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SHOCK

SHOCK. Dr.Mohammed Sharique Ahmed Quadri Assistant Prof.Physiology Almaarefa College. WHAT IS SHOCK?.

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SHOCK

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  1. SHOCK Dr.MohammedSharique Ahmed Quadri Assistant Prof.Physiology Almaarefa College

  2. WHAT IS SHOCK? • Shock is the term used to describe acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalized cellular hypoxia and/or an inability of the cells to utilize oxygen. Inadequate Tissue Perfusion SHOCK IS A SYNDROME THAT CAN OCCUR IN THE COURSE OF MANY LIFE THREATENING TRAUMATIC CONDITIONS OR DISEASE STATES

  3. Or it can be define simply as A clinical state in which tissues do not receive adequate blood flow and O2 to meet their metabolic needs.

  4. Physiological Principles MAP = CO X PVR Tissue perfusion is driven by mean arterial pressure MAP CO – Cardiac Output PVR – Peripheral Vascular resistance

  5. Cardiac Output CO = SV X HR This means that MAP= SV X HR X PVR Blood Pressure = Stroke Volume X Heart Rate X Peripheral Vascular Resistance • MAP= DP+ 1/3 PP and normal value for adult is between 60 and 110 mm Hg • Normal adult CO is about 5 L/ min& is equal for both ventricles

  6. Stroke Volume Stroke Volume • Volume of Blood pumped by the heart during 1 cycle What affects Stroke volume? Rhythm Problems Blood Volume Heart Muscle Damage MechanicalObstruction Mechanical Obstruction

  7. What makes up blood volume Plasma RBCs Platelets WBCs

  8. What Alters Blood Volume? • Haemorrhage • Plasma Loss • Loss /Redistribution of Extracellular Volume

  9. Heart Rate • Heart rate increases as a compensatory response to Shock Heart rate too fast to allow adequate refilling of heart between beats

  10. Peripheral Vascular Resistance PVR regulated by ARTERIOLAR tone. Dilatation opens Arteriovenous beds & increases volume of circulatory system

  11. What Alters PVR? • Circulating cytokines & Inflammatory mediators (e.g. Histamine) • Endotoxins • Drugs (e.g. Nitrates)

  12. So tissue and cellular perfusion is dependent on • Adequate preload • Functioning heart • Intact blood vessels

  13. TYPES OF SHOCK HYPOVOLEMIC CARDIOGENIC OBSTRUCTIVE DISTRIBUTIVE

  14. Pathophysiology: Overview Tissue perfusion is determined by Mean Arterial Pressure (MAP) MAP = CO x SVR Heart rate Stroke Volume

  15. Hypovolemic Shock: Pathophysiology Heart pumps well, but not enough blood volume to pump MAP = CO x SVR HR x Stroke volume

  16. Hypovolemic Shock:Pathophysiology Normal MAP = CO x SVR Hypovolemic MAP = ↓CO x SVR MAP = ↓CO x ↑SVR ↓MAP = ↓↓CO x ↑SVR

  17. Hypovolemic Shock: Causes ↓MAP =↓CO (HR x Stroke Volume) x ↑SVR Decreased Intravascular volume (Preload) leads to Decreased Stroke Volume Hemorrhagic - trauma, GI bleed, AAA rupture, ectopic pregnancy Hypovolemic - burns, GI losses, dehydration, third spacing (e.g. pancreatitis, bowel obstruction), Adesonian crisis, Diabetic Ketoacidosis

  18. Cardiogenic Shock: Pathophysiology Heart fails to pump blood out MAP = CO x SVR HR Stroke Volume

  19. Cardiogenic Shock: Pathophysiology Heart fails to pump blood out MAP = CO x SVR HR Stroke Volume

  20. Cardiogenic Shock: Pathophysiology Normal MAP = CO x SVR Cardiogenic MAP = ↓CO x SVR MAP = ↓CO x ↑SVR ↓MAP = ↓↓CO x ↑SVR

  21. Cardiogenic Shock: Causes ↓MAP =↓CO (HR x Stroke Volume) x ↑SVR Decreased Contractility (Myocardial Infarction, myocarditis, cardiomypothy, Post resuscitation syndrome following cardiac arrest) Mechanical Dysfunction – (Papillary muscle rupture post-MI, Severe Aortic Stenosis, rupture of ventricular aneurysms etc) Arrhythmia – (Heart block, ventricular tachycardia, SVT, atrial fibrillation etc.) Cardiotoxicity (B blocker and Calcium Channel Blocker Overdose)

  22. Obstructive Shock: Pathophysiology Heart pumps well, but the output is decreased due to an obstruction (in or out of the heart) MAP = CO x SVR HR x Stroke volume

  23. Obstructive Shock:Pathophysiology Normal MAP = CO x SVR Obstructive MAP = ↓CO x SVR MAP = ↓CO x ↑SVR ↓MAP = ↓↓CO x ↑SVR

  24. Obstructive Shock: Causes ↓MAP =↓CO (HR x Stroke Volume) x ↑SVR Heart is working but there is a block to the outflow Massive pulmonary embolism Aortic dissection Cardiac tamponade Tension pneumothorax Obstruction of venous return to heart Vena cava syndrome - eg. neoplasms, granulomatous disease Sickle cell splenic sequestration

  25. Distributive Shock: Pathophysiology Heart pumps well, but there is peripheral vasodilation due to loss of vessel tone MAP = CO x SVR HR x Stroke volume

  26. Distributive Shock:Pathophysiology Normal MAP = CO x SVR Distributive MAP = co x ↓SVR MAP = ↑co x ↓SVR ↓MAP = ↑co x ↓↓SVR

  27. Distributive Shock: Causes ↓MAP = ↑CO (HR x SV) x↓SVR • Loss of Vessel tone • Inflammatory cascade • Sepsis and Toxic Shock Syndrome • Anaphylaxis • Post resuscitation syndrome following cardiac arrest • Decreased sympathetic nervous system function • Neurogenic - C spine or upper thoracic cord injuries • Toxins • Due to cellular poisons -Carbon monoxide, methemoglobinemia, cyanide • Drug overdose (a1 antagonists)

  28. PATHOPHYSIOLOGY OF SHOCK • The manifestation of shock reflects both • The impaired perfusion of body tissue & • The body’s attempt to maintain tissue perfusion (compensatory mechanism) • So the pathophysiology of shock can be explained as cellular hypoxia resulting from impaired tissue perfusion

  29. COMPENSATORY MECHANISMS

  30. Compensatory mechanism and shock AFTER-LOAD PRE-LOAD Fluid Volume (CVP/JVP) Cardiac Output (SV x HR) Vascular Diameter (SVR)

  31. Hypovolaemic shock AFTER-LOAD PRE-LOAD Fluid Volume (CVP/JVP) Cardiac Output (SV x HR) Vascular Diameter (SVR) 1

  32. Hypovolaemic shock AFTER-LOAD PRE-LOAD Fluid Volume (CVP/JVP) Cardiac Output (SV x HR) Vascular Diameter (SVR) 1 2

  33. Hypovolaemic shock AFTER-LOAD PRE-LOAD Fluid Volume (CVP/JVP) Cardiac Output (SV x HR) Vascular Diameter (SVR) 1 2 3

  34. Cardiogenic shock AFTER-LOAD PRE-LOAD Fluid Volume (CVP/JVP) Cardiac Output (SV x HR) Vascular Diameter (SVR) 1

  35. Cardiogenic shock AFTER-LOAD PRE-LOAD Fluid Volume (CVP/JVP) Cardiac Output (SV x HR) Vascular Diameter (SVR) 1 2

  36. Cardiogenic shock AFTER-LOAD PRE-LOAD Fluid Volume (CVP/JVP) Cardiac Output (SV x HR) Vascular Diameter (SVR) 3 1 2

  37. Distributive shock AFTER-LOAD PRE-LOAD Fluid Volume (CVP/JVP) Cardiac Output (SV x HR) Vascular Diameter (SVR) 1

  38. Distributive shock AFTER-LOAD PRE-LOAD Fluid Volume (CVP/JVP) Cardiac Output (SV x HR) Vascular Diameter (SVR) 2 1

  39. Distributive shock AFTER-LOAD PRE-LOAD Fluid Volume (CVP/JVP) Cardiac Output (SV x HR) Vascular Diameter (SVR) 2 3 1

  40. Sympatho-Adrenal Response to Shock • Most immediate of compensatory mechanisms are those of sympathetic nervous system and renin angiotensin mechanism • Sympathetic nervous system • NE, epinephrine, and cortisol release • Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac output) • Renin-angiotensin axis • Water and sodium conservation and vasoconstriction • Increase in blood volume and blood pressure

  41. Sympatho-Adrenal Response to Shock

  42. Neuroendocrine response • Release of pituitary hormones such as adrenocorticotrophic hormone (ACTH), vasopressin(antidiuretic hormone, ADH). • There is release of cortisol, which causes fluid retention and antagonizes insulin. • There is release of glucagon, which raises the blood sugar level.

  43. Release of Pro- and Anti InflammatoryMediators Trigger an exaggerated inflammatory response (systemic activation of leucocytes & release of potentially damaging ‘mediators’) • Severe infection (bacteraemia/endotoxaemia), • Presence of large areas of damaged tissue (following trauma /extensive surgery) • Prolonged episodes of hypoperfusion

  44. Release of Pro- and Anti InflammatoryMediators (continued) • Pro inflammatory Mediators: • Proteases • Toxic free radicals & other reactive oxygen species • Cytokines • IL • TNF • Platelet activating factor • Hypotension, Inc. vascular permeability, platelet aggregation. • Anti inflammatory mediators: • Interleukin 10 ( IL-10) Are involved in leukocyte adhesion ,local inflammation, neutrophil activation, fever, lactic acidosis, ventilation perfusion abnormalities

  45. Release of Pro- and Anti InflammatoryMediators (continued) • Although beneficial when targeted against local areas of infection or necrotic tissue--dissemination of this ‘innate immune’ response can produce shock and widespread tissue damage. • Characteristically the initial episode of overwhelming inflammation is followed by a period of immune suppression--- increased risk of developing secondary infections.

  46. TO BE CONTINUED TOMORROW THANK YOU

  47. CLINICAL FEATURES OF SHOCK

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