shock various types features final ppt.pptx

MBBS shock topic various types and features pathophysiology

1. Shock Orthopaedics presentation By Roll no. 61 to 80

2. Introduction Shock is the most common cause of death of surgical patients. Hypovolemic shock is a commonest cause of death following fracture of major bones such as pelvis and femur. Death may occur rapidly because of a profound state of shock or may occur later because of the consequences of organ ischaemia and reperfusion injury.

3. Definition Shock is a systemic state of low tissue perfusion that is inadeq uate for normal cellular respiration. With insufficient delivery of oxygen and glucose, cells switch from aerobic to anaerobic metabolism. If perfusion is not restored in a timely fashion, cell death ensues.

4. Etiology (Types of Shock) Hypovolemic shock Cause: ↓ Intravascular volume (hemorrhage, trauma, burns, dehydration). Cardiogenic shock Cause: Pump failure (MI, arrhythmia, valvular disease, cardiomyopathy) Distributive shock ( Hampered distribution of blood flow) Septic shock – bacteria’s endotoxins/cytokines. Anaphylactic shock – Ig E mediated histamine release. Neurogenic shock – loss of sympathetic tone

5. Etiology 4. Obstructive shock Cause: Mechanical obstruction (cardiac tamponade , tension pneumothorax, massive PE). 5. Endocrine shock

6. Pathophysiology CELLULAR LEVEL ↓ Oxygen delivery → switch to anaerobic metabolism
Lactic acidosis develops
Glucose depletion → Na⁺/K⁺ pump failure
Lysosomal enzyme release → cell lysis
↑ Extracellular K⁺ → hyperkalemia

7. Pathophysiology 2..MICROVASCULAR LEVEL Hypoxia + acidosis → complement activation, leukocyte priming
Release of cytokines, free radicals
Endothelial injury → capillary leak → tissue edema Ischemic cell death → further K⁺ release + systemic inflammation

8. Pathophysiology 3.. SYSTEMIC LEVEL Cardiovascular As preload and afterload decrease, there is a compensatory baroreceptor response, resulting in increased sympathetic activity and release of catecholamines into the circulation. This results in tachycardia and systemic vasoconstriction (except in sepsis (vasodilation))

9. Pathophysiology Respiratory The metabolic acidosis and increased sympathetic response result in an increased respiratory rate and minute ventilation to increase the excretion of carbon dioxide (and so produce a compensatory respiratory alkalosis). Renal Decreased perfusion pressure → ↓ GFR → oliguria RAAS activation → vasoconstriction + Na⁺/water retention

10. Pathophysiology Endocrine As well as activation of the adrenal and renin–angiotensin systems, vasopressin (antidiuretic hormone) is released in response to decreased preload and results in vasoconstriction and resorption of water in the renal collecting system Cortisol is also released from the adrenal cortex, contributing to the sodium and water resorption and sensitising cells to catecholamines.

11. Stages of shock 3 stages Reversible shock Progressive shock I rreversible shock

12. Compensated (Non-progressive, Reversible) Shock Goal: Maintain blood flow to brain & heart.
Mechanisms:
Vasoconstriction (via baroreceptors, catecholamines, renin–angiotensin, etc.) → ↑ peripheral resistance, BP, HR.
Renal fluid conservation → aldosterone, ADH, ↓ GFR, fluid shift from tissues.
Adrenal medulla stimulation → catecholamines increase HR & cardiac output.
Clinical: Cool, pale skin. Recovery possible if cause treated.

13. Progressive (Decompensated) Shock Occurs with persistent shock + comorbidities.
Pathophysiology:
Pulmonary hypoperfusion → ↑ permeability, ARDS, tachypnea.
Tissue ischemia → anaerobic glycolysis, lactic acidosis, ineffective vasomotor tone, vasodilation, blood pooling.
Clinical: Confusion, worsening renal function.

14. Irreversible shock Severe, refractory to treatment; widespread cell injury.
Key effects:
Progressive vasodilatation & vascular permeability → pooling + edema.
Myocardial depressant factor (MDF) → ↓ cardiac output, ischemia.
Pulmonary edema/ARDS, worsening hypoxia.
Anoxic cell death in heart, kidney (tubular necrosis), brain (neurons).
Hypercoagulability & microthrombi → tissue necrosis.
Clinical: Coma, renal failure, severe myocardial depression.

15. Difference between stages

16. Classification Hypovolemic shock Cardiogenic shock Obstructive shock Distributive shock Neurogenic shock Anaphylactic shock Septic shock Endocrine shock

17. Hypovolemic shock

18. Irreversible (Refractory) Shock
‣ Severe hypotension, weak/absent pulse ●Respiratory distress / ARDS . ●Stupor, coma – ●Anuria ● Cold, cyanotic, mottled skin • ● Multi-organ failure, collapse Progressive (Decompensated) Shock
‣ Hypotension, tachycardia worsens ● Rapid, shallow breathing ●Confusion, lethargy ● Oliguria ●Mottled, cold extremities ● Nausea, vomiting, worsening diaphoresis Compensated (Reversible) Shock
• Tachycardia BP normal • Weak pulse • Anxiety, restlessness • Pale, cool, clammy skin • Thirst, mild sweating • Mild urine output Clinical features

19. Management of hypovolemic shock Basic Principles:-
Aim: Restore tissue perfusion & oxygen delivery
Maintain airway, breathing, circulation (ABC)
Rapid diagnosis & treatment of underlying cause
Prevent further injury/bleeding
Monitor response (BP, HR, urine output, lactate)
Provide definitive therapy after stabilization

20. Management of hypovolemic shock Resuscitation:-
Airway with cervical spine protection
Breathing: Oxygenation & ventilation
Circulation: IV access, fluids, blood
Disability: Neuro status (GCS, pupils)
Exposure: Fully expose, prevent hypothermia

21. Management of hypovolemic shock Airway Management Ensure patent airway in all patients
Supplemental oxygen to maintain SpO ₂ > 94%
Endotracheal intubation if GCS < 8, severe distress, or airway compromise
Cervical spine protection in trauma patients
Suction secretions, use adjuncts (OPA/NPA) if needed
Mechanical ventilation for refractory hypoxemia

22. Management of hypovolemic shock Fluid Resuscitation
First-line: Isotonic crystalloids (Ringer’s lactate, NS)
Colloids: Limited role, not superior to crystalloids
Bolus approach: 500–1000 ml adults → reassess → repeat if needed
Goal: Restore perfusion (MAP ≥ 65 mmHg, urine output ≥ 0.5 ml/kg/hr)
Avoid fluid overload (esp. Cardiogenic shock)

23. Management of hypovolemic shock Blood Transfusion (Massive Transfusion Protocol)
Indication: Ongoing hemorrhage + shock not controlled by fluids
Massive transfusion protocol (MTP): 1:1:1 ratio
Packed RBCs : Fresh Frozen Plasma : Platelets
Early use of tranexamic acid (TXA) in trauma (<3 hrs)
Monitor Hb , coagulation, Ca²⁺, electrolytes
Prevent hypothermia during transfusion

24. Management of hypovolemic shock Damage Control Resuscitation
Permissive hypotension: Maintain SBP 80–90 until bleeding controlled Hemostatic resuscitation: Early blood products, minimize crystalloids
Damage control surgery: Temporary control (packing, shunts, clamps)
Prevent lethal triad: Hypothermia, acidosis, coagulopathy
Transition to definitive repair after stabilization

25. Management of hypovolemic shock Vasoactive Drugs (Indications)
When to use: Persistent hypotension despite fluids
First choice: Norepinephrine (septic/distributive shock)
Dopamine/ Dobutamine : For cardiogenic shock with low CO
Adrenaline: Anaphylaxis, refractory shock
Vasopressin: Refractory septic shock (2 nd line)
Always use after adequate fluid resuscitation

26. Management of hypovolemic shock Orthopaedic Specifics
External fixation for long bone fractures – reduces bleeding
Pelvic binder/sheet wrap – stabilizes pelvic fractures, reduces venous bleeding
Pelvic packing in OR if binder insufficient Splintage of limbs – reduces pain, blood loss, fat embolism risk
Damage control orthopaedics (DCO): Temporary stabilization → definitive surgery later

27. Cardiogenic shock

28. Clinical features General: Restlessness, anxiety, altered sensorium (due to cerebral hypoperfusion )
Skin: Cold, clammy, mottled extremities; delayed capillary refill
Pulse & BP: Rapid, weak, thready pulse; systolic BP < 90 mmHg; narrow pulse pressure
Respiratory: Tachypnea , dyspnea , pulmonary crepitations (pulmonary edema )
Renal: Oliguria/anuria (< 0.5 ml/kg/hr)
Neck veins: Raised JVP (in LV failure / RV infarction)

29. Diagnosis and Investigation Diagnosis :
Clinical suspicion: Shock state with evidence of myocardial dysfunction
Hemodynamic parameters:
Cardiac index < 2.2 L/min/m²
Pulmonary capillary wedge pressure > 18 mmHg Investigations :
ECG: MI, arrhythmia, ischemia
Echocardiography: ↓ LV contractility, wall motion abnormality
Labs: Cardiac enzymes (troponin, CK-MB), ABG (lactic acidosis)

30. Management of cardiogenic shock

31. Distributive shock

32. Management of Distributive shock Recognize hypotension + warm extremities + low SVR
Resuscitation: Secure airway, give oxygen, IV crystalloids (first-line)
Vasopressors: Norepinephrine preferred if fluids inadequate
Septic shock: Early IV antibiotics + source control (drainage/surgery)
Anaphylactic shock: IM adrenaline (first), antihistamines, steroids, fluids
Neurogenic shock: IV fluids, vasopressors, atropine if severe bradycardia, spinal immobilization
Supportive care: Correct acidosis/electrolytes, organ support in ICU

33. Obstructive shock

34. Clinical Features General: Hypotension, tachycardia, weak thready pulse, cold clammy skin
Jugular venous distension (↑ venous pressure – tamponade , tension pneumothorax, PE) Pulsus paradoxus (↓ SBP >10 mmHg during inspiration, esp. Tamponade ) Dyspnea , tachypnea , hypoxia (PE, pneumothorax)
Absent breath sounds & hyperresonance on affected side (tension pneumothorax)
Muffled heart sounds + JVP + hypotension (Beck’s triad) in tamponade Signs of RV strain on ECG/Echo in pulmonary embolism

35. Management of Obstructive Shock Initial: Secure airway, give oxygen, IV access, fluids (temporary)
Tension pneumothorax: Immediate needle decompression → chest tube
Cardiac tamponade : Urgent pericardiocentesis or surgical drainage
Massive pulmonary embolism: Thrombolysis or surgical embolectomy , anticoagulation
Aortic dissection: BP control (beta-blockers), urgent surgical repair
Supportive: Vasopressors if hypotension persists, ICU monitoring

36. Comparison

37. Investigations Bedside / Rapid Tests Vital monitoring – HR, BP, SpO ₂, RR, urine output.
Capillary refill time – delayed in hypoperfusion .
Bedside glucose – hypoglycemia may mimic or worsen shock.
Arterial blood gas (ABG) – metabolic acidosis (↑ lactate).
ECG – arrhythmia, myocardial ischemia (cardiogenic shock).

38. Investigations 2.Laboratory Diagnosis Hemoglobin & Hematocrit – anemia , hemorrhage .
Complete Blood Count (CBC) – leukocytosis (sepsis), thrombocytopenia (DIC).
Serum Electrolytes, Urea, Creatinine – renal perfusion & dysfunction.
Liver function tests – hypoxic hepatitis in prolonged shock.
Serum Lactate – key marker of tissue hypoperfusion (↑ >2 mmol /L).
Coagulation profile (PT, INR, aPTT , D-dimer, fibrinogen) – for DIC or massive transfusion.
Blood culture – in suspected septic shock.
Cross-matching & Blood grouping – essential in hemorrhagic shock.

39. Investigations 3. Imaging Studies
Chest X-ray – pneumothorax, hemothorax , cardiomegaly, pulmonary edema .
Focused Assessment with Sonography in Trauma (FAST) – detect intraperitoneal bleed.
Echocardiography – cardiac contractility, tamponade , valvular lesions.
CT scan (where patient is stable enough) – trauma evaluation, PE suspicion. 4. Specialized Tests (as per suspected cause)
Troponin I/T, CK-MB – myocardial infarction (cardiogenic). Procalcitonin / CRP – sepsis marker.
Urine analysis – dehydration, sepsis.
Toxicology screen – poisoning, drug overdose.

40. Complications A. MODS – Multiple Organ Dysfunction Syndrome
Progressive failure of >2 organ systems
Commonly involves: lungs, kidneys, liver, heart, brain
Usually due to prolonged tissue hypoperfusion or sepsis
B. ARDS – Acute Respiratory Distress Syndrome (WRDS: Wrong term; it should be ARDS)
Severe lung injury due to inflammation and capillary leak
Hypoxia refractory to oxygen therapy
Common in septic or traumatic shock

41. Complications C.DIC – Disseminated Intravascular Coagulation
Systemic activation of clotting – microthrombi + bleeding tendency
Seen in septic shock, trauma, obstetric emergencies