1 / 126

SHOCK Phil Ukrainetz, MD, PGY5 Jeff Plant, MD, FRCPC Core Rounds, August 9, 2002

SHOCK Phil Ukrainetz, MD, PGY5 Jeff Plant, MD, FRCPC Core Rounds, August 9, 2002. Shock talk outline. In the trenches approach What’s the evidence What is on the horizon. Shock definition.

lei
Télécharger la présentation

SHOCK Phil Ukrainetz, MD, PGY5 Jeff Plant, MD, FRCPC Core Rounds, August 9, 2002

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. SHOCKPhil Ukrainetz, MD, PGY5Jeff Plant, MD, FRCPCCore Rounds, August 9, 2002

  2. Shock talk outline • In the trenches approach • What’s the evidence • What is on the horizon

  3. Shock definition A condition of the circulatory system whereby there is inadequate tissue nourishment and removal of toxic metabolites

  4. Better shock definition Inadequate blood flow secondary to decreased cardiac output or mal-distributed output that results in irreversible tissue damage

  5. Why is my sphincter tone so high? • Shock is the transition between life and death • Cornerstone of emergency medicine • You need to know it cold

  6. Shock:assert yourself and know your team Preparation: • Who’s the boss • Know names of staff • Assign tasks including reinforcing that you are running the code (AKA: shut-up or leave)

  7. Shock: the set up • T: Triage • V: Vitals including C/S and O2 sat • M: Pulse-ox, ACF IV x 2, cardiac monitor, O2 NRB

  8. Your role as code leader • Your position is at the foot of the bed with your hand on the pts femoral artery and your eyes on the monitor • Do not get roped into procedures • Direct specific people for specific tasks • Close the loop - “Please intubate the patient and let me know when it is done” - then check that tasks have been completed.

  9. Shock: it is as simple as ABC’s • C: quick look because early defibrillation makes such a difference • A: if they will take a tube give it (have sux on hand), confirm tube • B: adequate vent and ox • C: fluids then pressors • S: sugar and temp

  10. Shock: you want a directed history Do not wait for the info - ask these questions: • A: Allergies • M: Medications - cardiac CCB/BB/Dig • P: PMHX - surgery? • L: Last meal - who cares but it makes AMPLE a word • E: Events leading up

  11. Shock: how do I know they are in shock? Confirm shock • Encephalopathic - MAP of 50 before decr CBF - do not rely ALOC to diagnose shock • Hypotense • Tachypnea • Oliguria - sensitive at < 0.5cc/kg/hr • Cold skin

  12. Shock:how do I diagnose the etiology Head to toe etiologic clues: • Head: pupils, neck stiffness, JVD • Chest: muffled HS, S3, murmur, crackles • Abdo: peritonitis, tense • Skin: warm, cold, purpura fulminans

  13. Shock:how should I remember it? • S: Sepsis/distributive - warm skin? • H: Hypovolemic - hemorrhage/third space • O: Obstructive • C: Cardiogenic - pump, rhythm, valve • K: Anaphylactic - red, laryngospasm or wheeze?

  14. Shock: when can I call the code • Have I done everything? • Confirm ABC’s • ACLS and fluid / pressor resuscitation)

  15. H: Hypovolemic H: Hypoxia H: H+ ions/acidosis H: Hyperkalemia H: Hypothemia Fluids and pressors Tube / ox / vent HCO3 crapola Get I stat K+ Peaked T’s, sine wave? Rectal temp When can I call a code? - confirm 5 H’s and their treatment

  16. T: Tablets T: Tension ptx T: Tamponade T: Thrombo coronary T: Thrombo pulmo Digibind, glucagon Needle, tube Pericardiocentesis PTCA, lyse TPA 100mg? When can I call a code? - confirm 5 T’s and their treatment

  17. Confused Tachypnea Pulse pressure change Oliguria Anion gap Coagulopathy Coma ARDS Hypotension Anuria Metabo;ic acidosis DIC Remember shock is a spectrum - recognize its early symptoms

  18. Shock classifications: how to rally in an exam • Simplest: vasogenic, cardiogenic, hypovolemic • Quantitative vs qualitative • SHOCK mnemonic • It doesn’t matter how you do it just be comprehensive and be able to rattle it off

  19. Shock classifications: how to rally in an exam • Pre - heart • hypovolemia, venous pooling • Heart • contractility, arrythmias, mech obstruction • Post - heart • loss of vascular tone, inability to deliver to tissues, inability of tissues to utilize

  20. Quantitative shock: circulatory defect • Quantitative: large area of decreased tissue perfusion secondary to a circulatory defect • Vasogenic, hypovolemic and cardiogenic in origin • Compensate with hyperdynamic state; HR, CO increased and clamp down • Correct the circulatory defect

  21. Qualitative shock: altered milieau • Affects the metabolic milieau from the get-go • Sepsis, hemoglobinopathies, crush, heat, cell poisons • Do not necessarily have a compensatory period • Identify the toxin and customize management

  22. Shock unifying features: • Disrupted cellular homeostasis • Think failed anaerobic metabolism • Acidosis • Calcium influx, SR pukes • Failed ion gradients and cellular pumps • Cell edema and death

  23. Some other $25 cent words to throw around • Membrane lipid peroxidation • Free radicals • Nitric oxide damage • Enzymatic denaturation • “Inflammatory mediators”

  24. How does our body compensate? • Counter-regulatory mediators • Catecholamines, glucocorticoids, angiotensin, vasopressin, insulin • Increased substrates: glucose, TG and FFA • Anaerobic metabolism: incr CO2:02 ratio

  25. Oxygen metabolism • Shock is a state of oxidative phosphorylative failure • Loss of autoregulation • Inability to match demand • Paralyze paradoxers: 50-100% increase in 02 demands, 50% decrease in CBF • DELIVER 02!!!!!!!!!!!!!

  26. Hemorrhagic shock

  27. Case • 50 year old male MVA victim, HR is 120, BP is 100/75, RR is 20 complaining of abdominal and chest pain. What is the likely blood loss?

  28. What is the utility of the Hemorrhagic Shock Classification?

  29. Classification utility • It makes you consider the signs of shock • It makes you aware that you can have significant blood loss with very little signs or symptoms • It tells you that patients become hypotensive late so don’t wait

  30. Compensatory mechanisms for blood loss • Cardiac: increase rate to 150 then diminished returns • Resistance: catecholamines increase diastolic pressure, narrowed pulse pressure • Capacitance: shunt from catechol receptor rich gut and skin, decreased renal function means increased vascular colume

  31. Case • 14 year old male MVA victim, weighing 50 kg has a fractured femur, seat belt sign and a GCS of 14. The accident happened right outside ACH only minutes ago. His heart rate is 95, BP is 95/65, RR is 20. Do these vitals make you sweat?

  32. Supine vitals sensitivity I would sweat, supine vitals are: • Not very sensitive • 15% loss has no change in vitals • 30% loss before hypotense • Act early and aggressively - especially in kids. They crump late and fast.

  33. Case • Nurse comes to you saying “The girl involved in the slow speed (5km/hr) rear end MVC, the one who is complaining of abdominal pain has an orthostatic increase of 20 BPM”. Is this useful information?

  34. Orthostatic vitals • Consider the context, however in the absence of concerning trauma they are not sensitive • Normal euvolemic patients average an orthostatic increase of 15 BPM, therefore an orthostatic increase of 20 BPM is not helpful • A meaningful orthostatic increase is 30 BPM and this requires a 20% loss of blood volume.

  35. Hemorrhagic shock management • Management • ABCs, vascular access, crystalloid bolus X 2, blood transfusion prn • Search for the cause of blood loss: CXR, abdo and pelvis • controversies • crystalloid versus colloid • immediate versus delayed • small versus large volume resuscitation • Optimal endpoints of resuscitation

  36. Case • An ICU nurse gawks at you when you ask to give the hemorrhagic shock patient NS. She remarks you should pull up your MAST pants and start giving pentaspan, albumin or something useful - is she right?

  37. Colloids • Albumin, protoplasm protein fraction, hydroxyethylstarch, gelatin, dextran • Advantages • less fluid required, more volume in vascular space, potential to draw fluid in from tissues • Disadvantages • expensive, allergic reactions, coagulopathies

  38. Colloids • Cochrane Database of Systematic Reviews. BMJ 1998: 317:235-40. • Objective: effect of albumin on mortality • Study: 30 RCTs total 1419 patients • Results: RR of death 1.46 hypovolemia, 2.40 burns, 1.69 hypoalbuminemia • Pooled RR of death 1.68 (1.26,2.23) • Conclusion: albumin increases mortality

  39. Colloids • Cochrane Database 2000. Colloids versus crystalloids for fluid resuscitation. • Albumin: 18RCTs RR1.52 (1.08,2.13) • HES: 7 RCTs RR 1.16 (0.68,1.96) • Gelatin: 4 RCTs RR 0.50(.08,3.03) • Dextran: 8 RCTs RR 1.24 (.94,1.65) • Conclusion: No evidence that albumins reduce risk of death in trauma, burns, or surgery

  40. Colloid summary • There is NO evidence that colloids decrease mortality in the resuscitation of critically ill patients. • There IS evidence that colloids increase mortality in the resuscitation of critically ill patients.

  41. Hypertonic saline • Advantages • less volume, stays in vascular space, draws fluid • Disadvantages • hypernatremia, hyperosmolarity, seizures, coagulopathy, anaphylactoid rxns with dextran

  42. Hypertonic saline • Animal evidence • improved hemodynamics and mortality • Human evidence • Wade et al 1997: HS and HSD in trauma • Metanalysis of 8 RCTS of HSD and 6 HS • HS (7.5% saline): no difference in mortality • HSD (+6%dextran): decreased mortality in 7/8 trials overall 3.5%; trend only ---> Not stat sign

  43. Hypertonic saline • Cochrane Database 2001. Alderson P. • Objective: effect on mortality • Study: metanalysis of 8 RCTs • Results: pooled RR of 0.88 (0.74, 1.95) • Conclusion: there is a trend toward reduction in mortality with HSD although not statistically significant

  44. Hypertonic saline summary • There is evidence of TRENDS toward lower mortality in resuscitation with hypertonic saline but statistical significance has not been demonstrated ………… • More RCTs are needed………..

  45. Case • A 20 year old male comes in with a knife wound to his abdomen. He is bleeding profusely. The trauma surgeon will be here in 10 minutes. The patients systolic is 70. How much and what fluid would you like Doctor?

  46. Controlled fluid resuscitation • ATLS recommends 2 litres then switch to O negative blood. • Newer research suggests minimal fluids if there is a short time to the OR • Rationale: early, aggressive fluid resuscitation with large volume dislodges soft clots and dilutes clotting factors leading to increased hemorrhage and mortality

  47. Bickell et al 1990The Detrimental Effects of Intravenous Crystalloid after Aortotomy in Swine. Surgery 110: 529-36. • Objective: does rapid volume replacement inc mortality? • Study: 16 pigs, 8 controls (no fluid), 8 tx (RL 80 ml/kg ) • Results Mortality Hemorrhage • Controls 0/8 783 ml • RL tx grp 8/8 2142ml • Bickell et al 1992. HSD vs RL after Aortotomy • HSD tx grp 5/8 1340ml

  48. Bickell et al. NEJM 1994.Immediate versus Delayed Fluid Resuscitation for Hypotensive Patients with Penetrating Torso Trauma • Study: 598 patients SBP<90, odd/even day randomization, immediate fluids vs none until OR • Immediate fluids - mortality 110/303 (38%) • Delayed fluids - mortality 86/289 (30%) • ARR 8%, NNTT 12 • Statistically significant p = 0.04 • Conclusion: delayed fluid resuscitation reduces mortality in hypotensive patients with penetrating trauma

  49. Controlled Fluid Resuscitation • Cochrane Database 2001. Kwan I. Timing and volume of fluid administration for patients with bleeding following trauma. • 3 RCTs for early vs delayed fluids • 3 RCTs for large vs small volume • NO evidence for early or large volume fluid replacement and trends toward increased mortality

  50. Controlled Fluid Resuscitation - Conclusions • There is evidence (limited) that early, large volume aggressive fluid resuscitation increases mortality in penetrating trauma. • Further study needed on penetrating trauma without immediate access to OR and for blunt trauma and CHI

More Related