PATHOPHYSIOLOGY OF SHOCK PART II

1. 1 PATHOPHYSIOLOGY OF SHOCK PART II

2. 2 BACKGROUND TO SHOCK Basics Defined as inadequate tissue perfussion Can result from trauma, fluid loss, heart attack, infection, spinal cord injury Occurs first at cellular level If allowed, can progress to organ failure, and death

3. 3 PHYSIOLOGY OF PERFUSION Basics Body cells require a constant supply of oxygen and nutrients and elimination of carbon dioxide and waste products Needs fulfilled by circulatory system in conjunction with respiratory and gastrointestinal systems Perfusion is dependent on three components of the circulatory system

4. 4 THREE COMPONENTS Pump (heart) Fluid volume (blood) Container (blood vessels) Any derangement of any of these components can affect perfusion

5. 5 THE PUMP The heart The pump of the circulatory system Receives blood from venous system Pumps it to the lungs to receive oxygen Pumps it to the peripheral tissues Stroke volume is the amount of blood pumped by the heart in one contraction Affected by preload, contractile force, and afterload

6. 6 PRELOAD Defined as the amount of blood delivered to the heart during diastole Dependent on venous return Variable venous capacitance can increase or reduce blood return to the heart Increased preload = increased stroke volume

7. 7 CONTRACTILE FORCE Defined as the force generated by the heart during each contraction Frank - Starling mechanism The greater the preload, the more the ventricals are stretched The greater the stretch, the greater the contractile force

8. 8 AFTERLOAD Defined as resistane against which the heart must pump When the resistance is overcome, blood can be ejected Determined by the degree of arterial peripheral vasoconstriction Vasoconstriction = increased resistance = increased afterload = decreased stroke volume

9. 9 CARDIAC OUTPUT Defined as the amount of blood pumped by the heart in one minute or stroke volume x heart rate = cardiac output Expressed in liters per minute An increase in stroke volume or heart rate = increased cardiac output A decrease in stroke volume or heart rate = decreased cardiac output

10. 10 BLOOD PRESSURE Defined as cardiac output x peripheral vascular resistance (afterload) = blood pressure Increased afterload = increased blood pressure Decreased afterload = decreased blood pressure

11. 11 BARORECEPTORS Sensory fibers located in the aortic aortic and carotid bodies Monitor closely for changes in blood pressure If blood pressure, baroreceptors tell the brain to decrease heart rate, preload, and afterload If blood pressure falls, baroreceptors signal the brain to activate the sympathetic nervous system to increase heart rate, preload, contractile force, afterload, and cardiac output

12. 12 THE FLUID Blood is the fluid of the cardiovascular system Viscous fluid, thicker, more adhesive, slower moving than water Because cardiovascular system is closed, an adequate volume of blood must be present to fill system Blood transports oxygen, carbon dioxide, nutrients, horemones, metabolic waste products, and heat

13. 13 THE CONTAINER Blood vessels Serve as container for the cardiovascular system A continuous, closed, pressurized pipeline that moves blood Includes arteries, arterioles, capillaries, venules, and veins Under control of the autonomic nervous system, they regulate blood flow to different areas of the body by adjusting their size and rerouting blood flow through microcirculation

14. 14 MICROCIRCULATION Responsive to local tissue needs Capillary beds can adjust size to supply undernourished tissue and bypass tissue with no immediate need Pre-capillary sphincters and post capillary sphincters open and close to feed or bypass tissues

15. 15 BLOOD FLOW Occurs because of peripheral resistance and pressure within the system Peripheral resistance is dependent on inner diameter and length of the vessel, and blood viscosity Very little resistance in aorta and arteries Significant changes are seen in arterioles which can change size fivefold

16. 16 SYSTEM PRESSURES Contraction of the venous side increases prelaod and stroke volume Contraction of the arteriole side increases afterload and blood pressure

17. 17 OXYGEN TRANSPORT In addition to perfusion, oxygenation of peripheral tissues is essential Oxygen diffuses across the alveolar-capillary membrane Oxygen binds to the hemoglobin molecule of the red blood cells Ideally, 97-100% of hemoglobin saturated with oxygen Oxygen diffuses into cells at end organs

18. 18 FICK PRINCIPLE Conditions for effective movement and utilization of oxygen in the body Adequate FiO2 ( concentration of O2 in inspired air) Appropriate oxygen diffusion from alveoli into bloodstream Adequate number of red blood cells Proper tissue perfusion Efficient off-loading at the tissue level

19. 19 TISSUE PERFUSION Tissue perfusion dependent on circulatory system and oxygenation by respiratory system Inadequate tissue perfussion caused by Inadequate pump Inadequate preload Inadequate cardiac contractile strength Excessive afterload Inadequate heart rate Inadequate fluid volume Hypovolemia Inadequate container Excessive dilation without change in fluid volume Excessive systemic vascular resistance

20. 20 PHYSIOLOGICAL RESPONSE TO SHOCK Normally the body can compensate for some decreased tissue perfusion through a variety of mechanisms When composition fails, shock develops and if uncorrected becomes irreversible

21. 21 PHYSIOLOGICAL RESPONSE TO SHOCK Systemic response Progressive vasoconstriction Increased blood flow to major organs Increased cardiac output Increased respiratory rate and volume Decreased urine output Decreased gastric activity

22. 22 SHOCK AT THE CELLULAR LEVEL Metabolism in normal conditions Metabolism is aerobic Cell energy comes from glucose broken down through glycosis into pyruvic acid Pyruvic acid futher broken down in cycle into CO2, water, and energy

23. 23 METABOLISM/POOR PERFUSION STATES Metabolism is anaerobic Glucose breaks down into pyruvic acid, but not enough oxygen is present to enter into the Krebs cycle Pyruvic acid accumulates, degrades into lactic acid, which also accumulates along with other metabolic acids Cells die; tissues die; organs fail; organ systems fail; death ultimately ensues

24. 24 STAGES OF SHOCK

25. 25 COMPENSATED SHOCK Body defense mechanisms attempt to preserve major organs Precapillary sphincters close, blood is shunted Increased heart rate and strength of contractions Increased respiratory function, bronchodilation

26. 26 COMPENSATED SHOCK Will continue until problem solved or shock progresses to next stage Can be difficult to detect with subtle indicators Tachycardia Decreased skin perfusion Alterations in mental status Some medications such as propranolol can hide signs and symptoms

27. 27 UNCOMPENSATED SHOCK Physiological response Precapillary sphincters open, blood pressure falls Cardiac output falls Blood surges into tissue beds, blood flow stagnates Red cells stack up in rouleaux

28. 28 UNCOMPENSATED SHOCK Easier to detect than compensated shock Prolonged capillary refill time Marked increase in heart rate Rapid thready pulse Agitation, restlessness, confusion

29. 29 IRREVERSIBLE SHOCK Compensatory mechanisms fail, cell death begins, vital organs falter Patient may be resusitated but will die later of (ARDS, renal and liver failure, sepsis)

30. 30 TYPES OF SHOCK

31. 31 HYPOVOLEMIC SHOCK Shock due to loss of intravascular fluid volume Possible causes Internal or external hemorrhage Traumatic hemorrhage Long bone or open fractures Severe dehydration from GI losses Plasma losses from burns Diabetic ketoacidosis Excessive sweating

32. 32 HYPOVOLEMIC SHOCK Also can result from internal third-space loss Possible causes Bowel obstruction Peritonitis Pacreatitis Liver failure resulting in ascites

33. 33 CARDIOGENIC SHOCK Inability to pump enough blood to supply all body parts Primary cause is severe left ventricular failure (AMI, CHF) Accompanying hypotension decreases coronary artery perfusion, worsening the situation Other compensatory mechanisms-increased peripheral resistance, increased myocardial O2 demand -worsen situation

34. 34 CARDIOGENIC SHOCK Other causes Chronic progressive heart disease Rupture of papillary heart muscles or intraventricular septum End-stage valvular disease Patients may be normovolemic or hypovolemic

35. 35 NEUROGENIC SHOCK Shock resulting from inadequate peripheral resistance due to widespread vasodilation Common causes Sepsis Anaphylaxis Spinal cord injury Central nervous system injuries Insulin overdose Addisonian crisis No sympathetic response

36. 36 EVALUATION OF SHOCK VICTIM

37. 37 INITIAL APPROACH Be alert during initial approach to patient, information gleaned from the view at the door Mental status Respiratory effort Skin color

38. 38 PRIMARY ASSESSMENT Airway and breathing Check for airway patency; correct problems Assess breathing rate, quality, correct any problems

39. 39 PRIMARY ASSESSMENT Circulation Correct any obvious external breathing Location of palpable pulse as indicator of circulatory status Radial pulse - BP at least 80 mm Hg Femoral pulse - BP at least 70 mm Hg Carotid pulse - BP at least 60 mm Hg

40. 40 PRIMARY ASSESSMENT Assess skin color, temperature, and moisture Pale = decreased diffusion Cyanotic = inadequate oxygenation Mottled = late sign of shock Cool = indicates vasoconstriction Assess capillary refill time ( less than 2 seconds normal)

41. 41 PRIMARY ASSESSMENT Disability Level of consciousness is very early sign of impending circulatory collapse Manifestations of reduction in cerebral flow include Agitation Disorientation Confusion Inappropriateness of response Unresponsiveness

42. 42 PRIMARY ASSESSMENT While altered mental status may result from drug/alcohol intake, probably safest to assume cause is decreased cerebral perfusion

43. 43 SECONDARY ASSESSMENT Rapid transport for life-threatening conditions Ideally, expose the head, neck, chest , and abdomen Reassess vital signs Patient history

44. 44 GENERAL SHOCK MANAGEMENT

45. 45 ASSURE PATENT AIRWAY Maintain cervical spine support Maintain airflow through the use of airway adjuncts or intubation, preferred in unresponsive shock patients Provide suctioning as necessary

46. 46 MAINTAIN ADEQUATE RESPIRATORY FUNCTION Assist ventilations with BVM or other appropriate adjunct Perform other interventions as needed to correct shock-related conditions leading to respiratory compromise Bronchodilators

47. 47 OXYGENATE THE PATIENT Provide high flow oxygen as soon as possible BVM Nonrebreather Nasal Cannula if mask not tolerated Demand valve if necessary

48. 48 CONTROL MAJOR BLEEDING Direct pressure Pressure points Tourniquet (last resort) PASG for intra-abdominal and lower extremity bleeding

49. 49 TREAT HYPOTENSION Positioning of patient Supine with legs elevated 10-12 inches Upright if cardiogenic shock with pulmonary edema Check respirations and assist as needed

50. 50 PNEUMATIC ANTI-SHOCK GARMENT Three chambered unit wrapped around the lower body and inflated to provide circumferential pneumatic pressure to underlying structures

51. 51 PASG BENEFITS Increase in blood pressure Increased blood flow to the brain, heart, and lungs Bleeding control Stabilization of fractures of lower limb and pelvis

52. 52 PASG INDICATIONS Control of bleeding Stabilization of fractures in hypotensive patients with lower extremity injury Raising of blood pressure

53. 53 ABSOLUTE CONTRINIDICATIONS Acute pulmonary edema secondary to heart failure

54. 54 RELATIVE CONTRAINDICATIONS (Legs only) Third trimester pregnancy Abdominal eviscerations Impaled objects

55. 55 PASG COMPLICATIONS Lower extremity compartment syndrome Metabolic acidosis after prolonged use Decreased renal function Decreased respiratory function

56. 56 INTRAVENOUS THERAPY Reasons for procedure Administration of drugs Fluid replacement Obtaining blood samples

57. 57 INTRAVENOUS THERAPY Necessary supplies Protective gloves and eyewear IV solution Crystalloid most common in field Administration tubing Macrodrip (10gtts/ml) shock, fluid replacement Microdrip (60gtts/ml) cardiac, peds, medical emergencies Extension set

58. 58 CANNULAS Angiocath (catheter over a hollow needle) preferred in field 14 -16 gauge for rapid fluid replacement 18, 20, - 22 gauge for IV lifeline

59. 59 OTHER EQUIPMENT Venous constricting band Tape or Venigaurd device Antibiotic swab Antibiotic ointment Gauze dressing (2x2, 4x4) 10 TO 35 cc syringe Padded armboard

60. 60 VENOUS ACCESS Peripheral veins preferred Dorsal veins of hand Forearm Antecubital fossa

61. 61 VENOUS ACCESS Begin IV distally, move upwards if problems occur In cardiac arrest, use the antecubital fossa External jugular as an alternative Scalp veins in infants Intraosseus infusion

62. 62 INTRAVENOUS CANNULATION Troubleshooting points to keep in mind Did you remove the tourniquet? Is there swelling at the site? Are the tubing valves open? Is the cannula against a valve or wall of the vein? Is the IV bag high enough? Is the drip chamber completely filled with solution?

63. 63 COMPLICATIONS OF IV THERAPY Pain Due to needle puncture or extravasation Use smaller gauge catheter

64. 64 COMPLICATIONS OF IV THERAPY Hematoma or infiltration Remove catheter and establish another IV site Local infection Clean area properly before venipuncture

65. 65 COMPLICATIONS OF IV THERAPY Pyrogenic reaction Characterized by fever, chills, backache, headache, nausea/vomiting Immediately terminate the IV if suspected Catheter shear Never draw the catheter back over the needle

66. 66 COMPLICATIONS OF IV THERAPY Inadvertent arterial puncture Recognized by spurting bright red blood Withdraw catheter and apply direct pressure to site for 5 minutes

67. 67 COMPLICATIONS OF IV THERAPY Circulatory overload Closely monitor the IV flow rate Look for signs of pulmonary congestion and edema Reduce or terminate IV flow if signs appear

68. 68 COMPLICATIONS OF IV THERAPY Thrombophlebitis Inflamation of a vein common in long term IV therapy Redness, swelling, tenderness, pain at site Terminate IV and apply warm compress to site

69. 69 COMPLICATIONS OF IV THERAPY Air embolism Usually during central vein cannulation Can occur when air has not been cleared out of IV tubing

70. 70 FLOW RATES To keep open (TKO) rate for medication administration Rapid rate for hypovolemia, trauma where fluids are being used to replace circulatory volume 2-3 liters maximum that should be administered in field Flow rate can be increased in cases of severe blood loss by wrapping BP cuff around bag and inflating

71. 71 MAINTAINING BODY TEMP. Keep as close to normal as possible Protect patient from elements Remove wet clothing Cover patient, but don’t get them too warm, causing vasodilation