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SHOCK final.pptxbnsf.gns.atg.areststbathbadtbhi
- 1. Presented by -Dr. Aniruddh Jain (1st Year Resident) Under the guidance of - Dr. Neelkamal Gupta Sir Professor and Unit Head Department of General Surgery SHOCK
- 2. Introduction • Shock isthe most common cause of death of surgical patients. • Death may occur rapidly because of a profound state of shock or may occur later because of the consequences of organ ischemia and re- perfusion injury.
- 3. SHOCK • Shock isa systemic state of low tissue perfusion that is inadequate for normal cellular respiration. • Insufficient delivery of oxygen and glucose, cells switch from aerobic to anaerobic metabolism.
- 4. PATHOPHYSIOLOGY • CELLULAR • MICROVASCULAR •SYSTEMIC - CARDIOVASCULAR, RESPIRATORY, RENAL AND ENDOCRINE
- 5. CELLULAR Perfusion to tissuesis reduced Cells are deprived of oxygen Switch from aerobic to anaerobic metabolism Lactic acid is produced Accumulation of lactic acid in the blood Systemic metabolic acidosis PATHOPHYSIOLOGY
- 6. CELLULAR Glucose within thecells get exhausted Anaerobic respiration ceases Failure of sodium/potassium pumps in the cell membrane and intracellular organelles Intracellular lysosomes release auto digestive enzymes Cell lysis Intracellular contents (potassium) gets released into the bloodstream PATHOPHYSIOLOGY Hyperkalemia
- 7. MICROVASCULAR Hypoxia and acidosis Activatescomplement and prime leucocytes Generation of oxygen free radicals and cytokine release Leads to injury of the capillary endothelial cells Activates the immune and coagulation systems Damages endothelium loses its integrity and becomes ‘leaky’ Tissue edema Exacerbating cellular hypoxia PATHOPHYSIOLOGY
- 8. SYSTEMIC As preload andafter load decreases Compensatory baroreceptor response gets activated Increased sympathetic activity and release of catecholamines Tachycardia and systemic vasoconstriction (except in septic shock) CARDIOVASCULAR PATHOPHYSIOLOGY
- 9. SYSTEMIC Metabolic acidosis Increased respiratoryrate and minute ventilation (to increase the excretion of Co2) Compensatory respiratory alkalosis RESPIRATORY Increased sympathetic response PATHOPHYSIOLOGY
- 10. SYSTEMIC Decreased perfusion pressure Reducedfiltration at the glomerulus and decreased urine output Activation of renin-angiotensin-aldosterone system Vasoconstriction and increased sodium and water resorption RENAL PATHOPHYSIOLOGY
- 11. SYSTEMIC Decreased preload Release ofvasopressin (anti-diuretic hormone) Vasoconstriction and resorption of water ENDOCRINE Cortisol release from adrenal cortex Sensitizing cells to catecholamines PATHOPHYSIOLOGY
- 12. CLASSIFICATION OF SHOCK •Based on the initiating mechanism. • All states/types are characterized by systemic tissue hypo-perfusion. • Different states may coexist within the same patient.
- 13. CLASSIFICATION OF SHOCK HEMORRHAGIC/ HYPOVOLAEMIC CARDIOGENIC OBSTRUCTIVE DISTRIBUTIVE ENDOCRINE Based on the initiating mechanism
- 14. CLASSIFICATION OF SHOCK •Due to the reduced circulating volume. • Most common form of shock. • It is a component of all other forms of shock. • Causes - HEMORRHAGIC / HYPOVOLEMIC Hemorrhagic Non - Hemorrhagic 1. Poor fluid intake (dehydration) 2. Excessive fluid loss (vomiting, diarrhea) 3. Urinary loss (diabetes) 4. Evaporation 5. Third spacing (Bowel obstruction and pancreatitis)
- 15. CLASSIFICATION OF SHOCK •Due to primary failure of the heart to pump blood to the tissues. • Venous hypertension with pulmonary or systemic edema may coexist with the classical signs of shock. • Causes - 1. Myocardial infarction 2. Cardiac dysrhythmias 3. Valvular heart disease 4. Blunt myocardial injury 5. Cardiomyopathy 6. Myocardial depression caused by endogenous factors (bacterial and humoral agents released in sepsis) or exogenous factors (pharmaceutical agents or drug abuse) CARDIOGENIC
- 16. CLASSIFICATION OF SHOCK •Due to mechanical obstruction of cardiac filling. • Reduction in pre-load leading to low cardiac output. • Causes - 1. Cardiac tamponade 2. Tension pneumothorax 3. Massive pulmonary embolus / air embolus OBSTRUCTIVE
- 17. CLASSIFICATION OF SHOCK •Inadequate organ perfusion is accompanied by vascular dilatation with hypotension, low systemic vascular resistance, inadequate afterload and a resulting abnormally high cardiac output. • There is maldistribution of blood flow at a microvascular level, with arteriovenous shunting and dysfunction of cellular utilization go oxygen. • Can be further classified into - A. Anaphylactic shock - due to histamine release. B. Septic shock - due to release of endotoxins and activation of immune system. C. Neurogenic shock - due to failure of sympathetic outflow and adequate vascular tone. DISTRIBUTIVE
- 18. CLASSIFICATION OF SHOCK •Combination of hypovolemic, cardiogenic and distributive shock. • Causes A. Hypothyroidism - due to disordered vascular and cardiac responsiveness to circulating catecholamines. Cardiac output falls as a result go low inotropy and bradycardia. Associated cardiomyopathy may be present. B. Hyperthyroidism - causes high output cardiac failure. C. Adrenal Insufficiency - due to hypovolemia and a poor response to circulating and exogenous catecholamines. ENDOCRINE
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- 20. RECOGNITION AND DIAGNOSISOF SHOCK • COMPENSATED SHOCK - Body’s cardiovascular and endocrine compensatory responses reduces the flow to non-essential organs like skin, muscle and gastrointestinal tract to preserve preload. There will be adequate compensation to maintain central blood volume and preserve the flow to kidneys, lungs and brain. Clinically occult shock - There may be no clinical signs of hypovolemia apart from tachycardia and cool peripheries (vasoconstriction and circulating catecholamines). Occult hypo-perfusion (metabolic acidosis despite normal urine output and cardiorespiratory vital signs) for more than 12 hours have a significantly higher mortality rate. • DECOMPENSATED SHOCK - Loss of circulating volume overloads age body’s compensatory mechanisms. Loss of around 15% of the circulating volume is within normal compensatory mechanisms. Blood pressure is well maintained. Blood pressure only falls after 30 - 40% of circulating volume has been lost.
- 21. RECOGNITION AND DIAGNOSISOF SHOCK • MILD (COMPENSATED) SHOCK - Tachycardia, tachypnoea, mild reduction in urine output, mild anxiety. Blood pressure is maintained, decrease in pulse pressure. Peripheries are cool and sweaty with prolonged capillary refill times (except in septic distributive shock). • MODERATE SHOCK - Renal compensation mechanism fail, renal perfusion falls and urine output dips below 0.5 mL/kg/hour. Further tachycardia. Blood pressure starts to fall. Drowsy and mildly confused. • SEVERE SHOCK - Profound tachycardia and hypotension. Urine output falls to zero. Unconscious with labored respiration.
- 22. RECOGNITION AND DIAGNOSISOF SHOCK
- 23. RECOGNITION AND DIAGNOSISOF SHOCK • Not a specific marker. • Hypovolemic shock - cool, pale peripheries with prolonged capillary refill times. • Distributive (septic) shock - warm peripheries and capillary refill will be brisk, despite profound shock. CLINICAL FEATURES CAPILLARY REFILL
- 24. RECOGNITION AND DIAGNOSISOF SHOCK • Not always accompany shock. • Patients on beta-blockers or who have implanted pacemakers are unable to mount a tachycardia. • Young patients with penetrating trauma, where there is hemorrhage but little tissue damage, there may be paradoxical bradycardia rather than tachycardia. CLINICAL FEATURES TACHYCARDIA
- 25. RECOGNITION AND DIAGNOSISOF SHOCK • Hypotension is one of the last signs of shock. • Maintained until the final stages of shock by dramatic increase in stroke volume and peripheral vasoconstriction. CLINICAL FEATURES BLOOD PRESSURE
- 26. CLINICAL CONSEQUENCES OFSHOCK • Unresuscitatable shock • Ischemia-reperfusion and systemic inflammatory response syndrome (SIRS) • Multiple organ failure
- 27. CLINICAL CONSEQUENCES OFSHOCK • Profound shock for a prolonged period of time. • Ability of the body to compensate is lost. UNRESUSCITATABLE SHOCK Severe acidemia and hyperkalemia Poor coronary perfusion and myocardial depression Poor cardiac output and limited response to fluids or inotropic therapy Loss of ability to maintain systemic vascular resistance Further hypotension Peripheries no longer respond to appropriate vasopressor agents
- 28. CLINICAL CONSEQUENCES OFSHOCK • Injury occurs once normal circulation is restored. • Only be attenuated by reducing the extent and duration of tissue hypo- perfusion. ISCHAEMIA-REPERFUSION AND SIRS
- 29. CLINICAL CONSEQUENCES OFSHOCK ISCHAEMIA-REPERFUSION AND SIRS Acid and potassium load that has built up released into the circulation Sensed by and activate leukocytes Hypoxia Activation of complement, neutrophils and microvascular thrombi Overwhelms the local anti-inflammatory response Flushed back into the systemic circulation Injury to distant organs Acute lung injury, acute renal injury, cerebral edema, multiple organ failure and death
- 30. CLINICAL CONSEQUENCES OFSHOCK • Defined as two or more failed organ system. • Result of prolonged ischemia and re-perfusion injury is end organ damage and multiple organ failure. • No specific treatment. • Management is support of organ systems, with ventilation, cardiovascular support and hemofiltration/dialysis. • Mortality of 60%. MULTIPLE ORGAN FAILURE
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