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SHOCK PRESENTATION PPT EASY WAY TO UNDERSTAND
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- 2. SHOCK SHOCK A clinical syndromethat results from A clinical syndrome that results from inadequate tissue perfusion inadequate tissue perfusion Hypo perfusion tissue hypoxia Hypo perfusion tissue hypoxia Cellular dysfunction and injury Cellular dysfunction and injury Release of mediators of inflammation Release of mediators of inflammation Further aggravation of hypo perfusion Further aggravation of hypo perfusion Vicious cycle Vicious cycle
- 3. SHOCK SHOCK Clinical manifestationsattributable to Clinical manifestations attributable to 1) sympathetic neuro endocrine responses 1) sympathetic neuro endocrine responses 2) impaired organ function due to cellular 2) impaired organ function due to cellular injury injury Clinical hallmark of shock – Clinical hallmark of shock – HYPOTENSION HYPOTENSION i.e. a i.e. a MAP < 60 mmhg MAP < 60 mmhg in in previously normotensive patient previously normotensive patient
- 4. Types of Shock Typesof Shock 1) Hypo volemic 1) Hypo volemic 2) Traumatic 2) Traumatic 3) Cardiogenic – intrinsic , compressive 3) Cardiogenic – intrinsic , compressive 4) Septic – hyper / hypo dynamic 4) Septic – hyper / hypo dynamic 5) Neurogenic 5) Neurogenic 6) Hypo adrenal 6) Hypo adrenal
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- 6. Introduction Introduction Most commonform of shock Most common form of shock Caused by:- Caused by:- 1. Loss of RBC mass and plasma 1. Loss of RBC mass and plasma (hemorrhagic) (hemorrhagic)
- 7. Introduction Introduction 2. Loss ofplasma alone 2. Loss of plasma alone (non (non hemorrhagic) hemorrhagic) Extra vascular fluid sequestration Extra vascular fluid sequestration GIT losses GIT losses Urinary losses Urinary losses Insensible losses Insensible losses
- 8. Physiologic response Physiologic response AIMS:- AIMS:- 1.Restore effective circulating blood volume 1. Restore effective circulating blood volume 2. Maintain perfusion to the brain and heart 2. Maintain perfusion to the brain and heart Increased sympathetic activity Increased sympathetic activity - Tachycardia - Tachycardia - Tachypnoea - Tachypnoea - Collapse of venous capacitance vessels - Collapse of venous capacitance vessels
- 9. Physiologic response Physiologic response Release of stress hormones Release of stress hormones Expansion of intravascular volume Expansion of intravascular volume - Recruitment of interstitial and - Recruitment of interstitial and intracellular fluid intracellular fluid - Reduction in urine output - Reduction in urine output
- 10. Clinical Features Clinical Features Vary according to the amount of blood Vary according to the amount of blood volume lost volume lost Younger healthy patients tolerate larger Younger healthy patients tolerate larger volumes of blood loss volumes of blood loss Elderly patients have decreased ability Elderly patients have decreased ability to tolerate hemorrhage to tolerate hemorrhage Effect of medications Effect of medications
- 11. Clinical Features Clinical Features Mild Hypovolemia Mild Hypovolemia (<20% of blood (<20% of blood volume) volume) Mild tachycardia Mild tachycardia Few other signs especially in a supine Few other signs especially in a supine young patient young patient
- 12. Clinical Features Clinical Features Moderate Hypovolemia Moderate Hypovolemia (20 to 40% of (20 to 40% of blood volume) blood volume) Tachycardia increases Tachycardia increases Anxiety Anxiety BP – normal / postural hypotension BP – normal / postural hypotension
- 13. Clinical Features Clinical Features Severe Hypovolemia Severe Hypovolemia (> 40% of blood (> 40% of blood volume) volume) Classic signs of shock seen Classic signs of shock seen BP decreases, even in supine position BP decreases, even in supine position Marked tachycardia Marked tachycardia Oliguria Oliguria Agitation and confusion Agitation and confusion
- 14. Clinical Features Clinical Features Perfusion of the CNS is maintained till Perfusion of the CNS is maintained till shock becomes severe. Mental shock becomes severe. Mental obtundation is an ominous sign obtundation is an ominous sign
- 15. CLINICAL FEATURES CLINICAL FEATURES MILD MILD (<20% Blood (< 20% Blood Volume ) Volume ) MODERATE MODERATE (20 – 40%) (20 – 40%) SEVERE SEVERE (>40% (>40% Blood Volume) Blood Volume) Cool Cool extremities extremities Inc. capillary Inc. capillary refill time refill time Diaphoresis Diaphoresis Collapsed Collapsed veins veins Anxiety Anxiety Tachycardia Tachycardia Tachypnea Tachypnea Postural Postural hypotension hypotension oliguria oliguria Marked Marked tachycardia tachycardia Hypotension Hypotension Haemodynami Haemodynami c instability c instability Mental status Mental status deterioration deterioration
- 16. DIAGNOSIS DIAGNOSIS Easy whensource of volume loss is Easy when source of volume loss is obvious and there is haemodynamic obvious and there is haemodynamic instability instability May be difficult when source of volume May be difficult when source of volume loss is occult or when plasma volume loss is occult or when plasma volume alone is depleted alone is depleted
- 17. DIAGNOSIS DIAGNOSIS Shock ina trauma victim or post operative Shock in a trauma victim or post operative patient should be presumed to be due to patient should be presumed to be due to hemorrhage until proved otherwise hemorrhage until proved otherwise In Trauma – understanding the patterns of In Trauma – understanding the patterns of injury helps to direct the evaluation and injury helps to direct the evaluation and management management
- 18. DIAGNOSIS DIAGNOSIS Penetrating trauma Penetratingtrauma – source of – source of bleeding is usually located along the bleeding is usually located along the path of the wounding object. path of the wounding object. Operative intervention is required if Operative intervention is required if there are features of shock there are features of shock
- 19. DIAGNOSIS DIAGNOSIS Blunt trauma– Blunt trauma – may have multiple may have multiple sources of potential hemorrhage sources of potential hemorrhage Blood loss sufficient to cause shock Blood loss sufficient to cause shock usually occurs in the following sites:- usually occurs in the following sites:- - External - External - Intrabdominal – commonest - Intrabdominal – commonest contd… contd…
- 20. DIAGNOSIS DIAGNOSIS - Intrathoracic - Intrathoracic -Retroperitoneal - Retroperitoneal - extremities - extremities
- 21. DIAGNOSIS DIAGNOSIS The siteof bleeding should be looked The site of bleeding should be looked for aggressively and treated for aggressively and treated Severe hypovolemia, if untreated, leads Severe hypovolemia, if untreated, leads to irreversible cell injury and death to irreversible cell injury and death Time frame available is very narrow Time frame available is very narrow
- 22. DIAGNOSIS DIAGNOSIS Non trauma Nontrauma – usually the site of loss is – usually the site of loss is the GIT the GIT
- 23. DIAGNOSIS DIAGNOSIS Hypovolemic v/s cardiogenicshock Hypovolemic v/s cardiogenic shock Both forms have a similar picture Both forms have a similar picture Presence of raised JVP, rales, S3 gallop Presence of raised JVP, rales, S3 gallop rhythm in cardiogenic shock rhythm in cardiogenic shock Definitive therapy differs significantly Definitive therapy differs significantly Volume expansion is undesirable in Volume expansion is undesirable in cardiogenic shock cardiogenic shock
- 24. Treatment Treatment Initial treatmentis empiric Initial treatment is empiric Instituted concurrently along with Instituted concurrently along with diagnostic evaluation diagnostic evaluation Time is of essence Time is of essence Aims:- Aims:- Rapid re-expansion Rapid re-expansion Control ongoing losses Control ongoing losses
- 25. Treatment Treatment 1. 1. Volume Resuscitation VolumeResuscitation Place large bore IV lines Place large bore IV lines Rapid infusion of Normal Saline / Rapid infusion of Normal Saline / Ringer’s lactate solution Ringer’s lactate solution No distinct benefit demonstrated from No distinct benefit demonstrated from use of colloids use of colloids
- 26. Treatment Treatment Infusion of2 to 3 liters should restore Infusion of 2 to 3 liters should restore normal haemodynamic parameters, if the normal haemodynamic parameters, if the bleeding has stopped bleeding has stopped If haemodynamic instability persists If haemodynamic instability persists ? Ongoing losses / inadequate replacement ? Ongoing losses / inadequate replacement
- 27. Treatment Treatment Inadequate replacement Inadequate replacement Blood transfusion – if Hb < 10gm% with Blood transfusion – if Hb < 10gm% with continuing blood loss continuing blood loss Fully cross matched blood preferred Fully cross matched blood preferred In extreme emergencies, type specific In extreme emergencies, type specific or ‘O’ negative packed red cells may be or ‘O’ negative packed red cells may be given given
- 28. Treatment Treatment Ongoing losses Ongoing losses – –prompt surgical intervention required prompt surgical intervention required to control persistent bleeding, usually to control persistent bleeding, usually from a large vessel. from a large vessel.
- 29. Treatment Treatment Patients whorespond to initial Patients who respond to initial resuscitation but then deteriorate also resuscitation but then deteriorate also have injuries that require control by have injuries that require control by surgery or interventional radiology surgery or interventional radiology
- 30. Treatment Treatment Persistent haemodynamicinstability Persistent haemodynamic instability despite control of bleeding and despite control of bleeding and restoration of intravascular volume restoration of intravascular volume Presence of the trauma triad of Presence of the trauma triad of hypothermia, acidosis and hypothermia, acidosis and coagulopathy coagulopathy Mortality inevitable Mortality inevitable
- 31. Treatment Treatment 2. Ionotropic support 2.Ionotropic support Dopamine, vasopressin and Dopamine, vasopressin and dobutamine dobutamine To maintain adequate ventricular To maintain adequate ventricular performance, after blood volume has performance, after blood volume has been replaced been replaced
- 32. Treatment Treatment 3. Support ofrespiratory function 3. Support of respiratory function Also required for successful Also required for successful resuscitation resuscitation Supplemental oxygen Supplemental oxygen Endotracheal intubation, if required Endotracheal intubation, if required
- 33. Treatment Treatment 4) 4) Adjunctivemeasures Adjunctive measures Positioning Positioning PASG and MAST PASG and MAST Re warming Re warming
- 34. Treatment Treatment Recovery afterresuscitation from Recovery after resuscitation from hemorrhagic shock is usually better hemorrhagic shock is usually better than following Septic or traumatic shock than following Septic or traumatic shock – because of less severe activation of – because of less severe activation of the inflammatory mediator response the inflammatory mediator response system system
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- 36. TRAUMATIC SHOCK TRAUMATIC SHOCK Caused by bleeding and loss of plasma Caused by bleeding and loss of plasma in the injured tissues in the injured tissues In addition – In addition – injury induced injury induced inflammatory responses inflammatory responses contribute to contribute to secondary micro circulatory injury secondary micro circulatory injury Mal distribution of blood flow Mal distribution of blood flow Tissue hypoxia and MOSF Tissue hypoxia and MOSF
- 37. Traumatic Shock -Treatment Traumatic Shock - Treatment A – ensure airway A – ensure airway B – breathing and adequate ventilation B – breathing and adequate ventilation C – restore blood volume, support C – restore blood volume, support circulation circulation Control haemorrhage Control haemorrhage Reduce inflammatory response by Reduce inflammatory response by fracture stabilization, debridement and fracture stabilization, debridement and haematoma evacuation haematoma evacuation
- 38. HYPO ADRENAL SHOCK HYPOADRENAL SHOCK
- 39. HYPO ADRENAL SHOCK HYPOADRENAL SHOCK Causes Causes :- :- 1) Chronic exogenous steroid intake 1) Chronic exogenous steroid intake 2) Prolonged critical state 2) Prolonged critical state 3) Idiopathic atrophy of adrenals 3) Idiopathic atrophy of adrenals 4) other causes of adrenal insufficiency 4) other causes of adrenal insufficiency like Tuberculosis , bilateral like Tuberculosis , bilateral haemorrhage, metastases and haemorrhage, metastases and amyloidosis amyloidosis
- 40. TREATMENT- Hypo adrenalshock TREATMENT- Hypo adrenal shock Steroids – Dexamethasone / Steroids – Dexamethasone / Hydrocortisone Hydrocortisone Volume resuscitation Volume resuscitation Vasopressor support Vasopressor support
- 41. Conclusion Conclusion What isshock What is shock Hypovolemic shock – commonest type Hypovolemic shock – commonest type Hemorrhagic / non hemorrhagic Hemorrhagic / non hemorrhagic Shock in a trauma victim / post Shock in a trauma victim / post operative patient should be considered operative patient should be considered due to bleeding unless disproved due to bleeding unless disproved
- 42. Conclusion Conclusion C/F dependupon volume of blood loss C/F depend upon volume of blood loss Untreated severe hypovolemia leads to Untreated severe hypovolemia leads to cell injury and death cell injury and death Diagnosis may be difficult when the Diagnosis may be difficult when the blood loss is not external blood loss is not external
- 43. Conclusion Conclusion The patternof injury may help to The pattern of injury may help to discover site of blood loss discover site of blood loss Therapy aims at re-expansion of Therapy aims at re-expansion of intravascular volume and control of intravascular volume and control of ongoing losses, along with supportive ongoing losses, along with supportive measures measures
Editor's Notes
- #3 MAP – 1/3 of pulse pressure plus diastolic BP