1、Sections Introduction to Hemorrhage&Shock Hemorrhage Shock Hemorrhage Abnormal internal or external loss of blood Homeostasis Tendency of the body to maintain a steady and normal internal environment Shock INADEQUATE TISSUE PERFUSION Transition between homeostasis and deathIntroduction to Hemorrhage
2、&Shock1800s Injury to one part of the body results in often fatal effect Strychnine to stimulate NS;seizures Electrical current alcohol“shock was not a process of dying,rather a marshaling of the bodily defenses in a struggle to live”Realized a fall in BP could account for all symptoms of shock Repr
3、esents a generalized failure of the body to deliver sufficient amounts of O2 to its tissues S/S represent compensation measures utilized by the body to maintain delivery of O2 to vital organs Delay of appropriate therapy,cascade of events results in damage to organsTreatment Goals Recognition of ear
4、ly shock Appropriate airway management Rapid transportation to appropriate facilityHemorrhage Circulatory System Hemorrhage Classification Clotting Factors Affecting Clotting Hemorrhage Control Stages of Hemorrhage Hemorrhage Assessment Hemorrhage ManagementCardiovascular System Delivery of nutrient
5、s and O2 to tissues and cells Transportation of waste products produced by metabolism to liver and kidneys Delivery of CO2 to lungsComponentsHeart or pumpBlood vessels or pipesBlood or fluidCirculatory System Review Terminology Stroke Volume Preload Ventricular Filling Frank-Starling Mechanism After
6、load Cardiac Output SVxHR=CO 5L/min Fick Principle Heart Parasympathetic Nervous System Slows rate Vagus Nerve Sympathetic Nervous System Increases rate Cardiac PlexusCardiac Output Volume of blood pumped in 1 minute=4-6L SV x HR SV=amount of blood ejected from left ventricle with each contractionBl
7、ood Pressure Directly proportional to the product of the CO multiplied by SVR BP=CO x SVR SVR,resistance to flow in the system(systemic vascular resistance)Stroke Volume Preload Represents filling of the ventricle Volume of blood delivered to atria prior to ventricular diastole Dependent on venous r
8、eturn Afterload Amount of resistance heart must overcome to eject blood Contractility Ability to contract,inotropy Frank Starlings LawInotropy Negative Scar tissue,CHF Beta adrenergic blockers Calcium channel blockers Positive Beta adrenergic agonists,B1 List some B blockers,Ca channel blockers,B ag
9、onists Names Indications Contraindications What would you expect to see if you administered this medication?Why?Fick Principle Factors necessary for systemic O2 delivery Ability of O2 to diffuse across alveolar membrane into blood stream Adequate number of RBCs to transport O2 Adequate blood flow to
10、 transport RBCs Ability of RBCs to off-load O2O2 Delivery Normal circumstances body extracts about 20%of O2 and 80%returned to heart for reoxygenation Normal ratio of delivered to consumed 5:1 Shock may increase extraction to 50%Ratio drops to 2:1Cellular Metabolism Glycolysis Krebs Cycle Electron T
11、ransportGlycolysis Occurs in cytoplasm Glucose converted to pyruvic acid 2 ATP created O2 present further aerobic metabolism No O2 present,hypoperfusion,pyruvic acid converted to lactic acid Liver converts some lactic acid Generalized shock Amount of lactic acid exceeds the livers ability to convert
12、 it Muscle and skin can function in aerobic conditions for short period Brain most sensitive to hypoxiaKrebs CycleAerobic conditions pyruvic acid enters mitochondriaProduces 6 CO2 molecules and 4 ATPElectron Transport Occurs in proteins bound to mitochondrial membrane Additional 32 ATP produced Prim
13、ary site of O2 utilization within cell Produce very little ATP on anarerobic conditionsCellular Metabolism Two Step Process Glycolysis Cell utilizing energy source Releases energy Aerobic Metabolism:95%of cellular Energy Requires oxygen and glucose Krebs cycle(citric acid cycle)Uses carbohydrates,pr
14、oteins and fats to release energy Other Processes Anaerobic Metabolism Inadequate oxygen pathway Byproducts:Pyruvic Acid Lactic Acid Cellular death eventually occurs due to inadequate perfusionCirculatory System Vascular System Arteries Tunica Adventitia Tunica Media Tunica Intima Arteriole Capillar
15、y:7%of blood volume Venule Vein Constriction returns 20%(1 L)of blood to active circulation13%of blood volume64%of blood volumeBlood Vessels Sympathetic innervation Vasoconstriction Alpha 1 agonist List some drugs that have alpha 1 agonsist/blocker effects Names Indications Contraindications What ph
16、ysiological response would you expect?Why?Hydrostatic and Oncotic Pressure Two opposing forces that control net flow of fluid and nutrients out of proximal capillaries and flow of waste products and fluid into distal capillaries Hydrostatic pressure Pressure of fluid(BP)serves to drive fluid out of
17、capillary into interstitial space Oncotic pressure Force exerted by large protein molecules in blood that draws fluid into vascular systemProximal capillaryHydrostatic pressure prevailsAllows intravascular fluid and nutrients to diffuse out of capillaryDistal capillaryOncotic pressure is dominantDra
18、ws fluid from interstitial fluid and waste of metabolism into capillariesBlood Components Erythrocyte:45%Hemoglobin Hematocrit Other Formed Elements:2 sec Decreased BP Nausea,vomitingHemorrhage Control Internal Hemorrhage Epistaxis:Nose Bleed Causes:Trauma,Hypertension Treatment:Lean forward,pinch n
19、ostrils,roll gauze under upper lip Hemoptysis Esophageal Varices Melena Chronic Hemorrhage AnemiaStages of Hemorrhage 60%of body weight is fluid 7%circulating blood volume(CBV):Male 5 L(10 units)6.5%CBV in women 4.6 L(9-10 units)15%loss of CBV 70 kg pt=500-750 mL Compensation Vasoconstriction Normal
20、 BP,Pulse Pressure,Respirations Slight Elevation of Pulse Release of catecholamines Epinephrine Norepinephrine Anxiety,slightly pale and clammy skinStages of Hemorrhage Stage 1 15-25%loss of CBV 750-1250 mL Early Decompensation Unable to maintain BP Tachycardia&TachypneaStages of Hemorrhage Stage 2(
21、continued)Decreased pulse strength Narrowing pulse pressure Significant catecholamine release Increase PVR Cool,clammy skin&thirst Increased anxiety and agitation Normal renal output MAP 70 25-35%loss of CBV 1250-1750 mL Late Decompensation(Early Irreversible)Compensatory mechanisms unable to cope w
22、ith loss of Blood VolumeStages of Hemorrhage Stage 3(continued)Classic Shock Weak,thready,rapid PULSE Narrowing pulse pressure=35%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
23、 Unlikely survivalStages of Hemorrhage Stage 4Stages of Hemorrhage 35%4 25-35%3 15-25%2 50%blood volume than normal Fetal circulation is impaired when mother is compensating Athletes Greater fluid and cardiac capacity Obese CBV is based on IDEAL weight(less CBV)Stages of Hemorrhage Concomitant Facto
24、rs(continued)Stages of Hemorrhage Concomitant Factors Children CBV 8-9%of body weight Poor compensatory mechanisms TREAT AGGRESIVELY Elderly Decreased CBV Medications:BP,&AnticoagulantsHemorrhage Assessment Scene Size-up Is it Safe?BSI Blood Loss Law Enforcement Mechanism of Injury/Nature of Illness
25、 Number of Patients Need for Additional ResourcesHemorrhage Assessment Initial Assessment General Impression Obvious Bleeding Mental Status CABC Interventions Manage as you go O2 Bleeding Control Shock BLS before ALS!Hemorrhage Assessment Focused H&P Rapid Trauma Assessment Full Head to Toe Consider
26、 Air Medical if Stage 2+Blood Loss Focused Physical Exam Guided by c/c Vitals,SAMPLE,&OPQRST Additional Assessment Orthostatic Hypotension Tilt Test:20 BP or P from supine to sitting Pelvic fracture:2,000 mL Femur fracture:1,500 mL Tibia/Fibula fracture:500-750 mL Hematomas&Contusions:500 mLHemorrha
27、ge Assessment Fractures and Blood LossHemorrhage Assessment Ongoing Assessment Reassess Vitals&Mental Status Q 5 min:UNSTABLE patients Q 15 min:STABLE patients Reassess Interventions Oxygen ET IV Medication Actions Trending:Improvement vs DeteriorationHemorrhage Management ABCs O2,ET,IV,CM Protect C
28、-Spine Full immobilization Best splint is the body CPR:BLS&ALS care If multiple casualties,do not begin unless adequate resources are available Bleeding Control PASGAny injury to the head or torso is ALSO considered an injury to the spine.Head Wounds Presentation Severe bleeding Skull Fracture Manag
29、ement Gentle Direct Pressure Fluid drainage from Ears and Nose DO NOT Pack Cover and bandage looselySpecific Wound Considerations Neck Wounds Presentation Large vessel can entrain air.Management Consider direct digital pressure Occlusive dressing Gaping Wounds Presentation Multiple sites Gaping prev
30、ents uniform pressure Management Bulky Dressing Trauma Dressing Sterile,non-adherent surface to wound Compression dressingSpecific Wound Considerations Crush Injury Presentation Difficult to locate source of bleeding Normal hemorrhage control mechanism non-functional Management Consider an air-splin
31、t and pressure dressing Consider constricting band or tourniquetTransport Considerations Consider Rapid Transport Suspected serious blood loss Suspected serious internal bleeding Decompensating Shock AMS,pulse,Narrowing pulse pressure WHEN IN DOUBT TRANSPORT Other Considerations Sympathetic Response
32、 AnxietySHOCK isINADEQUATETISSUEPERFUSIONIn a Nutshell.Circulation Systolic Pressure Strength and volume of cardiac output Diastolic Pressure More indicative of the state of constriction of the arterioles Mean Arterial Pressure 1/3 pulse pressure added to the diastolic pressure Tissue Perfusion Pres
33、sureCompensation Respiratory Cardiovascular Sympathetic NS activation Neuroendocrine Response Transcapillayr refillRespiratory Compensation Chemoreceptors located in carotid body and aortic arch Communicate respiratory center via CN IX,X PaO2 50mmHg,hypoxemia PaCo2 increased,hypercarbia acidosis Inc
34、reased rate,depth or respirationsCirculation Vascular Control Increased sympathetic tone results in increased vasoconstriction Microcirculation Blood flow in the arterioles,capillaries and venules Sphincter Functioning Most organ tissue requires blood flow 5 to 20%of the timeSphincter FunctioningSph
35、inctersConstrictO2 returnsCO2 removedpH normalSphinctersDilateCO2increasesO2 fallsMASTCellsHISTAMINE ReleaseMASTCellsStop ReleasingHISTAMINERespiratory Control Increased blood CO2 Decreased blood O2 Decrease CSF pH(acidosis)Mast cells release histamine Vasodilation Increase O2/decrease CO2/pH Histam
36、ine release halted Stop vasodilationHistamine Release Eventually:Vasodilation Increased venous capacitance Blood pooling Increased vascular permeability Leaking into tissues Edema Circulation Thoracoabdominal Pump Respirations assist blood return to the heart Changing intrathoracic pressure Changing
37、 pressures draw blood back to heart Blood Volume:5L 7%heart 13%major arteries 7%capillaries 64%venous system 9%pulmonary circulation In shock,the blood return to the heart is diminished?Preload and AfterloadParasympathetic Nervous SystemDecrease Heart rate strength of contractions blood pressureIncr
38、ease Digestive system KidneysCardiovascular System RegulationSympathetic Nervous SystemIncrease Body activity Heart rate Strength of contractions Vascular constriction Bowel&Digestive Viscera Decreased urine production Respirations BronchodilationIncreases skeletal muscle perfusionCardiac Innervatio
39、n Primarily innervated by sympathetic NS Parasympathetic innervates atria Vagal response Vagal stimulation PNS&SNS always act in balance Baroreceptors:Monitor BP Location Aortic Arch Carotid Sinuses Send Impulses to the Medulla Cardioacceleratory Center SNS:controls release of E and NE Cardioinhibit
40、ory Center PNS:controls the vagus nerve Vasomotor Center Arterial and Venous toneCardiovascular System Regulation Chemoreceptors Monitors level of CO2 in CSF pH CSF Monitors level of O2 in bloodCardiovascular System RegulationSympathetic NS Activation Baroreceptors monitor BP Communicate with brain
41、CN IX Carotid arch thru CN X Increased activity of SNS,decreased vagal activity Account for many S/S associated with shock Compensate for inadequate O2 deliveryCatecholamines Epinephrine Norepinephrine Actions Alpha 1 Alpha 2 Beta 1 Beta 2Cardiovascular System RegulationHormone RegulationAlpha 1 Vas
42、oconstriction Increased peripheral vascular resistance Increased preloadAlpha 2 Regulates release of NEBeta 1 Positive inotropy Positive chronotropy Positive dromotopyBeta 2 Bronchodilation Smooth muscle dilation in bowel Activation A1 Vasoconstriction Blood shunted from non-vital tissues Skin-pale,
43、cool,clammy GI-nausea,vomiting Activation B1 Increased chronotropy,inotropy,maintain BP Stimulation B2 Bronchodilation Improve oxygenation Antidiuretic Hormone(ADH)aka:Arginine Vasopressin(AVP)Released Posterior Pituitary Drop in BP or Increase in serum osmolarity Action Increase in peripheral vascu
44、lar resistance Increase water retention by kidneys Decrease urine output Splenic vasoconstriction 200 mL of free blood to circulationCardiovascular System RegulationHormone Regulation Angiotensin II Released Primary chemical from Kidneys Lowered BP and decreased perfusion Action Converted from Renin
45、 into Angiotensin I Modified in lungs to Angiotensin II 20 minute process Potent systemic vasoconstrictor 1 hour duration Causes release of ADH,Aldosterone and EpiCardiovascular System RegulationHormone Regulation Aldosterone Release Adrenal Cortex Stimulated by Angiotensin II Action Maintain kidney
46、 ION balance Retention of sodium and water Reduces insensible fluidCardiovascular System RegulationHormone Regulation(continued)Cardiovascular System RegulationHormone Regulation Glucagon Release Alpha Cells of Pancreas Triggered by Epi Action Causes liver and skeletal muscles to convert glycogen in
47、to glucose Gluconeogenesis Insulin Release Beta Cells of Pancreas Action Facilitates transport of glucose across cell membraneCardiovascular System RegulationHormone Regulation Erythropoietin Release Kidneys Hypoperfusion or hypoxia Action Increases production and maturation of RBCs in the bone marr
48、owNeuroendocrine Response ACTH(adrenocorticotropic hormone)secreted by pituitary Stimulates adrenal cortex to produce aldosterone and cortisol Aldosterone causes reabsorption of Na&H2O in kidney Kidney releases renin when cells of juxtaglomerular apparatus(JGA)are hypoperfused Renin acceleerates con
49、version angiotensin to angiotensin I Lung tissue converts angiotensin I to angiotensin II,potent vasoconstrictor and stimulates release aldosteroneCortisol Stimulates protein synthesis Adrenal medulla secretes epi and NE Vasopressin(ADH)released by posterior pituitary in response to increased osmola
50、lity Causes distal renal tubules to increase H2O absorption Greater Loss Cellular Ischemia Capillary Microcirculation Possibility of Capillary Washout Buildup of lactic acid and CO2 Relaxation of post capillary sphincters Release of byproducts into circulation PROFOUND METABOLIC ACIDOSISThe Bodys Re
