1. SHOCK , PATHOPHYSIOLOGY Prof.M.H.MUMTAZ.
Energy Metabolism
Perfusion
Shock

2. Topics Define shock in terms of cellular function
Review the requirements for adequate cellular perfusion (Fick principle)
Review the mechanisms for starling’s law
Preload vs. afterload
Muscle contraction

3. Topics Continued Discuss the mechanisms for oxygen transport
oxyhemoglobin dissociation curve
Define the stages of shock
Describe different causes of shock
Define multiple organ dysfunction syndrome

4. Shock Defined Inadequate tissue perfusion Anaerobic metabolism
Final Common Pathway!

5. Aerobic Metabolism 6 CO2 6 O2 6 H2O METABOLISM 36 ATP GLUCOSE
HEAT (417 kcal)

6. Anaerobic Metabolism 2 LACTIC ACID GLUCOSE METABOLISM 2 ATP
HEAT (32 kcal)

7. Anaerobic? So What? Inadequate Cellular Oxygenation Anaerobic
Metabolism
Inadequate
Energy
Production
Lactic Acid
Production
Metabolic
Failure
Metabolic
Acidosis
Cell Death!

8. Homeostasis is maintenance of balance
Requires proper functioning systems
Cardiovascular
Respiratory
Renal

9. Physiology of Perfusion
Dependant on 3 components of circulatory system
Pump
Fluid
Container

10. Factors Affecting The Pump
Preload
Contractile force
Frank-starling mechanism
Afterload

11. Muscle Anatomy

12. Contraction: Sliding Filaments
image from:

13. What Is Blood Pressure? BP = Cardiac Output
X Systemic Vascular Resistance
CO = Stroke Volume
X Heart Rate

14. What Affects Blood Pressure?
ANS balance
Contractility
Preload
Starling’s law
Afterload

15. Autonomic Nervous System Review…
Quiz Time! Yeah!

16. parasympathetic nervous system?
Jeopardy
Controls vegetative functions,exits the CNS at high in the neck and low in the back.
What is the
parasympathetic nervous system?

17. Jeopardy The chief neurotransmitter of the sympathetic nervous system.
What is
Norepinephrine?

18. Jeopardy The ‘cutesy’ name for the parasympathetic nervous system.
What is
‘Feed or Breed’?

19. Jeopardy Two types of parasympathetic receptors.
What is nicotinic (NMJ)
and muscarinic (organs)?

20. Jeopardy Two types classes of sympathetic receptors. What is
alpha and beta?

21. Jeopardy The ‘cutesy name’ for the sympathetic nervous system. What is
‘fight or flight’?

22. Jeopardy
Stimulation of this receptor causes an increase in peripheral vasoconstriction.
What is alpha 1?

23. Jeopardy
Stimulation of this receptor causes an increase in myocardial contractility.
What is beta 1?

24. Jeopardy
Stimulation of this receptor causes an increase in bronchodilation.
What is beta 2?

25. Jeopardy
Stimulation of this receptor causes a decrease in the sympathetic activation.
What is alpha 2?

26. Jeopardy Two types of parasympathetic receptors.
What is nicotinic (NMJ)
and muscarinic (organs).

27. Changes in Afterload and Preload
 Peripheral vasoconstriction…
 peripheral vascular resistance…
 afterload…
 blood pressure.

28. Changes in Afterload and Preload
 
 Peripheral vasodilation…
 peripheral vascular resistance…
 afterload…
 blood pressure.

29. Changes in Afterload and Preload
 fluid volume…
 preload…
 contractility (Starling’s Law)…
 cardiac output.
 blood pressure.

30. Changes in Afterload and Preload
 fluid volume…
 preload…
 contractility (Starling’s Law)…
 cardiac output.
 blood pressure.

31. Fluid Must have adequate amounts of hemoglobin
Must have adequate intravascular volume

32. Maintenance of Fluid Volume
Renin-Angiotensin-Aldosterone system.
Works through kidneys to regulate balance of Na+ and water.

33. Renin-Angiotensin-Aldosterone
Plasma
volume
Kidney
(juxtaglomerular
apparatus)
Detected by
&/Or
 [Na+]
Releases
Renin
Via ACE
(Angiotensin
Converting
Enzyme)
Angiotensin II…
Angiotensinogen
Angiotensin I…
Converts

34. Renin-Angiotensin-Aldosterone
 vasoconstriction
 PVR
Angiotensin II…
 BP!
 thirst
Adrenal
cortex
Releases
Aldosterone
ADH
(anti-diuretic
hormone)
Fluid
volume
Na+
reabsorption

35. Hemostasis The stoppage of bleeding. Three methods
Vascular constriction
Platelet plug formation
Coagulation

36. Coagulation Formation of blood clots Prothrombin activator
Prothrombin  thrombin
Fibrinogen  fibrin
Clot retraction

37. Fibrinolysis
Plasminogen
Tissue plasminogen activator (tPA)
Plasmin

38. Disseminated Intravascular Coagulation
“A systemic thrombohemorrhagic disorder … with evidence of:
Procoagulant activation
Fibrinolytic activation
Inhibitor consumption
End-organ failure”
Bick, R.L. Seminars in Thrombosis and Hemostasis 1996

39. Pathophysiology of DIC
Uncontrolled acceleration of clotting cascade
Small vessel occlusion
Organ necrosis
Depletion of clotting factors
Activation of fibrinolysis
Ultimately severe systematic hemorrhage

40. Container Vasculature is continuous, closed and pressurized system
Microcirculation responds to local tissue needs
Blood flow dependent on PVR

41. Fick Principle Effective movement and utilization of O2 dependent on:
Adequate fio2
Appropriate O2 diffusion into bloodstream
Adequate number of RBCs
Proper tissue perfusion
Efficient hemoglobin ‘loading’

42. Fick Principle Perfusion = Arterial O2 Content - Venous O2 Content
Affected by:
Hemoglobin levels
circulation of RBCs
distance between alveoli and capillaries
pH and temperature

46. Onloading Oxygen in Lungs
oxyhemeglobin
pH 7.45
Remember:
CO2  [H+]
pH 7.4
Saturation
 pH shifts curve to left
 ‘onloading’ in lungs
deoxyhemeglobin
Pressure

47. Offloading Oxygen in Tissues
oxyhemeglobin
pH 7.4
Remember:
CO2  [H+]
pH 7.35
Saturation
pH shifts curve to right
 ‘offloading’ to tissues
deoxyhemeglobin
Pressure

48. Causes of Inadequate Perfusion
Inadequate pump
Inadequate preload
Poor contractility
Excessive afterload
Inadequate heart rate
Inadequate fluid volume
Hypovolemia
Inadequate container
Excessive dilation
Inadequate systematic vascular resistance

49. Responses to Shock Normal compensation includes:
Progressive vasoconstriction
Increased blood flow to major organs
Increased cardiac output
Increased respiratory rate and volume
Decreased urine output

50. Cellular Response to Shock
use
Tissue
perfusion
Impaired cellular
metabolism
Anaerobic
metabolism
Stimulation of
clotting cascade &
inflammatory
response
Impaired
glucose
usage
ATP
synthesis
 Intracellular Na+
& water
Na+ Pump
Function
Cellular edema
 Vascular volume

51. Stages of Shock
Compensated
Uncompensated
Irreversible

52. Compensated Shock
Defense mechanisms are successful in maintaining perfusion
Presentation
Tachycardia
Decreased skin perfusion
Altered mental status

53. Uncompenstated Shock Defense mechanisms begin to fail Presentation
Hypotension
Prolonged Cap refill
Marked increase in heart rate
Rapid, thready pulse
Agitation, restlessness, confusion

54. Irreversible Shock Complete failure of compensatory mechanisms
Death even in presence of resuscitation

55. Types of Shock
Hypovolemic
Cardiogenic
Neurogenic
Anaphylactic
Septic

56. Hypovolemic Shock “Fluid failure” Decreased intravascular volume
Causes?
“Third spacing”

57. Cardiogenic Shock Catecholamine R.A.S.  CO Release Activation  SVR
Impaired
myocardial function
 SVR
Volume/
Preload
Myocardial
O2 demand O2
supply
Peripheral
& pulmonary
edema
 Dyspnea

58.  Parasympathetic Tone
Neurogenic Shock
 Sympathetic Tone Or
 Parasympathetic Tone
Vascular Tone
Massive Vasodilation
Tissue
perfusion
 SVR & Preload
 Cardiac Output

59. Anaphylactic Shock “Container failure”
Massive & systemic allergic reaction
Large release of histamine
Increases membrane permeability & vasodilation

60. Septic Shock
“Container failure”
Systemic infection

61. Multiple Organ Dysfunction System
Progressive dysfunction of two or more organ systems
Caused by uncontrolled inflammatory response to injury or illness
Typically sepsis

62. References New York Presbyterian hospital hypertension center:
Biographics Gallery:
RAS (Renin-Angiotensin-Aldosterone System):
A graduate student’s hypertension page: