Pathophysiology of shock and reperfusion injury

2. Pathophysiology of Shock &
Reperfusion Injury
Presented By:
Dr Maryam Shamal Ghalib
(1st Year General Surgery Resident - WAKH)
Supervised By: Sp Dr Naseema Azami

3. Contents
Definition of Shock
Pathophysiology
Classification of Shock
Reperfusion Injury
References

4. What is SHOCK? (Schwartz)
Definition:
It is the failure to meet the metabolic needs
of the cells and tissues and the consequences
that ensue.
Tissue hypo-perfusion:
1. Decreased delivery of metabolic substrates
2. Inadequate removal of cellular waste
products
“Shock is the
manifestation
of the rude
unhinging of
machinery of
life”
Sameul V.
Gross, 1872

5. What is SHOCK?(Bialey and Love’s)
Definition:
Shock is a systemic state of low tissue perfusion,
which is inadequate for normal cellular
respiration.​
Tissue hypo-perfusion:
1. Insufficient delivery of oxygen and glucose: Cells
switch from aerobic to anaerobic metabolism.​
2. If perfusion is not restored in a timely fashion,
cell death ensues.​

6. Pathophysiology
Levels:
1. Cellular
2. Microvascular
3. Systemic

7. Cellular
Level
Tissue Perfusion↓
(Cellular Hypoxia)
Aerobic to
Anaerobic
Metabolism (Lactic
Acid ↑)
Lactic acid in
Blood↑ (Metabolic
Acidosis)
Cellular Glucose ↓
(Anaerobic Resp
Ceases)
Na-K Pumps fail +
Intracellular
organelles fail +
Lysosomes lyse cell
Cell contents inc.
Potassium release in
blood

8. Micro
Vascular
Level
Immune & Coagulation Sys. ↑
- Complement & Prime
Neutrophils are activated
- Oxygen free radicals ↑
- Cytokine ↑ - Capillary
endothelial cells injury
- Immune and Coagulation sys.
↑↑
Endothelium becomes ‘leaky’ Tissue Edema Cellular Hypoxia Exacerbated

9. Systemic
Level
Preload &
Afterload ↓
Compensatory
Baroreceptor
Respond
Sympathetic
activity ↑
Catecholamin in
circulation↑
Tachycardia &
Systemic
vasoconstriction
(except in sepsis)
Perfusion Pres
in kidney↓
 GFR↓
 Urine
Output↓
Ren–Ang–Ald
axis is
stimulated
 Vasocons↑↑
 Na & H2O
Reabsorption
in kidney↑
Metabolic
Acidosis &
Sympathetic
response↑
RR ↑ &
Ventilation↓
CO2
Excretion↑
Compensatory
Resp Alkalosis
Preload↓
Ren–Ang &
Adrenal Sys
Activate
ADH↑
Vasocons & H2O
Reabs in kid↑
Cortisol↑
(Adrenal cortex)
Na & H2O
Reabs↑
Sensitizes cells
to
Catecholamines

10. Classification of Shock
• Hypovolemic
•Cardiogenic
• Obstructive
•Distributive
• Endocrine

11. Hypovolemic Shock
Causes:
1. Hemorrhagic
2. Non-Hemorrhagic
• Poor fluid intake (dehydration) (Cont.)

12. Hypovolemic Shock
Causes: (Cont.)
• Excessive fluid loss
o Vomiting
o Diarrhoea
o Urinary loss (e.g. diabetes)
o Evaporation
o Third-Spacing (Fluid is lost in GIT & interstitial
spaces, e.g. bowel obstruction or pancreatitis)

13. Hypovolemic Shock
Hypovolemia
Venous Return ↓
Preload↓
Cardiac Output
↓
CO= SV * HR
Hypotension
BP= CO * TPR
Perfusion
Failure + Tissue
Hypoxia
Organ
Dysfunction
Multiorgan
Failure
May end in
Death

14. Classification of Hemorrhage
D. Neurologic: Slightly anxious
E. Skin
1.Warm and pink
2.Capillary Refill brisk (<2
seconds)
F.Renal: Normal urine output
1.Adults: >0.5 ml/kg/hour (>30
cc/hour)
2.Children: >1 ml/kg/hour
3.Infants <1yo: >2 ml/kg/hour
Class I : Minimal Blood Loss
A. Characteristics
1.Blood Volume Loss <15%
2.Adult blood loss <750 ml
B. Cardiovascular
1.Heart Rate normal or mild
increase
2.Pulses normal
3.Blood Pressure normal
4.pH normal
C. Respiratory: Rate normal

15. Classification of Hemorrhage
Class II : Mild Blood Loss
A. Characteristics
1.Blood Volume Loss: 15-30%
2.Adult: 750-1500 ml of blood
loss
B. Cardiovascular
1.Tachycardia
2.Diminished peripheral pulses
3.Blood Pressure normal
4.Normal pH
C. Respiratory:
Mild Tachypnea
D. Neurologic:
1.Irritable
2.Confused
3.Combative
E. Skin
1.Cool extremities
2.Mottling
3.Delayed Capillary Refill
F.Renal:
1.Oliguria
2.Increased specific gravity

16. Classification of Hemorrhage
Class III : Moderate Blood Loss
A. Characteristics
1.Blood Volume Loss: 30-40%
2.Adults: 2000 ml blood loss
B. Cardiovascular
1.Significant Tachycardia
2.Thready peripheral pulses
3.Hypotension
4.Metabolic Acidosis
C. Respiratory:
Moderate Tachypnea
D. Neurologic:
1.Irritable
2.Lethargic
3.Diminished pain response
E. Skin
1.Cool extremities, mottling or pallor
2.Prolonged Capillary Refills
F.Renal:
1.Oliguria
2. Blood Urea Nitrogen (BUN)
increased

17. Classification of Hemorrhage
Class IV : Severe Blood Loss
A. Characteristics
1. Blood Volume Loss: >40%
B. Cardiovascular
1. Severe Tachycardia
2. Thready central pulses
3. Significant Hypotension
4. Significant acidosis
C. Respiratory:
Severe Tachypnea
D. Neurologic:
1.Lethargic
2.Coma
E. Skin
1.Cold extremities
2.Pallor
3.Cyanosis
F.Renal:
1.Anuria

18. Cardiogenic Shock
State of primary failure of heart to pump blood to
the tissues
Causes:
1. Myocardial Infarction
2. Cardiac Dysrhythmias
3. Valvular Heart Disease
(Cont.)

19. Cardiogenic Shock (Cont.)
4. Blunt Myocardial Injury
5. Cardiomyopathy
6. Myocardial Depression
• Endogenous factors (e.g. bacterial and humoral agents
released in sepsis)
• Exogenous factors (Pharmaceutical agents or drug
abuse)

20. Obstructive Shock
State of reduction in preload because of mechanical
obstruction of cardiac filling.
Causes:
1. Cardiac Tamponade
2. Tension Pneumothorax
3. Massive Pulmonary Embolus
4. Air Embolus

21. Obstructive Shock
Filling ↓ of Left
+/- Right sides
of the heart
Preload↓
Cardiac Output
↓
CO= SV * HR
Hypotension
BP= CO * TPR
Perfusion
Failure + Tissue
Hypoxia
Organ
Dysfunction
Multiorgan
Failure
May end in
Death

22. Distributive Shock
It is the pattern of cardiovascular responses
characterising a variety of conditions:
• Septic shock (Unclear Cause)
o Release of endotoxins + Activation of cellular
& humoral components of immune system
(Cont.)

23. Distributive Shock (Cont.)
o Maldistribution of blood flow at a
microvascular level + arteriovenous shunting +
dysfunction of the cellular utilisation of
oxygen
o Later - Hypovolaemia from fluid loss into the
interstitial spaces +/- concomitant myocardial
depression, which complicates the clinical
picture

24. Distributive Shock
• Anaphylaxis
o Histamine Release - Vasoconstriction – Tissue
Perfusion↓ - Tissue Hypoxia….. Shock
• Spinal Cord Injury (Neurogenic)
o Sympathetic Outflow + Adequate Vascular Tone ????

25. Endocrine Shock
May present as a combination of Hypovolemic,
Cardiogenic and Distributive shock
Causes:
1. Hypothyroidism
• Similar to Neurogenic Shock
• Caused by disordered vascular and cardiac
responsiveness to circulating catecholamines
• CO falls because of low inotropy and bradycardia
(Cont.)

26. Endocrine Shock (Cont.)
2. Hyperthyroidism
• Cause a high-output cardiac failure.
3. Adrenal Insufficiency
• Caused by hypovolaemia and a poor response
to circulating and exogenous catecholamines
• Pre-existing Addison’s disease
• Relative insufficiency caused by a pathological
disease state such as systemic sepsis.

27. Severity of Shock
• Compensated Shock
• Decompensated Shock
1. Mild
2. Moderate
3. Severe

28. Clinical Features of Shock
Compensated Mild Moderate Severe
Lactic Acidosis + + ++ +++
Urine Output Normal Normal Reduced Anuric
Level of
Consciousness
Normal Mild Anxiety Drowsy Comatous
Respiratory Rate Normal Increased Increased Laboured
Pulse Rate Mild Increased Increased Increased Increased
Blood Pressure Normal Normal Mild Hypotension Severe HypoTN

29. Consequences of Shock
• Unresuscitable Shock
• Multiple Organ Failure
Effects of Organ Failure
Lungs ARDS
Kidney Acute Renal Insufficiency
Liver Acute Liver Insufficiency
Clotting Coagulopathy
Cardiac Cardiovascular Failure

30. Resuscitation
1. Airway and Ventilation first
2. Conduct of Resuscitation
• Don’t Wait to diagnose the type and find source
• Good Clinical Examination
Patient’s Response
to be observed
during resuscitation:
• HR
• BP
• CVP

31. Resuscitation (Cont.)
3. Fluid Therapy (Cont.)
• IV Fluid in all cases
• Wide Bore IV Cannula
• Crystalloid (RL or NS or BT in hemorrhage)
• No hypotonic Solutions (Dextrose)
(Cont.)
Patient’s Response
to be observed
during resuscitation:
• HR
• BP
• CVP

32. Resuscitation (Cont.)
• IV Fluid Bolus Infusion: 250-500ml in 5-10 mins
(Observe the Patient’s Response)
o Responders (Improve + No active fluid loss)
o Transient Responders (Improve + Return to
previous state in 10-20 mins due to
hemorrhage)
o Non-Responders (Severe Volume Deficit + No
Significant Response + Persistent Uncontrolled
Hemorrhage)
Patient’s Response
to be observed
during resuscitation:
• HR
• BP
• CVP

33. Resuscitation (Cont.)
• Blood and Blood Products
o Whole Blood
o Packed RBC
o FFP (Rich in Coagulation factors)
o Cryoprecipitate (FFP rich in Factor VIII and
Fibrinogen)
o Platelets
o Prothrombin Complex Concentrates
(Concentrate pooled plasma having Factor II, VII,
IX, X)
o Autologous Blood
Patient’s Response
to be observed
during resuscitation:
• HR
• BP
• CVP

34. Resuscitation (Cont.)
4. Vasopressor & Inotropic Support
• Not first line therapy in Hypovolemia
• Adequate preload before it
• Phenylephrine & Noradrenal in Septic and Neurogenic
shock
• Inotropic therapy in Cardiogenic shock to increase
cardiac output
Patient’s Response
to be observed
during resuscitation:
• HR
• BP
• CVP

35. Resuscitation (Cont.)
5. Monitoring
• Minimum
• ECG
• Pulse Oximetry (Continously for PR and
Oxygen Saturation)
• BP (Frequently, non invasive)
• Urine Output (Hourly)
Patient’s Response
to be observed
during resuscitation:
• HR
• BP
• CVP

36. Resuscitation (Cont.)
• Additional
• CVP
• Invasive BP
• Cardiac Output
• Base Deficit and Serum Lactate
Patient’s Response
to be observed
during resuscitation:
• HR
• BP
• CVP

37. Ischemia–Reperfusion Syndrome
Sys.
Hypo-
perfusion
Tissue
Hypoxia
Local
Inflamm-
ation
Organ
Damage
Restored
normal
circulation
Acid
and K+
Build up
Myocardial
Depression
Vascular
Dilatation
Further
HypoTN
-Hypoxia
-Cellular &
humoral
activation
Further
endothelial
Injury
Mult.OrganFailure

38. Ischemia–Reperfusion Syndrome
Reperfusion injury can currently only be attenuated by
reducing the extent and duration of tissue
hypoperfusion.

39. References
• Bialey and Love’s Short Practice of Surgery
(25th Edition)
• Schwartz’s Principles of Surgery
(11th Edition)