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Ch04 hemorrhage and shock
- 1. Paramedic Care: Death byPowerPoint Part 2 Shock !
- 2. EMT class shock lecture: “Airgoes in and out… blood goes around and around…. Anything that gets in the way is a big problem….”
- 3.
- 4. Hemorrhage Loss of bloodfrom the vascular space – EXTERNAL – INTERNAL
- 5.
- 6. CARDIAC OUTPUT STROKE VOLUMEX HEART RATE
- 7.
- 8. Heart Stroke volume isthe amount of blood pumped from the ventricle with each contraction.
- 9. WHAT IS STROKEVOLUME DEPENDENT ON?
- 10. PRELOAD AFTERLOAD CONTRACTILITY The normal heart,at rest, beats about 70 times per minute and moves about 70 mL of blood with each beat.
- 11. The Circulatory System TheVascular System – Consists of arteries, capillaries, and veins
- 12. Arteries Consist of three distincttissue layers – Tunica adventicia – Tunica media – Tunica intima
- 13. Capillaries Capillary flow provides essentialnutrients and oxygen and removes waste products. – Only one-cell thick Hydrostatic pressure pushes the plasma into the interstitial space. – Filtration
- 14. Veins Collect blood andreturn it to the heart Contains the vast majority of the total blood volume Able to constrict in early stages of hemorhage
- 15. The Circulatory System Progressivereduction in pressure as blood is moved through the circulatory system
- 16. Blood Blood is thetissue that circulates within the cardiovascular system – A mixture of cells, proteins, water, and other suspended elements Blood Volume – Average adult male has a blood volume of 7% of total body weight – Average adult female has a blood volume of 6.5% of body weight – Normal adult blood volume is 4.5–5 L Remains fairly constant in the healthy body
- 17. Blood Components Erythrocytes: 45% –Hemoglobin – Hematocrit Miscellaneous blood products: <1% – Platelets – Leukocytes Plasma: 54%
- 18. Blood Components Erythrocytes (RBC’s) –The major blood Contains hemoglobin A molecule to which oxygen attaches – Efficient transporter of oxygen from the lungs to body cells.
- 19. Blood Components Plasma – Approximately92% water – Circulates salts, minerals, sugars, fats, and proteins throughout the body
- 20. Blood Components Leukocytes (WBC’s) –Defend the body against various pathogens – Produced in bone marrow and lymph glands
- 21. Blood Components Platelets – Partof the body’s defense mechanism – Formed in red bone marrow – Work by swelling and adhering together to form sticky plugs (initiating the clotting phenomenon)
- 22.
- 23. Clotting Three-Step Process – Vascularphase Vasoconstriction – Platelet phase – Coagulation Release of enzymes Normal coagulation in 7–10 minutes
- 24.
- 25. Clotting The nature ofthe wound also affects how rapidly and well the clotting mechanisms respond. – Transverse wound – Longitudinal wound
- 26. What affects clotting? Bloodthinners Body temperature Movement Aggressive fluid therapy
- 27. Hemorrhage Control External Hemorrhage –External hemorrhage is relatively easy to recognize and control. Bleeding from small vessels can often be controlled by firmly bandaging a dressing in place. Fingertip pressure – With careful application of direct pressure you can halt virtually all hemorrhage.
- 28.
- 29. Hemorrhage Control External Hemorrhage(cont.) – If you consider using a tourniquet, be extremely cautious. The need for a tourniquet is rare. – In the absence of perfusion, lactic acid, potassium, and other anaerobic metabolites accumulate Will be released into the circulation when released – Use a wide-band if considering use
- 30. Internal Hemorrhage Can resultfrom: – Blunt or penetrating trauma – Acute or chronic medical illnesses Internal bleeding that can cause hemodynamic instability usually occurs in one of four body cavities: – Chest – Abdomen – Pelvis – Retroperitoneum
- 31. Internal Hemorrhage Signs andsymptoms that suggest significant internal hemorrhage include: – Bright red blood from mouth, rectum, or other orifice – Coffee-ground appearance of vomitus – Melena (black, tarry stools) – Orthostatic hypotension Chronic hemorrhage may result in anemia
- 32. Internal Hemorrhage Control General Management –Immobilization, stabilization, elevation – Epistaxis: Nose Bleed Causes: trauma, hypertension Treatment: lean forward, pinch nostrils
- 33. How Much BloodLoss? Humerus 500-750 mL Femur up to 1500 mL Pelvis up to 2000 mL
- 34. Know These Numbers! 15 25 35
- 35. Stages of Hemorrhage Stage1 – 15% loss of CBV (circulating blood volume) 70 kg pt = 500–750 mL – Compensation Vasoconstriction Normal BP, pulse pressure, respirations Slight elevation of pulse Release of catecholamines Epinephrine Norepinephrine Anxiety, slightly pale and clammy skin
- 36. Stages of Hemorrhage Stage2 – 15–30% loss of CBV 750–1500 mL – Early decompensation Unable to maintain BP Tachycardia and tachypnea – Decreased pulse strength – Narrowing pulse pressure – Significant catecholamine release Increase PVR Cool, clammy skin and thirst Increased anxiety and agitation Normal renal output
- 37. Stages of Hemorrhage Stage3 – 30–40% loss of CBV 1500–2000 mL – Late decompensation (early irreversible) – Classic Shock Weak, thready, rapid pulse Narrowing pulse pressure Tachypnea Anxiety, restlessness Decreased LOC and AMS Pale, cool, and clammy skin
- 38. Stages of Hemorrhage Stage4 – >40% CBV loss >1750 mL – Irreversible Pulse: Barely palpable Respiration: Rapid, shallow, and ineffective LOC: Lethargic, confused, unresponsive GU: Ceases Skin: Cool, clammy, and very pale Unlikely survival
- 39. Different People, Different BloodVolumes Pregnant Athletic Obese Elderly Children
- 40. Geriatric Patients Discussed inanother chapter Old people take beta blockers and other medications that slow heart rate. May not show typical signs of shock. Break bones easily Have curvy spines Can’t hear very well
- 41. Pediatric Trauma Discussed inanother presentation PALS CONCEPT: 70 + (2 X Patient’s Age) is cutoff for hypotension in a pediatric patient Compensate well, then decline rapidly – (don’t circle the drain like adults)
- 42. Stages of Hemorrhage ConcomitantFactors – Pre-existing condition – Rate of blood loss – Patient Types Pregnant >50% greater blood volume than normal Fetal circulation impaired when mother compensating Athletes Greater fluid and cardiac capacity Obese CBV is based on IDEAL weight (less CBV)
- 43. Stages of Hemorrhage ConcomitantFactors – Children CBV 8–9% of body weight Poor compensatory mechanisms – Elderly Decreased CBV Medications BP Anticoagulants
- 44. Hemorrhage Assessment Assessment ofthe hemorrhage patient is directed at identifying the source of the hemorrhage. – Halt any serious and controllable loss. Examine the nature of the injury.
- 45. Hemorrhage Assessment Scene Size-up –Standard precautions are essential – Evaluate the mechanism of injury Time elapsed since injury Determine the amount and rate of blood loss © Jeff Forster
- 46. Hemorrhage Assessment Primary Assessment –General Impression Obvious Bleeding – Mental Status – CABC – Interventions Manage as you go O2 Bleeding control Shock BLS before ALS!
- 47. Hemorrhage Assessment Secondary Assessment –Rapid Trauma Assessment Full head to toe Consider air medical if stage 2+ blood loss – Focused Physical Exam Guided by c/c – Vitals, SAMPLE, and OPQRST – Additional Assessment Search for signs of internal bleeding Bleeding from body orifice, melena, hematochezia Orthostatic hypotension
- 48. Hemorrhage Assessment Ongoing Assessment –Reassess vitals and mental status: Q 5 min: UNSTABLE patients Q 15 min: STABLE patients – Reassess interventions: Oxygen ET IV Medication actions – Trending: improvement vs. deterioration Pulse oximetry End-tidal CO2 levels
- 49. Hemorrhage Management Assure thatthe airway is patent and breathing is adequate. – Maintain the airway and provide the necessary ventilatory support. – Administer high-flow oxygen. Assure that the patient has a palpable carotid pulse. Care for serious (arterial and heavy venous) hemorrhage, immediately after you correct airway and breathing problems.
- 50. Hemorrhage Management Direct Pressure –Controls all but the most persistent hemorrhage – If bleeding saturates the dressing, cover it with another dressing If ineffective, may be necessary to visualize wound to apply pressure directly to site
- 51.
- 52.
- 53.
- 54. Bleeding Assessment Click hereto view an animation on bleeding assessment.
- 55. Specific Wound Considerations Head Wounds –Presentation Severe bleeding Skull fracture – Management Gentle direct pressure Fluid drainage from ears and nose DO NOT pack Cover and bandage loosely Neck Wounds – Presentation Large vessel can entrap air – Management Consider direct digital pressure Occlusive dressing
- 56. Specific Wound Considerations Gaping Wounds –Presentation Multiple sites Gaping prevents uniform pressure – Management Bulky dressing Trauma dressing Sterile, non- adherent surface to wound Compression dressing Crush Injury – Presentation Difficult to locate source of bleeding Normal hemorrhage control mechanism non-functional – Management Consider an air- splint and pressure dressing Consider tourniquet
- 57. Transport Considerations Consider rapidtransport if: – Suspected serious blood loss – Suspected serious internal bleeding – Decompensating shock – If in doubt, rapid transport indicated Other Considerations – Sympathetic response – Anxiety
- 58.
- 59. Shock Inadequate tissue perfusion –Transitional stage between normal life, called homeostasis, and death – Can result from a variety of disease states and injuries – Can affect the entire organism, or it can occur at a tissue or cellular level
- 60. Biology 101 Cellular Metabolism –Glycolysis – Kreb’s Cycle – Electron Transport Chain
- 61. Biology for Paramedics Glycolysis –Anaerobic (no Oxygen needed) – Produces pyruvic acid and 2 ATPs
- 62. Don’t Degrade MyPyruvate
- 63. Cellular Metabolism ATP isa product of the cellular breakdown of glucose – Breakdown occurs in three steps Glycolysis Does not require oxygen Produces pyruvic acid and 2 ATP’s Kreb’s Cycle Requires oxygen Converts pyruvic acid into water, carbon dioxide and 2 ATP’s Electron transport chain Occurs in mitochondria Results in the production of 32 ATPS
- 64. Biology 101.b Kreb’s Cycle –Requires Oxygen – Converts pyruvic acid to H20, CO2, and 2 ATP
- 66. Electron Transport Chain (ITSCOMPLICATED)
- 67.
- 68. WHY IS AEROBIC RESPIRATIONSO GOOD?
- 69.
- 70. Oxygen Transport Oxygen mustuptake on the hemoglobin molecule. – Efficiently carries 97% of the oxygen – Remaining 3% dissolves in plasma The cardiovascular system then moves the red blood cells from the pulmonary system, through the heart, through the arterial system and into the tissues.
- 71. Oxygen Transport In thecapillaries oxygen diffuses across the capillary wall, into the interstitial fluid and then to the cell. – Internal respiration
- 72. Cellular Metabolism The cardiovascularsystem is also responsible to help maintain other elements of the homeostatic environment – Removal of CO2 and water – Heat regulation – Provides the glucose necessary for the cellular metabolism
- 73. Digestion, Filtration, Hormone Production,Excretion The digestive system absorbs carbohydrates and lipids (fats), moving them through the portal system to the liver for processing. The pancreas regulates blood glucose. – Glucagon increases blood glucose – Insulin decreases blood glucose
- 74. Digestion, Filtration, Hormone Production,Excretion Role of the Kidneys – Regulating the body’s fluid/electrolyte balance Excreting excess sodium, potassium, chloride, calcium, bicarbonate, and magnesium – Excreting the waste products of metabolism – Excrete or retain water
- 75. Circulation The cardiovascular system –Responsible for assuring that the necessary materials travel to and from the body’s cells – Cardiac output Preload, cardiac contractility, and afterload Systolic blood pressure is most indicative of the strength and volume of cardiac output Lowest pressure in the arteries is the diastolic blood pressure
- 76.
- 77. Circulation Microcirculation – Blood flowin the arterioles, capillaries, and venules – Sphincter functioning
- 78. Microcirculation Venules and veinsserve as collecting channels and storage vessels (capacitance) Normally contain 70% of the blood volume Muscular movement aids in blood return to the heart
- 79. Circulation Respiration also facilitatesblood return to the heart – Changes in pressure draws blood towards the heart Thoracoabdominal pump In states of hypovolemia, blood return to the heart is diminished – Reduces cardiac output, arterial blood pressure, and the body’s ability to direct blood flow to critical organs
- 80. Cardiovascular System Regulation The humanbody is controlled by the autonomic branch of the nervous system. – Parasympathetic branch – Sympathetic branch These two systems act in balance Many sympathetic nervous system activities are aimed at defending the organism. – These mechanisms may be detrimental in shock states
- 81. Cardiovascular System Regulation Parasympathetic NervousSystem FEED AND BREATHE Decrease – Heart rate – Strength of contractions – Blood pressure Increase – Digestive system – Kidneys
- 82. Cardiovascular System Regulation Sympathetic NervousSystem FIGHT OR FLIGHT Increase – Body activity – Heart rate – Strength of contractions – Vascular constriction Bowel and digestive viscera Decreased urine production – Respirations – Bronchodilation Increases skeletal muscle perfusion
- 83. Cardiovascular System Regulation A systemof receptors, autonomic centers, and nervous and hormonal interventions maintains control over the cardiovascular system
- 84.
- 85. Chemoreceptors Aortic Arch Carotid Sinus Brain(monitoring CSF) Monitors CO2 (and Oxygen) levels
- 86. Cardiovascular System Regulation Hormonal Regulation –Epinephrine and norepinephrine are sympathetic agents Most rapid hormonal response to hemorrhage Both have A1 properties causes vasoconstriction Epinephrine has beta-1 and beta-2 properties B1= increased rate, strength, and conductivity B2= broncodilation
- 87. Hormonal Regulation Antidiuretic Hormone(ADH) – Arginine Vasopressin (AVP) – Released Posterior pituitary Drop in BP or increase in serum osmolarity – Action Increase in peripheral vascular resistance Increase water retention by kidneys Decrease urine output Splenic vasoconstriction 200 mL of free blood to circulation
- 88. Hormonal Regulation Angiotensin – Released Primarychemical from kidneys Stimulus is lowered BP and decreased perfusion – Action Converted from renin into angiotensin I Modified in lungs to angiotensin II Potent systemic vasoconstrictor Causes release of ADH, aldosterone, and epinephrine
- 90. Hormonal Regulation Aldosterone – Release Adrenalcortex Stimulated by angiotensin II – Action Maintain kidney ion balance Retention of sodium and water Reduce insensible fluid loss
- 91. Hormonal Regulation Glucagon – Release Alphacells of pancreas Triggered by epinephrine – Action Causes liver and skeletal muscles to convert glycogen into glucose Gluconeogenesis
- 92. Hormonal Regulation Insulin – Release Betacells of pancreas – Action Facilitates transport of glucose across cell membrane Erythropoietin – Release Kidneys Hypoperfusion or hypoxia – Action Increases production and maturation of RBCs in the bone marrow
- 93. Hormonal Regulation Adrenocorticotropic hormone –Stimulates the release of glucocorticoids from the adrenal cortex Increases glucose production Reduces the body’s inflammation response Prolongs clotting time, wound healing, and infection fighting processes Growth hormone – Promotes the uptake of glucose and amino acids in the muscle cells
- 94. The Body’s Response toBlood Loss As stroke volume decreases, cardiac output decreases resulting in decreased systolic BP – Carotid and aortic baroreceptors recognize this decrease in blood pressure Stimulate the cardiovascular center of the medulla oblongata Mechanisms compensate for small blood losses
- 95. The Body’s Response toBlood Loss Cellular Ischemia – Constriction of arterioles means that less and less blood is directed to the noncritical organs Results in hypoxia – Anaerobic metabolism results Followed by ischemia
- 96. Cellular Ischemia If bloodloss continues, waste products accumulate and blood becomes acidic. – Increase in depth and rate of respirations – Decreased LOC – Increased circulating catecholamines causes anxiousness, restlessness, and possibly a combative patient – Decreased myocardial oxygen supply
- 97. Cellular Ischemia If theblood loss stops, the blood draws fluid from within the interstitial space – Up to 1 L per hour Kidneys reduce urine output
- 98. The Body’s Response toBlood Loss Capillary Microcirculation – Sympathetic stimulation and reduced perfusion to the kidneys, pancreas, and liver cause the release of hormones Angiotensin II causes reduced blood flow – Perfusion is further limited to only those organs most critical to life More cells begin to use anaerobic metabolism for energy = Increased acids
- 99. Capillary Microcirculation The build-upof lactic acid and carbon dioxide relaxes the precapillary sphincters Postcapillary sphincters remain closed Capillary and cell membranes begin to break down Red blood cells begin to clump together – Rouleaux
- 101.
- 102. Capillary Washout Acidosis finallycauses relaxation of the postcapillary sphincters Washout causes profound metabolic acidosis and microscopic emboli Body moves quickly and then irreversibly toward death
- 103. Stages of Shock Threestages: – Compensated – Decompensated – Irreversible Stages are progressively more serious
- 104. Stages of Shock CompensatedShock Size of container is reduced – The body is capable of meeting its critical metabolic needs through a series of progressive compensating actions.
- 105. Compensated High pulse rate Narrowingpulse pressure Vasoconstriction Tachypnea Air hunger Thirst Pale, ashen skin Restlessness
- 106. Stages of Shock DecompensatedShock (Progressive) – Mechanisms that compensate for blood loss fail – Systolic BP drops significantly – Vital organs are no longer perfused – Patient displays a rapidly dropping level of responsiveness
- 107. Stages of Shock IrreversibleShock – The body’s cells die. – Cell membrane lyses. – Toxic chemicals released. – Aggressive resuscitation will be ineffective. – The longer a patient is in decompensated shock, the more likely he has moved to irreversible shock.
- 108. Etiology of Shock Shockcan have many causes Classifications according to origin: – Hypovolemic, – distributive – obstructive – cardiogenic – respiratory
- 109. Hypovolemic Shock Big container Lessvolume Causes – Bleeding – Dehydration – Third space issues
- 110. Distributive Shock Distributive Shock –Mechanisms that interfere with the ability of the vascular system to distribute the cardiac output – Causes Neurogenic Anaphylactic Sepsis
- 111. We will talkabout this after spring break
- 112. Obstructive Obstructive – Results frominterference with the blood flowing through the cardiovascular system – Causes Tension pneumothorax Cardiac tamponade Pulmonary emboli
- 113. Obstructive Shock Tension pneumothorax Cardiactamponade Pulmonary emboli
- 114. Etiology of Shock CardiogenicShock – Results from a problem with the cardiovascular pump – Causes Infarction Disturbances in the cardiac electrical system Failure of the valves Cardiac rupture Reduced cardiac pumping action – May present with the signs and symptoms of myocardial infarction or pulmonary edema
- 115. Etiology of Shock RespiratoryShock – Occurs when the respiratory system is not able to bring oxygen into the alveoli and remove carbon dioxide – Causes Flail chest Respiratory muscle paralysis Pneumothorax Pulmonary edema Tension pneumothorax
- 116. Respiratory Shock Flail chest Respiratorymuscle paralysis Pneumothorax Pulmonary edema Tension pneumothorax
- 117. Etiology of Shock NeurogenicShock – Results from an interruption in the communication pathway between the central nervous system and the rest of the body – Causes Spinal injury Skin remains warm and dry above injury site Head injury Temporary or permanent – Body’s compensatory mechanisms are often affected Tachycardia and increased diastolic are not present
- 118. Let’s Look atthe #s Type of Shock Heart Rate BP Hemorrhagic/hypovole mic Cardiogenic Neurogenic Anaphylactic Warm septic shock Late septic shock
- 119. Had Enough Yet? CardiacOutput: Heart rate X stroke volume MAP = 1/3 (2 X diastolic + systolic) SVR= MAP ÷ Cardiac Output Type of Shock Cardiac Output SVR Hemorrhagic/hypovole mic Cardiogenic Neurogenic Anaphylactic Warm septic shock Late septic shock
- 120. Shock Assessment You mustbe able to recognize shock as early as possible in your patient assessment. Search out the signs and symptoms of shock in each phase of the assessment process. Carefully monitor for the development or progression of shock.
- 121. The Lethal Triad AcidosisHypothermia Coagulopathy Death Brohi, K, et al. J Trauma, 2003.
- 122. Shock Assessment Scene Size-up –Analyze the forces that caused the trauma. Possibility of both external and internal injury. – Look for mechanisms that might result in internal chest, abdominal, or pelvic injuries. – Observe for external hemorrhage.
- 123. Shock Assessment Initial Assessment –Determine the patient’s level of consciousness, responsiveness, and orientation. – Assess the airway for patency and breathing for adequacy. Administer high-concentration oxygen. – Note the heart rate and pulse strength. Skin color and temperature.
- 124. Initial Assessment Pulse oximetry –If you note erratic or intermittent readings with the device, suspect increasing cardiovascular compensation. Capnography – Decreased ETCO2 levels Reflect cardiac arrest, shock, pulmonary embolism, or incomplete airway obstruction – Increased ETCO2 levels Reflect hypoventilation, respiratory depression, or hyperthermia
- 125. Focused History and PhysicalExam Vary with the patient’s priority as determined by the initial assessment Patients who have no significant mechanism of injury : focused trauma assessment Trauma patients who have signs or symptoms of serious injury : rapid trauma assessment
- 126. Assessment Techniques Orthostatic Hypotension TiltTest- increase by 20
- 127. Rapid Trauma Assessment Whenyou have a trauma patient with significant signs and symptoms of injury, perform a rapid trauma assessment. © Jeff Forster
- 128. Rapid Trauma Assessment Inspectand palpate the patient head to toe. Pay special attention to the areas most likely to produce serious, life-threatening injury. Rule out the possibility of obstructive shock. Set the patient’s priority for transport and for injury care.
- 129. Detailed Patient Assessment Considerthe detailed physical exam only after all priorities have been addressed and the patient is either en route to the trauma center or during prolonged extrication.
- 130. Ongoing Assessment Perform serialongoing assessments – Mental status, airway, breathing, and circulation – Perform the ongoing assessment every 5 minutes in the serious trauma patient Pay particular attention to the pulse rate and pulse pressure Check the adequacy and effectiveness of any interventions you have performed
- 131. Airway and Breathing Management Assuregood ventilations with supplemental high-flow, high-concentration oxygen Overdrive respiration may be indicated with: – Rib fractures – Flail chest – Spinal injury with diaphragmatic respirations – Head injury © Craig Jackson/In the Dark Photography
- 132. Airway and Breathing Management Positiveend-expiratory pressure (PEEP) and continuous positive airway pressure (CPAP) Protect the airway with an oral airway, nasal airway or possibly, endotracheal intubation Provide pleural decompression as necessary
- 133. Hemorrhage Control Provide ongoinghemorrhage control as previously described.
- 134. Fluid Resuscitation Basics Warmfluid if possible After 250-500 mL, check BP and lung sounds Permissive hypotension -80 mmHg Children- 20 mL/kg BP cuff on IV bag or pressure infuser Large bore IV
- 135. Fluid Replacement The fieldtreatment of choice for significant blood loss in trauma is whole blood. – Generally not practical in the field setting – Most practical fluid for prehospital administration is an isotonic crystaloid Polyhemoglobins – Contain either animal or human hemoglobin – Prolonged shelf life – Relatively inexpensive – Efficacy not well established
- 136. Fluid Replacement Isotonic FluidReplacement – The standard for shock treatment in the prehospital setting – Current approach to fluid administration Begin fluid resuscitation when blood pressure falls to below 75 percent of normal or about 90mmHg systolic. Observe the patient’s level of consciousness and other signs and symptoms.
- 137. Isotonic Fluid Replacement Employaggressive fluid resuscitation – Use lactated Ringer’s solution or normal saline via two lines – Administer until blood pressure returns to 100 mmHg and the level of consciousness increases In children, infuse 20 mL/kg of body weight
- 138.
- 139. Isotonic Fluid Replacement Considerthe internal lumen size of both the catheter and the administration set – Utilize largest bore possible – Catheter length and fluid pressure Ideal catheter for the shock patient is relatively short, 1 1/2" or shorter Cautiously control fluid – Maintain V/S – don’t increase them
- 140. Treat the Patient… Don’tFix the Patient
- 141. Shock Management Temperature Control –Conserve core temperature – Warm IV fluids PASG – Action Increase PVR Reduce vascular volume Increase central CBV Immobilize lower extremities – Assess Pulmonary edema Pregnancy Vital signs © Craig Jackson/In the Dark Photography
- 142. Shock Management Pharmacological Intervention –Pharmacological interventions are generally limited – Cardiogenic shock Fluid challenge Dopamine – Distributive shock Fluid challenge Dopamine PASG
- 143. Trauma Score See page505 Based on BP, respirations, GCS Maximum of 12 Points
- 144.
- 145. Helicopter Transport Follow localprotocol Have helicopter enroute while you are enroute Cancel if needed Used designated LZ