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[ Pathophysiology,Types & Mgt ]
Prof. Utham Murali. M.S; M.B.A](https://image.slidesharecdn.com/shock-types-141009102815-conversion-gate01/75/Shock-Pathophysiology-Types-Management-1-2048.jpg)
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Shock - Pathophysiology / Types & Management
The document provides a detailed overview of shock, including its definition, pathophysiology, various etiologies, clinical features, and management strategies. It categorizes shock into types such as hypovolemic, cardiogenic, obstructive, neurogenic, anaphylactic, and septic shock, along with their respective causes and symptoms. Management emphasizes monitoring, treatment goals to improve oxygen delivery, fluid therapy, use of vasopressors, and the importance of early recognition and intervention.
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Shock - Pathophysiology / Types & Management
- 1. SHOCK [ Pathophysiology,Types &Mgt ] Prof. Utham Murali. M.S; M.B.A
- 2. Objectives Definition Reviewbasic physiologic aspects of shock Different categories with Etiology &Clinical features Management aspects
- 3. Definition Shock is aphysiologic state characterized by systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery. 3
- 4. Other Ways * It’sa condition, in which circulation fails to meet the metabolic need of the tissue & at the same time fails to remove the metabolic waste products. • Inadequate tissue perfusion to meet tissue demands • Usually result of inadequate blood flow and/or oxygen delivery • Inadequate peripheral perfusion leading to failure of tissue oxygenation • Lead to anaerobic metabolism 4
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- 6. 6 Demand Supply Shock
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- 8. Cells switch fromaerobic to anaerobic metabolism lactic acid production Cell function ceases & swells membrane becomes more permeable electrolytes & fluids seep in & out of cell Na+/K+ pump impaired mitochondria damage cell death
- 9. Shock – Effectson Organ Heart – ↓ CO / hypotension / myocardial depressants Lung - ↓gas exchange / tachypnoea / pulmonary edema Endocrine – ADH → ↑ reabsorption of water CNS – perfusion ↓ – drowsy Blood - Coagulation abnormalities – DIC Renal - ↓ GFR - ↓ urine output GIT – mucosal ischaemia – bleeding & hepatic - ↑ enzyme levels
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- 12. HYPOVOLAEMIC ETIOLOGY Blood loss. haemorrhage Plasma / body water loss. Electrolytes imbalance. Vomiting. Diarrhea. Dehydration.
- 13. Valvular heart disease Myocardialinfarction. Cardiac arrhythmias. Cardiomyopathy CARDIOGENIC ETIOLOGY
- 14. OBSTRUCTIVE ETIOLOGY Cardiac Tamponade Pulmonary Embolism Tension Pneumothorax Air embolism
- 15. NEUROGENIC ETIOLOGY Paraplegia. Quadriplegia. Trauma to spinalcord. Spinal anesthesia.
- 16.
- 17. Gram + Gram - Fungi/ Virus Protozoa SEPTIC ETIOLOGY
- 18. ENDOCRINE ETIOLOGY Hypo & Hyperthyroidism. Adrenalinsufficiency.
- 19. Clinical Features Features ofshock depend on the degree of loss of volume & on duration of shock. Types Mild shock. Moderate shock. Severe shock.
- 20. Mild Shock Features Collapseof subcutaneous veins of extremities esp. the feet, which become pale and cool Sweat on forehead, hand and feet Urine output normal. Pulse rate normal. Blood pressure normal. Patient feels thirsty and cold.
- 21. Moderate Shock Features Mildshock features + drowsy & confused Oliguria Pulse rate increased usually less then 100/min. Blood pressure normal initially then falls in later stage.
- 22. Severe Shock Features Unconscious. Gasping respiration. Anuria. Rapid pulse. Profound hypotension.
- 23. Stages of shock Initial : The cells become leaky and switch to anaerobic metabolism. Non-progressive:(compensated stage) Attempt to correct the metabolic upset of shock. Progressive: (decompensated stage ) Eventually the compensation will begin to fail. Refractory : Organs fail and the shock can no longer be reversed.
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- 26. Monitoring Blood pressure Heart rate Respiratoryrate Urine output Blood CBC Pulse- oximetry ECG U/S , CT , X-ray
- 27. Special Monitoring CARDIO– VASCULAR - Central venous pressure Normal ; 5-10cmH2O, If CVP<5cmH2O Inadequacy of blood volume CVP>12cmH2O Cardiac dysfunction - Cardiac output Pulmonary catheter Doppler ultrasound Pulse waveform analysis
- 28. Special Monitoring SYSTEMIC& ORGAN PERFUSION Clinical : urine output & LOC Sr. Lactate estimation & Base defecit Blood gas analysis PO2 / PCO2 / ph Mixed venous O2 saturation – N – 50-70% Newer methods Muscle tissue O2 probes Near –infrared spectroscopy Sublingual capnometry
- 29. Guidelines Treat thecause Improve Cardiac function Improve Tissue perfusion
- 30. Goals of Resuscitation Overall goal: increase O2 delivery decrease demand Treatment O2 content Cardiac output Blood pressure Sedation/analgesia
- 31. Principles of Resuscitation A:Airway patent upper airway B: Breathing adequate ventilation and oxygenation C: Circulation placement of adequate IV access cardiac function oxygenation
- 32. Fluid Therapy inShock Crystalloid Solutions Normal saline Ringers Lactate solution Hartmann’s solution Colloid Solutions Blood transfusion
- 33. Oxygen Carrying Capacity Only RBC contribute to oxygen carrying capacity (hemoglobin) Replacement with all other solutions will support volume Improve end organ perfusion Will Not provide additional oxygen carrying capacity
- 34. Dynamic Fluid Response Infusing 250-500ml of Fluid rapidly in 5 - 10 mts. Responders – Improvement Transient responders – revert back Non – responders
- 35. Vasopressors / InotropicDrugs Vasopressors – Phenylephrine / NA Distributive shock states Septic shock / Neurogenic Inotropics - Dobutamine Cardiogenic shock / Severe septic shock To increase the cardiac output
- 36. Other Treatments Correctionof Acid – base balance Steriods - Hydrocortisone Antibiotics Catheterisation Nasal O2 / Ventilatory support CVP Line Control of Pain ICU – Critical care management
- 37. End Points ofResuscitation Classic / Traditional Restoration of blood pressure Normalization of heart rate and urine output Appropriate mental status Improved / Global All of the above plus Normalization of serum lactate levels Resolution of base deficit Adequate - MVS Goal directed approach Urine output > 0.5 mL/kg/hr CVP 5 -10 cm H2o MAP 65 to 90 mmHg Central venous oxygen concentration > 70%
- 38. Practically Speaking…. Know howto distinguish different types of shock and treat accordingly. Look for early signs of shock. Monitor the patient using the HR, MAP, mental status, urine output. SHOCK is not equal to hypotension. Start antibiotics within an hour ! Do not wait for cultures or blood work.
- 40. 1.All of thefollowing are causes related to Obstructive shock except - A Cardiac tamponade. B Air embolism. C Cardiac arrhythmias. D Pulmonary embolism.
- 41. 2.Which of thefollowing is the agent of choice in Severe septic shock ? A Vasopressin. B Adrenaline. C Phenylephrine. D Dobutamine.
- 42. 3. A 19-year-oldmale is brought to the hospital after sustaining an abdominal injury while playing rugby. He is complaining of left upper abdominal pain and has some bruising over the same area. His pulse is 140/min and his BP is 100/82mmHg. What is the type of shock? A Septic shock. B Cardiogenic shock. C Hypovolaemic shock. D None of the above.
- 43. 4.Which of thefollowing is not a newer methods for monitoring tissue perfusion - A Muscle tissue O2 probe. B Doppler ultrasound. C Infrared spectroscopy. D Sublingual capnometry.
- 44. 5.Which of thefollowing is one of the last signs of shock ? A Profound hypotension. B Tachycardia. C Prolonged capillary refill. D All of the above.
- 45. THANK YOU THANK YOU. . .