorax , pneumomediastinum , or arterial gas embolism. Pulmonary barotrauma during HBO therapy is extremely rare, probably due to slow decompression rates typically used. Although a pneumothorax would be expected to diminish in size and resorb more quickly after compression, continuing leakage of air from the lung might result in tension pneumothorax during decompression.

26. Pneumothorax detected before treatment is usually treated by insertion of a chest tube and water seal or Heimlich-type valve. Caution must be exercised when using certain commercially available pleural suction regulators, which can exert high negative pleural pressures during chamber compression. Such excessive suction can be relieved by an attendant inside a multiplace chamber by activating the manual pressure relief valve on the chest drainage unit.

27. Effects of increased PaO2 Increased Pa o 2 has at least four pharmacologic effects: 1. Increased blood O 2 content, 2. Vasoconstriction, 3. Antibacterial action, particularly against anaerobic bacteria 4. Inhibition of endothelial neutrophil adhesion in injured tissue.

28. The elevation in Pa o 2 leads to an increase in arterial content thereby inc. tissue P o 2 , even in ischemic tissue. The mechanism of HBO-induced vasoconstriction appears to be inactivation of nitric oxide due to increased production of superoxide and possibly decreased release of NO from circulating S- nitrosohemoglobin . The second effect is an explanation for the effectiveness of HBO in the treatment of traumatic edema (e.g., crush injury). These two effects, increased O 2 content and vasoconstriction, lead to a slight increase in mean arterial pressure. heart rate and cardiac output may be decreased and systemic vascular resistance is increased. pulmonary vascular resistance is decreased. Cerebral blood flow is decreased by O 2 administration over a range of pressures,At 2 ATA, hepatic, renal, and mesenteric flows are unchanged.

29. Conditions for Which Hyperbaric Oxygen Has Been Used Gas-bubble disease : Air embolism Decompression sickness Poisoning : Carbon monoxide Cyanide Carbon tetrachloride Hydrogen sulfide Infections : Clostridial myonecrosis Other soft tissue necrotizing infections Refractory chronic osteomyelitis Intracranial abscess Mucormycosis Acute ischemia : Crush injury Compromised skin flaps Central retinal artery occlusion, Central retinal vein occlusion

30. Chronic ischemia : Radiation necrosis (soft tissue, radiation cystitis and osteoradionecrosis ) Ischemic ulcers, including diabetic ulcers Acute hypoxia : Exceptional blood loss anemia (when transfusion is delayed or unavailable) Support of oxygenation during therapeutic lung lavage Thermal injury : Burns Envenomation : Brown recluse spider bite

31. Primary Effects of Hyperbaric Oxygen Mechanism Effect Clinical Utility Hyperoxygenation Greater oxygen carrying capacity Increased oxygen defusion in tissue fluid Diffusion distance proportional to the square root of dissolved oxygen Severe blood loss anemia (unable to carry oxygen) Crush injury, compartment syndrome graft, and flap salvage (decreased perfusion) Edema (increased diffusion barrier) Decrease gas bubble size Decompression sickness Air embolus syndrome

32. Secondary Effects of Hyperbaric Medicine Mechanism Effect Clinical Application Vasoconstriction Decreased inflow into tissues Decreased edema Crush injuries Acute burns Compartment syndrome Angiogenesis Inc. O2 gradient b/w wound and surrounding environment Inc. fibroblast proliferation leading to inc. collagen deposition and inc. fibronectin , which aids in neovascularization Graft and flap salvage Osteoradio -necrosis Radiation endarteritis obliterans Chronic wounds

33. Mechanism Effect Clinical Application Fibroblast proliferation Oxygen-dependent proliferation Chronic wounds Radiation-induced injury Leukocyte oxidative killing Increased oxygen free radicals Anaerobes lack superoxide dismutase to control oxygen free radicals Necrotizing soft-tissue infections Chronic osteomyelitis Toxin inhibition Decreased clostridial alpha toxins Clostridial gas gangrene Decreased cardio toxins Antibiotic synergy Fluoroquinolones, amphotericin B, and aminoglycosides - Use oxygen to transport across cell membranes Sepsis Necrotizing infections

34. Rationale for the Treatment of Selected Specific Syndromes 1) Carbon Monoxide Poisoning : Hb has high affinity for CO than O2 (200 times). Forms carboxyhemoglobin ( HbCO ) which has two major effects. a) Functional anemia – d/t dec . in O2 transport b) The avidity with which the remaining Hb binds O 2 is increased leading to dec . in O2 unloading in tissues. binding of CO to intracellular pigments (e.g., cytochrome aa 3 , myoglobin ) and oxidative stress may contribute significantly to CO toxicity. CO exposure also triggers intravascular platelet- neutrophil aggregation and neutrophil activation. These mechanisms result in toxicity to multiple organ systems, including brain and heart. Immune-mediated effects have also been described.

35. Clinical effects include headache, nausea, vomiting, dizziness, myocardial ischemia, loss of consciousness, and, during pregnancy, fetal distress. Persistent or delayed neurologic sequelae can occur in older age (≥36 years) and longer CO exposure. The diagnosis of CO poisoning is made by a history of exposure (internal combustion engine exhaust, fire, improperly adjusted gas or oil heating, charcoal or gas grills, or exposure to paint stripper containing methylene chloride, which is metabolized by the liver to CO). Confirmation - ↑ HbCO level in either arterial or venous blood. Fetal hemoglobin ( HbF ) can produce a falsely elevated reading for HbCO on certain four-wavelength laboratory co- oximeters . In the first few weeks of life, blood from normal infants may therefore falsely indicate 7% to 8% HbCO .

36. O2 is the primary treatment modality for CO poisoning. High Pa o 2 hastens the removal of CO from blood, as indicated by a reduced half-life of HbCO . HBO reduces the half-time even further, to around 20 minutes at 2.5 ATA . Additionally, the increased dissolved O 2 in plasma may support tissue oxygenation pending removal of CO from Hb and other proteins important for O 2 transport. Although the treatment of CO poisoning with HBO remains somewhat controversial, there is mounting evidence that for poisoning in which neurologic symptoms occur, HBO treatment may decrease both early and late morbidity.

37. Commonly used guidelines for the application of HBO therapy in CO poisoning include the following: A history of neurologic impairment (including dizziness, loss of consciousness) • Evidence of cardiac abnormalities (ischemia, arrhythmias, ventricular failure) • An HbCO level that has been greater than 25% Fetuses are particularly susceptible to CO toxicity. Pregnant women who fulfill the criteria just listed or in whom there is fetal distress should be treated with HBO as the benefits of HBO outweigh the theoretical risks to the fetus of HBO treatment.

38. 2. Gas Embolism and Decompression Sickness : Arterial gas embolism has been associated with scuba divers and attributed to pulmonary barotrauma during ascent from a dive while breathing compressed gas, during cardiopulmonary bypass or as a result of inadvertent injection of air during a diagnostic arteriogram or hemodialysis . Venous air embolism may occur during neurosurgical procedures with the patient in the sitting position, hemodialysis , major back surgery, total hip replacement, cesarean section, laparoscopy, intrauterine laser surgery, arthroscopy, hydrogen peroxide irrigation , central venous catheter, patients with ARDS being ventilated with PEEP. The effects of gas embolism are due to vessel obstruction by bubbles, Bubble-endothelial interaction causes increased capillary permeability and extravasation of fluid and impairment of endothelial function.

39. A related syndrome that results from pathologic effects of tissue and blood gas bubbles is decompression sickness (DCS) seen in aviators and compressed gas divers. The gas bubbles occur because of a decrease in ambient pressure at a rate sufficient to induce local inert gas supersaturation , resulting in formation of bubbles in situ from tissue stores. Symptoms of arterial gas embolism classically consist of impaired consciousness, hemiparesis , or seizures but may be of a less severe nature. DCS most commonly presents as any combination of joint pain, paresthesias , motor weakness, bladder or bowel sphincter dysfunction, vertigo, tinnitus, or hearing loss.

40. O2 therapy causes High P o 2 which results in increased rate of resolution of gas bubbles because of the resulting higher partial pressure gradient for diffusion of inert gas from the interior of the bubble into the surrounding tissue or blood. Treatment of arterial gas embolism is usually performed at ambient pressures from 2.8 to 6 ATA. HBO therapy is the definitive treatment for arterial gas embolism and DCS. The increased pressure will cause a diminution in gas volume and thus further hasten resolution. Fluid resuscitation will replenish intravascular volume, reduce hemoconcentration , and facilitate microcirculatory flow, However, excessive fluid administration can worsen pulmonary gas exchange in cardiorespiratory DCS (pulmonary edema due to venous gas embolism) and aggressive fluid therapy is not indicated for isolated arterial gas embolism.

41. 3.Acute Infections : Anaerobic bacteria are especially sensitive to increased tissue P o 2 . High O 2 tensions inhibit clostridial α-toxin production. Other mechanisms include reversal of hypoxia-induced neutrophil function, enhanced macrophage interleukin (IL)-10 expression,and anti-inflammatory effects. 4.Maintenance of Oxygen Transport in Severe Anemia : The ability of HBO to increase arterial O 2 content in plasma to clinically useful levels may allow support of tissue O 2 delivery even without hemoglobin . HBO can therefore be used for temporary support of severely anemic patients pending availability of definitive therapy in the form of crossmatched blood.

42. 5.Support of Arterial Oxygenation : HBO is a safe and effective method of supporting arterial oxygenation during therapeutic lung lavage , during which oxygenation has to be maintained by the contralateral ( nonlavaged ) lung. A reversible simulation of pulmonary gas exchange during the lavage procedure can be provided by temporarily ventilating the lung to be lavaged with 5% to 6% O 2 /balance N 2 , which reduces P ao 2 in that lung to approximately the level of mixed venous P o 2 and confining O 2 exchange to the contralateral lung. Hypoxemia within 5 minutes is predictive of hypoxemia during the actual lavage .

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