This document discusses shock and its classifications and pathophysiology. It defines shock as an imbalance between oxygen delivery and demand. There are four main classifications of shock: cardiogenic, hypovolemic, distributive, and obstructive. The pathophysiology involves a progression from compensated shock to end organ dysfunction as the body's compensatory mechanisms become insufficient to maintain adequate tissue perfusion and oxygen delivery. Treatment involves initial stabilization and assessment followed by definitive care, which may include fluid resuscitation, vasopressor therapy, treating the underlying cause, and monitoring for complications.

1. SHOCK AND ITS COMPLICATIONS
Dr Kyegombe Willy MBChB MMED SURG
Soroti University
MBChB iii lecture

2. Definition of Shock:
• Imbalance between oxygen delivery and demand.
• Philosophically transition between life and death
• Globally represents 1% of emergency ward
presentation
• Mortality exceeds 20%

3. Classification
• ATLS(severity)(4 classes)
• Degree of
compensation(compassated/uncompassated)
• Aetiology(3broad types)

4. ATLS CLASSIFICATION

5. Aetiology(3broad types)
• Cardiogenic Shock
– Cardiac tamonade
– Tension pneumothorax
– Arrythmias and MI
– Obstructive shock ; Pulmonary emboli.
• Heamorrhagic shock and hypovolemic
shock.Leaking vessel or third space loss from
vessel(
– Burns,
– Trauma related heamorrhage
– Vommiting diahoerrhea
– Upper and lower GI bleeding.
– Ectopic pregnancy
• Distributive shock.
– Endocrine shock
– Septic shock
– Anaphylactic shock
– Neurogenic shock

6. Aetiology(cardiogenic shock)
Cardiogenic Shock:
Intrinsic abnormality in the heart renders the heart
incapable of delivering blood into the vasculature
with adequate power
• Problems arise with the muscle or rhythm
• Normovolemic
• Examples include MI, myocarditis, cardiac contusion,
bradyarrhythmias, tachyarrythmias

7. Aetiology(distributive shock)
Neurogenic Shock:
Loss of autonomic innervation of the vasculature
Results in
1. Low ventricular end diastolic pressure
2. Hypotension
3. Bradycardia
Examples: spinal cord injury, regional anesthesia,
antiadrenergic agents, neurologic disorders, fainting

8. Aetiology(distributive shock)
Inflammatory Shock:
Arises from the release of inflammatory and coagulatory
mediators (cytokines, TNF-a, IL-1, IL-6, etc)
resulting from
•trauma
•infection
•ischemia reperfusion
Examples include major fractures, burns, anaphylaxis,
peritonitis, pneumonia, wet gangrene

9. Aetiology(Heamorrhagic and
distributive shock)
Hypovolemic Shock:
Small ventricular end diastolic volumes
leads to:
inadequate cardiac generation of pressure, flow,
and ultimately power
Examples include bleeding, GI losses (vomiting, diarrhea, etc),
fluid sequestration, diabetes insipidus, adrenal insufficiency,
dehydration

10. Aetiology(Heamorrhagic shock)
Do not overlook:
1. Internal Bleeding
Ectopic pregnancy
Hemoperitoneum (abdomen can hold >3 liters)
Hemothorax (thorax can hold >3 liters)
2. Fracture losses

11. Aetiology(Heamorrhagic shock)
0
0.2
0.4
0.6
0.8
1
1.2
1.4
1.6
1.8
2
Liters
Pelvic
Femur
Tib-Fib
Humerus
Radius/U
lna
Rib
Open
Fracture
Blood
Losses
Adult Fist = 500ml

12. PATHOPHYSIOLOGY
• Hypoxia at the cellular level causes a series of
physiologic and biochemical changes,resulting in
• acidosis
• decrease in regional blood flow, which further
worsens the tissue hypoxia.
• Cellular injury with further release of
inflammatory mediators and end organ failure
• In hypovolemic, obstructive, and cardiogenic shock,
there is a decrease in cardiac output and decreased
oxygen transport.

13. PATHOPHYSIOLOGY
• In distributive shock, there is decreased peripheral
vascular resistance and abnormal oxygen extraction.
• Generally, shock has the following three stages of
stress response:
– Pre shock (reversible)
– Shock(Transition)
– Endorgan dysfunction(Irreversible shock)

14. PATHOPHYSIOLOGY–
• Pre-shock or compensated shock
• compensatory mechanisms to counter the decrease
in tissue perfusion.
• Decreased blood flow to skin, gut, and periphery
to increase venous return to the heart
• Increased catecholamines and sympathetic
activity to increase heart rate and contractility
• Increased sympathetic tone to arterial system and
vasoconstrictors (e.g. angiotensin II) increase the
SVR to maintain BP

15. Fluid Conserving Measures in
hypovolemia
ADH secretion in posterior pituitary increased due to:
1. afferent nerve impulses from site of injury
2. Increased plasma osmolality
3. Atrial stretch receptors responding to reduced volume and
aortic and carotid baroreceptors responding to reduce
pressure
ADH promote retention of free water (without electrolytes)

16. Fluid Conserving Measures in
hypovolemia
Aldosterone secretion from adrenal cortex increases
and acts on distal renal tubular cells to increase
reabsorption of sodium and increase excretion of
potassium and hydrogen in urine.
Net Result: concentrated urine in reduced amounts for
48-72 hours after injury with general body edema

17. Pathophysiology
Shock
• progression of the pre-shock stage as the
compensatory mechanisms become insufficient.
• most of the classic signs and symptoms of shock
appear due to early organ dysfunction

18. Pathophysiology
• End-organ dysfunction -
• Final stage, leading to irreversible organ
dysfunction, multiorgan failure, and death
– gut mucosal barrier breakdown occurs and translocation of bacteria or
their endproducts(endotoxin) is possible
– Triad of death sets(Hypothermia, coagulopathy and acidosis)

19. EVALUATION
History, PE, and Investigation

20. History
• HPC from the patient (if feasible) and/or patient's relatives.
• Also, a review of the patient’s outpatient medical records
(information regarding risk factors, medications, and trend of
baseline vital signs including blood pressure
• Cinical features and symptoms.
– Hypotension, (30mmhg below base line)
– Tachycardia(20b/m from baseline and physical activity)
– Modified shock index( HR/MAP,
– tachypnea

21. History and physical
examination
– obtundation or
abnormal mental
status,(Donot use GCS)
– cold, clammy
extremities, mottled
skin,
– oliguria,(adults.0.5-
1ml/kg/hr, Children 1-2
ml/kg/hr)
– metabolic acidosis, and
hyperlactatemia(greater
than 4mmol/L)

22. History and physical
examination
• Stigmata chronic liver disease (in case of variceal bleeding).
• Source of infection (example-skin manifestations of primary
infection such as erysipelas, cellulitis, necrotizing soft-tissue
infections), and cutaneous manifestations of infective
endocarditis.
• Anaphylactic shock can have hypotension, flushing, urticaria,
tachypnea, hoarseness of voice, oral and facial edema, hives,
wheeze, inspiratory stridor, and history of exposure to
common allergens such as medications or food items the
patient is allergic to or insect stings.

23. Conditions that Kill Quickly:
1. Airway
2. Ventilation (e.g. tension
pneumothorax)
3. Arrhythmia (e.g. ventricular
fibrillation)
4. Heart compression (e.g. cardiac
tamponade)
5. Compression of great vessels
(arteries or veins)
6. Bleeding
7. Severe anaphylaxis
8. Electrolyte abnormalities (e.g.
hypo or hyperkalemia)
4H
• Hypotension
• Hypothermia
• Hypoxia
• Hypoglycemia

25. INVESTIGATIONS
HEMATOLOGICAL
• CBC(pay attention to HB and heamatocrit)
• RFT
• LFT
• Dynamic coagulation studies
• Serum lactacte
• ABG
• Grouping and x matching
• Cultures(urine,blood)
• Cardiac enzymes
• RBS
• Markers of pancreatitis

27. RADIOLOGICAL.
• EFAST
• Xrays(CXR and abdominal USS)
• Cardiac Echo
• Abdominal USS
• CT scan.
• ECG

28. TREATMENT
• 2stages
– Initial assessment and stabilization.
– Definitive Care
• stabilization of the airway and breathing with oxygen
and oral mechanical ventilation when needed.

29. • Intravenous access.
– 2 Large bore Peripheral IV , intraosseous infusion
(IO) .
– Central venous access : if there is difficulty
securing peripheral venous access, or the patient
needs prolonged vasopressor therapy , large-
volume resuscitation and dynamic monitoring.
Urinary Catheterization to monitor urine out put.
Keep patient

30. • Immediate treatment with intravenous (IV) fluid should be
initiated, followed by vasopressor therapy, if needed, to
maintain tissue perfusion.
– 20ML/KG/in 30 minutes for hypovolemic shock or Blood to
crystalloid ratio 1;3
– Better to replace blood with blood.
– Other colloids can be used to restore volume especially for
truma
• Reasses response to fluids( Heamodynamic parameters, urine
out put,level of counciousness, cvp, serum lactate)

31. • Keep patient warm
• Elevate the limbs
• Treat coagulopathies
• Attend to other life
threatening
emergencies.

32. Definitive care
Septic shock –
• IV isotonic crystalloids 30 mL/kg within 3 hrs
• empiric antibiotic therapy within one hr.
• For patients with septic shock requiring
vasopressors, target a mean arterial pressure (MAP)
of 65 mmHg.

33. • Anaphylactic shock
– aggressive IV fluid resuscitation with 4 to 6 L of IV
crystalloids.
– Stop the offending agent, intramuscular
epinephrine, antihistamines, corticosteroids,
nebulized albuterol.
• In adrenal crisis - judicious fluid resuscitation, IV
dexamethasone.

35. • Hypovolemic shock –
– two large-bore IVs or central line.
– Place the patient in the Trendelenburg position.
– Aggressive IV fluid resuscitation with 2 to 4 L of isotonic
crystalloids.
– PRBC transfusion if ongoing bleed.
– Appropriate medical or interventional strategies to treat
the underlying etiology. Continue with isotonic crystalloids
and use vasopressors if needed
• Heamorrhagic shock we do heamostatic
resuscitation in addition to IV fluid therapy and
blood transfusion.

36. Obstructive shock -
• the judicious use of IV crystalloids.
• If shock persists, early initiation of vasopressors-
norepinephrine is the first choice and add
vasopressin if refractory.
• Continue IV fluids but monitor very closely

37. Acute massive pulmonary embolism
• thrombolysis.
• Judicious use of IV fluids has a paradoxical
worsening of hypotension; it may develop due to
severe right ventricular dilatation and septal bowing
compromising left ventricle filling.

38. Tension pneumothorax -
• needle thoracotomy followed by tube thoracotomy.
Cardiac tamponade-
• pericardiocentesis, significant clinical improvement is
possible, even with minimal fluid removal
Cardiogenic shock

39. Shock & Body Fluid Requirements
Vasopressors:
act to increase BP by increasing SVR and decreasing
tissue perfusion
Dopamine: inotropic at low doses (3ug/kg/hr),
vasopressor at high doses
Dobutamine: increases cardiac input with less
tachycardia and arrhythmias than dopamine…its B
adrenergic effect results in vasodilatation
Norepinephrine: A receptor agonist…increases BP
Epinephrine: catecholamine, A and B
adrenergic…increases BP

40. Shock & Body Fluid Requirements

41. Questions??