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Environmental Emergencies Provincial Reciprocity Attainment Program Environmental Emergencies A medical emergency caused by or exacerbated due to exposure to environmental, terrain, or atmospheric pressure Common terms Thermoregulation The maintenance of internal body temperature at or near the set point of 36.5 ºC Thermogenesis The regulation of heat production Thermolysis Regulation of heat loss Thermoregulation Regulatory centre located in posterior hypothalamus Central thermoreceptor (stimulated by blood temp) near anterior hypothalamus, peripheral thermoreceptors of skin, and some mucous membranes Control temperature through vasoconstriction / vasodilation, perspiration, and increased circulation to skin Regulating heat production Heat is generated through mechanical, chemical, metabolic, and endocrine activities Mechanical Shivering Chemically Cellular metabolism Endocrine Hormone release Regulating heat production Cell metabolism Breathing Sweating Arrector pilli (piloerection) ↑ HR Shunting of blood Dilation/constriction of blood vessels Core shunting Muscle movement Fluid intake ↑ food intake Sleep ADH release ↑ urination Catecholamine release Regulating heat loss Heat is naturally lost through Radiation Convection Conduction Evaporation Body Temperature Maintenance Physiologic responses — controlled by the brain (involuntary, such as shivering and vasoconstriction) Deliberate actions — (such as exerting yourself or putting on layers of clothing to retain heat when you stop exercising) Regulating Heat Loss Heat is lost from the body to the external environment through the skin, lungs, and excretions The skin is most important in regulating heat loss Radiation, conduction, convection, and evaporation are the major sources of heat loss Convection Happens when air or water with a lower temperature than the body comes into contact with the skin and then moves on You use convection when you blow on hot food or liquids to cool them Amount of heat lost depends on the temperature difference between your body and the environment, plus the speed with which the air or water is moving Convection If you are not moving, and the air is still, you can tolerate a cold environment quite well Air in motion takes away a LOT of heat With air in motion, the amount of heat lost increases as a square of the wind’s speed A breeze of 8 mph (12.8 km/h) will take away FOUR times as much heat as a breeze of 4 mph (6.4 km/h) Convection Above wind speeds of 30 mph (48 km/h), the point becomes moot, because the air does not stay in contact with the body long enough to be warmed to skin temperature Convective cooling is much more rapid in cold water because the amount of heat needed to warm the water is far greater than the amount of heat needed to heat the same volume of air Conduction Transfer of heat away from the body to objects or substances it comes into contact with This is the one where grabbing a door handle with a moist hand at -40º gives you a chance to stick around... Stones and ice are good heat conductors, which is why you get cold when you sit on them Conduction Air conducts heat poorly — still air is an excellent insulator Water conductivity is 240 times greater than that of dry air The ground is also a good heat conductor, which is why you need a foam pad or other insulating barrier under a sleeping bag if you want to stay warm overnight Conduction Alcohol is an excellent heat conductor that remains liquid well below the freezing temperature of water At very cold temperatures, drinking alcohol (ethanol) can result in flashfreezing of tissues inside the mouth If the back of the throat and the esophagus become frozen this way, the resulting injury is often lethal Evaporation Responsible for 20% - 30% of heat loss in temperate conditions About 2/3 of evaporative heat loss takes place from the skin in thermoneutral conditions Remaining evaporative heat loss happens in the lungs and airway In cold weather, airway evaporative heat loss increases as the incoming air is humidified and warmed Evaporation In cold weather, 3 - 4 litres of water per day are required to humidify inhaled air 1500 - 2000 kilocalories (Cal) of heat are lost in this way on a cold day This fluid loss, if not replaced, results in dehydration, causing a lowered blood volume and increased risk of developing hypothermia Evaporation Wet clothing enhances heat loss Sweat-drenched clothing conducts heat toward surface layers of clothing Wet outer clothing layers enhance heat loss to the environment through evaporation A combination of sweat-soaked inner clothing layers and wet outer clothing can be quite lethal Radiation Direct emission or absorption of heat Heat radiates from the body to the clothing, then from the clothing to the environment The greater the difference between body and environmental temperatures, the greater the rate of heat loss Clothing that adequately controls the rates of conductive and convective heat loss will compensate for the radiation heat loss Cold / aquatic emergencies Localized cold injuries Hypothermia Hyperthermia Drowning Diving Emergencies Localized cold Injuries Classifications/Symptoms A common classification separates localized cold injury into three categories Frostnip (the mildest form of cold exposure) may be treated without loss of tissue Superficial frostbite there is at least some minimal tissue loss Deep frostbite there is significant tissue loss even with appropriate therapy Frost nip AKA chilblains The mildest and most common form of localized cold injury Fingertips, ears, nose and toes commonly affected, characterized by numbness, coldness, and pain without swelling Re-warming is safe even with friction if sure not superficial frostbite Frostbite A localized injury that results from environmentally induced freezing of body tissues Pathophysiology Ice tissues form Vascular abnormalities occur Cellular injury caused Increased sensitivity to reoccurrence Frostbite Predisposing factors Peripheral neuropathies PVD Alcohol / tobacco use Inadequate protection Nutritional deficiencies Medication administration PmHx frostbite Injury / illness / fatigue Superficial Frostbite Some freezing of dermal tissue Initial redness followed by blanching Diminished tactile sensation Pain Deep Frostbite Freezing of dermal and subcutaneous layers White appearance Hard (frozen) to palpation Loss of sensation Management ? Frostbite Edema and blister formation 24 hours after frostbite injury in area covered by tightly fitted boot. . Deep Frostbite Gangrenous necrosis 6 weeks after frostbite injury Hypothermia Hypothermia Is defined as a core temperature less than 35°C (95º F). Most commonly seen in cold climates, but can develop without exposure to extreme environmental conditions May result from: A decrease in heat production An increase in heat loss A combination of these factors Hypothermia If left untreated, hypothermia can kill. Nobody ever froze to death — instead, they died of hypothermia. The freezing part came later… ...and only if the temperature of the surrounding environment was below freezing. Predisposing Factors Age Medical conditions Prescription and over-the-counter medications Alcohol or recreational drugs Previous rate of exertion Environmental Factors External environmental factors that may contribute to a medical emergency Climate Season Weather Atmospheric pressure Terrain Progression Clinical signs and symptoms may be divided into three classes: Mild core temperature between 34º and 36º C (93.2º and 96.8º F) Moderate core temperature between 30º and 34º C (86º and 93º F) Severe core temperature below 30º C (86 º F) Clinical Features Mild (34º and 36º C) - ( pissed off stage ) LOC Withdrawn Slurred Speech HR Normal (May increase initially) BP Normal (May increase initially) Other Shivering Clinical Features Moderate (30º and 34º C) - ( stupid ass stage ) LOC Confused, sleepy, irrational, Clumsy, Stumbling HR Slow and/or weak May see EKG changes BP Decreasing RR Bradypnea Other Cyanosis Dilated Pupils Clinical Features Severe (below 30º C) - ( I’m going to die stage ) LOC Stupor to Unconscious HR Slow (may be irregular), Absent EKG Changes (high risk) BP Hypotensive RR Bradypnea or apnea Other Cyanosis Dilated Pupils EKG Changes Hypothermia causes characteristic EKG changes: T-Wave inversion PR, QRS, QT intervals may increase Muscle Tremor Artifact Arrhythmias Sinus Brady, AFib, AFlut, AV Block, PVC’s, VFib, Asystole Complications While the risk of complications are low in healthy people, there are a few to be aware of Most of these result from pre-existing health problems Pneumonia Acute pancreatitis Thromboses Complications Pulmonary edema Acute renal failure due to tubular necrosis Increased renal potassium excretion leading to alkalosis Hemolysis (breakdown of red blood cells) Depressed bone marrow function Inadequate blood clotting Low serum phosphorus Complications Seizures Hematuria (blood in the urine) Myoglobinuria (muscle pigment that looks like blood in the urine) Simian deformity of the hand Temporary adrenal insufficiency Gastric erosion or ulceration Stages of Hypothermia Shivering Apathy or Decreased Muscle Function Decreased Level of Consciousness Decreased Vital Signs Death Immersion Hypothermia In relation to hypothermia, cold water has two specific threat characteristics: Extreme thermal conductivity The specific heat of water Worsened with saturation of clothing by water The body cannot maintain temperature is water less than 92 degrees F Immersion Hypothermia Sudden immersed in cold water causes; Peripheral vasoconstriction causing increased BP Tachycardia due to anxiety Lethal dysrhythmias often occur, especially in patients with cardiovascular / cardioelectrical abnormalities Immersion Hypothermia Immersion hyperventilation is the first risk… Immersion in cold water initially causes a breathing pattern of deep, involuntary gasps Followed by a minute or more of deep, rapid breaths, with tidal volumes about five times normal Drowning often occurs especially in conjunction with deep immersion or rough water Immersion Hypothermia Hyperventilation causes alkalosis Alkalosis increases the blood’s pH Physiologic responses causes cerebral hypoxia to alkalosis Syncope increases the risk of drowning Immersion Hypothermia In 15°C (60°F) water breath can only be held approx. 1/3 normal increasing the risk of drowning when submersion occurs for more than a few seconds Mammalian diving reflex phenomenon occurs as a mode of self preservation Mammalian Diving Reflex Cold water ( < 68 degrees F ) immersion causes Results in apnea, vasoconstriction, bradycardia and slowed metabolism without the risk of aspiration Vascular bed also becomes engorged with blood in attempt to equalize pressure from outside the body Mammalian Diving Reflex 20 - 30 % reduction in heart rate Complete recovery after 60 min possible Redistribution of blood flow from the periphery to the core Mammalian Diving Reflex Muscles cool and nerve impulses slow, causing slow, weak, poorly coordinated movements Treading water or swimming much more difficult Dysfunction increases as the tissues cool, causing inability to swim or tread water after 10-15 minutes in 10°C (50°F) water Immersion Hypothermia This stage is reached in as little as 5 minutes in icy water The patient is no longer able to assist in his or her rescue In such cases water rescue is imperative Hypothermia does not cause deaths early in cold water immersion emergencies Death results from drowning or cardiac dysrhythmias Immersion Hypothermia After 10-15 minutes of immersion, shivering is constant and obvious Core temp cooling has not occurred Shivering may temporarily prevent heat loss in dry air, but not in cold water ( remember 240 x ) Core temp fall commonly occurs around 15-20 minutes in cold (50°F (10°C)) water Immersion Hypothermia 68 59 50 41 32 Water Temperature ºF ºC 20 15 10 5 0 Cooling Rate ºC/hr 0.5 1.5 2.5 4.0 6.0 Non-exercising adults, light clothing, wearing PFDs Immersion Hypothermia Once immersed, swimming is a dangerous choice to make An average person who can ordinarily swim well probably will not be able to swim more than 1 km (.062 mi) in 50°F (10°C) water on a calm day People who tread water lose heat about 30% faster than people holding still while wearing a PFD Systemic Heat Related Illness Hyperthermia Heat illness results from one of two basic causes: Normal thermoregulatory mechanisms are overwhelmed by environment Excessive exercise Failure of the thermoregulatory mechanisms Elderly, ill or debilitated Maintenance of Thermoregulation Hyperthermic compensation Increased heat loss Vasodilatation of skin vessels Sweating Decreased heat production Decreased muscle tone and voluntary activity Decreased hormone secretion Decreased appetite Heat Illness Heat Illness can be described by three basic forms: Heat Cramps Heat Exhaustion Heat Stroke Classic Exertional Heat Cramps Brief, intermittent, and often severe muscular cramps or spasms Believed to be caused primarily by a rapid loss of salt during profuse sweating Cramps may worsen if salts are not replenished When Ca levels are low Too much water is drunk by patient ( Na / H2O ratio disruption ) Heat Cramps Signs and Symptoms A/O X3 Hot Sweaty Skin Tachycardia Normotensive Normal Body Core Temp (BCT) Heat Cramps Treatment Remove Pt from environment Remove excess clothing Replace salt and water if conscious (First Aid treatment) 1 – 2 tsp of sugar in 1 liter of water Gatorade et al If Severe, IV N/S Heat Exhaustion A more severe form of heat illness Mild-to-moderate core temperature elevation (less than 39ºC) A relative state of shock Most commonly associated with: Profuse sweating Water and salt deficiencies cause electrolyte imbalance Vasomotor response causes inadequate peripheral and cerebral perfusion from pooling S / S of Heat Exhaustion LOC (Irritable, poor judgment, dizziness, headache) Pale, Cool, Clammy Skin Tachycardia Tachypnea Cramps Nausea/Vomiting Blurred Vision or Dilated pupils In severe cases may see orthostatic hypotension and syncope Treatment of Heat Exhaustion Remove Pt from environment Remove excess clothing Replace salt and water if conscious Oxygen (100% NRB) Begin Cooling (Slowly) IV N/S Heat Stroke A syndrome that occurs when the thermoregulatory mechanisms break down entirely Body temperature elevated to extreme levels (usually greater than 41º C) This produces multi-system tissue damage and physiological collapse Heat stroke is a true medical emergency Heat Stroke Classic heat stroke Occurs during periods of sustained high ambient temperatures and humidity Pts are unable to dissipate heat adequately Examples: Children left in enclosed vehicle on hot afternoon Elderly person confined to a hot room Predisposing factors: Age Chronic disease (DM, IHD, Alcoholism and schizophrenia) Medications Heat Stroke Exertional heat stroke Patients are usually young and healthy Heat is accumulated faster than the body can dissipate it Exacerbated by drugs i.e. Ephedra in athletes S / S Heat Stroke LOC (Restless, Headache, Fatigue, Dizziness) Pt may be unconscious or in coma Tachycardia, progress to weak Noisy respirations Classic Heat Stroke: Hot, Dry Skin Exertional Heat Stroke: Hot, Sweaty Skin Nausea/Vomiting Seizures Will lead to DEATH if left untreated Treatment of Heat Stroke Primary Survey and ABC’s Early recognition important Move pt to cool environment Remove excessive clothing Begin cooling Watch for rebound hypothermia IV access May require fluid challenge Near-Drowning Incidence 551 drowning accidents in 1998 (Canadian) Classifications Drowning is defined as death by asphyxia after submersion Near-drowning is submersion with at least temporary survival Drowning Pathophysiology Sequence of drowning: After submersion and panic Victim takes several deep breaths to conserve oxygen Holds breath until reflex takes over Water is aspirated causing laryngospasm This results in hypoxia Hypoxia leads to arrhythmias and CNS anoxia Hypercapnia begins Acidosis Cardiac Arrest Progression of a drowning incident. Salt Water Hypertonic Causes rapid shift of plasma and fluid into the alveoli and interstitial spaces Causes: Pulmonary Edema Poor Ventilatory ability Hypoxia Fresh Water Hypotonic Passes readily out of alveoli into circulation If sufficient amounts are aspirated may causes: Increase of blood volume causing hemolysis Surfactant Washout Hemolysis may result in hyperkalemia and anemia May lead to dangerous / lethal electrolyte imbalances Near-Drowning Hypothermic considerations Common concomitant syndrome May be organ protective in cold-water near-drowning Always treat hypoxia first Treat all near-drowning patients for hypothermia Factors That Affect Clinical Outcome Temperature of the water Length of submersion Cleanliness of the water Age of the victim Near-Drowning Management ABC’s CPR if needed IV Possible sodium bicarbonate Trauma considerations Immersion episode of unknown etiology warrants trauma management Post-resuscitation complications ARDS or renal failure often occur post-resuscitation Symptoms may not appear for 24 hours or more postresuscitation All near-drowning patients should be transported for evaluation Diving Emergencies Medical emergencies unique to pressure-related diving include those caused by: Mechanical effects of barotrauma Air embolism Decompression sickness and nitrogen narcosis Mechanical Effects of Pressure Water is denser than air Pressure changes are greater underwater (even shallow depths) Gas-filled organs are directly affected by changes Every 33 feet of water adds one atmosphere of pressure (14 psi) Atmosphere mmHg Volume 1 760 1 volume 2 1520 (2 X) ½ volume 3 2280 (3 X) ⅓ volume 4 3050 (4 X) ¼ volume Mechanical Effects of Pressure Basic properties of gases Increased pressure dissolves gases into blood, oxygen metabolizes; nitrogen dissolves Boyle's Law Charles’ Law Dalton's Law Henry's Law Boyle’s Law The volume of a gas is inversely proportional to its pressure. If the pressure is increased the volume will decrease May be written in the form of an expression: P1V1=P2V2 Pressures in ventilation Atmospheric pressure Intra-alveolar (intrapulmonary) pressure Intra-pleural pressure Charles’ Law Volume is directly proportional to the temperature as long as the pressure is constant So as air is heat within the respiratory system it will expand Dalton’s Law of Partial Pressures Dalton surmises that the total partial pressure of a gas (if its mixture) is the sum of all the partial pressures of its components pTotal=pgas1+pgas2+pgas3+pgas4 p(air) = p(N2) + p(O2) + p(CO2) + ... 760 mmHg = 592.8 mmHg + 159.6 mmHg + 0.2 mmHg + ... 100 % = 76 % + 21 % + 0.03 % + … Henry’s Law The concentration of a gas in a solution depends on the partial pressure of the gas and its solubility (as long as the temperature stays constant) The higher the solubility, the more gas will dissolve The higher the pressure the more gas will dissolve Barotrauma Tissue damage caused by compression or expansion of gas spaces Can occur with in a descent or a ascent Most common diving emergency Barotrauma of descent Aka "squeeze" Compressed gas in enclosed spaces causes vacuum effect Can occur in: Ears (Most common) Sinuses Lungs and airway GI tract Thorax Teeth (decay or recent extractions) Added spaces (Mask and diving suit) S / S of squeeze Pain Sensation of fullness Headache Disorientation Vertigo Nausea Bleeding from the nose or ears Management of squeeze Begins with gradual ascent to shallower depths Prehospital care primarily revolves around management of findings and transport in reverse Trendelenburg Definitive care may include bed rest with the head elevated avoidance of strain and strenuous activity use of decongestants and possibly antihistamines and antibiotics surgical repair possibly required Barotrauma of ascent Aka "reverse squeeze” The reverse process Assume pressures were equalized with a slow descent As the diver ascends pressure decreases causing volume to increase If air is not allowed to escape because of obstruction the expanding gases distend the tissues surrounding them Reverse squeeze ( cont’d ) Common causes include Holding breath Mucous plug Brochospasm (Panic) Last 6 feet are the most dangerous Reverse squeeze ( cont’d ) May result in Pulmonary Over Pressurization Syndrome (POPS) This may cause alveolar rupture or movement of air into other locations S / S of POPS Gradually increasing chest pain Hoarseness Neck fullness Dyspnea Dysphagia Subcutaneous emphysema Complications of POPS Pneumomediastinum Subcutaneous emphysema Pneumopericardium Pneumothorax Pneumoperitoneum Systemic arterial air embolism Management of reverse squeeze Oxygen administration Hyperbaric chamber if emboli present Reevaluate q 5 for changes Transport Air Embolism The most serious complication of pulmonary barotrauma Results as expanding air disrupts tissues and air is forced into the circulatory system The emboli become lodged in small arterioles, occluding distal circulation More likely to occur with a rapid ascent or holding breath Leading cause of death and disability of sport divers S / S Air Embolism Focal paralysis (stroke-like symptoms) Aphasia Confusion Blindness or other visual disturbances Convulsions Loss of consciousness Dizziness Vertigo Abdominal pain Cardiac arrest Management of Air Embolism Unchanged regardless of color of tag Rapid transport for recompression treatment Assess for S/S of POPS Should be transported in a LLR position with a 15-degree elevation of the thorax Decompression Sickness AKA the bends, dysbarism, caisson disease, and diver's paralysis Nitrogen in compressed air is dissolved into tissues and blood from the increase in its partial pressure at depth DS is a multi-system disorder that results when nitrogen in compressed air converts back from solution to gas, forming bubbles in the tissues and blood Decompression Sickness Occurs with a rapid ascent and ambient pressure decreases Equilibrium between the dissolved nitrogen in tissue and blood and the partial pressure of nitrogen in the inspired gas cannot be established Decompression Sickness The most significant mechanical effect of bubbles is vascular occlusion, which impairs arterial venous flow Since bubbles can form in any tissue, lymphedema, cellular distention, and cellular rupture also can occur The net effect of all these processes is poor tissue perfusion and ischemia The joints and the spinal cord are the areas most often affected S / S Decompression Sickness SOB Itch, rash Joint pain Crepitus Fatigue Vertigo Paresthesias Paralysis Seizures Unconsciousness Management of Decompression Sickness Should be suspected in any patient who has symptoms within 12 to 36 hours after a scuba dive that cannot adequately be explained by other conditions Support of vital functions Oxygen administration Rapid transport for recompression Nitrogen Narcosis “Rapture of the deep” A condition in which nitrogen becomes dissolved in solution as a result of greaterthan-normal atmospheric pressure Produces neurodepressant effects similar to those of alcohol and may impair the diver's judgment and discrimination Nitrogen Narcosis Signs and Symptoms Impaired judgment Sensation of alcohol intoxication Slowed motor response Loss of proprioception Euphoria Nitrogen Narcosis Symptoms of nitrogen narcosis usually become evident at depths between 75 and 100 feet 300 feet and over with standard air will cause unconsciousness Affects all divers but can be tolerated by experienced divers Helium-oxygen mixtures are used to improve the nitrogen complication for deep dives The syndrome is a common precipitating factor in diving accidents and may be responsible for memory loss at depth about events Diving Injuries Depth of dive? Bottom time? Rapid or controlled ascent? # of dives that day? Fresh or salt water? C-Spine? Blood in mask from eyes, ears or nose? Hx? Amount of psi left in diver’s tank? Was diver trained and/or experienced? Recreation or commercial dive? Gas mixtures? High-Altitude Illness Principally occurs at altitudes of 8000 feet or more above sea level Caused by reduced atmospheric pressure, resulting in hypobaric hypoxia Activities associated with these syndromes include: Mountain climbing Aircraft or glider flight Hot-air balloons Low-pressure or vacuum chambers High-Altitude Illness Some Types Acute Mountain Sickness High Altitude Pulmonary Edema High Altitude Cerebral Edema Acute Mountain Sickness (AMS) A common high-altitude illness that results from rapid ascent of an unacclimatized person to high altitudes Usually develops within 4 to 6 hours of reaching high altitude Attains maximal severity within 24 to 48 hours Ceases in 3-4 days with gradual acclimatization S / S AMS Headache (most common symptom) Malaise Anorexia Vomiting Dizziness Irritability Impaired memory DOE ( Dyspnea on exertion ) S / S AMS ( cont’d ) Tachycardia or bradycardia Postural hypotension Ataxia the most useful sign for recognizing the progression of the illness May see coma within 24 hours of ataxia onset Management of AMS Oxygen administration Descent to lower altitude Should see physician High-Altitude Pulmonary Edema (HAPE) Caused by increased pulmonary artery pressure that develops in response to hypoxia Results in: Increase pulmonary arteriolar permeability Leakage of fluid into extravascular locations Initial symptoms usually begin 24 to 72 hours after exposure to high altitudes and are often preceded by strenuous exercise S / S HAPE Dyspnea, cyanosis Cough (with or without frothy sputum) Generalized weakness Lethargy Disorientation Tachypnea Crackles, rhonchi Tachycardia Management of HAPE Oxygen administration to increase arterial oxygenation and reduce pulmonary artery pressure Descent to lower altitude Should be seen by physician May require hospitalization for observation High-Altitude Cerebral Edema (HACE) Most severe form of acute high-altitude illness A progression of global cerebral signs in the presence of AMS Related to increased ICP from cerebral edema and swelling Progression from mild AMS to unconsciousness associated with HACE may be as fast as 12 hours but usually requires 1 to 3 days of exposure to high altitudes S / S HACE Headache Ataxia Altered consciousness Confusion Hallucinations Drowsiness Stupor Coma Management of HACE Delay in treatment will result in death Airway support Circulatory support Descent to a lower altitude