Shock

1. Shock Ghiath Al Saied (adapted from D Dovic, U of A)

2. Inadequate tissue perfusion Sustained loss of effective circulatory blood volume Breakdown of cellular metabolism and microcirculatory homeostasis Hypoperfusion of peripheral tissue that leads to a diminutive transcapillary exchange function Disproportion between VO2 and DO2

3. Mediators of shock Toxins Endotoxins Oligo- and polypeptides Complement Factors Opiods TNF, Interleukins Fatty Acid Derivatives Arachidonic acid metabolites Varia Calcium

4. What is Shock? Theoretical Inability of to meet cellular need for oxygen. Practical When the RN call you for low BP

5. In the beggining - What do you need to maintain a nice garden? WATER How? 1. Water pump 2. Valve 3. Hose 4. Water

6. Types of shock Think about the garden: The garden will die without enough water Pump failure Release valve failure Hose failure Water failure

7. What do I mean? Pump failure = Cardiogenic shock Release valve failure = Obstructive shock Hose failure = Distributive shock Water failure = Hypovolemic shock

8. Cardiogenic Shock Causes Muscle Valve Heart rate Too fast or too slow Poor coordination

9. Obstructive Shock Causes Tension pneumothorax Massive pulmonary embolism Cardiac tamponade HOCM

10. Distributive Shock Inappropriate vasodilation of peripheral blood vessels Causes Septic shock Neurogenic shock Anaphylaxis Adrenal insufficiency Others Cyanide toxicity Beri beri AVM�s High output failure (fistula, pregnancy

11. Hypovolemic Shock Not enough fluid Blood Plasma

12. Fluids Two broad categories related to a shock discussion Crystalloids colloids

13. Crystalloids Osmotic balance Hypo Iso Hyper Hypo- not helpful for our patient in shock D5, 2/3 1/3, � NS Iso: NS, RL Ringer�s lactate has lower chloride concentration vs. normal saline Tendency of the former to produce a non-anion gap metabolic acidosis when given in significant amounts Hyper: mannitol, 3%NS

14. Colloids Natural vs Synthetic Natural Blood FFP Platelets Human albumin 5%, 25 % Derived from pooled human plasma Heated & sterilized (ultrafiltration) Drawbacks: Limited supply High cost Possible allergic reactions Risk of infection

15. Colloids Synthetic (hydroxy ethyl starches) Pentaspan Endless variety in other countries Categorized into low, medium and high molecular weight subgroups Differences exist in molar substitution, C2:C6 ratio Relatively little data available on individual HES preparations Larger molecular weight HES seem to have longer half-lives Smaller HES molecules exert a greater oncotic pressure

16. Colloids Some colloids can potentially induce renal failure by increasing the plasma colloid oncotic pressure Likely due to oncotic injury and more likely to occur with higher MWt HES HES have clear antihemostatic effects Lower molecular weight solutions have less effect on coagulation than higher molecular weight solutions

17. Albumin has modest antithrombotic and anticoagulant effects, ? inactivation of nitric oxide and prolongation of antiplatelet effects

18. Which is best? Crystalloid vs Colloid debate Evidence has been conflicting

19. Cochrane Injuries Group Albumin Reviewers. Human albumin administration in critically ill patients: systematic review of randomized controlled trials. BMJ 1998; 317: 235-240 Albumin is bad, causes death

20. The SAFE Study Investigators. �A Comparison of Albumin and Saline for Fluid Resuscitation in the Intensive Care Unit�. NEJM 2004; 350: 2247-2256 No mortality benefit subgroup analysis suggestions Trauma could be harmful

21. The choice of fluids is indeterminate, but the rate of administration is clear. An increase in maintenance fluid is inadequate to cause significant volume expansion during the resuscitative phase Fluid must be given as a rapid bolus, and patient assessment and recording of vital signs must be completed after each bolus.

22. Vasopressors / Inotropes Essentially a few important principles to understand Alpha Peripheral squeeze on vessels Beta Inotropic and/or chronotropic effect on heart ie increase cardiac contractility or increased heart rate

23. A few other considerations With most beta effect, comes a degree of vasodilation Ie decreased afterload Other pathways exist cAMP hosphodiesterase inhibitors

24. Epinephrine Alpha and beta effect Great increase on cardiac O2 demand Splanchnic vasoconstriction appears to be greater than with equipotent doses of dop or levo Should be 2nd or 3rd line trope (exept cardiac surgery)

25. Dopamine Alpha and beta depending on dose BUT Overall alpha effect is weaker than levo Beta effect increases cardiac O2 requirements Beta also increases amount of dysrhythmias

26. Dopamine AND works indirectly at nerve endings to release norepi and epi In critically ill patient, stores of nor/epi are depleted Get increase in HR without much increase in BP and CO

27. Norepinephrine (Levophed) Mostly alpha, some beta Potent vasoconstrictor, less effect on increase in HR Reflex bradycardia in response to increase in MAP Mild chronotropy cancelled out HR remains unchanged or slightly decreased

28. Vasopressin Mechanism: vasoconstriction of peripheral blood vessels via V1 receptor Weak pressor in normal patients Patel 1999, Sharshar 2003- 1/3 of septic patients have relative vasopressin deficiency 0.02-0.04 U/min IV Although used commonly, still experimental, look for studies in the future (VASST) which showed no mortality difference

29. Dobutamine Mostly beta effect Increase in inotropy Increase in chronotropy Peripheral vasodilation Overall will increase cardiac output and decrease afterload Good for weak hearts, careful with low or borderline blood pressures

30. Others Milrinone Nitroglycerine Nitroprusside High dose insulin/glucose ephedrine Phenylephrine Pulmonary vasodilators Nitric oxide

31. So� Now we understand shock types We understand fluid principles We understand pressors/tropes Let�s put it all together to treat �shock�

32. Case 1 52 yr old male with crushing retrosternal chest pain, diaphoresis. ECG: depression in V56, II, III, aVF Inferolateral ischemia BP 110/70, HR 110 Admitted to CCU

33. 0300 in CCU BP drops to 80/60 Possible causes? Likely cardiogenic shock Treatment? Principles of fluid, pressors/tropes?

34. Cardiogenic Shock Judicious fluid Inotropes Little need for pressors ie if heart muscle is the problem, use something that helps the muscle

35. Case 2 60 yr female with chest pain and shortness of breath Sa02 82% BP 75/50 Clear CXR and chest exam Elevated JVP, S1Q3T3 CT chest: massive saddle pulmonary embolism

36. Obstructive Shock Treatment: using fluids, pressors, tropes Obstruction to right heart emptying Tamponade, tension pneumo are left heart obstructions RELIEVE THE OBSTRUCTION Thrombolysis Needle decompression and chest tube pericardiocentesis

37. Obstructive Shock Fluids? Judicious Stop once evidence of right heart backing up Can cause further RV expansion andcompression of LV

38. Obstructive Shock Vasopressors vs inotropes Do we need the heart to work harder or the peripheral vessels to squeeze tighter to maintain forward flow? Heart likely working as hard as it can Peripheral squeeze to buy time until relieve obstruction Adjunctive treatments: Pulmonary vasodilation, surgery

39. Case 3 78 yr female with productive cough, fever, confusion BP 85/35, HR 125 CXR: RLL infiltrate, 25% bands, urea 19 Treatment: fluids, pressors, inotropes? ANTIBIOTICS (in under one hour)

40. Distributive Shock Fill the tank A dry patient not in heart failure will die much sooner than a resuscitated patient in heart failure 250cc boluses are for wussies and willcontribute to the death of your patient 1-2L boluses will make you a real man!!

41. Rivers et al. Early Goal Directed Therapy in theTreatment of Severe Sepsis and Septic Shock.NEJM 2001; 345: 1368-1377 SWAT team approach to sepsis in the ED randomized partially blinded 263 patients; 130 Tx, 133 control Standard therapy vs. six hours of early goal directed therapy CVP 8-12 MAP >65 SvO2>70 Urine output>0.5cc/kg/hr Used a combination of fluid, vasopressors, red cell transfusion and inotropes

42. Early Goal DirectedTherapy Total fluids(L) 0-6hr 7-72hr 0-72hr Standard 3.5L 10.6L 13.3L EGDT 5.0L 8.6L 13.4L In hospital mortality standard group: 46.5% In hospital mortality EGDT group: 30.5%

43. Distributive Shock What about pressors/inotropes? If your MAP <70, likely will need vasopressor If your MAP>70, and Scv02<70, may benefit from inotrope

44. Case 4 53 yr old male on GI ward Hx of portal hypertension, esophageal varices, recent hematemesis 0400: massive hematemesis HR 135, BP 80/60, 8L 02. Anxious, confused, diaphoretic Treatment?

45. Your staff will bring the scope in about 30 minutes The MET team will respond in 15 minutes Your patient will be dead in 10 minutes

46. 1. Stop the bleeding 2. Fluid resus Crystalloids- NS, RL Colloids- blood, FFP 3. IV? Central line? Poiselle�s Law Flow is: directly proportional to radius indirectly proportional to length

47. 4. Pressor vs inotrope? Heart can�t work any harder, so why squeeze it? Squeeze the vessels to buy you time. Pressors are NOT a substitute for volume resuscitation, but a bridge

48. Hemorrhagic Shock initial uncompensated response

49. MAP response to blood volume loss

50. Hemorrhagic shock classification Class I hemorrhage (loss of 0-15%) � Little tachycardia � Usually no significant change in BP, pulse pressure, respiratory rate � Class II hemorrhage (loss of 15-30%) � HR >100 beats per minute, tachypnea, decreased pulse pressure � Class III hemorrhage (loss of 30-40%) � Marked tachycardia and tachypnea, decreased systolic BP, oliguria � Class IV hemorrhage (loss of >40%) � Marked tachycardia and decreased systolic BP, narrowed pulse pressure, markedly decreased (or no) urinary output � Immediately life threatening

51. Compensatory mechanisms � Baroreceptor reflexes � Circulating vasoconstrictors � Chemoreceptor reflexes � Reabsorption of tissue fluids � Renal reabsorption of sodium and water � Activation of thirst mechanisms � Cerebral ischemia � Hemapoiesis

52. Baroreceptor actions

53. Overview of compensatory mechanisms

54. Plasma volume expansion � Capillary pressure falls � Reduced arterial and venous pressures � Increased precapillary resistance � Transcapillary fluid reabsorption (up to 1 liter/hr autoinfused) � Capillary plasma oncotic pressure can fall from 25 to 15 mmHg due to autoinfusion thereby limiting capillary fluid reabsorption � Hemodilution causes hematocrit to fall which decreases blood viscosity

55. Cerebral ischemia role � When mean arterial pressure falls below 60 mmHg, cerebral perfusion decreases because the pressure is below the autoregulatory range � Cerebral ischemia produces very intense sympathetic discharge that is several-fold greater than the maximal sympathetic activation caused by the baroreceptor reflex

56. What if the blood loss continues?? � Cardiogenic Shock � Impaired coronary perfusion causing myocardial hypoxia, systolic and diastolic dysfunction, arrhythmias � Sympathetic Escape � Loss of vascular tone (?SVR) causing progressive hypotension and organ hypoperfusion � Increased capillary pressure causing increased fluid filtration and hypovolemia � Cerebral Ischemia � Loss of autonomic outflow due to severe cerebral hypoxia

57. The vicious cycle

58. � Metabolic Acidosis � Rheological � Increased microvascular viscosity � Microvascular plugging by leukocytes and platelets � Intravascular coagulation � Systemic Inflammatory Response � Endotoxin release into systemic circulation � Cytokine formation � TNF, IL, etc. � Enhanced nitric oxide formation � Reactive oxygen-induced cellular damage � Increased capillary permeability � Multiple organ failure