Hemorrhage & Shock.

Hemorrhage & Shock

Sections Introduction to Hemorrhage & Shock Hemorrhage Shock

Introduction to Hemorrhage & Shock
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 death

SHOCK “a momentary pause in the act of death”

“But a more careful examination soon serves to show that deep mischief is lurking in the system; 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)

1800’s 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 Heart 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 Afterload Contractility
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 Starling’s Law

Inotropy Negative Positive
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 RBC’s to transport O2 Adequate blood flow to transport RBC’s Ability of RBC’s 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 Kreb’s 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 liver’s ability to convert it Muscle and skin can function in aerobic conditions for short period Brain most sensitive to hypoxia

Kreb’s 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 Other Processes Glycolysis
Cell utilizing energy source Releases energy Aerobic Metabolism: 95% of cellular Energy Requires oxygen and glucose Kreb’s 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 Arteriole
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 Distal 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% Other Formed Elements: <1%
Hemoglobin Hematocrit Other Formed Elements: <1% Platelets Leukocytes Monocytes, Basophils, Eosinophils, Neutrophils Plasma: 54%

Function Delivers O2 and nutrients to tissues and transports waste to kidneys and liver for detoxification Rids body of invading microorganisms

Acidosis Hgb has a decreased affinity for O2 in an acidotic state
Therefore, hgb will release more O2 into acidotic tissue Oxyhgb saturation will be lower

Alkolosis Causes Hgb to have a higher affinity for O2
Decreased amount of O2 released into alkalotic tissue

Hemorrhage Classification
Capillary Slow, even flow Venous Steady, slow flow Dark red Arterial Spurting blood Pulsating flow Bright red color

Clotting Three Step Process Vascular Phase Platelet Phase
Vasoconstriction Reduction lumen size = reduction blood loss Platelet Phase Tunica intima damaged Turbulent blood flow Frictional damage to platelets Agglutination and aggregation Coagulation Phase Release of enzymes Extrinsic=nearby tissue Intrinsic=damaged platelets FIBRIN release Normal coagulation = 7-10 minutes

Clotting Other Factors Nature of Wound Transverse Longitudinal
Vessels constrict and draw inward Reduction of lumen Reduction of blood loss Example: Clean Tear Longitudinal Constriction of smooth muscle Enlarges wound Increased blood loss Example: Crushing Trauma

Factors Affecting Clotting
Movement of the wound site Aggressive Fluid Therapy Increases BP and pushes clots Fluid dilutes clotting factors Low Body Temperature Ineffective clot formation Medications ASA, heparin, warfarin (Coumadin)

Hemorrhage Control External Hemorrhage
Direct Pressure & Pressure Dressing General Management Direct Pressure Elevation Ice Pressure Points Constricting Band Tourniquet Release may send toxins to heart Lactic acid, and electrolytes

Tourniquets are ONLY used as a last resort!

Hemorrhage Control Internal Hemorrhage Hematoma
Pocket of blood between muscle and fascia Humerus or Tibia/Fibula fracture: mL Femur fracture: 1,500mL UNEXPLAINED SHOCK is BEST attributed to abdominal trauma General Management Immobilization, Stabilization, Elevation

Early S/S Internal Hemorrhage
Pain, tenderness, swelling, discoloration Bleeding from mouth, nose, rectum, vagina Hematemesis Tender, rigid, distended

Late S/S Internal Hemorrhage
Anxiety, restlessness, combative, AMS Weak, faint, dizzy Pale, cool, clammy Dilated pupils, sluggish Thirst Shallow, tachypnic respirations Rapid, weak pulse Cap refill > 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)

Stages of Hemorrhage Stage 1
15% loss of CBV 70 kg pt = mL Compensation Vasoconstriction Normal BP, Pulse Pressure, Respirations Slight Elevation of Pulse Release of catecholamines Epinephrine Norepinephrine Anxiety, slightly pale and clammy skin

15-25% loss of CBV mL Early Decompensation Unable to maintain BP Tachycardia & Tachypnea (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 hypoperfusion

MAP Mean Arterial Pressure Systolic + 2(diastolic) 3
Map should be maintained > 70

25-35% loss of CBV mL Late Decompensation (Early Irreversible) Compensatory mechanisms unable to cope with loss of Blood Volume (continued)

Classic Shock Weak, thready, rapid PULSE Narrowing pulse pressure = < MAP Tachypnea Anxiety, restlessness Decreased LOC and AMS Pale, cool and clammy skin

>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

Pulse Pressure/ Strength
Stages of Hemorrhage    >35% 4   25-35% 3   15-25% 2 <15% 1 Resp. Volume Resp. Rate BP Pulse Pressure/ Strength Pulse Rate Vasocon-striction Blood Loss Stage Average Blood Volume = 5 L

Stages of Hemorrhage Concomitant Factors
Pre-existing condition Rate of blood loss Patient Types Pregnant >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) (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

Initial Assessment General Impression Obvious Bleeding Mental Status CABC Interventions Manage as you go O2 Bleeding Control Shock BLS before ALS!

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

Hemorrhage Assessment Fractures and Blood Loss
Pelvic fracture: ,000 mL Femur fracture: ,500 mL Tibia/Fibula fracture: mL Hematomas & Contusions: mL

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
ABC’s 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.

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 entrain air. Management Consider direct digital pressure Occlusive dressing

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 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….. SHOCK is… INADEQUATE TISSUE PERFUSION

Circulation Systolic Pressure Diastolic 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 Microcirculation
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 Dilate CO2 increases O2 falls O2 returns CO2 removed pH normal HISTAMINE Release Drop in pH MAST Cells Stop Releasing HISTAMINE MAST Cells Sphincter Functioning Sphincters Constrict

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 Blood Volume: 5L
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

Cardiovascular System Regulation
Parasympathetic Nervous System Decrease Heart rate strength of contractions blood pressure Increase Digestive system Kidneys 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

Chemoreceptors Monitors level of CO2 in CSF pH CSF Monitors level of O2 in blood

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

Cardiovascular System Regulation Hormone Regulation
Catecholamines Epinephrine Norepinephrine Actions Alpha 1 Alpha 2 Beta 1 Beta 2 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 Activation B1 Stimulation B2 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

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

Aldosterone Release Adrenal Cortex Stimulated by Angiotensin II Action Maintain kidney ION balance Retention of sodium and water Reduces insensible fluid (continued)

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 Erythropoietin Release Kidneys Hypoperfusion or hypoxia Action Increases production and maturation of RBC’s 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

The Body’s Response to Blood Loss
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

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

RBC’s clump, rouleax Build up of acids results in relaxation of post capillary sphincters Byproducts, K+ released by cells, agglutinated RBC’s 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 actively bleeding patients Anemia present with hemodilution due to resuscitation, transcapillary refill

Stages of Shock Compensated Shock Decompensated Shock
Minimal Change Decompensated Shock System beginning to fail Irreversible Shock Ischemia and death imminent

Decompensation Body’s compensatory mechanisms overwhelmed O2 delivery falls again

Host Factors May limit ability to compensate Age: Neonate, infants
Mechanism undeveloped Geriatrics Underlying disease Medications B blockers, Ca channel blockers Alcohol intoxication Peripheral vasodilation Hypothermia Physiacl conditioning Compensate well until decompensation

Etiology of Shock Hypovolemic Shock Distributive Shock
Loss of blood volume Distributive Shock Prevent appropriate distribution of nutrients and removal of wastes Anaphylactic Septic Hypoglycemia Neurogenic Shock Loss of nervous control from CNS to peripheral vasculature Cardiogenic Shock Pump failure Obstructive Shock Interference with the blood flowing through the cardiovascular system Tension Pneumothorax Cardiac Tamponade Pulmonary Emboli Respiratory Shock Respiratory system not able to bring oxygen into the alveoli Airway obstruction Pneumothorax

Respiratory Failure Hypoxia Airway obstruction Mechanical failure
Foreign body Mechanical failure Interfere with pulmonary mechanics Open pneumothorax, massive flail chest

Diffusion failure Toxic
Interfere with O2 diffusion across alveolar membrane Pulmonary contusion, pulmonary burns, pneumonia Toxic Interfere with O2 delivery and utilization Co, cyanide

Perfusate Failure Hypovolemic shock Hemorrhage Plasma loss Internal
External Plasma loss Thermal burns, severe crush injury, burns, diabetes insipidus, dehydration

Vascular Failure Distributive shock Sepsis Neurogenic Anaphylaxis
Systemic inflammation Severe infection Neurogenic High spinal cord injury Brain stem injury Anaphylaxis Severe allergic reaction

Septic Shock Toxins associated associated with bacterial infection
vasodilation Immune response Increased permeability Relative hypovolemia Decreased preload, CO

Shock Assessment Scene Size-up Initial Assessment Focused H&P
Rapid Trauma Detailed H&P Ongoing Assessment

Shock Management Airway & Breathing Hemorrhage Control
NRB PPV (overdrive respiration) ET Difficult Airway Devices LMA, PtL, Combitube Needle Decompression Hemorrhage Control Fluid Resuscitation Catheter Size & length Large Bore 20ml/kg of NS or LR STABILIZE VITALS

Shock Management Temperature Control PASG Conserve core temperature
Warm IV Fluids PASG Action Increase PVR Reduce Vascular. Volume Increase central CBV Immobilize lower extremities Assess Pulmonary Edema Pregnancy Baseline Vitals

Shock Management Pharmacology ONLY after Fluid Resuscitation
Hypovolemic Fluid challenge Cardiogenic Shock Fluid Challenge except in PE Vasopressors: Dopamine Cardiac Drugs: Epi, Atropine Obstructive Shock IV resuscitation: NS & LR Distributive Shock IV Resuscitation Dopamine PASG

Hemorrhage & Shock.

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Hemorrhage & Shock.

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