1 / 85

SHOCK

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

yeva
Download Presentation

SHOCK

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  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 • 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. 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 ECF Loss - Vomiting & Diarrhoea

  16. Cardiogenic • Pump Failure May be due to • Inability of heart to Contract or • 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 control on vascular tone) • ANAPHYLACTIC shock (presence of vasodilator substances like histamine)

  18. 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)

  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 • 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

  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, 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). • 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. 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 • systemic metabolic lactic acidosis that overcomes the body’s compensatory mechanisms

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

  45. BREAK !

  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

  49. HypovolaemicShock

More Related