Ch04 hemorrhage and shock

15 de Oct de 2015

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Ch04 hemorrhage and shock

  1. Paramedic Care: Death by PowerPoint Part 2 Shock !
  2. EMT class shock lecture: “Air goes in and out… blood goes around and around…. Anything that gets in the way is a big problem….”
  3. Hemorrhage
  4. Hemorrhage Loss of blood from the vascular space – EXTERNAL – INTERNAL
  5. The Circulatory System Heart
  8. Heart Stroke volume is the amount of blood pumped from the ventricle with each contraction.
  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 The Vascular System – Consists of arteries, capillaries, and veins
  12. Arteries Consist of three distinct tissue layers – Tunica adventicia – Tunica media – Tunica intima
  13. Capillaries Capillary flow provides essential nutrients and oxygen and removes waste products. – Only one-cell thick Hydrostatic pressure pushes the plasma into the interstitial space. – Filtration
  14. Veins Collect blood and return 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 Progressive reduction in pressure as blood is moved through the circulatory system
  16. Blood Blood is the tissue 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 – Approximately 92% 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 – Part of 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. Hemmorhage Classification
  23. Clotting Three-Step Process – Vascular phase Vasoconstriction – Platelet phase – Coagulation Release of enzymes Normal coagulation in 7–10 minutes
  24. Clotting
  25. Clotting The nature of the wound also affects how rapidly and well the clotting mechanisms respond. – Transverse wound – Longitudinal wound
  26. What affects clotting? Blood thinners 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. Hemorrhage Control
  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 result from: – 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 and symptoms 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 Blood Loss? 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 Stage 1 – 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 Stage 2 – 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 Stage 3 – 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 Stage 4 – >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 Blood Volumes Pregnant Athletic Obese Elderly Children
  40. Geriatric Patients Discussed in another 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 in another 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 Concomitant Factors – 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 Concomitant Factors – Children CBV 8–9% of body weight Poor compensatory mechanisms – Elderly Decreased CBV Medications BP Anticoagulants
  44. Hemorrhage Assessment Assessment of the 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 that the 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. Hemorrhage Management Topical Hemostatic Agents
  52. Hemorrhage Management Elevation Pressure Point
  53. Hemorrhage Management Tourniquet
  54. Bleeding Assessment Click here to 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 rapid transport if: – Suspected serious blood loss – Suspected serious internal bleeding – Decompensating shock – If in doubt, rapid transport indicated Other Considerations – Sympathetic response – Anxiety
  58. Shock!
  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 My Pyruvate
  63. Cellular Metabolism ATP is a 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
  65. Electron Transport Chain (ITS COMPLICATED)
  66. Electron Transport Chain 32 ATP
  68. Answer: More ATP No lactic acid
  69. Oxygen Transport Oxygen must uptake 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.
  70. Oxygen Transport In the capillaries oxygen diffuses across the capillary wall, into the interstitial fluid and then to the cell. – Internal respiration
  71. Cellular Metabolism The cardiovascular system 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
  72. 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
  73. 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
  74. 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
  75. Circulation
  76. Circulation Microcirculation – Blood flow in the arterioles, capillaries, and venules – Sphincter functioning
  77. Microcirculation Venules and veins serve as collecting channels and storage vessels (capacitance) Normally contain 70% of the blood volume Muscular movement aids in blood return to the heart
  78. Circulation Respiration also facilitates blood 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
  79. Cardiovascular System Regulation The human body 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
  80. Cardiovascular System Regulation Parasympathetic Nervous System FEED AND BREATHE Decrease – Heart rate – Strength of contractions – Blood pressure Increase – Digestive system – Kidneys
  81. Cardiovascular System Regulation Sympathetic Nervous System 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
  82. Cardiovascular System Regulation A system of receptors, autonomic centers, and nervous and hormonal interventions maintains control over the cardiovascular system
  83. Baroreceptors Aortic Arch Atria Carotid Sinus Monitors pressure
  84. Chemoreceptors Aortic Arch Carotid Sinus Brain (monitoring CSF) Monitors CO2 (and Oxygen) levels
  85. 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
  86. 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
  87. Hormonal Regulation Angiotensin – Released Primary chemical 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
  88. Hormonal Regulation Aldosterone – Release Adrenal cortex Stimulated by angiotensin II – Action Maintain kidney ion balance Retention of sodium and water Reduce insensible fluid loss
  89. Hormonal Regulation Glucagon – Release Alpha cells of pancreas Triggered by epinephrine – Action Causes liver and skeletal muscles to convert glycogen into glucose Gluconeogenesis
  90. Hormonal Regulation Insulin – Release Beta cells 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
  91. 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
  92. The Body’s Response to Blood 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
  93. The Body’s Response to Blood 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
  94. Cellular Ischemia If blood loss 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
  95. Cellular Ischemia If the blood loss stops, the blood draws fluid from within the interstitial space – Up to 1 L per hour Kidneys reduce urine output
  96. The Body’s Response to Blood 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
  97. Capillary Microcirculation The build-up of 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
  98. Rouleaux
  99. Capillary Washout Acidosis finally causes relaxation of the postcapillary sphincters Washout causes profound metabolic acidosis and microscopic emboli Body moves quickly and then irreversibly toward death
  100. Stages of Shock Three stages: – Compensated – Decompensated – Irreversible Stages are progressively more serious
  101. Stages of Shock Compensated Shock Size of container is reduced – The body is capable of meeting its critical metabolic needs through a series of progressive compensating actions.
  102. Compensated High pulse rate Narrowing pulse pressure Vasoconstriction Tachypnea Air hunger Thirst Pale, ashen skin Restlessness
  103. Stages of Shock Decompensated Shock (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
  104. Stages of Shock Irreversible Shock – 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.
  105. Etiology of Shock Shock can have many causes Classifications according to origin: – Hypovolemic, – distributive – obstructive – cardiogenic – respiratory
  106. Hypovolemic Shock Big container Less volume Causes – Bleeding – Dehydration – Third space issues
  107. Distributive Shock Distributive Shock – Mechanisms that interfere with the ability of the vascular system to distribute the cardiac output – Causes Neurogenic Anaphylactic Sepsis
  108. We will talk about this after spring break
  109. Obstructive Obstructive – Results from interference with the blood flowing through the cardiovascular system – Causes Tension pneumothorax Cardiac tamponade Pulmonary emboli
  110. Obstructive Shock Tension pneumothorax Cardiac tamponade Pulmonary emboli
  111. Etiology of Shock Cardiogenic Shock – 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
  112. Etiology of Shock Respiratory Shock – 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
  113. Respiratory Shock Flail chest Respiratory muscle paralysis Pneumothorax Pulmonary edema Tension pneumothorax
  114. Etiology of Shock Neurogenic Shock – 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
  115. Let’s Look at the #s Type of Shock Heart Rate BP Hemorrhagic/hypovole mic Cardiogenic Neurogenic Anaphylactic Warm septic shock Late septic shock
  116. Had Enough Yet? Cardiac Output: 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
  117. Shock Assessment You must be 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.
  118. The Lethal Triad Acidosis Hypothermia Coagulopathy Death Brohi, K, et al. J Trauma, 2003.
  119. 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.
  120. 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.
  121. 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
  122. Focused History and Physical Exam 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
  123. Assessment Techniques Orthostatic Hypotension Tilt Test- increase by 20
  124. Rapid Trauma Assessment When you have a trauma patient with significant signs and symptoms of injury, perform a rapid trauma assessment. © Jeff Forster
  125. Rapid Trauma Assessment Inspect and 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.
  126. Detailed Patient Assessment Consider the 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.
  127. Ongoing Assessment Perform serial ongoing 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
  128. Airway and Breathing Management Assure good 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
  129. Airway and Breathing Management Positive end-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
  130. Hemorrhage Control Provide ongoing hemorrhage control as previously described.
  131. Fluid Resuscitation Basics Warm fluid 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
  132. Fluid Replacement The field treatment 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
  133. Fluid Replacement Isotonic Fluid Replacement – 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.
  134. Isotonic Fluid Replacement Employ aggressive 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
  135. Permissive Hypotension
  136. Isotonic Fluid Replacement Consider the 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
  137. Treat the Patient… Don’t Fix the Patient
  138. 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
  139. Shock Management Pharmacological Intervention – Pharmacological interventions are generally limited – Cardiogenic shock Fluid challenge Dopamine – Distributive shock Fluid challenge Dopamine PASG
  140. Trauma Score See page 505 Based on BP, respirations, GCS Maximum of 12 Points
  141. Revised Trauma Score
  142. Helicopter Transport Follow local protocol Have helicopter enroute while you are enroute Cancel if needed Used designated LZ