1. SHOCK DOOMSDAY

2. Vicken Y. Totten • Shock lecture • Thanks to David Cheng MD • And all who taught me

3. Definition SHOCK: inadequate organ perfusion to meet the tissue’s oxygenation demand

4. PATHOPHYSIOLOGY OF SHOCK SYNDROME Cells switch from aerobic to anaerobic metabolism lactic acid production Cell function ceases & cells swell membranes becomes more permeable electrolytes & fluids seep in & out of cell Cells Die in Many Organs Death

5. Stages of shock • Compensated /Early Shock • Vasoconstriction  (renin & carotid sinus baroceptor • Increase in HR and RR <- sympthatic activation) • Normotensive usually <- (aldosterone/ADH Na+/h20 retention) • Decompensated / late Shock • Cool, clammy , hypotenisve. • Vital organ preservation • Worsening LOC • Continued increase in HR and RR <-----(Chemreceptor respose to metabolic acidosis) • Irreversible- • HR and RR drop Multi Organ Failure Impending death)

6. Fevers / Rigors (sepsis) SSCP (cardiogenic) Wheezing (anaphylaxis) Trauma pain (hypovolemia) Symptoms of Shock • Anxious • Dizziness • Weakness • Faintness • Thirsty • “I am sick” General Symptoms Specific Symptoms

7. Early Signs of Shock in Non Complicated Patients • WARM EARLY STAGE / PRESHOCK • Need high index of suspicion b/c lack of signs +/- tachycardia +/- orthostatics (HR more sensitive than BP) +/- pulse pressure narrowing +/-restless

8. “Hypoperfusion can be present in the absence of significant hypotension.”(Don’t only relay on BP for diagnosisng shock) -fccs course

9. Signs of Late Shock Hypotension COLD LATE STAGE • Cold, clammy and pale skin • Rapid, weak, thready pulse • Rapid breathing (blow off CO2 met acidosis) • Cyanotic • AMS->Coma • Anuria

10. GI Ischemic bowel Hepatic Increased LFT’s, liver failure Hematologic Neutropenia, Thrombocytopenia DIC (Gm- > Gm+) CNS coma End Stage Clinical effects • Cardiovascular • Myocardial depression • Vasogenic effects • Pulmonary • ARDS • Renal • ARF

11. Multiple Organ Dysfunction Syndrome *Adapted from Irwin and Rippe’s Critical Care Medicine 5th Edition, pg 1837

12. Circumferential Subendocardial Infarction due to Shock

13. Shock Lung

14. Acute congestion of liver due to shock

15. Acute tubular necrosis of the kidney due to shock

16. Intestinal mucosal hemorrhages due to shock

17. Adrenal gland hemorrhage due to shock

18. Remember • History and Physical often limited by patient’s condition • Patient presentation can be variable secondary to • Severity of the perfusion defect • Underlying cause • Prior organ dysfunction • Exam should be tailored to be performed quickly with highest yield for uncovering the cause of shock.

19. Components (fluids, pump, pipes)

20. Components: • Blood (fluid) • Heart (pump) • Blood Vessels (pipes)

21. Types of Shock Hypovolemic (fluids) Cardiogenic (pump) Redistributive (pipes) (septic, neurogenic, anaphylactic)

22. Adequate circulating blood volume depends on 3 components; A minor impairment in one can be compensated for by the other 2 for a limited time. Prolonged or severe impairments will lead to SHOCK.

23. An Approach to Shock – Know this! BP = SVR x CO BP = blood pressure CO = cardiac output (pump & fluids) SVR = systemic vascular resistance (pipes)

24. An Approach to Shock If the blood pressure is low, then either the: CO is low or SVR is low or BOTH

25. Low SVR There are only a few causes of low SVR. They ALL cause vasodilation: • Septic shock • Neurogenic (spinal cord injury) shock • Anaphylaxis Shock • Vasodilator (antihypertensive) Posioning

26. How do you assess SVR? Look at and feel the patient! Low SVR has the features: • warm !!! • pink • Bounding pulses • hyperdynamic heart (fast and pounding)

27. What if the SVR is high? • Pale • Poor cap refill (>2 seconds) • Cool arms/legs (>2 degree C difference) • Thready pulses (narrow pulse pressure (incr DBP)) Cause of shock (low BP) is then: low CO

28. What are factors of CO? CO = HR x SV CO = cardiac output HR = heart rate SV = stroke volume

29. HR Problems • Heart Rate problems are easy to diagnose • Rate: bradycardia versus tachycardia

30. Low SV (stroke volume) Most difficult to diagnose and manage

31. Stroke Volume depends on Preload--is the ventricle full? Hypovolemic Shock Obstructive Shock (ie Tension PTX, Tamponade) Cardiac function SqueezeContractility–can the ventricle contract? Can blood get out?  Valve function: normal? regurgitation? stenosis?

32. Perfusion (blood pressure) depends on: BP = CO x SVR CO = HR x SV SV = preload & cardiac contractility-valve

33. Components of BP summary

34. Why Monitor? • Essential to understanding their disease • Describe the patient’s physiologic status • Serial monitoring • Facilitates diagnosis and treatment of shock

35. Monitoring clinical shock parameter Noninvasive： • Blood pressure (SBP, MAP) • Urine output • Heart rate • Shock index Invasive： • Pulmonary artery catheter: CVP, PAWP, CO, SVR, DO2I, VO2I, SvO2 • Arterial catheter: ABP, Serum lactate, Base deficit

36. Diagnosis of Shock • MAP < 60 or decrease of 20 from baseline • systolic BP  90 •  systolic BP > 40 mm Hg from the patient’s baseline pressure • Shock index (HR>SBP) • Clinical s/s of hypoperfusion of vital organs

37. Mean Arterial Pressure • MAP is the mean perfusion pressure for the tissues • Most require a MAP of 60 or greater! • Dependent only on the elastic properties of the arterial walls and the mean blood volume in the arterial tree • MAP = (2 x DBP) + SBP 3

38. Wide Normal 30-50 mmHg Commonly seen with fever, anemia, exercise and hyperthyroidism AR (aortic regurgitation) is also a cause Narrow May indicate an increase in vascular resistance with decreased stroke volume (ie aortic stenosis or decreased intravascular volume) Pulse Pressure=SBP-DBPThe difference between the systolic (fxn of ejection fraction) and diastolic pressures (function of SVR and distensibility (elastic recoil) of the aorta

39. Invasive Markers • Global Markers • Base Deficit • Lactate • Regional Markers • Gastric pH • Sublingual CO2

40. Base Deficit • Inadequate tissue perfusion leads to tissue acidosis • Amount of base required to titrate 1 L of whole arterial blood to a pH of 7.4 • Normal range +3 to –3 mmol per L • Elevated base deficit correlates with the presence and severity of shock

41. Base Deficit • Inadequate tissue perfusion leads to tissue acidosis • Amount of base required to titrate 1 L of whole arterial blood to a pH of 7.4 • Normal range +3 to –3 mmol per L • Elevated base deficit correlates with the presence and severity of shock

42. Initial LactateWeil and Afifi. (Circulation 1970)

43. Lactate and OutcomesAdult Patients A peak blood lactate level of >4.0 mmol/L was identified as a strong independent predictor of mortality and morbidity and suggests that tissue hypoperfusion Demmers Ann Thorac Surg 70:2082-6:2000

45. Gastric Intramucosal pH • Blood flow is not uniformly distributed to all tissue beds • Regions with inadequate tissue perfusion may exist while global markers are ‘normal’ • Gut mucosa among the first to be affected during shock and the last to be restored to normal • Intramucosal pH falls when perfusion becomes inadequate

46. Sublingual capnometry: • A new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock hypercarbia is a universal indicator of critically reduced tissue perfusion.

47. Sublingual CO2 • Decrease gut perfusion • Gastric tissue = esophagus = sublingual tissue • Non-invasive, hand held monitor • Rapid measurement • Sensitive marker of decreased blood flow

48. Sublingual capnometry: • A new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock P SL CO2 provides a prompt indication of the reversal of tissue hypercarbia when circulatory shock is reversed

49. Direct arterial pressureA-line

50. Pulmonary Artery Catheter • INDICATIONS • volume status • cardiac status • COMPLICATIONS • technical • anatomic • physiologic