Upload
sadie
View
27
Download
0
Embed Size (px)
DESCRIPTION
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 Presentation
Citation preview
Hemorrhage & ShockTerry White, RN
Review of HemorrhageLocationAnatomical Type & TimingCoagulationFibrinolysisAssessmentManagement
Review of HemorrhageLocationExternalInternalTraumaticNon-TraumaticExamples?
Review of HemorrhageAnatomical TypeArterialVenousCapillaryTimingAcuteChronic
Severity of HemorrhageComparison of Adult vs Child
Hematocrit% of RBC in blood (hematocrit)Normal: 37% - 47% (Female)40% - 54% (Male)
ThrombocytesPlateletsForm platelet plugscontact collagen & adhere to injured surfaceactivate plateletsaggregate to form platelet plug
CoagulationFormation of blood clotsProthrombin activatorProthrombin ThrombinFibrinogen Fibrinentrap platelets, blood cells & plasmaClot retraction
FibrinolysisBreaking up the clottissue plasminogen activator (tPA)plasminogen plasmin
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
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
ShockA rude unhinging of the machinery of lifeA brief pause in the act of dying
ShockInadequate peripheral perfusion leading to failure of tissue oxygenation may lead to anaerobic metabolism
ShockHomeostasiscellular state of balanceperfusion of cells with oxygen is one of its cornerstones
ShockAdequate Cellular OxygenationRed Cell OxygenationRed Cell Delivery To TissuesFick Principle
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
Fick PrincipleAirs gotta go in and out.Bloods gotta go round and round.Any variation of the above is not a good thing!
ShockRed Cell OxygenationOxygen delivery to alveoliAdequate FiO2Patent airwaysAdequate ventilation
ShockRed Cell OxygenationOxygen exchange with bloodAdequate oxygen diffusion into bloodAdequate RBC flow past alveoliAdequate RBC mass/Hgb levelsAdequate RBC capacity to bind O2pHTemperature
ShockRed Cell Delivery To TissuesAdequate perfusionBlood volumeCardiac outputHeart rateStroke volume (pre-load, contractility, after-load)ConductanceArterial resistanceVenous capacitance
ShockRed Cell Delivery To TissuesAdequate RBC massAdequate Hgb levelsAdequate RBC capacity to unbind O2pHTemperatureDistance between capillaries and cells
ShockInadequate oxygenation or perfusion causes:Inadequate cellular oxygenationShift from aerobic to anaerobic metabolism
AEROBIC METABOLISMGlycolysis: Inefficient source of energy production; 2 ATP for every glucose; produces pyruvic acidOxidative phosphorylation: Each pyruvic acid is converted into 34 ATP
ANAEROBIC METABOLISMGlycolysis: Inefficient source of energy production; 2 ATP for every glucose; produces pyruvic acid
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
Ultimate Effects of Anaerobic Metabolism
Maintaining perfusion requires:VolumePumpVesselsFailure of one or more of these causes shock
ShockHypovolemic Shock = Low VolumeTraumaNon-traumatic blood loss VaginalGIGUBurnsDiarrheaVomitingDiuresisSweatingThird space lossesPancreatitisPeritonitisBowel obstruction
ShockCardiogenic Shock = Pump Failure
Acute M ICHFBradyarrhythmiasTachyarrhythmiasMechanical obstruction (distributive shock)Cardiac tamponadeTension pneumothoraxPulmonary embolism
ShockVasogenic Shock = Low Resistance
Spinal cord traumaneurogenic shockDepressant drug toxicitySimple fainting
ShockMixed ShockSeptic ShockOverwhelming infectionInflammatory response occursBlood vesselsDilate (loss of resistance)Leak (loss of volume)
ShockMixed ShockSeptic ShockFeverIncreased O2 demandIncreased anaerobic metabolismBacterial toxinsImpaired tissue metabolism
ShockMixed ShockAnaphylactic ShockSevere allergic reactionHistamine is releasedBlood vesselsDilate (loss of resistance)Leak (loss of volume)
ShockMixed ShockAnaphylactic ShockHistamine releaseExtravascular smooth muscle spasmLaryngospasmBronchospasm
ShockProgressive syndromeThree phasesCompensatedDecompensatedIrreversible
ShockSigns and symptoms due to:HypoperfusionCompensatory responses
Compensated ShockBaroreceptors detect fall in BPUsually 60-80 mm Hg (adult)Sympathetic nervous system activatesWhat are the primary SNS Neurotransmitters & their effects?
Compensated ShockCardiac effectsIncreased force of contractionsIncreased rateIncreased cardiac output
Compensated ShockPeripheral effectsArteriolar constrictionPre-/post-capillary sphincter contractionIncreased peripheral resistanceShunting of blood to core organs
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
Compensated ShockDecreased blood flow to hypothalamusRelease of antidiuretic hormone (ADH or Arginine Vasopressin) from posterior pituitaryRetention of salt, waterPeripheral vasoconstriction
Compensated ShockInsulin secretion caused by epinephrinecontributes to hyperglycemiaGlucagon release caused by epinephrinepromotes liver glycogenolysis & gluconeogenesisACTHstimulates adrenal cortex release of cortisol glucose production
Compensated ShockPeripheral capillaries contain minimal bloodStagnationAerobic metabolism changes to anaerobicExtracellular potassium shifts begin
Compensated ShockPresentationRestlessness, anxiety Earliest sign of shockTachycardia ?Bradycardia in cardiogenic, neurogenic
Compensated ShockPresentationNormal BP, narrow pulse pressure Falling BP = late sign of shockMild orthostatic hypotension (15 to 25 mm Hg)Possible delay in capillary refill
Compensated ShockPresentationPale, cool skin CardiogenicHypovolemicFlushed skin AnaphylacticSepticNeurogenic
Compensated ShockPresentationSlight tachypneaRespiratory compensation for metabolic acidosis
Compensated ShockPresentationNausea, vomitingThirstDecreased body temperatureFeels coldWeakness
Decreased Cardiac OutputAldosterone, ADH ReleaseCatecholamine ReleaseIncreased Blood VolumeIncreased PVRIncreased Cardiac OutputIncreased Myocardial Work, O2 DemandIncreased Volume LossMyocardial IschemiaCompensated Shock Leading to Decompensation
Decompensated ShockPresentationCardiac EffectsDecreased RBC oxygenationDecreased coronary blood flowMyocardial ischemiaDecreased force of contraction
Decompensated ShockPresentationPeripheral effectsRelaxation of precapillary sphinctersContinued contraction of postcapillary sphinctersPeripheral pooling of bloodPlasma leakage into interstitial spaces
Decompensated ShockPresentationPeripheral effectsContinued anaerobic metabolismContinued increase in extracellular potassiumRouleaux formations of RBCspile up like coinsCold, gray, waxy skin
Decompensated ShockPresentationListlessness, confusion, apathy, slow speechTachycardia; weak, thready pulseDecreased blood pressureModerate to severe orthostatic hypotensionDecreased body temperatureTachypnea
Irreversible ShockPost-capillary sphincter relaxationLoss of peripheral vascular resistance
Irreversible ShockWashout of accumulated productsHydrogen ionPotassiumRouleaux formationsCarbon dioxideRouleaux formations microembolize in lungsSystemic metabolic acidosis occursCardiac Output decreases further
Irreversible ShockPresentationConfusion, slurred speech, unconsciousSlow, irregular, thready pulseFalling BP; diastolic goes to zeroCold, clammy, cyanotic skinSlow, shallow, irregular respirationsDilated, sluggish pupilsSeverely decreased body temperature
Irreversible ShockIrreversible shock leads to:Renal failureHepatic failureDisseminated intravascular coagulation (DIC)Multiple organ systems failureAdult respiratory distress syndrome (ARDS)Death
Disseminated Intravascular Coagulation (DIC)Decreased perfusion causes tissue damage/necrosisTissue necrosis triggers diffuse clottingDiffuse clotting consumes clotting factorsFibrinolysis beginsSevere, uncontrolled systemic hemorrhage occurs
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
Shock ClassificationsHypovolemicCardiogenicVasogenic (Distributive)Neurogenic
Shock ClassificationsHypovolemic CausesHemorrhagePlasmaFluid & ElectrolytesEndocrine
Shock ClassificationsCardiogenic CausesContractilityRateObstructive (Preload/Afterload)Tension pneumothoraxPericardial tamponadePulmonary embolismSevere Hypertension
Shock ClassificationsVasogenic (distributive)Increased venous capacitancelow resistance, vasodilationanaphylaxissepsis
Shock ClassificationsNeurogenic (spinal shock)loss of spinal cord function below site of injuryloss of sympathetic tonecutaneous vasodilationrelative bradycardia
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!
Key Issues In ShockRecognize & Treat during compensatory phaseBest indicator of resuscitation effectiveness = Level of ConsciousnessRestlessness, anxiety, combativeness = Earliest signs of shock
Key Issues In ShockFalling BP = LATE sign of shockBP is NOT same thing as perfusionPallor, tachycardia, slow capillary refill = Shock, until proven otherwise
Key Issues In ShockIsolated head trauma does NOT cause shock(possible in peds)
General Shock ManagementAirwayOpen, Clear, MaintainedConsider Intubation
General Shock ManagementHigh concentration oxygen Oxygen = Most Important Drug in ShockAssist ventilation as needed When in Doubt, VentilateBVMDecompress Tension Pneumothorax
General Shock ManagementEstablish venous access Replace fluidGive drugs, as appropriateDont delay definitive therapy Maintain body temperatureCover patient with blanket if neededAvoid cold IV fluids
General Shock ManagementMonitorMental StatusPulseRespirationsBlood PressureECG
Hypovolemic ShockControl severe external bleedingElevate lower extremities Avoid TrendelenburgPneumatic anti-shock garment
Hypovolemic ShockTwo large bore IV linesInfuse Lactated Ringers solutionTitrate BP to 90-100 mm Hg
Hypovolemic ShockDo NOT delay transport Start IVs enroute to hospitalWhere does stabilization of critical trauma occur?
Cardiogenic ShockSupine, or head and shoulders slightly elevatedDo NOT elevate lower extremities
Cardiogenic ShockKeep open line, micro-drip setFluid challenge based on cardiovascular mechanism and historyTitrate to BP ~ 90 mm Hg
Cardiogenic ShockTreat the underlying cause if possibleTreat rate, then rhythm, then BPCorrect bradycardia or tachycardiaCorrect irregular rhythmsTreat BPCardiac contractilityDobutamine, DopaminePeripheral resistanceDopamine, Norepinephrine
Cardiogenic ShockObstructive ShockTreat the underlying causeTension PneumothoraxPericardial TamponadeIsotonic fluids titrated to BP w/o pulmonary edemaControl airwayIntubation
Shock Management Avoid vasopressors until hypovolemia ruled out, or corrected
Shock ManagementSqueezing partially empty tank can cause ischemia, necrosis of kidney and bowel
Vasogenic ShockConsider need to assist ventilationsPatient supine; lower extremities elevatedAvoid Trendelenburg
Vasogenic ShockInfuse isotonic crystalloid Top off tankConsider PASGConsider possible hypovolemiaConsider vasopressors
Vasogenic ShockMaintain body temperature Hypothermia may occur
Vasogenic ShockAnaphylaxisSuppress inflammatory responseAntihistaminesCorticosteroidsOppose histamine responseEpinephrinebronchospasm & vasodilationReplace intravascular fluidIsotonic fluid titrated to BP ~ 90 mm
Pneumatic AntiShock Garment (PASG)FunctionPrimary effect is increased PVRHemorrhage control throughDirect pressureFracture stabilizationIncreased intra-abdominal pressureLittle effect from autotransfusion
Pneumatic AntiShock GarmentIndicationsMultiple lower extremity fracturesPelvic fracturesAbdominal injuriesAbdominal aortic aneurysmRefractory decompensated shock
Pneumatic Antishock GarmentContraindicationsAbsolutePulmonary edema
Pneumatic Antishock GarmentContraindicationsRelativeClosed head injuryThoracic hemorrhageImpaled object (abdomen, chest?)Pregnancy (abdominal section)EviscerationRuptured diaphragmCardiogenic shock
Shock in ChildrenSmall blood volumeIncreased hypovolemia riskVery efficient compensatory mechanisms Failure may cause sudden shockPallor, altered LOC, cool skin = shock UPO
Shock in ChildrenAvoid massive fluid infusionUse 20 cc/kg bolusesHigh surface to volume ratioIncreased hypothermia risk
Shock in the ElderlyPoor cardiovascular condition Rapid decompensationSepsis more likelyHypoperfusion can cause: CVAAMISeizuresBowel InfarctionsRenal failure
Shock in the ElderlyAssessment more difficultPeripheral vascular diseaseWeak pulsesAltered sensoriumHypertension masking hypoperfusionBeta-blockers masking hypoperfusionFluid infusion may produce volume overload/CHF
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
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
Transport ConsiderationsIndications for Rapid TransportIndications for Trauma Center TransportConsiderations for Air Medical Transport