1. SHOCK

2. Case study
You are dispatched to a report of an overturned bulldozer, trapping a 39 y/o male.
On arrival, you find the patient CAO PPTE. His airway, respirations and pulse are normal. His pelvis and lower extremities are pinned under the side of the bulldozer. The FD tells you it will be at least 10 minutes before they can lift the bulldozer.

3. HMM??
The pt. has O2 at 15 lpm/nrb. His BBS are =, clear and he complains that he can’t feel his feet.
Your DDX?

4. His BP is 110/68, HR 90, RR 24, and Sa02 99%. Because of the extended extrication time, you request Lifeflight response. You establish 2 IV’s w/NS; one at full flow. You check his vitals q 5 min. – they remain stable.
As the bulldozer is lifted, you realize that the pt. has pelvic, bilateral femur and L tibia Fx.
The pt. c/o increased pain, is restless and attempts to get up, then becomes lethargic. His Sa02 is now 94%; his HR is 130 and weak. You increase the IV flow rate, and his mentation improves, but his HR remains elevated.

5. The pt. is moved to the helicopter, and the IV’s are placed in pressure infuser bags.
At the hospital, his systolic BP is 90, and he is still tachycardic.
The pt. goes to surgery, tolerates the surgery well, and is in rehab for one year.

6. SHOCK
Inadequate Tissue Perfusion
Cells die>tissues die>organs die>patient dies
The transition between homeostasis and death

7. Causes Trauma spinal cord injury fluid loss Infection
Allergic reaction
etc

8. Perfusion
The pump
The fluid
The container

9. The pump Stroke Volume = one beat = 70 mls SV x HR = CO
70 x 80 = 5,600 ml/min
Preload
Cardiac contractility
Afterload

10. Preload
Blood delivered to heart during diastole (between contractions)
Depends on venous return
The greater the preload, the greater the stroke volume

11. Contractile force
The greater the preload, the more the ventricles are stretched
The greater the stretch (to a point) the greater the contraction
Frank - Starling law
Contractile force is affected by catecholamines (controlled by sympathetic nervous system) – affect beta adrenergic receptors

12. Arterial resistance (PVR)
Afterload
Arterial resistance (PVR)
Vasoconstriction/vasodilation

13. Afterload
Vasopressor drugs
Epinephrine
Dopamine
Norepinephrine

14. Blood pressure BP Baroreceptors Adrenergic responses
Nerve tissue in Carotids & Aorta
Adrenergic responses
Low B/P Releases Epi/Norepi
Rising B/P slows release of …

15. Blood
Adequate quantity
Adequate quality

16. The container
Closed system –Supposed 2B
Dynamic in nature

17. Capillaries – Still The Container
The Dam Pre-capillary sphincter
Responds to local needs
The Dam Post-capillary sphincter

18. Peripheral resistance
Length of vessel
Diameter of vessel
Viscosity of blood

19. Oxygen transport
Tidal volume mls
21% oxygen in air
Hemoglobin

20. Adequate concentration inspired Appropriate diffusion into blood
The Fick Principle
Adequate concentration inspired
Appropriate diffusion into blood
More O2 in Stream than cells

21. The Fick Principle
Adequate RBCs
Adequate on-loading

22. The Fick Principle
Proper perfusion
Adequate off-loading

23. Brief Relation to SaO2
Oxygen - Hemoglobin
Saturation

24. Decreased Perfusion
Pump
Container
Fluid

25. Decreased perfusion-Pump
Inadequate preload
Inadequate contraction
Excessive afterload
Inadequate rate

26. Inadequate fluid
Hypovolemia
Inadequate RBCs
Toxic – 3rd Spaced

27. Inadequate container
Dilated
Constricted
Leaking

28. Systemic response to shock
Early signs
Late signs

29. Compensated shock
Vasoconstriction
Increased cardiac output
Increased contractility

30. Compensated shock, cont.
Renin-angiotension system
Activated by hypotension
Renin released from kidneys into systemic circulation
Acts on special plasma protein angiotension to produce angiotension I and is converted to angiotension II by enzyme in lungs – angiotension converting enzyme (ACE). – a potent vasoconstrictor.
angiotension II stimulates production of aldosterone from adrenal gland – stimulates kidneys to readsorb sodium (water follows salt)

31. Compensated shock, cont.
Pituitary gland secretes ADH
Spleen (can store > 300 ml of blood – can expel up to 200 ml blood into venous circulation

32. Decompensated shock (Progressive shock)
BP begins to fall
Slow refill
Pre-capillary sphincters relax
Post-remain closed
No pressure to open
Rouleaux
Can’t limbo through capillaries

33. Bad news, baby
Cardiac depression – 2ndary to compensatory mechanisms –
Greatly increased demand for oxygen
Low arterial blood pressure = coronary blood flow too low to adequately perfuse the myocardium
Heart is weakened – CO falls
Vasomotor center of brain is depressed
Sympathetic activity slows, then stops

34. We ain’t done yet
Metabolic wastes are released into slower-flowing blood. Capillary beds become aciditic = microemboli
Generalized, systemic acidosis develops
Further deterioration of calls and tissues = increased permeability = shift into 3rd spaces

35. Irreversible shock Death is inevitable
Short term save vs Long term save

36. Types of shock
Hypovolemic
Distributive
Obstructive
Cardiogenic
Respiratory
Neurogenic

37. Assessment
ABCDEs
Intervene early

38. Hypovolemic Shock Internal or external hemorrhage Traumatic injury
Long-bone or open fractures
Severe dehydration 2ndary to vomiting or diarrhea
Plasma loss – burns
Sweating
DKA with osmotic diuresis
3rd spacing –
Bowel obstruction
Peritonitis, pancreatitis
Liver failure - ascites

39. Management - Hypovolemic
ABCs
C-spine O2
ECG
IVs
PASG?

40. Management - Distributive
ABCs O2
ECG
Ivs
Meds?
PASG?

41. Management - Obstructive
ABCs O2
ECG IV
Correct obstruction?

42. Management - Cardiogenic
If BP is low, what is pulse?
Fluid challenge
If lungs are dry
Vasopressors?
Dopamine (Inotropin)

43. Management - Respiratory
ABCs O2
ECG IV
Correct condition?

44. Management - Neurogenic
Usually spinal cord injury
Spinal-immobilize
IV fluids
EKG

45. Shock Assessment