hemorrhage & shock
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Hemorrhage & Shock. Terry White, RN. Review of Hemorrhage. Location Anatomical Type & Timing Coagulation Fibrinolysis Assessment Management. Review of Hemorrhage. Location External Internal Traumatic Non-Traumatic Examples?. Review of Hemorrhage. Anatomical Type Arterial Venous - PowerPoint PPT PresentationTRANSCRIPT
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Hemorrhage & ShockTerry White, RN
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Review of HemorrhageLocationAnatomical Type & TimingCoagulationFibrinolysisAssessmentManagement
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Review of HemorrhageLocationExternalInternalTraumaticNon-TraumaticExamples?
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Review of HemorrhageAnatomical TypeArterialVenousCapillaryTimingAcuteChronic
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Severity of HemorrhageComparison of Adult vs Child
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Hematocrit% of RBC in blood (hematocrit)Normal: 37% - 47% (Female)40% - 54% (Male)
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ThrombocytesPlateletsForm platelet plugscontact collagen & adhere to injured surfaceactivate plateletsaggregate to form platelet plug
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CoagulationFormation of blood clotsProthrombin activatorProthrombin ThrombinFibrinogen Fibrinentrap platelets, blood cells & plasmaClot retraction
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FibrinolysisBreaking up the clottissue plasminogen activator (tPA)plasminogen plasmin
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Assessing HemorrhageCluesBright red blood from wound, mouth, rectum or other orificeHematemesisCoffee ground appearance of vomitusHematocheziaMelenaOrthostatic hypotensionDizziness or syncope on sitting or standingSigns and symptoms of hypovolemic shock
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Management of HemorrhageAirway and Ventilatory SupportCirculatory SupportFrom nose or ears after head trauma = loose drsgControl bleedingdirect pressure, elevation, pressure pointstourniquetpacking of large woundssplintingPASGtransport to appropriate facility
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ShockA rude unhinging of the machinery of lifeA brief pause in the act of dying
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ShockInadequate peripheral perfusion leading to failure of tissue oxygenation may lead to anaerobic metabolism
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ShockHomeostasiscellular state of balanceperfusion of cells with oxygen is one of its cornerstones
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ShockAdequate Cellular OxygenationRed Cell OxygenationRed Cell Delivery To TissuesFick Principle
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VO2COThe following variables are measured:VO2 consumption per minute using a spirometer (with the subject re-breathing air) and a CO2 absorber Cv, the oxygen content of blood taken from the pulmonary artery (representing deoxygenated blood blood) Ca, the oxygen content of blood from a cannula in a peripheral artery (representing oxygenated blood)
From these values, we know that:where CO = Cardiac Output, CA = Oxygen concentration of arterial blood and CV = Oxygen concentration of venous blood.
= xCA ()COxCV)(CO=VO2CACVThis allows us to say
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Fick PrincipleAirs gotta go in and out.Bloods gotta go round and round.Any variation of the above is not a good thing!
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ShockRed Cell OxygenationOxygen delivery to alveoliAdequate FiO2Patent airwaysAdequate ventilation
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ShockRed Cell OxygenationOxygen exchange with bloodAdequate oxygen diffusion into bloodAdequate RBC flow past alveoliAdequate RBC mass/Hgb levelsAdequate RBC capacity to bind O2pHTemperature
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ShockRed Cell Delivery To TissuesAdequate perfusionBlood volumeCardiac outputHeart rateStroke volume (pre-load, contractility, after-load)ConductanceArterial resistanceVenous capacitance
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ShockRed Cell Delivery To TissuesAdequate RBC massAdequate Hgb levelsAdequate RBC capacity to unbind O2pHTemperatureDistance between capillaries and cells
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ShockInadequate oxygenation or perfusion causes:Inadequate cellular oxygenationShift from aerobic to anaerobic metabolism
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AEROBIC METABOLISMGlycolysis: Inefficient source of energy production; 2 ATP for every glucose; produces pyruvic acidOxidative phosphorylation: Each pyruvic acid is converted into 34 ATP
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ANAEROBIC METABOLISMGlycolysis: Inefficient source of energy production; 2 ATP for every glucose; produces pyruvic acid
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Anaerobic MetabolismOccurs without oxygenoxydative phosphorylation cant occur without oxygenglycolysis can occur without oxygencellular death leads to tissue and organ deathcan occur even after return of perfusion organ or organism death
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Ultimate Effects of Anaerobic Metabolism
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Maintaining perfusion requires:VolumePumpVesselsFailure of one or more of these causes shock
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ShockHypovolemic Shock = Low VolumeTraumaNon-traumatic blood loss VaginalGIGUBurnsDiarrheaVomitingDiuresisSweatingThird space lossesPancreatitisPeritonitisBowel obstruction
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ShockCardiogenic Shock = Pump Failure
Acute M ICHFBradyarrhythmiasTachyarrhythmiasMechanical obstruction (distributive shock)Cardiac tamponadeTension pneumothoraxPulmonary embolism
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ShockVasogenic Shock = Low Resistance
Spinal cord traumaneurogenic shockDepressant drug toxicitySimple fainting
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ShockMixed ShockSeptic ShockOverwhelming infectionInflammatory response occursBlood vesselsDilate (loss of resistance)Leak (loss of volume)
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ShockMixed ShockSeptic ShockFeverIncreased O2 demandIncreased anaerobic metabolismBacterial toxinsImpaired tissue metabolism
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ShockMixed ShockAnaphylactic ShockSevere allergic reactionHistamine is releasedBlood vesselsDilate (loss of resistance)Leak (loss of volume)
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ShockMixed ShockAnaphylactic ShockHistamine releaseExtravascular smooth muscle spasmLaryngospasmBronchospasm
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ShockProgressive syndromeThree phasesCompensatedDecompensatedIrreversible
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ShockSigns and symptoms due to:HypoperfusionCompensatory responses
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Compensated ShockBaroreceptors detect fall in BPUsually 60-80 mm Hg (adult)Sympathetic nervous system activatesWhat are the primary SNS Neurotransmitters & their effects?
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Compensated ShockCardiac effectsIncreased force of contractionsIncreased rateIncreased cardiac output
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Compensated ShockPeripheral effectsArteriolar constrictionPre-/post-capillary sphincter contractionIncreased peripheral resistanceShunting of blood to core organs
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Compensated ShockDecreased renal blood flowRenin released from kidney arterioleRenin & Angiotensinogen combineConverts to Angiotensin IAngiotensin I converts to Angiotensin IIPeripheral vasoconstrictionIncreased aldosterone release (adrenal cortex)promotes reabsorption of sodium & water
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Compensated ShockDecreased blood flow to hypothalamusRelease of antidiuretic hormone (ADH or Arginine Vasopressin) from posterior pituitaryRetention of salt, waterPeripheral vasoconstriction
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Compensated ShockInsulin secretion caused by epinephrinecontributes to hyperglycemiaGlucagon release caused by epinephrinepromotes liver glycogenolysis & gluconeogenesisACTHstimulates adrenal cortex release of cortisol glucose production
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Compensated ShockPeripheral capillaries contain minimal bloodStagnationAerobic metabolism changes to anaerobicExtracellular potassium shifts begin
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Compensated ShockPresentationRestlessness, anxiety Earliest sign of shockTachycardia ?Bradycardia in cardiogenic, neurogenic
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Compensated ShockPresentationNormal BP, narrow pulse pressure Falling BP = late sign of shockMild orthostatic hypotension (15 to 25 mm Hg)Possible delay in capillary refill
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Compensated ShockPresentationPale, cool skin CardiogenicHypovolemicFlushed skin AnaphylacticSepticNeurogenic
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Compensated ShockPresentationSlight tachypneaRespiratory compensation for metabolic acidosis
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Compensated ShockPresentationNausea, vomitingThirstDecreased body temperatureFeels coldWeakness
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Decreased Cardiac OutputAldosterone, ADH ReleaseCatecholamine ReleaseIncreased Blood VolumeIncreased PVRIncreased Cardiac OutputIncreased Myocardial Work, O2 DemandIncreased Volume LossMyocardial IschemiaCompensated Shock Leading to Decompensation
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Decompensated ShockPresentationCardiac EffectsDecreased RBC oxygenationDecreased coronary blood flowMyocardial ischemiaDecreased force of contraction
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Decompensated ShockPresentationPeripheral effectsRelaxation of precapillary sphinctersContinued contraction of postcapillary sphinctersPeripheral pooling of bloodPlasma leakage into interstitial spaces
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Decompensated ShockPresentationPeripheral effectsContinued anaerobic metabolismContinued increase in extracellular potassiumRouleaux formations of RBCspile up like coinsCold, gray, waxy skin
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Decompensated ShockPresentationListlessness, confusion, apathy, slow speechTachycardia; weak, thready pulseDecreased blood pressureModerate to severe orthostatic hypotensionDecreased body temperatureTachypnea
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Irreversible ShockPost-capillary sphincter relaxationLoss of peripheral vascular resistance
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Irreversible ShockWashout of accumulated productsHydrogen ionPotassiumRouleaux formationsCarbon dioxideRouleaux formations microembolize in lungsSystemic metabolic acidosis occursCardiac Output decreases further
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Irreversible ShockPresentationConfusion, slurred speech, unconsciousSlow, irregular, thready pulseFalling BP; diastolic goes to zeroCold, clammy, cyanotic skinSlow, shallow, irregular respirationsDilated, sluggish pupilsSeverely decreased body temperature
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Irreversible ShockIrreversible shock leads to:Renal failureHepatic failureDisseminated intravascular coagulation (DIC)Multiple organ systems failureAdult respiratory distress syndrome (ARDS)Death
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Disseminated Intravascular Coagulation (DIC)Decreased perfusion causes tissue damage/necrosisTissue necrosis triggers diffuse clottingDiffuse clotting consumes clotting factorsFibrinolysis beginsSevere, uncontrolled systemic hemorrhage occurs
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Adult Respiratory Distress Syndrome (ARDS)AKA: Shock Lung, Da Nang LungDecreased perfusion damages alveolar and capillary wallsSurfactant production decreasesFluid leaks into interstitial spaces and alveoliGas exchange impairedWork of breathing increases
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Shock ClassificationsHypovolemicCardiogenicVasogenic (Distributive)Neurogenic
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Shock ClassificationsHypovolemic CausesHemorrhagePlasmaFluid & ElectrolytesEndocrine
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Shock ClassificationsCardiogenic CausesContractilityRateObstructive (Preload/Afterload)Tension pneumothoraxPericardial tamponadePulmonary embolismSevere Hypertension
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Shock ClassificationsVasogenic (distributive)Increased venous capacitancelow resistance, vasodilationanaphylaxissepsis
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Shock ClassificationsNeurogenic (spinal shock)loss of spinal cord function below site of injuryloss of sympathetic tonecutaneous vasodilationrelative bradycardia
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Key Issues In ShockTissue ischemic sensitivityHeart, brain, lung: 4 to 6 minutesGI tract, liver, kidney: 45 to 60 minutesMuscle, skin: 2 to 3 hoursResuscitate Critical Tissues First!
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Key Issues In ShockRecognize & Treat during compensatory phaseBest indicator of resuscitation effectiveness = Level of ConsciousnessRestlessness, anxiety, combativeness = Earliest signs of shock
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Key Issues In ShockFalling BP = LATE sign of shockBP is NOT same thing as perfusionPallor, tachycardia, slow capillary refill = Shock, until proven otherwise
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Key Issues In ShockIsolated head trauma does NOT cause shock(possible in peds)
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General Shock ManagementAirwayOpen, Clear, MaintainedConsider Intubation
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General Shock ManagementHigh concentration oxygen Oxygen = Most Important Drug in ShockAssist ventilation as needed When in Doubt, VentilateBVMDecompress Tension Pneumothorax
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General Shock ManagementEstablish venous access Replace fluidGive drugs, as appropriateDont delay definitive therapy Maintain body temperatureCover patient with blanket if neededAvoid cold IV fluids
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General Shock ManagementMonitorMental StatusPulseRespirationsBlood PressureECG
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Hypovolemic ShockControl severe external bleedingElevate lower extremities Avoid TrendelenburgPneumatic anti-shock garment
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Hypovolemic ShockTwo large bore IV linesInfuse Lactated Ringers solutionTitrate BP to 90-100 mm Hg
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Hypovolemic ShockDo NOT delay transport Start IVs enroute to hospitalWhere does stabilization of critical trauma occur?
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Cardiogenic ShockSupine, or head and shoulders slightly elevatedDo NOT elevate lower extremities
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Cardiogenic ShockKeep open line, micro-drip setFluid challenge based on cardiovascular mechanism and historyTitrate to BP ~ 90 mm Hg
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Cardiogenic ShockTreat the underlying cause if possibleTreat rate, then rhythm, then BPCorrect bradycardia or tachycardiaCorrect irregular rhythmsTreat BPCardiac contractilityDobutamine, DopaminePeripheral resistanceDopamine, Norepinephrine
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Cardiogenic ShockObstructive ShockTreat the underlying causeTension PneumothoraxPericardial TamponadeIsotonic fluids titrated to BP w/o pulmonary edemaControl airwayIntubation
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Shock Management Avoid vasopressors until hypovolemia ruled out, or corrected
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Shock ManagementSqueezing partially empty tank can cause ischemia, necrosis of kidney and bowel
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Vasogenic ShockConsider need to assist ventilationsPatient supine; lower extremities elevatedAvoid Trendelenburg
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Vasogenic ShockInfuse isotonic crystalloid Top off tankConsider PASGConsider possible hypovolemiaConsider vasopressors
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Vasogenic ShockMaintain body temperature Hypothermia may occur
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Vasogenic ShockAnaphylaxisSuppress inflammatory responseAntihistaminesCorticosteroidsOppose histamine responseEpinephrinebronchospasm & vasodilationReplace intravascular fluidIsotonic fluid titrated to BP ~ 90 mm
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Pneumatic AntiShock Garment (PASG)FunctionPrimary effect is increased PVRHemorrhage control throughDirect pressureFracture stabilizationIncreased intra-abdominal pressureLittle effect from autotransfusion
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Pneumatic AntiShock GarmentIndicationsMultiple lower extremity fracturesPelvic fracturesAbdominal injuriesAbdominal aortic aneurysmRefractory decompensated shock
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Pneumatic Antishock GarmentContraindicationsAbsolutePulmonary edema
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Pneumatic Antishock GarmentContraindicationsRelativeClosed head injuryThoracic hemorrhageImpaled object (abdomen, chest?)Pregnancy (abdominal section)EviscerationRuptured diaphragmCardiogenic shock
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Shock in ChildrenSmall blood volumeIncreased hypovolemia riskVery efficient compensatory mechanisms Failure may cause sudden shockPallor, altered LOC, cool skin = shock UPO
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Shock in ChildrenAvoid massive fluid infusionUse 20 cc/kg bolusesHigh surface to volume ratioIncreased hypothermia risk
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Shock in the ElderlyPoor cardiovascular condition Rapid decompensationSepsis more likelyHypoperfusion can cause: CVAAMISeizuresBowel InfarctionsRenal failure
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Shock in the ElderlyAssessment more difficultPeripheral vascular diseaseWeak pulsesAltered sensoriumHypertension masking hypoperfusionBeta-blockers masking hypoperfusionFluid infusion may produce volume overload/CHF
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Shock in OB PatientsPulse increases 10 to 15 bpmBP lower than in non-pregnant patientBlood volume increased by 45% Slower onset of shock signs/ symptomsFluid resuscitation requires greater volume
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Shock in OB PatientsOxygen requirement increased 10 to 20%Pregnant uterus may compress vena cava, decreasing venous return to heart Place women in late-term pregnancy on left-sideFetus can be in trouble even though mother looks well-perfused
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Transport ConsiderationsIndications for Rapid TransportIndications for Trauma Center TransportConsiderations for Air Medical Transport