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Hemorrhage & Shock
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Review of Hemorrhage Location Anatomical Type & Timing Coagulation
Fibrinolysis Assessment Management
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Review of Hemorrhage Location External Internal Examples? Traumatic
Non-Traumatic Examples?
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Review of Hemorrhage Anatomical Type Timing Arterial Venous Capillary
Acute Chronic
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Severity of Hemorrhage
Comparison of Adult vs Child
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Hematocrit % of RBC in blood (hematocrit) Normal: 37% - 47% (Female)
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Thrombocytes Platelets Form platelet plugs
contact collagen & adhere to injured surface activate platelets aggregate to form platelet plug
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Coagulation Formation of blood clots Prothrombin activator
Prothrombin Thrombin Fibrinogen Fibrin entrap platelets, blood cells & plasma Clot retraction
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Fibrinolysis Breaking up the clot tissue plasminogen activator (tPA)
plasminogen plasmin
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Assessing Hemorrhage Clues
Bright red blood from wound, mouth, rectum or other orifice Hematemesis Coffee ground appearance of vomitus Hematochezia Melena Orthostatic hypotension Dizziness or syncope on sitting or standing Signs and symptoms of hypovolemic shock
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Management of Hemorrhage
Airway and Ventilatory Support Circulatory Support From nose or ears after head trauma = loose drsg Control bleeding direct pressure, elevation, pressure points tourniquet packing of large wounds splinting PASG transport to appropriate facility
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Shock “A rude unhinging of the machinery of life”
“A brief pause in the act of dying”
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Shock Inadequate peripheral perfusion leading to failure of tissue oxygenation may lead to anaerobic metabolism
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Shock Homeostasis cellular state of balance
perfusion of cells with oxygen is one of its cornerstones
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Shock Fick Principle Adequate Cellular Oxygenation
Red Cell Oxygenation Red Cell Delivery To Tissues Fick Principle
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Fick Principle Air’s gotta go in and out.
Blood’s gotta go round and round. Any variation of the above is not a good thing!
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Shock Red Cell Oxygenation Oxygen delivery to alveoli Adequate FiO2
Patent airways Adequate ventilation
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Shock Red Cell Oxygenation Oxygen exchange with blood
Adequate oxygen diffusion into blood Adequate RBC flow past alveoli Adequate RBC mass/Hgb levels Adequate RBC capacity to bind O2 pH Temperature
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Shock Red Cell Delivery To Tissues Adequate perfusion Blood volume
Cardiac output Heart rate Stroke volume (pre-load, contractility, after-load) Conductance Arterial resistance Venous capacitance
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Shock Red Cell Delivery To Tissues Adequate RBC mass
Adequate Hgb levels Adequate RBC capacity to unbind O2 pH Temperature Distance between capillaries and cells
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Shock Inadequate oxygenation or perfusion causes:
Inadequate cellular oxygenation Shift from aerobic to anaerobic metabolism
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AEROBIC METABOLISM 6 O2 GLUCOSE METABOLISM 6 CO2 6 H2O 36 ATP HEAT (417 kcal) Glycolysis: Inefficient source of energy production; 2 ATP for every glucose; produces pyruvic acid Oxidative phosphorylation: Each pyruvic acid is converted into 34 ATP
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ANAEROBIC METABOLISM GLUCOSE METABOLISM 2 LACTIC ACID 2 ATP HEAT (32 kcal) Glycolysis: Inefficient source of energy production; 2 ATP for every glucose; produces pyruvic acid
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Anaerobic Metabolism Occurs without oxygen
oxydative phosphorylation can’t occur without oxygen glycolysis can occur without oxygen cellular death leads to tissue and organ death can occur even after return of perfusion organ or organism death
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Ultimate Effects of Anaerobic Metabolism
Inadequate Cellular Oxygen Delivery Lactic Acid Production Inadequate Energy Production Anaerobic Metabolism Metabolic Failure Metabolic Acidosis CELL DEATH
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Maintaining perfusion requires:
Volume Pump Vessels Failure of one or more of these causes shock
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Shock Hypovolemic Shock = Low Volume Trauma Vomiting
Non-traumatic blood loss Vaginal GI GU Burns Diarrhea Vomiting Diuresis Sweating Third space losses Pancreatitis Peritonitis Bowel obstruction
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Shock Cardiogenic Shock = Pump Failure
Mechanical obstruction (“distributive shock”) Cardiac tamponade Tension pneumothorax Pulmonary embolism Acute M I CHF Bradyarrhythmias Tachyarrhythmias
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Shock Vasogenic Shock = Low Resistance Spinal cord trauma
neurogenic shock Depressant drug toxicity Simple fainting
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Shock Mixed Shock Septic Shock Overwhelming infection
Inflammatory response occurs Blood vessels Dilate (loss of resistance) Leak (loss of volume)
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Shock Mixed Shock Septic Shock Fever Increased O2 demand
Increased anaerobic metabolism Bacterial toxins Impaired tissue metabolism
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Shock Mixed Shock Anaphylactic Shock Severe allergic reaction
Histamine is released Blood vessels Dilate (loss of resistance) Leak (loss of volume)
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Shock Mixed Shock Anaphylactic Shock Histamine release
Extravascular smooth muscle spasm Laryngospasm Bronchospasm
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Shock Progressive syndrome Three phases Compensated Decompensated
Irreversible
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Shock Signs and symptoms due to: Hypoperfusion Compensatory responses
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Compensated Shock Baroreceptors detect fall in BP
Usually mm Hg (adult) Sympathetic nervous system activates What are the primary SNS Neurotransmitters & their effects?
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Compensated Shock Cardiac effects Increased force of contractions
Increased rate Increased cardiac output
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Compensated Shock Peripheral effects Arteriolar constriction
Pre-/post-capillary sphincter contraction Increased peripheral resistance Shunting of blood to core organs
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Compensated Shock Decreased renal blood flow
Renin released from kidney arteriole Renin & Angiotensinogen combine Converts to Angiotensin I Angiotensin I converts to Angiotensin II Peripheral vasoconstriction Increased aldosterone release (adrenal cortex) promotes reabsorption of sodium & water
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Compensated Shock Decreased blood flow to hypothalamus
Release of antidiuretic hormone (ADH or Arginine Vasopressin) from posterior pituitary Retention of salt, water Peripheral vasoconstriction
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Compensated Shock Insulin Glucagon ACTH
secretion caused by epinephrine contributes to hyperglycemia Glucagon release caused by epinephrine promotes liver glycogenolysis & gluconeogenesis ACTH stimulates adrenal cortex release of cortisol glucose production
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Compensated Shock Peripheral capillaries contain minimal blood
Stagnation Aerobic metabolism changes to anaerobic Extracellular potassium shifts begin
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Compensated Shock Presentation Restlessness, anxiety Tachycardia
Earliest sign of shock Tachycardia ?Bradycardia in cardiogenic, neurogenic
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Compensated Shock Presentation Normal BP, narrow pulse pressure
Falling BP = late sign of shock Mild orthostatic hypotension (15 to 25 mm Hg) “Possible” delay in capillary refill
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Compensated Shock Presentation Pale, cool skin Flushed skin
Cardiogenic Hypovolemic Flushed skin Anaphylactic Septic Neurogenic
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Compensated Shock Presentation Slight tachypnea
Respiratory compensation for metabolic acidosis
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Compensated Shock Presentation Nausea, vomiting Thirst
Decreased body temperature Feels cold Weakness
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Compensated Shock Leading to Decompensation
Decreased Cardiac Output Aldosterone, ADH Release Catecholamine Release Increased Blood Volume Increased PVR Increased Cardiac Output Increased Myocardial Work, O2 Demand Increased Volume Loss Compensated Shock Leading to Decompensation Myocardial Ischemia
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Decompensated Shock Presentation Cardiac Effects
Decreased RBC oxygenation Decreased coronary blood flow Myocardial ischemia Decreased force of contraction
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Decompensated Shock Presentation Peripheral effects
Relaxation of precapillary sphincters Continued contraction of postcapillary sphincters Peripheral pooling of blood Plasma leakage into interstitial spaces
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Decompensated Shock Presentation Peripheral effects
Continued anaerobic metabolism Continued increase in extracellular potassium Rouleaux formations of RBCs “pile up like coins” Cold, gray, “waxy” skin
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Decompensated Shock Presentation
Listlessness, confusion, apathy, slow speech Tachycardia; weak, thready pulse Decreased blood pressure Moderate to severe orthostatic hypotension Decreased body temperature Tachypnea
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Irreversible Shock Post-capillary sphincter relaxation
Loss of peripheral vascular resistance
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Irreversible Shock Washout of accumulated products
Hydrogen ion Potassium Rouleaux formations Carbon dioxide Rouleaux formations microembolize in lungs Systemic metabolic acidosis occurs Cardiac Output decreases further
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Irreversible Shock Presentation Confusion, slurred speech, unconscious
Slow, irregular, thready pulse Falling BP; diastolic goes to zero Cold, clammy, cyanotic skin Slow, shallow, irregular respirations Dilated, sluggish pupils Severely decreased body temperature
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Irreversible Shock Irreversible shock leads to: Renal failure
Hepatic failure Disseminated intravascular coagulation (DIC) Multiple organ systems failure Adult respiratory distress syndrome (ARDS) Death
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Disseminated Intravascular Coagulation (DIC)
Decreased perfusion causes tissue damage/necrosis Tissue necrosis triggers diffuse clotting Diffuse clotting consumes clotting factors Fibrinolysis begins Severe, uncontrolled systemic hemorrhage occurs
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Adult Respiratory Distress Syndrome (ARDS)
AKA: “Shock Lung”, “Da Nang Lung” Decreased perfusion damages alveolar and capillary walls Surfactant production decreases Fluid leaks into interstitial spaces and alveoli Gas exchange impaired Work of breathing increases
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Shock Classifications
Hypovolemic Cardiogenic Vasogenic (Distributive) Neurogenic
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Shock Classifications
Hypovolemic Causes Hemorrhage Plasma Fluid & Electrolytes Endocrine
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Shock Classifications
Cardiogenic Causes Contractility Rate Obstructive (Preload/Afterload) Tension pneumothorax Pericardial tamponade Pulmonary embolism Severe Hypertension
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Shock Classifications
Vasogenic (distributive) Increased venous capacitance low resistance, vasodilation anaphylaxis sepsis
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Shock Classifications
Neurogenic (spinal shock) loss of spinal cord function below site of injury loss of sympathetic tone cutaneous vasodilation relative bradycardia
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Resuscitate Critical Tissues First!
Key Issues In Shock Tissue ischemic sensitivity Heart, brain, lung: 4 to 6 minutes GI tract, liver, kidney: 45 to 60 minutes Muscle, skin: 2 to 3 hours Resuscitate Critical Tissues First!
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Best indicator of resuscitation effectiveness = Level of Consciousness
Key Issues In Shock Recognize & Treat during compensatory phase Restlessness, anxiety, combativeness = Earliest signs of shock Best indicator of resuscitation effectiveness = Level of Consciousness
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Key Issues In Shock Falling BP = LATE sign of shock
BP is NOT same thing as perfusion Pallor, tachycardia, slow capillary refill = Shock, until proven otherwise
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Isolated head trauma does NOT cause shock (“possible” in peds)
Key Issues In Shock Isolated head trauma does NOT cause shock (“possible” in peds)
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General Shock Management
Airway Open, Clear, Maintained Consider Intubation
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General Shock Management
High concentration oxygen Oxygen = Most Important Drug in Shock Assist ventilation as needed When in Doubt, Ventilate BVM Decompress Tension Pneumothorax
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General Shock Management
Establish venous access Replace fluid Give drugs, as appropriate Don’t delay definitive therapy Maintain body temperature Cover patient with blanket if needed Avoid cold IV fluids
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General Shock Management
Monitor Mental Status Pulse Respirations Blood Pressure ECG
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Hypovolemic Shock Control severe external bleeding
Elevate lower extremities Avoid Trendelenburg Pneumatic anti-shock garment
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Hypovolemic Shock Two large bore IV lines
Infuse Lactated Ringer’s solution Titrate BP to mm Hg
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Where does stabilization of critical trauma occur?
Hypovolemic Shock Do NOT delay transport Start IVs enroute to hospital Where does stabilization of critical trauma occur?
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Cardiogenic Shock Supine, or head and shoulders slightly elevated
Do NOT elevate lower extremities
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Cardiogenic Shock Keep open line, micro-drip set
Fluid challenge based on cardiovascular mechanism and history Titrate to BP ~ 90 mm Hg
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Cardiogenic Shock Treat the underlying cause if possible
Treat rate, then rhythm, then BP Correct bradycardia or tachycardia Correct irregular rhythms Treat BP Cardiac contractility Dobutamine, Dopamine Peripheral resistance Dopamine, Norepinephrine
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Cardiogenic Shock Obstructive Shock Treat the underlying cause
Tension Pneumothorax Pericardial Tamponade Isotonic fluids titrated to BP w/o pulmonary edema Control airway Intubation
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Avoid vasopressors until hypovolemia ruled out, or corrected
Shock Management Avoid vasopressors until hypovolemia ruled out, or corrected
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Shock Management Squeezing partially empty tank can cause ischemia, necrosis of kidney and bowel
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Vasogenic Shock Consider need to assist ventilations
Patient supine; lower extremities elevated Avoid Trendelenburg
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Vasogenic Shock Infuse isotonic crystalloid “Top off tank”
Consider PASG Consider possible hypovolemia Consider vasopressors
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Vasogenic Shock Maintain body temperature Hypothermia may occur
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Vasogenic Shock Anaphylaxis Suppress inflammatory response
Antihistamines Corticosteroids Oppose histamine response Epinephrine bronchospasm & vasodilation Replace intravascular fluid Isotonic fluid titrated to BP ~ 90 mm
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Pneumatic AntiShock Garment (PASG)
Function Primary effect is increased PVR Hemorrhage control through Direct pressure Fracture stabilization Increased intra-abdominal pressure Little effect from autotransfusion
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Pneumatic AntiShock Garment
Indications Multiple lower extremity fractures Pelvic fractures Abdominal injuries Abdominal aortic aneurysm Refractory decompensated shock
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Pneumatic Antishock Garment
Contraindications Absolute Pulmonary edema
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Pneumatic Antishock Garment
Contraindications Relative Closed head injury Thoracic hemorrhage Impaled object (abdomen, chest?) Pregnancy (abdominal section) Evisceration Ruptured diaphragm Cardiogenic shock
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Shock in Children Small blood volume Increased hypovolemia risk
Very efficient compensatory mechanisms Failure may cause “sudden” shock Pallor, altered LOC, cool skin = shock UPO
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Shock in Children Avoid massive fluid infusion Use 20 cc/kg boluses
High surface to volume ratio Increased hypothermia risk
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Shock in the Elderly Poor cardiovascular condition Sepsis more likely
Rapid decompensation Sepsis more likely Hypoperfusion can cause: CVA AMI Seizures Bowel Infarctions Renal failure
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Shock in the Elderly Assessment more difficult
Peripheral vascular disease Weak pulses Altered sensorium Hypertension masking hypoperfusion Beta-blockers masking hypoperfusion Fluid infusion may produce volume overload/CHF
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Shock in OB Patients Pulse increases 10 to 15 bpm
BP lower than in non-pregnant patient Blood volume increased by 45% Slower onset of shock signs/ symptoms Fluid resuscitation requires greater volume
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Shock in OB Patients Oxygen requirement increased 10 to 20%
Pregnant uterus may compress vena cava, decreasing venous return to heart Place women in late-term pregnancy on left-side Fetus can be in trouble even though mother looks well-perfused
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Transport Considerations
Indications for Rapid Transport Indications for Trauma Center Transport Considerations for Air Medical Transport
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