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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 BP = CO X PVR Tissue perfusion is driven by blood pressure CO – Cardiac Output PVR – Peripheral Vascular resistance

  5. Cardiac Output CO = SV X HR This means that BP= SV X HR X PVR Blood Pressure = Stroke Volume X Heart Rate X Peripheral Vascular Resistance

  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 • 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? • Circulation cytokines & Inflammatory mediators (e.g. Histamine) • Endotoxins • Drugs (e.g. Nitrates)

  12. Blood Volume Mechanical Obstruction Heart Damage / Rhythm Stroke Volume Heart Rate PVR Blood Pressure

  13. TYPES OF SHOCK HYPOVOLEMIC CARDIOGENIC OBSTRUCTIVE DISTRIBUTIVE

  14. DISTRIBUTIVE SHOCK

  15. Hypovolaemic • Volume Loss • Blood loss -Haemorrhage Plasma Loss -Burns / Pancreatitis ECF Loss - Vomiting & Diarrhoea

  16. Cardiogenic • Pump Failure May be due to • Inability of heart to Contract • Inability of heart to pump blood • Myocardial damage ( M.I) • Arrhythmias • Valvular damage

  17. Distributive • Decreased Peripheral Vascular Resistance • Septic Shock (inflammatory mediators) • Neurogenic Shock (loss of sympathetic vascular tone) • ANAPHYLACTIC shock (presence of vasodilator substances)

  18. PATHOPHYSIOLOGY OF SHOCK

  19. COMPENSATORY MECHANISMS

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

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

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

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

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

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

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

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

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

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

  30. Sympatho-Adrenal Response to Shock • Hypotension stimulates autonomic responses to maintain blood flow and systemic oxygen delivery • 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

  31. Sympatho-Adrenal Response to Shock

  32. Compensatory reactions activated by hemorrhage. • Vasoconstriction • Tachycardia • Venoconstriction • Tachypnea→increased thoracic pumping • Restlessness→increased skeletal muscle pumping (in some cases) • Increased movement of interstitial fluid into capillaries • Increased secretion of norepinephrine and epinephrine • Increased secretion of vasopressin • Increased secretion of renin and aldosterone • Increased secretion of erythropoietin • Increased plasma protein synthesis

  33. Effect of hemorrhage on mean arterial pressure

  34. Sympathetic activation • Tachycardia • Increased myocardial contractility (β1) • α-adrenergic receptor-mediated vasoconstriction (β2-receptor-mediated vasodilatation in skeletal muscle, bronchodialatation ) • Overall increased COP and redistribution of flow: cardiac, cerebral, hepatic and muscle vascular beds

  35. Points to Ponder • Goal is to maintain cerebral and cardiac perfusion • Vasoconstriction of splanchnic, musculoskeletal, and renal blood flow • Compensatory mechanisms are not effective over the long term and fails when shock state is prolonged.

  36. Neuroendocrine response • Release of pituitary hormones such as adrenocorticotrophic hormone (ACTH), vasopressin(antidiuretic hormone, ADH) and endogenous opioid peptides. • There is release of cortisol, which causes fluid retention and antagonizes insulin. • There is release of glucagon, which raises the blood sugar level. • Absolute adrenocortical insufficiency due to bilateral adrenal hemorrhage or necrosis is rare(in septic shock) and that this may be associated with an impaired pressor response to norepinephrine(noradrenaline) and a worsen the prognosis. cause of this phenomenon remain unclear.

  37. Pathophysiology of shockcellular responses Inadequate tissue perfusion Decreased oxygen supply Anaerobic metabolism Accumulation metabolic waste & lactate Cellular failure (limited ATP produce)

  38. BREAK !

  39. 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

  40. 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

  41. 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.

  42. Harmful effects of inflammatory mediators • Damage to cell membranes • Impaired mitochondrial respiration • DNA strand breakage • Apoptosis, which may contribute to the organ damage • Vasodilatation • Maldistribution of regional blood flow • Abnormalities in the microcirculation: – capillaries are obstructed – increased capillary permeability with interstitial oedema. • and immune hypo-responsiveness associated with sepsis. • Coagulation disorders

  43. VICIOUS CYCLE

  44. Understanding Shock • Cellular responses to decreased systemic oxygen delivery • ATP depletion → Na+/ K+ pump dysfunction • Cellular edema – Due to accumulation of Na+ inside the cell • Hydrolysis of cellular membranes and cellular death • Mitochondrial activity severely depressed and lysosomal rupture may occur • Leads to systemic metabolic lactic acidosis that overcomes the body’s compensatory mechanisms

  45. Global Tissue Hypoxia • Endothelial inflammation and disruption • Inability of O2 delivery to meet demand • Result: • Lactic acidosis • Cardiovascular insufficiency • Increased metabolic demands

  46. CLINICAL FEATURES OF SHOCK

  47. Anxiety /Nervousness Dizziness Weakness Faintness Nausea & Vomiting Thirst Confusion Decreased UO Hx of Trauma / other illness Vomiting & Diarrhoea Chest Pain Fevers / Rigors SOB Symptoms of Shock General Symptoms Specific Symptoms

  48. Signs of Shock Pale Cold & Clammy skin Sweating Cyanosis Tachycardia Tachypnoea Confused / Aggiatated Unconscious Hypotensive Stridor / SOB

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