This document defines and describes shock, its causes, clinical features, assessment, pathophysiology, classification, management, complications, SIRS and MODS. Shock is defined as a state of poor perfusion with impaired cellular metabolism due to inadequate end-organ perfusion and tissue oxygenation. The main causes of shock include hypovolemia, cardiogenic, obstructive, distributive, endocrine and septic origins. Management involves resuscitation of airway, breathing and circulation through fluid administration and treatment of the underlying cause. Complications can include multiple organ failure if not treated promptly.

1. SHOCK
SENGOOBA DENNIS NYANZI
WAMALA RODNEY RAWPOWER

2. …

3. DEFINITION
 Shock is a state of poor perfusion with impaired cellular metabolism
manifesting with severe pathophysiological abnormalities
 Inadequate end-organ perfusion and tissue oxygenation.
 Most common and most important cause of death in surgical patients.
 Death may occur rapidly due to profound state, or be delayed due to
consequences of ischaemia and reperfusion injury.

4. Clinical Features of Shock
 In early stage—tachycardia, sweating, cold periphery, hypotension,
restlessness, air hunger, tachypnoea, oliguria, collapsed veins.
 In late stage—cyanosis, anuria, jaundice, drowsiness.
Clinically shock may be:
• Compensated with mild tachycardia, normal blood pressure, urine output,
normal respiration and mild lactic acidosis. Mild shock with mild lactic
acidosis, tachycardia, tachypnoea and anxiousness.
• Moderate shock with significant lactic acidosis, decreased urine, tachycardia,
tachypnoea, drowsiness, and mild hypotension.
• Severe shock with severe lactic acidosis, anuria, tachypnoea with gasping,
severe tachycardia, profound hypotension and unconsciousness.

5. Assessment
 Always assess for the above features.
 Shock index is ratio of pulse rate to blood pressure; normal shock index is <
1. In shock it reverses.

6. Pathophysiology
 At cellular level hypoxia causes change of normal aerobic to anaerobic
metabolism causing lactic acidosis. Intracellular potassium is released into
circulation. Lysosomes from cells get released into blood causing cell lysis.
 Hypoxia and acidosis through complements release free oxygen radicals and
cytokines which damage capillary endothelium. Eventually cardiovascular,
respiratory, renal, endocrine and GIT will be affected presenting as systemic
features.
 Damaged endothelium loses its integrity and becomes ‘leaky’, which leads to
tissue oedema which exacerbates hypoxia

7. …

8. Ischaemia Reperfusion Syndrome/Injury
(IRS) or (IRI)
 This is further injury that occurs once normal circulation is restored to the
ischemic tissues.
 The acid and potassium load that has built up can lead to direct myocardial
depression, vascular dilatation and further hypotension
 The cellular and humoral elements activated by the hypoxia (complement,
neutrophils, microvascular thrombi) are flushed back into the circulation
where they cause further endothelial injury to organs such as the lungs and
the kidneys.
 This leads to acute lung injury, acute renal injury, multiple organ failure and
death

9. Classification
 All states are characterised by systemic tissue hypoperfusion and different
states might coexist within the patient.
1. Hypovolemic
2. Cardiogenic
3. Obstructive
4. Distributive
5. Endocrine
6. Septic

10. Hypovolemic
 Due to reduction in total blood volume.
 It may be due to: Haemorrhage –
External from wounds, open fractures –
Internal from injury to spleen, liver,
mesentery or pelvis Severe burns, which
results in loss of plasma Peritonitis,
intestinal obstruction Vomiting and
diarrhoea of any cause
 cause may be Haemorrhagic or Non-
haemorrhagic.
 Most common

11. …

12. Cardiogenic
 Cardiogenic shock is due to primary failure of the heart to pump blood to the
tissues.
 Causes include myocardial infarction, cardiac dysrhythmias, valvular heart
disease, blunt myocardial injury and cardiomyopathy.
 Cardiac insufficiency may also be due to myocardial depression caused by
endogenous factors (e.g. bacterial and humoral agents released in sepsis) or
exogenous factors, such as pharmaceutical agents or drug abuse.
 Evidence of venous hypertension with pulmonary or systemic oedema may
coexist with the classical signs of shock.

13. Obstructive
 Caused due to a mechanical obstruction of cardiac filling that impedes
preload. Reduced cardiac output ensues.
 Common causes of obstructive shock include cardiac tamponade, tension
pneumothorax, massive pulmonary embolus or air embolus.
 Cardiac tamponade; Pericardial fluid collects  intrapericardial pressure
rises heart cannot fill pumping stops.
 Very similar to cardiogenic

14. Septic
 Septic shock may be due to gram-positive organisms, gram negative
organisms, fungi, viruses or protozoal origin. x Gram-negative
septicaemia/gram-negative septic shock is called as endotoxic shock. It
occurs due to gram-negative bacterial infections, commonly seen in
strangulated intestines, peritonitis, gastrointestinal fistulas, biliary and
urinary infections, pancreatitis, major surgical wounds, diabetic wounds and
crush injuries.

15. Distributive
 Distributive shock is one in which there is vasodilatation, decreased vascular
resistance, hypotension, altered micro-vascular perfusion with arteriovenous
shunting, altered cellular oxygen metabolism.
 It is seen in septic shock, spinal trauma, adrenal crisis and anaphylaxis

16. Endocrine
 Endocrine shock may present as a combination of hypovolaemic, cardiogenic
or distributive shock.
 Causes of endocrine shock include hypo- and hyperthyroidism and adrenal
insufficiency. Hypothyroidism causes a shock state similar to that of
neurogenic shock due to disordered vascular and cardiac responsiveness to
circulating catecholamines. Cardiac output falls due to low inotropy and
bradycardia.
 Thyrotoxicosis may cause a high-output cardiac failure. Adrenal insufficiency
leads to shock due to hypovolaemia and a poor response to circulating and
exogenous catecholamines.
 Adrenal insufficiency may be due to pre-existing Addison’s disease or be a
relative insufficiency due to a pathological disease state, such as systemic
sepsis.

17. Anaphylactic
 Injections—penicillins, anaesthetics, stings, venom, shellfish may be having
antigens which will combine with IgE of mast cells and basophils, releasing
histamine and large amount of SRS-A (Slow releasing substance of
anaphylaxis).
 They cause bronchospasm, laryngeal oedema, respiratory distress,
hypotension and shock.
 Mortality is 10%. Rashes all over the body are commonly observed
 An example of distributive

18. Management
 Immediate resuscitation manoeuvres for patients presenting in shock are to
ensure a patent airway and adequate oxygenation and ventilation.
 Once ‘airway’ and ‘breathing’ are assessed and controlled, attention is
directed to cardiovascular resuscitation.
 Make sure to arrest haemorrhage first before you start running fluids.

19. Fluids…
 In all cases of shock, regardless of classification, hypovolemia and inadequate
preload must be addressed before other therapy is instituted.
 Administration of inotropic or chronotropic agents to an empty heart will
rapidly and permanently deplete the myocardium of oxygen stores and
dramatically reduce diastolic filling and therefore coronary perfusion.
 DO NOT ADMINISTER THEM AS FIRST LINE or else Patients will enter the
unresuscitatable stage.
 First-line therapy, therefore, is intravenous access and administration of
intravenous fluids through short wide bore catheters that allow rapid fluid
infusion.

20. When to give what.
 You can administer either crystalloids (normal saline, Hartmann’s solution,
Ringer’s lactate) or colloids (albumin or commercially available products).
 Although, there is less volume benefit to administration of colloids.
 The oxygen carrying capacity of crystalloids and colloids is zero. If blood is
being lost, the ideal replacement fluid is blood, although crystalloid therapy
may be required while awaiting blood products.
 Hypotonic solutions (dextrose etc.) are poor volume expanders and should not
be used in the treatment of shock unless the deficit is free water loss (e.g.
diabetes insipidus) or patients are sodium overloaded (e.g. cirrhosis).

21. Dynamic fluid loss
 The shock status can be determined dynamically by the cardiovascular
response to the rapid administration of a fluid bolus.
 In total, 250–500 mL of fluid is rapidly given (over 5–10 minutes) and the
cardiovascular responses in terms of heartrate, blood pressure and central
venous pressure are observed.
 Patients can be divided into ‘responders’, ‘transient responders’ and ‘non-
responders’.
 Responders have an improvement in their cardiovascular status that is
sustained. These patients are not actively losing fluid but require filling to a
normal volume status.

22. …
 Transient responders have an improvement, but this then reverts to the
previous state over the next 10–20 minutes. These patients have moderate
ongoing fluid losses (either overt haemorrhage or further fluid shifts reducing
intravascular volume).
 Non-responders are severely volume depleted and are likely to have major
ongoing loss of intravascular volume, usually through persistent uncontrolled
hemorrhage.

23. Complications
 Acute respiratory distress syndrome and respiratory failure
 ™
Acute renal failure
 ™
Hypoxia, metabolic acidosis
 ™
Stress ulcers, ileus, liver failure
 ™
Disseminated intravascular coagulation (DIC) and thrombocytopenia
 ™
Systemic inflammatory response syndrome and multiorgan dysfunction
syndrome (MODS)

24. SIRS AND MODS
 SIRS (Systemic inflammatory response syndrome) is due to vasodilatation,
increased endothelial permeability, thrombosis, leucocyte migration and
activation. ↓
 All these lead to altered cytokines level, abnormal NO (nitric oxide) synthesis,
abnormal arachidonic acid metabolism, neutrophil activation, free radical
production, altered complement activation, failure to have a localisation of
inflammation. It is severe type of reversible shock. ↓
 Which will lead to established microvascular occlusion, cellular dysfunction,
sick cell syndrome, DIC and PUMP failure. ↓
 MODS (Multiorgan dysfunction syndrome) (Irreversible shock)—of lungs,
kidneys, liver, clotting system and brain.