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Hemorrhage & Shock. Review of Hemorrhage n Location n Anatomical Type & Timing n Coagulation n Fibrinolysis n Assessment n Management.

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Presentation on theme: "Hemorrhage & Shock. Review of Hemorrhage n Location n Anatomical Type & Timing n Coagulation n Fibrinolysis n Assessment n Management."— Presentation transcript:

1 Hemorrhage & Shock

2 Review of Hemorrhage n Location n Anatomical Type & Timing n Coagulation n Fibrinolysis n Assessment n Management

3 Review of Hemorrhage n Location –External –Internal Traumatic Non-Traumatic n Examples?

4 Review of Hemorrhage n Anatomical Type –Arterial –Venous –Capillary n Timing –Acute –Chronic

5 Severity of Hemorrhage Comparison of Adult vs Child

6 Hematocrit n % of RBC in blood (hematocrit) n Normal: –37% - 47% (Female) –40% - 54% (Male)

7 Thrombocytes n Platelets –Form platelet plugs contact collagen & adhere to injured surface activate platelets aggregate to form platelet plug

8 Coagulation n Formation of blood clots –Prothrombin activator –Prothrombin  Thrombin –Fibrinogen  Fibrin entrap platelets, blood cells & plasma –Clot retraction

9 Fibrinolysis n Breaking up the clot –tissue plasminogen activator (tPA) –plasminogen  plasmin

10 Assessing Hemorrhage n 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

11 Management of Hemorrhage n Airway and Ventilatory Support n 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

12 Shock “A rude unhinging of the machinery of life” “A brief pause in the act of dying”

13 Shock Inadequate peripheral perfusion leading to failure of tissue oxygenation  may lead to anaerobic metabolism

14 Shock n Homeostasis –cellular state of balance –perfusion of cells with oxygen is one of its cornerstones

15 Shock n Adequate Cellular Oxygenation –Red Cell Oxygenation –Red Cell Delivery To Tissues Fick Principle

16 Air’s gotta go in and out. Blood’s gotta go round and round. Any variation of the above is not a good thing!

17 Shock n Red Cell Oxygenation –Oxygen delivery to alveoli Adequate F i O 2 Patent airways Adequate ventilation

18 Shock n 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 O 2 –pH –Temperature

19 Shock n 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

20 Shock n Red Cell Delivery To Tissues –Adequate RBC mass –Adequate Hgb levels –Adequate RBC capacity to unbind O 2 pH Temperature –Distance between capillaries and cells

21 Shock Inadequate oxygenation or perfusion causes: uInadequate cellular oxygenation uShift from aerobic to anaerobic metabolism

22 AEROBIC METABOLISM 6 O 2 GLUCOSE METABOLISM 6 CO 2 6 H 2 O 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

23 ANAEROBIC METABOLISM GLUCOSEMETABOLISM 2 LACTIC ACID 2 ATP HEAT (32 kcal) Glycolysis: Inefficient source of energy production; 2 ATP for every glucose; produces pyruvic acid

24 Anaerobic Metabolism n 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

25 Inadequate Cellular Oxygen Delivery Anaerobic Metabolism Inadequate Energy Production Metabolic Failure Lactic Acid Production Metabolic Acidosis CELL DEATH Ultimate Effects of Anaerobic Metabolism

26 Maintaining perfusion requires: n Volume n Pump n Vessels n Failure of one or more of these causes shock

27 Shock n Hypovolemic Shock = Low Volume –Trauma –Non-traumatic blood loss  Vaginal  GI  GU –Burns –Diarrhea –Vomiting –Diuresis –Sweating –Third space losses  Pancreatitis  Peritonitis  Bowel obstruction

28 Shock n Cardiogenic Shock = Pump Failure –Acute M I –CHF –Bradyarrhythmias –Tachyarrhythmias –Mechanical obstruction (“distributive shock”)  Cardiac tamponade  Tension pneumothorax  Pulmonary embolism

29 Shock n Vasogenic Shock = Low Resistance –Spinal cord trauma neurogenic shock –Depressant drug toxicity –Simple fainting

30 Shock n Mixed Shock –Septic Shock Overwhelming infection Inflammatory response occurs Blood vessels –Dilate (loss of resistance) –Leak (loss of volume)

31 Shock n Mixed Shock –Septic Shock Fever –Increased O 2 demand –Increased anaerobic metabolism Bacterial toxins –Impaired tissue metabolism

32 Shock n Mixed Shock –Anaphylactic Shock Severe allergic reaction Histamine is released Blood vessels –Dilate (loss of resistance) –Leak (loss of volume)

33 Shock n Mixed Shock –Anaphylactic Shock Histamine release Extravascular smooth muscle spasm –Laryngospasm –Bronchospasm

34 Shock n Progressive syndrome n Three phases –Compensated –Decompensated –Irreversible

35 Shock n Signs and symptoms due to: –Hypoperfusion –Compensatory responses

36 Compensated Shock n Baroreceptors detect fall in BP –Usually 60-80 mm Hg (adult) n Sympathetic nervous system activates –What are the primary SNS Neurotransmitters & their effects?

37 Compensated Shock n Cardiac effects Increased force of contractions Increased rate Increased cardiac output

38 Compensated Shock n Peripheral effects Arteriolar constriction Pre-/post-capillary sphincter contraction Increased peripheral resistance Shunting of blood to core organs

39 Compensated Shock n 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

40 Compensated Shock n Decreased blood flow to hypothalamus n Release of antidiuretic hormone (ADH or Arginine Vasopressin) from posterior pituitary –Retention of salt, water –Peripheral vasoconstriction

41 Compensated Shock n Insulin –  secretion caused by epinephrine –contributes to hyperglycemia n Glucagon –  release caused by epinephrine –promotes liver glycogenolysis & gluconeogenesis n ACTH –stimulates adrenal cortex release of cortisol –  glucose production

42 Compensated Shock n Peripheral capillaries contain minimal blood n Stagnation n Aerobic metabolism changes to anaerobic n Extracellular potassium shifts begin

43 Compensated Shock n Presentation –Restlessness, anxiety Earliest sign of shock –Tachycardia ?Bradycardia in cardiogenic, neurogenic

44 Compensated Shock n 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

45 Compensated Shock n Presentation –Pale, cool skin Cardiogenic Hypovolemic –Flushed skin Anaphylactic Septic Neurogenic

46 Compensated Shock n Presentation –Slight tachypnea –Respiratory compensation for metabolic acidosis

47 Compensated Shock n Presentation –Nausea, vomiting –Thirst –Decreased body temperature –Feels cold –Weakness

48 Decreased Cardiac Output Aldosterone, ADH Release Catecholamine Release Increased Blood Volume Increased PVR Increased Cardiac Output Increased Myocardial Work, O2 Demand Increased Volume Loss Myocardial Ischemia Compensated Shock Leading to Decompensation

49 Decompensated Shock n Presentation –Cardiac Effects Decreased RBC oxygenation Decreased coronary blood flow Myocardial ischemia Decreased force of contraction

50 Decompensated Shock n Presentation –Peripheral effects Relaxation of precapillary sphincters Continued contraction of postcapillary sphincters Peripheral pooling of blood Plasma leakage into interstitial spaces

51 Decompensated Shock n Presentation –Peripheral effects Continued anaerobic metabolism Continued increase in extracellular potassium Rouleaux formations of RBCs –“pile up like coins” Cold, gray, “waxy” skin

52 Decompensated Shock n Presentation –Listlessness, confusion, apathy, slow speech –Tachycardia; weak, thready pulse –Decreased blood pressure –Moderate to severe orthostatic hypotension –Decreased body temperature –Tachypnea

53 Irreversible Shock n Post-capillary sphincter relaxation n Loss of peripheral vascular resistance

54 Irreversible Shock n Washout of accumulated products Hydrogen ion Potassium Rouleaux formations Carbon dioxide n Rouleaux formations microembolize in lungs n Systemic metabolic acidosis occurs n Cardiac Output decreases further

55 Irreversible Shock n 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

56 Irreversible Shock n Irreversible shock leads to: –Renal failure –Hepatic failure –Disseminated intravascular coagulation (DIC) –Multiple organ systems failure –Adult respiratory distress syndrome (ARDS) –Death

57 Disseminated Intravascular Coagulation (DIC) n Decreased perfusion causes tissue damage/necrosis n Tissue necrosis triggers diffuse clotting n Diffuse clotting consumes clotting factors n Fibrinolysis begins n Severe, uncontrolled systemic hemorrhage occurs

58 Adult Respiratory Distress Syndrome (ARDS) n AKA: “Shock Lung”, “Da Nang Lung” n Decreased perfusion damages alveolar and capillary walls n Surfactant production decreases n Fluid leaks into interstitial spaces and alveoli n Gas exchange impaired n Work of breathing increases

59 Shock Classifications n Hypovolemic n Cardiogenic n Vasogenic (Distributive) n Neurogenic

60 Shock Classifications n Hypovolemic Causes –Hemorrhage –Plasma –Fluid & Electrolytes –Endocrine

61 Shock Classifications n Cardiogenic Causes –Contractility –Rate –Obstructive (Preload/Afterload) Tension pneumothorax Pericardial tamponade Pulmonary embolism Severe Hypertension

62 Shock Classifications n Vasogenic (distributive) –Increased venous capacitance –low resistance, vasodilation anaphylaxis sepsis

63 Shock Classifications n Neurogenic (spinal shock) –loss of spinal cord function below site of injury –loss of sympathetic tone cutaneous vasodilation relative bradycardia

64 Key Issues In Shock n 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!

65 Key Issues In Shock n Recognize & Treat during compensatory phase Best indicator of resuscitation effectiveness = Level of Consciousness Restlessness, anxiety, combativeness = Earliest signs of shock

66 Key Issues In Shock n Falling BP = LATE sign of shock n BP is NOT same thing as perfusion n Pallor, tachycardia, slow capillary refill = Shock, until proven otherwise

67 Key Issues In Shock Isolated head trauma does NOT cause shock (“possible” in peds)

68 General Shock Management n Airway –Open, Clear, Maintained –Consider Intubation

69 General Shock Management n High concentration oxygen –Oxygen = Most Important Drug in Shock n Assist ventilation as needed –When in Doubt, Ventilate BVM n Decompress Tension Pneumothorax

70 General Shock Management n Establish venous access –Replace fluid –Give drugs, as appropriate –Don’t delay definitive therapy n Maintain body temperature –Cover patient with blanket if needed –Avoid cold IV fluids

71 General Shock Management n Monitor –Mental Status –Pulse –Respirations –Blood Pressure –ECG

72 Hypovolemic Shock n Control severe external bleeding n Elevate lower extremities n Avoid Trendelenburg n Pneumatic anti-shock garment

73 Hypovolemic Shock n Two large bore IV lines –Infuse Lactated Ringer’s solution –Titrate BP to 90-100 mm Hg

74 Hypovolemic Shock n Do NOT delay transport n Start IVs enroute to hospital Where does stabilization of critical trauma occur?

75 Cardiogenic Shock n Supine, or head and shoulders slightly elevated n Do NOT elevate lower extremities

76 Cardiogenic Shock n Keep open line, micro-drip set n Fluid challenge based on cardiovascular mechanism and history –Titrate to BP ~ 90 mm Hg

77 Cardiogenic Shock n Treat the underlying cause if possible n Treat rate, then rhythm, then BP  Correct bradycardia or tachycardia  Correct irregular rhythms  Treat BP Cardiac contractility –Dobutamine, Dopamine Peripheral resistance –Dopamine, Norepinephrine

78 Cardiogenic Shock n Obstructive Shock –Treat the underlying cause Tension Pneumothorax Pericardial Tamponade –Isotonic fluids titrated to BP w/o pulmonary edema –Control airway Intubation

79 Shock Management Avoid vasopressors until hypovolemia ruled out, or corrected

80 Shock Management Squeezing partially empty tank can cause ischemia, necrosis of kidney and bowel

81 Vasogenic Shock n Consider need to assist ventilations n Patient supine; lower extremities elevated n Avoid Trendelenburg

82 Vasogenic Shock n Infuse isotonic crystalloid –“Top off tank” n Consider PASG n Consider possible hypovolemia n Consider vasopressors

83 Vasogenic Shock n Maintain body temperature n Hypothermia may occur

84 Vasogenic Shock n Anaphylaxis –Suppress inflammatory response Antihistamines Corticosteroids –Oppose histamine response Epinephrine –bronchospasm & vasodilation –Replace intravascular fluid Isotonic fluid titrated to BP ~ 90 mm

85 Pneumatic AntiShock Garment (PASG) n Function –Primary effect is increased PVR –Hemorrhage control through Direct pressure Fracture stabilization –Increased intra-abdominal pressure –Little effect from autotransfusion

86 Pneumatic AntiShock Garment n Indications –Multiple lower extremity fractures –Pelvic fractures –Abdominal injuries –Abdominal aortic aneurysm –Refractory decompensated shock

87 Pneumatic Antishock Garment n Contraindications –Absolute Pulmonary edema

88 Pneumatic Antishock Garment n Contraindications –Relative Closed head injury Thoracic hemorrhage Impaled object (abdomen, chest?) Pregnancy (abdominal section) Evisceration Ruptured diaphragm Cardiogenic shock

89 Shock in Children n Small blood volume –Increased hypovolemia risk n Very efficient compensatory mechanisms –Failure may cause “sudden” shock n Pallor, altered LOC, cool skin = shock UPO

90 Shock in Children n Avoid massive fluid infusion –Use 20 cc/kg boluses n High surface to volume ratio –Increased hypothermia risk

91 Shock in the Elderly n Poor cardiovascular condition –Rapid decompensation n Sepsis more likely n Hypoperfusion can cause: –CVA –AMI –Seizures –Bowel Infarctions –Renal failure

92 Shock in the Elderly n Assessment more difficult –Peripheral vascular disease –Weak pulses –Altered sensorium –Hypertension masking hypoperfusion –Beta-blockers masking hypoperfusion n Fluid infusion may produce volume overload/CHF

93 Shock in OB Patients n Pulse increases 10 to 15 bpm n BP lower than in non-pregnant patient n Blood volume increased by 45% –Slower onset of shock signs/ symptoms n Fluid resuscitation requires greater volume

94 Shock in OB Patients n Oxygen requirement increased 10 to 20% n Pregnant uterus may compress vena cava, decreasing venous return to heart –Place women in late-term pregnancy on left-side n Fetus can be in trouble even though mother looks well-perfused

95 Transport Considerations n Indications for Rapid Transport n Indications for Trauma Center Transport n Considerations for Air Medical Transport

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