外科急诊创伤（英文）休克及出血

Hemorrhage that the machinery of life has been rudely unhinged, and the whole system profoundly shocked; in a word, that the nervous fluid has been exhausted” ( A System of Surgery, 1859) 1800s 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 Represents 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 organs Treatment Goals Recognition of early shock Appropriate airway management Rapid transportation to appropriate facility Hemorrhage Circulatory System Hemorrhage Classification Clotting Factors Affecting Clotting Hemorrhage Control Stages of Hemorrhage Hemorrhage Assessment Hemorrhage Management Cardiovascular System Delivery of nutrients and O2 to tissues and cells Transportation of waste products produced by metabolism to liver and kidneys Delivery of CO2 to lungs Components Heart or pump Blood vessels or pipes Blood or fluid Circulatory System Review Terminology Stroke Volume Preload Ventricular Filling Frank-Starling Mechanism Afterload Cardiac Output SVxHR=CO 5L/min Fick Principle Heart Parasympathetic Nervous System Slows rate Vagus Nerve Sympathetic Nervous System Increases rate Cardiac Plexus Cardiac Output Volume of blood pumped in 1 minute = 4-6L SV x HR SV = amount of blood ejected from left ventricle with each contraction Blood 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 return Afterload Amount of resistance heart must overcome to eject blood Contractility Ability to contract, inotropy Frank Starlings Law Inotropy Negative Scar tissue, CHF Beta adrenergic blockers Calcium channel blockers Positive Beta adrenergic agonists, B1 List some B blockers, Ca channel blockers, B agonists 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 transport RBCs Ability of RBCs to off-load O2 O2 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 2:1 Cellular Metabolism Glycolysis Krebs Cycle Electron Transport Glycolysis 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 it Muscle and skin can function in aerobic conditions for short period Brain most sensitive to hypoxia Krebs Cycle Aerobic conditions pyruvic acid enters mitochondria Produces 6 CO2 molecules and 4 ATP Electron Transport Occurs in proteins bound to mitochondrial membrane Additional 32 ATP produced Primary site of O2 utilization within cell Produce very little ATP on anarerobic conditions Cellular 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, proteins and fats to release energy Other Processes Anaerobic Metabolism Inadequate oxygen pathway Byproducts: Pyruvic Acid Lactic Acid Cellular death eventually occurs due to inadequate perfusion Circulatory System Vascular System Arteries Tunica Adventitia Tunica Media Tunica Intima Arteriole Capillary: 7% of blood volume Venule Vein Constriction returns 20% (1 L) of blood to active circulation 13% of blood volume 64% of blood volume Blood Vessels Sympathetic innervation Vasoconstriction Alpha 1 agonist List some drugs that have alpha 1 agonsist/ blocker effects Names Indications Contraindications What physiological 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 capillary into interstitial space Oncotic pressure Force exerted by large protein molecules in blood that draws fluid into vascular system Proximal capillary Hydrostatic pressure prevails Allows intravascular fluid and nutrients to diffuse out of capillary Distal capillary Oncotic pressure is dominant Draws fluid from interstitial fluid and waste of metabolism into capillaries Blood Components Erythrocyte: 45% Hemoglobin Hematocrit Other Formed Elements: 2 sec Decreased BP Nausea, vomiting Hemorrhage Control Internal Hemorrhage Epistaxis: Nose Bleed Causes: Trauma, Hypertension Treatment: Lean forward, pinch nostrils, roll gauze under upper lip Hemoptysis Esophageal Varices Melena Chronic Hemorrhage Anemia Stages 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 BP, Pulse Pressure, Respirations Slight Elevation of Pulse Release of catecholamines Epinephrine Norepinephrine Anxiety, slightly pale and clammy skin Stages of Hemorrhage Stage 1 15-25% loss of CBV 750-1250 mL Early Decompensation Unable to maintain BP Tachycardia & Tachypnea Stages of Hemorrhage Stage 2 (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 with loss of Blood Volume Stages 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 Unlikely survival Stages of Hemorrhage Stage 4 Stages 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 Factors (continued) Stages of Hemorrhage Concomitant Factors Children CBV 8-9% of body weight Poor compensatory mechanisms TREAT AGGRESIVELY Elderly Decreased CBV Medications: BP, & Anticoagulants Hemorrhage Assessment Scene Size-up Is it Safe? BSI Blood Loss Law Enforcement Mechanism of Injury/Nature of Illness Number of Patients Need for Additional Resources Hemorrhage 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 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 mL Hemorrhage Assessment Fractures and Blood Loss Hemorrhage 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 Deterioration Hemorrhage Management ABCs O2, ET, IV, CM Protect C-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 PASG Any injury to the head or torso is ALSO considered an injury to the spine. Head Wounds Presentation Severe bleeding Skull Fracture Management Gentle Direct Pressure Fluid drainage from Ears and Nose DO NOT Pack Cover and bandage loosely Specific Wound Considerations Neck Wounds Presentation Large vessel can entrain air. Management Consider direct digital pressure Occlusive dressing Gaping Wounds Presentation Multiple sites Gaping prevents uniform pressure Management Bulky Dressing Trauma Dressing Sterile, non-adherent surface to wound Compression dressing Specific Wound Considerations Crush Injury Presentation Difficult to locate source of bleeding Normal hemorrhage control mechanism non-functional Management Consider an air-splint and pressure dressing Consider constricting band or tourniquet Transport 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 Anxiety SHOCK is INADEQUATE TISSUE PERFUSION In 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 Pressure Compensation Respiratory Cardiovascular Sympathetic NS activation Neuroendocrine Response Transcapillayr refill Respiratory Compensation Chemoreceptors located in carotid body and aortic arch Communicate respiratory center via CN IX, X PaO2 50mmHg, hypoxemia PaCo2 increased, hypercarbia acidosis Increased rate, depth or respirations Circulation 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 time Sphincter Functioning Sphincters Constrict O2 returns CO2 removed pH normal Drop in pH Sphincters Dilate CO2 increases O2 falls MAST Cells HISTAMINE Release MAST Cells Stop Releasing HISTAMINE Respiratory Control Increased blood CO2 Decreased blood O2 Decrease CSF pH (acidosis) Mast cells release histamine Vasodilation Increase O2/ decrease CO2/ pH Histamine release halted Stop vasodilation Histamine 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 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 Afterload Parasympathetic Nervous System Decrease Heart rate strength of contractions blood pressure Increase Digestive system Kidneys Cardiovascular System Regulation Sympathetic Nervous System Increase Body activity Heart rate Strength of contractions Vascular constriction Bowel & Digestive Viscera Decreased urine production Respirations Bronchodilation Increases skeletal muscle perfusion Cardiac Innervation 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 Cardioinhibitory Center PNS: controls the vagus nerve Vasomotor Center Arterial and Venous tone Cardiovascular System Regulation Chemoreceptors Monitors level of CO2 in CSF pH CSF Monitors level of O2 in blood Cardiovascular System Regulation Sympathetic NS Activation Baroreceptors monitor BP Communicate with brain 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 delivery Catecholamines Epinephrine Norepinephrine Actions Alpha 1 Alpha 2 Beta 1 Beta 2 Cardiovascular System Regulation Hormone Regulation Alpha 1 Vasoconstriction Increased peripheral vascular resistance Increased preload Alpha 2 Regulates release of NE Beta 1 Positive inotropy Positive chronotropy Positive dromotopy Beta 2 Bronchodilation Smooth muscle dilation in bowel Activation A1 Vasoconstriction Blood shunted from non-vital tissues Skin- pale, 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 vascular resistance Increase water retention by kidneys Decrease urine output Splenic vasoconstriction 200 mL of free blood to circulation Cardiovascular System Regulation Hormone Regulation Angiotensin II Released Primary chemical from Kidneys Lowered BP and decreased perfusion Action Converted from Renin into Angiotensin I Modified in lungs to Angiotensin II 20 minute process Potent systemic vasoconstrictor 1 hour duration Causes release of ADH, Aldosterone and Epi Cardiovascular System Regulation Hormone Regulation Aldosterone Release Adrenal Cortex Stimulated by Angiotensin II Action Maintain kidney ION balance Retention of sodium and water Reduces insensible fluid Cardiovascular System Regulation Hormone Regulation (continued) Cardiovascular System Regulation Hormone Regulation Glucagon Release Alpha Cells of Pancreas Triggered by Epi Action Causes liver and skeletal muscles to convert glycogen into glucose Gluconeogenesis Insulin Release Beta Cells of Pancreas Action Facilitates transport of glucose across cell membrane Cardiovascular System Regulation Hormone Regulation Erythropoietin Release Kidneys Hypoperfusion or hypoxia Action Increases production and maturation of RBCs in the bone marrow Neuroendocrine 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 conversion angiotensin to angiotensin I Lung tissue converts angiotensin I to angiotensin II, potent vasoconstrictor and stimulates release aldosterone Cortisol Stimulates protein synthesis Adrenal medulla secretes epi and NE Vasopressin (ADH) released by posterior pituitary in response to increased osmolality 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 ACIDOSIS The Bodys Response to Blood Loss Systemic Response to Shock Sympathetic NS response Hormone release Result of hemorrhage R atrium does not fill completely Ventricle not filled Decreased contractility Decreased SV Decreased SBP Reduced perfusion of capillary beds Baroreceptors signal medulla Increased PVR Increased venous tone Increased HR Increased contractility BP returns to normal If blood loss is controlled no ill effects Cellular Ischemia Blood loss continues Venous constriction PVR increases maintaining SBP DBP also rises resulting in narrowing pulse pressure Pulse weakens Less blood directed to non-critical organs Skin- pale, cool, clammy Anaerobic metabolism ensues CO2 and lactic acid produced and accumulate Cellular hypoxialeads to cellular ischemia HR increases Blood becomes more acidotic Chemoreceptors increase RR/ depth Circulating catecholamines and acidosis results in AMS Arterioles hypoxic and fatigued Hemestasis occurs blood is drawn from interstitium 1L/hr Erythropoieten increases RBC production Recovery possible Sympathetic stimulation, reduced perfusion to kidneys, pancreas, liver cause hormone release Angiotensin II increases PVR reduces blood flow Lactic acid build up Hydrostatic pressure forces fluid into interstitium Compensatory mechanisms fail Interstitial edema decreases ability to provide O2 and remove CO2 Capillary cell membranes break down RBCs clump, rouleax Build up of acids results in relaxation of post capillary sphincters Byproducts, K+ released by cells, agglutinated RBCs released in venous circulation Results in profound metabolic acidosis and microscopic emboli CO= 0, PVR= 0, decrease BP, decrease cellular perfusion to critical organs irreversible Transcapillary Refill Following hypovolemia osmosis allows movement of fluid from intracellular and interstitial spaces into intravascular space 2L self limiting Hgb, Hct values inaccurate in