1. 1 SHOCK Prof.M.H.MUMTAZ

2. 2 SHOCK Inadequate perfusion (blood flow) leading to inadequate oxygen delivery to tissues

3. 3 Physiology l Basic unit of life = cell l Cells get energy needed to stay alive by reacting oxygen with fuel (usually glucose) l No oxygen, no energy l No energy, no life

4. 4 Aerobic Metabolism 6 O 2 GLUCOSE METABOLISM 6 CO 2 6 H 2 O 36 ATP HEAT (417 kcal)

5. 5 Anaerobic Metabolism GLUCOSEMETABOLISM 2 LACTIC ACID 2 ATP HEAT (32 kcal)

6. 6 Anaerobic? So What? InadequateCellularOxygenationInadequateCellularOxygenation AnaerobicMetabolismAnaerobicMetabolism MetabolicFailureMetabolicFailureMetabolicAcidosisMetabolicAcidosis InadequateEnergyProductionInadequateEnergyProduction Lactic Acid Production Production Cell Death!

7. 7 Homeostasis is maintenance of balance l Requires proper functioning systems Cardiovascular Respiratory Renal

8. 8 Cardiovascular System l Transports oxygen, fuel to cells l Removes carbon dioxide, waste products for elimination from body Cardiovascular system must be able to maintain sufficient flow through capillary beds to meet cell’s oxygen and fuel needs

9. 9 Flow = Perfusion Adequate Flow = Adequate Perfusion Inadequate Flow = Indequate Perfusion (Hypoperfusion) Hypoperfusion = Shock

10. 10 What is needed to maintain perfusion? l Pump l Pipes l Fluid Heart Blood Vessels Blood

11. 11 How can perfusion fail? l Pump Failure l Pipe Failure l Loss of Volume

12. Factors Affecting The Pump l Preload l Contractile force Frank-starling mechanism l Afterload l Preload l Contractile force Frank-starling mechanism l Afterload

13. 13 Muscle Anatomy

14. 14 Contraction: Sliding Filaments image from: http://www.accessexcellence.com/AB/GG/muscle_Contract.html

15. What Is Blood Pressure? BP = COxSVR CO = Stroke Volume X Heart Rate SVR= B.vessel calibre +viscosity CO = Stroke Volume X Heart Rate SVR= B.vessel calibre +viscosity

16. 16 What Affects Blood Pressure? l ANS balance l Contractility Preload Starling’s law l Afterload

17. 17 Types of Shock and Their Causes CARDIOGENIC HYPOVOLAEMIC SEPTIC NEUROGENIC PSYCHOGENic obstructive ANAPHYLACTIC

18. 18 Cardiogenic Shock l Pump failure l Heart’s output depends on How often it beats (heart rate) How hard it beats (contractility) l Rate or contractility problems cause pump failure

19. 19 Cardiogenic Shock l Causes Acute myocardial infarction Very low heart rates (bradycardias) Very high heart rates (tachycardias) Why would a high heart rate caused decreased output? Hint: Think about when the heart fills.

20. 20 Neurogenic Shock l Loss of peripheral resistance l Spinal cord injured l Vessels below injury dilate What happens to the pressure in a closed system if you increase its size?

21. 21 Hypovolemic Shock l Loss of volume l Causes Blood loss: trauma Plasma loss: burns Water loss: Vomiting, diarrhea, sweating, increased urine, increased respiratory loss If a system that is supposed to be closed leaks, what happens to the pressure in it?

22. 22 Psychogenic Shock l Simple fainting (syncope) l Caused by stress, pain, fright l Heart rate slows, vessels dilate l Brain becomes hypoperfused l Loss of consciousness occurs What two problems combine to produce hypoperfusion in psychogenic shock?

23. 23 Septic Shock l Results from body’s response to bacteria in bloodstream l Vessels dilate, become “leaky” What two problems combine to produce hypoperfusion in septic shock?

24. 24 Anaphylactic Shock l Results from severe allergic reaction l Body responds to allergen by releasing histamine l Histamine causes vessels to dilate and become “leaky” What two problems combine to produce hypoperfusion in anaphylaxis?

25. 25 OBSTRUCTIVE SHOCK PUMONARY EMBOLISM ? CRDIAC TEMPONADE ? PNEUMOTHORAX ?

26. 26 Shock: Signs and Symptoms l Restlessness, anxiety l Decreasing level of consciousness l Dull eyes l Rapid, shallow respirations Why are these signs and symptoms present? Hint: Think hypoperfusion l Nausea, vomiting l Thirst l Diminished urine output

27. 27 Shock: Signs and Symptoms l Hypovolemia will cause Weak, rapid pulse Pale, cool, clammy skin l Cardiogenic shock may cause: Weak, rapid pulse or weak, slow pulse Pale, cool, clammy skin l Neurogenic shock will cause: Weak, slow pulse Dry, flushed skin l Sepsis and anaphylaxis will cause: Weak, rapid pulse Dry, flushed skin Can you explain the differences in the signs and symptoms?

28. 28 Shock: Signs and Symptoms l Patients with anaphylaxis will: Develop hives (urticaria) Itch Develop wheezing and difficulty breathing (bronchospasm) What chemical released from the body during an allergic reaction accounts for these effects?

29. 29 Shock: Signs and Symptoms Shock is NOT the same thing as a low blood pressure! A falling blood pressure is a LATE sign of shock!

30. 30 Treatment l Secure, maintain airway l Apply high concentration oxygen l Assist ventilations as needed l Keep patient supine l Control obvious bleeding l Stabilize fractures l Prevent loss of body heat

31. 31 Treatment l Elevate lower extremities 8 to 12 inches in hypovolemic shock l Do NOT elevate the lower extremities in cardiogenic shock Why the difference in management?

32. 32 Management of Shock l Shock begins when DO2 to the cells is inadequate to meet metabolic demand l The major therapeutic goals in shock therefore are sufficient tissue perfusion and oxygenation l Early diagnosis remains a major problem

33. 33 Treatment l Administer nothing by mouth, even if the patient complains of thirst

34. 34 Hemodynamic Characteristics in Different Types of Shock TypePreloadCOPVRSVR Hemmorrhagic LOW Anaphylactic LOW Cardiogenic HIGH Septic (Hyperdynamic ) LOW Septic (Hypodynamic) LOW /

35. 35 Inotropic Agents and Vasodilators l Vasoactive drugs are an important pharmacologic defense in the treatment of shock. l May be required to support BP in the early stages of shock. l These agents may be needed to: Enhance CO through the use of inotropic agents Increase SVR through the use of vasopressors

36. 36 Effects of Inotropic Agents and Vasodilators Epinephrin e        0.02 – 0.5 Norepinep hrine     0 -0.05 – 0.5 Dopamine    DR  2 -12 Dobutamin e     2 - 12 Dopexamin e      DR0 -0.9 - 5 Vasopressi n Angiotensi n III 5 - 20 AmrinonePDI5 -10 Drug Receptor CO SVR Dose Range 0 - (  g/kg/min) 1

37. 37 Effects of Inotropic Agents and Vasodilators Nifedipine0 - 0.5 - 10 Nitroglycerin0 - 3 - 5 Nitroprusside0 - 0.5 - 5 Prostacyclin 10 - 40 2 Drug CO SVRDose Range (  g/kg/min)

38. 38 Dopamine An endogenous precursor of norepinephrine with multiple dose-related effects l Low Dose (0.5 - 3 mg/kg/min)  2 and dopaminergic (DR) effects Enhanced blood flow to renal and splanchnic beds l Moderate Dose (5 -10 mg/kg/min) Positive inotropic effects l High Dose (>20 mg/kg/min)  -actions (vasoconstriction)

39. 39 MANAGEMENT GUIDE l 1,Haemodynamic monitoring Blood pressure/HR SV,HR,CI,CO SVR,SVRI TOOLS ; SWAN GANZ TEMPERATURE LIDCO CENTRAL VENOUS PRESSURE 2, OXYGENATION STATUS FIO2/PAO2/PaO2/DO2/VO2/ Lactate 3, ACID BASE STATUS

40. 40 HAEMODYNAMIC TRUTHS l 1,TACHYCARDIA IS NEVER AGOOD THING. l 2,HYPOTENSION IS ALWAYS PATHOLOGIC l 3,THERE IS NO SUCH THING AS NORMAL CARDIAC OUTPUT. l 4,CENTRAL VENOUS PRESSURE IS ONLY ELEVATED IN DISEASE. l 5,PERIPHERA EDEMA IS OF COSMETIC CONCERN. PINKSY..Chest.2007; 132;2020-2029

41. 41 Bleeding

42. 42 Bleeding Significance l If uncontrolled, can cause shock and death

43. 43 Identification of External Bleeding l Arterial Bleed Bright red Spurting l Venous Bleed Dark red Steady flow l Capillary Bleed Dark red Oozing What is the physiology that explains the differences?

44. 44 Control of External Bleeding l Direct Pressure gloved hand dressing/bandage l Elevation l Arterial pressure points

45. 45 Arterial Pressure Points l Upper extremity: Brachial l Lower extramity: Femoral

46. 46 Control of External Bleeding l Splinting Air splint Pneumatic antishock garment

47. 47 Control of External Bleeding l Tourniquets Final resort when all else fails Used for amputations 3-4” wide write “TK” and time of application on forehead of patient Notify other personnel

48. 48 Control of External Bleeding l Tourniquets Do not loosen or remove until definitive care is available Do not cover with sheets, blankets, etc.

49. 49 Epistaxis l Nosebleed l Common problem

50. 50 Epistaxis l Causes Fractured skull Facial injuries Sinusitis, other URIs High BP Clotting disorders Digital insertion (nose picking)

51. 51 Epistaxis l Management Sit up, lean forward Pinch nostrils together Keep in sitting position Keep quiet Apply ice over nose 15 min adequate

52. 52 Epistaxis Epistaxis can result in life- threatening blood loss

53. 53 Internal Bleeding l Can occur due to: Trauma Clotting disorders Rupture of blood vessels Fractures (injury to nearby vessels)

54. 54 Internal Bleeding Can result in rapid progression to hypovolemic shock and death

55. 55 Internal Bleeding l Assessment Mechanism? Signs and symptoms of hypovolemia without obvious external bleeding

56. 56 Internal Bleeding l Signs and Symptoms Pain, tenderness, swelling, discoloration at injury site Bleeding from any body orifice

57. 57 Internal Bleeding l Signs and Symptoms Vomiting bright red blood or coffee ground material Dark, tarry stools (melena) Tender, rigid, or distended abdomen

58. 58 Internal Bleeding l Management Open airway High concentration oxygen Assist ventilations Control external bleeding Stabilize fractures Transport rapidly to appropriate facility