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Hemorrhagic Shock PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Hemorrhagic Shock".

This medical PowerPoint presentation talks about hemorrhagic shock, a medical emergency that occurs when a person loses a large amount of blood, typically more than 20% of their total blood volume. This can happen as a result of traumatic injuries, such as car accidents or gunshot wounds, or medical conditions that cause internal bleeding, such as ulcers or ruptured blood vessels.

When the body loses blood, it goes into a state of shock, which means that it is not getting enough oxygen and nutrients to function properly. Symptoms of hemorrhagic shock can include rapid heartbeat, low blood pressure, confusion, dizziness, pale skin, and rapid breathing.

Treatment for hemorrhagic shock typically involves stopping the bleeding and replenishing lost fluids and blood through intravenous fluids and blood transfusions. In severe cases, surgery may be necessary to repair the source of bleeding.

Prompt and effective treatment is crucial in cases of hemorrhagic shock, as it can quickly become life-threatening if left untreated.

Tags : Hemorrhagic Shock, medical emergency, traumatic injuries, Emergency Medicine, Emergency Medicine PowerPOint presentation

Published on : Apr 03, 2023 | Views : 3701 | Downloads : 4

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Slide 2-

Hemorrhagic Shock
Slide 3-

Objectives At the conclusion of this presentation the participant will be able to: Recognize hemorrhagic shock signs and symptoms Explain the importance of early control of hemorrhage in trauma patients Describe the management and ongoing evaluation of hemorrhagic shock List the components of damage control resuscitation
Slide 4-

Hemorrhagic Shock Feared by all Respected by many Foreign to none
Slide 5-

Time to Trauma Death 50% deaths occur at scene within minutes: CNS injury 40-50% Hemorrhage 30-40% 50% after hospital arrival: 60% die within first 4 hrs 84% die within first 12 hrs 90% die within first 24 hrs Hemorrhage accounts for 50% Deaths in the first 24 hours
Slide 6-

Historic Trauma Trimodal Death Distribution DEATH Minutes Hours Days Weeks 50% 30% 20% Immediate Early Late
Slide 7-

Hemorrhage Trauma Deaths
Slide 8-

Trimodal Moving Toward Bimodal Death Distribution Historical (Pre 2000) Current (Post 2000)
Slide 9-

New Bimodal Trauma Death Distribution 30% HOURS WEEKS 0 4 1 4 60% 30% 10%
Slide 10-

Hemorrhagic Shock Definition Hemorrhagic Shock Reduction in tissue perfusion below that necessary to meet metabolic needs Inadequate Perfusion
Slide 11-

Injuries Prone to Hemorrhage Quickly Rule Out Blood Loss Chest – CXR / FAST Abdomen - FAST Pelvis – Xray Femur – exam / Xray
Slide 12-

Humerus 750 ml Tibia 750 ml Femur 1500 ml Pelvis > 3 L Fracture Associated Blood Loss Associated Soft Tissue Trauma Release of Cytokines Increased permeability Magnify fluid loss
Slide 13-

Confounding Factors In Response To Hemorrhage Patients age Pre-existing disease / meds Severity of injury Access to care Duration of shock Amount prehospital fluid Presence of hypothermia
Slide 14-

Hemorrhagic Shock Pathophysiology
Slide 15-

Heart Rate (beats/min) Stroke Volume (cc/beat) Cardiac Output (L/min) X = Cardiac Output
Slide 16-

Sympathetic Nervous System Heart Rate Contractility Vasoconstriction
Slide 17-

Sympathetic Nervous System Progressive Vasoconstriction: Skin Muscle Splanchnic Bed
Slide 18-

Important Hormones in Shock Catecholamines: Epinephrine & Norepinephrine Increased heart rate & contractility Vasoconstriction & narrowed pulse pressure Renin-Angiotensin Axis: Aldosterone and ADH Water & sodium conservation & vasoconstriction Increase in blood volume and blood pressure Decreased urine output
Slide 19-

Sympathetic Nervous System Increased shunting of blood to: Heart & Brain
Slide 20-

Cellular Response to Shock
Slide 21-

Hemorrhagic Shock Assessment
Slide 22-

Classic Signs & Symptoms of Shock Changing mentation Tachycardia Cool, clammy, skin Prolonged capillary refill Narrowed pulse pressure Decreased urine output Hypotension
Slide 23-

Normal Vitals do not r/o Occult Hypo Perfusion
Slide 24-

ATLS Classification of Hemorrhagic Shock
Slide 25-

Effects of Blood Volume Loss on Mean Arterial Pressure in Classes of Shock Most die by 6 hrs
Slide 26-

pH Serum Lactate Base Deficit Echocardiography Arterial Wave Analsyis StO2 (NIRS) Mentation Skin Perfusion Pulse Blood Pressure Pulse Pressure Shock Index Urine Output Initial Assessment Resuscitation Endpoints Assessment vs. Resuscitation Endpoints Traditional vs. New Acute vs. Ongoing Static vs. Dynamic Global vs. End Organ
Slide 27-

Response Fluid Resuscitation
Slide 28-

Value of Manual Vital Signs GCS Motor Verbal Pulse Character Most Predictive for Need of Life Saving Interventions
Slide 29-

Rough BP Estimation from Pulse If you can palpate this pulse, you know the SBP is roughly this number
Slide 30-

Occult Hypoperfusion State of O2 delivery in the setting of grossly normal physiologic criteria Patients don’t suddenly deteriorate, rather we suddenly notice…
Slide 31-

Changing Mentation Indicator of perfusion Affected by drugs & alcohol Hypoxia/Head Injury Until proven otherwise
Slide 32-

Skin Perfusion Pale, cool, mottled Vasoconstriction Most sensitive in pediatrics Starts distal extremities Ascends towards trunk Capillary Refill Unreliable to measure Normal < 2 seconds
Slide 33-

Blood Pressure BP response to volume loss Non-linear due to compensatory mechanisms Insensitive sign of early shock NTDB study SBP did not decrease < 90 Until base deficit was > 20 Infrequently & or inadequately monitored First BP should always be manual Automated BP overestimated by 10 mm Hg
Slide 34-

Blood Pressure Systolic BP drop a late sign Systolic BP does not fall until: Adults 30% blood loss Pediatrics 40-45% blood loss SBP < 90 mm Hg: mortality approaches 65%
Slide 35-

Beware Dismissal of Prehospital BP Skepticism
Slide 36-

Hypotension Redefined?The New Hypotension: SBP < 110 Associated with onset of physiologic changes Use only to diagnose shock Not as resuscitation endpoint
Slide 37-

Research demonstrates that optimal SBP for improved mortality in hemorrhagic shock increases with age
Slide 38-

New SBP Sweet Spot for Early Diagnosis of Shock? 60 70 80 90 100 110 120 130 90 100 110 120 130 140 150 160 Adult Trauma Geriatric Trauma
Slide 39-

Pulse Pressure Narrowed pulse pressure suggests significant blood loss Result of increasing diastolic pressure from compensatory catecholamine release 100/66 100/74 100/77 100/84
Slide 40-

Pulse Lacks specificity alone Age dependent Affected by: Emotion Fever Pain Drugs Pulse & character together more reliable Trended over time may? have sensitivity When to be concerned? 80 90 100 110 > 120 Any patient who is cool & tachycardic is in shock until proven otherwise (ATLS)
Slide 41-

Relative Bradycardia(Paradoxical Bradycardia) Defined as Pulse < 90 with SBP < 90 Occurs in up to 45% of all hypotensive trauma Cause remains unclear: Sign of rapid & severe internal bleeding? Increased vagal tone from blood in abd cavity? Protective reflex designed to increase diastolic filing in the presence of severe hypovolemia?
Slide 42-

Shock Index (SI) SI = HR / SBP Elevated early in shock Normal 0.5 - 0.7 SI > 0.9 predicts: Acute hypovolemia in presence of normal HR & BP Marker of injury severity & mortality Caution in Geriatrics May underestimate shock due to higher baseline SBP Uses Prehospital use → triage Predict risk for mass transfusion?
Slide 43-

Urine Output Adult 0.5 ml / kg / hour Child 1.0 ml / kg / hour Toddler 1.5 ml / kg / hour Infant 2.0 ml / kg / hour
Slide 44-

Pulmonary Artery Catheter Not advocated for hemorrhagic shock Dynamic response of the systems too slow to guide therapy Use: May benefit geriatric trauma Sepsis goal directed therapy Hemodynamic Monitoring Central Venous Pressure Not advocated for hemorrhagic shock Poor relationship between CVP and blood volume Unreliable for assessing response to fluid Use: Acute air embolus Acute PE Rt Ventricular infarction Acute lung injury
Slide 45-

Doppler Echocardiography(Transthoracic or Transesophageal) Allows for physician bedside assessment: Ventricular function Volume status Stroke volume Cardiac output Dependent on: Technology investment Technical expertise Intra-observer variability Excellent diagnostic tool Poor monitoring device
Slide 46-

Physiologic Variability as Predictors Subtle patterns of variation produced by healthy biological systems is normal Loss of this variability is seen in critical illness Early loss of HR variability predicts mortality in trauma
Slide 47-

Arterial Pressure Waveform Systems Measures pulse pressure & stroke volume variation Reliable predictors of volume responsiveness Determines where the patient lies on their own individual Starling curve Examples of systems: PiCCO (Phillips) pulseCO (LiDCO,Ltd.) FloTrac/Vigileo (Edwards)
Slide 48-

Near Infrared Spectroscopy (NIRS) Skeletal muscle StO2 Measures hemoglobin oxygen saturation in tissue Tracks systemic O2 delivery Continuously and Noninvasively Comparable results to BD and Lactate Predicts MSOF Predicts Mortality Research ongoing as resuscitation endpoint
Slide 49-

Hemorrhagic Shock Lab Values
Slide 50-

Hemoglobin / Hematocrit Unreliable estimation acute blood loss Lag time of several hours Baseline value for comparison only
Slide 51-

Arterial pH Acidosis - Serum pH < 7.20 Ongoing Marker of Severe Physiologic Derangement Decreased cardiac contractility Decreased cardiac output Vasodilation and decreased BP Decreased hepatic and renal blood flow
Slide 52-

Lactate Indirect measure of oxygen debt Normal value = 1.0 mEq/L Values > 1.0 correlate to magnitude of shock Lactate Levels > 5 = ↑ mortality Ability to clear lactate within 24 hours: Predictive of survival Inability to clear lactate within 12 hours: Predictive of multisystem organ failure
Slide 53-

Base Deficit Sensitive measure of inadequate perfusion Normal range -3 to +3 Run on blood gases Admission BD correlates to blood loss Worsening BD: Ongoing bleeding Inadequate volume replacement
Slide 54-

Base Deficit Classification
Slide 55-

International Normalized Ratio (INR) Test of clotting (extrinsic pathway) Internationally accepted method of reporting prothrombin (PT) results worldwide
Slide 56-

Thromboelastogram (TEG) Measures global function of clotting components Dynamically: clot formation to clot dissolution Pattern recognition
Slide 57-

TEG Uses Predicts need for transfusion Targets use of blood components Identify hyperfibrinolytic patients Assess LMWH monitoring in high risk ICU pts Assess impact of platelet inhibitors (aspirin and Plavix) with Platelet Mapping Possibly the only method for detecting degree of anticoagulation by Dabigatran (Pradaxa)
Slide 58-

TEG Rapid, clinician operated, point of care test Allows for individualized quick monitoring Where used: ED, OR, Angio, ICU Flat screen monitors Project results in all areas Large volume of research coming that will establish TEG protocols in trauma resuscitation
Slide 59-

Hemorrhagic Shock Treatment
Slide 60-

airway… breathing… circulation…
Slide 61-

Is There a Shock Position? Dr. Friedrich Trendelenburg 1800’s To improve surgical exposure - pelvic organs No Benefit in Shock
Slide 62-

Mechanical Means of Stopping Hemorrhage Pelvic Binders Reduce pelvis volume Tamponade effect Tourniquets Studied extensively in war Good outcomes Safe and effective
Slide 63-

Mechanical Means of Stopping Hemorrhage Hemostatic Dressings Research advancing quickly Made of volcanic rock, clay, shells Actions: Direct compression Activation of clotting Adhesion Utility Speed of application (under fire) Pliable, Z Fold conformation
Slide 64-

IV Access Principles in Shock Fastest, simplest route best (antecubital) Large bore, short length (14-16 gauge, 2inch length) Flow limited by IV gauge & length not size of vein Optimally Two people attempting simultaneously Two different sites (above & below diaphragm) Two to three sites required per major trauma Progression [PIV → Femoral → Subclavian] Consider Intraosseous (IO) early as rescue device
Slide 65-

Avoid IV Access Injured limb Distal to possible vascular wound Femoral access with injury below diaphragm
Slide 66-

IV Access in Shock Femoral Vein 8.5/9.0 French Introducer Side port removed ↑ flow rate Out of the way of intubation or chest procedures Subclavian/Internal Jug Higher risk (pneumothorax) Lower success rate In chest injuries, place on side of injury
Slide 67-

Intraosseous Devices Temporary access Children & adults Insert within 1 minute Manual or power drill Prox tibia/humerus/sternum Avoid fracture /injury sites Good for fluid/blood/meds Flow rates up to 125 mL/min w pressure bag Risk: extravasation → compartment syndrome
Slide 68-

Pre Hospital IV Placement in Trauma?EAST 2009 Guideline No evidence to support IV placement at scene Enroute OK Limit 2 attempts → I.O. Saline lock/Keep open Avoid continuous IV Use small boluses (250cc) Titrate to palpable radial
Slide 69-

Fluid Resuscitation
Slide 70-

Fluid Administration Balance Too little… Ongoing shock Continued acidosis Coagulopathy Myocardial dysfunction Renal failure Death Too much… Increased bleeding Clot disruption Dilution coagulation factors Compartment syndromes Transfusion concerns Inflammation Immunosuppression Transfusion Related Acute Lung Injury (TRALI)
Slide 71-

IV’s & Fluid Distribution Total Body Water = 60% of Total Body Wt Intracellular (ICF) 2/3 Extracellular (ECF) 1/3 ISS IVS 75% 25% D5W 90% 90% <10% NS 0% 75% <25% LF 0% 75% <25%
Slide 72-

NS vs. LR Normal Saline Na,Cl Fluid of choice for blood Con: Hyperchloremic acidosis Lactated Ringers Na, Cl, K, Ca, Lactate Fluid of choice per ATLS Con: Immune modulation
Slide 73-

Crystalloids (Isotonic Solutions) Balanced electrolyte solutions similar to ECF Rapidly equilibrates across compartments Only 25% remain in IVS after 17 minutes!
Slide 74-

Small Volume ResuscitationParadigm Shift Using hypertonic/hyperosmotic fluid Remains in vascular space longer Restores vascular volume Without flooding patient Started by military → civilian trauma Examples: Hetastarch (Hespan/Hextend) Hypertonic Saline (3% to 7.5%)
Slide 75-

Small Volume Resuscitation:Hetastarch/Hespan/Hextend Plasma volume expander 500cc hetastarch expands blood volume 800cc Safe and effective at 500cc bolus Cons: May cause coagulopathy in large doses (>2L dose) Renal tubular dysfunction concern 2-3 L LR 500ml Hetastarch Equivalent
Slide 76-

Small Volume Resuscitation Hypertonic Saline Type: 3.0% and 7.5% Sodium Chloride Action: Rapidly pulls fluid from tissues into bloodstream Stabilizes BP & CO and controls ICP ~ Results: Large RCT unable to show survival benefit 250 ml 1 Liter NS or LR
Slide 77-

If it doesn’t carry oxygen or it doesn’t clot! Don’t give it to me!
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Slide 79-

Blood Administration
Slide 80-

Massive Transfusion Definition Old Definition New Definition 10 units of PRBC within 24 hours 10 units of PRBC within 6 hours
Slide 81-

Component Therapy vs. Whole Blood 1 u PRBC 335ml, Hct 55% 1u Plasma 275ml, 80% Coags 1 u Platelets 50ml, 5.5X1010 Total: 650 ml Hct 29% Platelest 88,000 Coag Factors 65% Whole Blood 500 ml Hct 38-50% PLTs 150-400,000 Coag Factors 100%
Slide 82-

Blood Progression in Hemorrhage O+ Males O- Females/ Peds ABO & Rh Compatible ABO & Rh Type Antibodies Immediate 10 minutes 50 minutes
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Slide 86-

Hemorrhagic Shock Drugs: Is there a role?
Slide 87-

Recombinant Factor VIIaNovoSeven Refractory bleeding in trauma Activates Extrinsic Pathway Off label use in trauma Research Results in Trauma: Numerous anecdotal reports 1 RCT published trauma: ↓ blood use ↓ MSOF ↓ ARDS Trend toward ↓ mortality No ↑ thrombotic events Correct before use: Hypofibrinogenemia: Give Cryoprecipitate Thrombocytopenia Give Platelets Hypothermia Correct Temperature Acidosis Consider Bicarbonate
Slide 88-

Factor VIIa Include in Massive Transfusion Protocol: Do not use to early or too late Administer between 8 - 20 PRBC’s Recommended dose: 100 mcg/kg Expensive: 100mcg X 70kg =7,000mcg = $7,700 Repeated at 1-2 hour intervals if required
Slide 89-

Tranexamic acid (TXA) Derivative of AA Lysine - inhibits fibrinolysis Inexpensive ( $80/dose) and proven safety profile Cochrane review (2007) 53 RCT’s Cardiac/Ortho Sig reduction in bleeding without thrombotic complications CRASH2 trial (2010) Prospective RCT, > 20,000 pts Stat sig 1.5% reduction in mortality (overall) Subgroup analysis (Severe bleeding & early admin) Reduced bleeding by 30% IF given within 1 hour MATTERs trial (2011) Camp Bastion in Afghanistan Marked improvement in survival in most severely injured compared to those who did not receive it Soldiers to carry autoinjectors on battlefield
Slide 90-

Tranexamic Acid (TXA)Example Protocols Military Protocol Give within 1-3 hours of injury 1 unit of blood 1 Gm of Bolus of TXA 1 Gm Infusion over 8 hrs Oregon Health & Science University Protocol MTP activated Pt has received > 4 units within 2 hours Give 1 Gm bolus Start 1 Gm drip over 8 hrs
Slide 91-

Hemorrhagic Shock Evolving Treatment Concepts
Slide 92-

Coagulopathy Hypothermia Acidosis Trauma Triad Death
Slide 93-

Hypothermia Defined: Core Temp < 35C (95F) Action: ↓ coagulation factors ↑ platelet dysfunction Classification: Mod 32-34 C (90-93 F) Severe <32 C (< 90 F)T < 32C = 100% mortality Moderate to Severe Hypo-thermia Occurs In <10% of Trauma
Slide 94-

Acidosis Effects: Altered hemostasis Myocardial depression Correlates with: Depth of shock Degree of tissue injury Assessed: pH Base Deficit Lactate pH < 7.2 Initial BD > 6 Predicts transfusion Increased ICU days Risk for MSOF Initial BD > 7.5 ↑ mortality
Slide 95-

Changing Paradigm ED OR death Traditional ED OR ICU OR ICU Damage Control
Slide 96-

Damage Control Surgery (1990’s) Stage I Initial Control of Hemorrhage Stage II Stabilization Stage III Definitive Treatment
Slide 97-

1/3 trauma arrive coagulopathic on arrival 4 X more likely to die 2003 Realization That Coagulopathy Starts Early
Slide 98-

Trauma Coagulopathy Theory Trauma Hemorrhage Shock Resuscitation Dilution Hypothermia Acute Coagulopathy of Trauma & Shock (ACoTS) or Acute Trauma Coagulopathy (ATC) Acidosis Fibrinolysis Factor consumption Trauma Induced Coagulopathy (TIC) Pre-existing Disease Meds Genetics Inflammation Hypothermia Now termed… Activation Protein C
Slide 99-

Permissive Hypotension Hemostatic Resuscitation Damage Control Surgery Damage Control Resuscitation
Slide 100-

Permissive Hypotension Restricted fluid administration Avoid “popping the clot” Accepting limited period (< 2 hours) of suboptimum end organ perfusion Titrate to Mean Arterial Pressure (MAP)
Slide 101-

Mean Arterial Pressure (MAP) Animal studies indicate a MAP of 50-60 as a resuscitation target 40 50 60 70 80 Pop the Clot Fatal Hypoperfusion MAP
Slide 102-

Human RCT Studies: Permissive Hypotension Bickell, 1994 NEJM (Houston) Randomized trial (n=598) Penetrating hypotensive EMS study Dutton, 2002 JT (Baltimore) Randomized trial (n=110) Blunt + Penetrating hypotensive Emergency Department study EMS Fluid EMS No Fluid 62% Survival 70% Survival ED SBP 80 ED SBP 100 92% Survival 92% Survival
Slide 103-

Permissive HypotensionRCT Intraoperative Morrison, 2011, J of T (Houston) Prelim Results n=90 Blunt & Pen, Hypotensive, To OR for chest or abd Maintaining target minimum MAP 50 vs. 65 Results: Hypotensive resuscitation is safe Decreased Coagulopathy and early death
Slide 104-

BP Measurements Normal MAP 70-100 Coming Soon? New Target MAP 50-70
Slide 105-

Traumatic Brain Injury? Geriatric Patients?
Slide 106-

Hemostatic Resuscitation Early diagnosis in ED 1:1 ratio (PRBC to FFP) Early frequent: Cryoprecipitate Platelets Minimal crystalloids Stop the bleeding
Slide 107-

ATLS: After 20 years of high volume fluid resuscitation Chasing tachycardia Using Crystalloid > Blood Little evidence of improved survival Blood Loss Current consensus: Damage Control Resuscitation Permissive Hypotension Hemostatic Resuscitation Damage Control Surgery
Slide 108-

Resuscitate New Treatment Paradigm Stop The Bleeding
Slide 109-

Component Therapy vs. Whole Blood 1 u PRBC 335ml, Hct 55% 1u Plasma 275ml, 80% Coags 1 u Platelets 50ml, 5.5X1010 Total: 650 ml Hct 29% Platelest 88,000 Coag Factors 65% Whole Blood 500 ml Hct 38-50%, PLTs 150-400,000 Coag Factors 100%
Slide 110-

Hemorrhagic Shock Putting it all together!
Slide 111-

Prehospital FluidsEAST 2009 Guideline Penetrating Stable (pulse/coherent) No Fluids Penetrating Unstable Titrate 250ml Boluses: radial pulse/coherent Traumatic Brain Injury Titrate 250ml Boluses: SBP >90 (MAP>60)
Slide 112-

Identifying The Patient At Risk In ED High ISS SI > 0.9 SBP < 90 mm Hg Acidosis Base Deficit > 6 Hypothermia T < 35C (95 F) INR > 1.5 Elevated Lactate Required Labs For Major Activations: ABG BD Lactate INR
Slide 113-

Putting It All Together Hemorrhaging (Non TBI) SBP 80-90 TBI SBP > 90 Hemorrhage + TBI No Recommendation
Slide 114-

Summary Assess for coagulopathy early LR is fluid of choice in trauma Utilize Massive Transfusion Protocol Small volume resuscitation techniques Consider Tranexamic acid and Factor VIIa Correct acidosis and hypothermia STOP THE BLEEDING!