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Pathopysiology of Shock

Pathopysiology of Shock. Dr H. Harding-Goldson Lecturer/Consultant, Sec. Anesthesia & Intensive Care, UWI. Circulatory Shock. State of cardiovascular dysfunction generalized inadequate tissue perfusion & oxygenation relative to metabolic requirements.

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Pathopysiology of Shock

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  1. Pathopysiology of Shock Dr H. Harding-Goldson Lecturer/Consultant, Sec. Anesthesia &Intensive Care, UWI

  2. Circulatory Shock • State of cardiovascular dysfunction generalized inadequate tissue perfusion & oxygenation relative to metabolic requirements

  3. Circulatory Shock • Tissue hypoxia progressive failure cellular metabolism. • initially reversible but if not corrected, progresses to irreversible multiple organ failure & death

  4. Clinical Types of Circulatory Shock • Hypovolaemic- circulating blood volume (15-25%) with inadequate L ventricular preload • Cardiogenic- myocardial failure (insufficient cardiac output despite adequate ventricular filling press) • Septic- peripheral vasodilatation (usu N orCardiac Output & filling pressure)

  5. Clinical Types of Circulatory Shock • Neurogenic-spinal cord trauma peripheral vasodilatation • Anaphylactic- allergic rxn peripheral vasodilatation

  6. Aetiology of Hypovolaemic Shock • Heamorrhage- commonest cause • Internal shifts of Plasma/Body Fluids-ac pancreatitis, intestinal obstruction • External Loss Protein-free ECF-burns, severe vomiting/diarrhoea, fistulae, excessive diuresis

  7. Aetiology of Cardiogenic Shock • Myocardial Infarction (most common) • Valve Failure • Myocarditis • Cardiomyopathy • Cardiac Tamponade

  8. Aetiology of Septic Shock • Usu severe infection, bacteremia • Gram neg organisms • May occur as aftermath of cardiogenic or hypovolaemic shock • Unlike other types, often assd with other pathological complications eg ac respiratory failure, pulmonary oedema, DIC

  9. Pathopysiology of Circulatory Shock • Most of the cellular changes & compensatory mechanisms are common to all forms of shock but the detailed pathophysiological changes & clinical picture may vary • Hypovolaemic shock- prototype of clinical shock

  10. Pathogenesis Haemodynamic & metabolic changes result from: • Low Cardiac Output • Hypotension • Stagnant Hypoxia

  11. Circulatory Effects Circulating Blood Volume • CVP, PVP • VR • SV, CO • aBP

  12. Compensatory Responses CVP & aBP • HR, myocardial contractility • Generalized vaso/venoconstriction • Flow skin, kidney, splanchnic organs • Release adrenal catecholamines

  13. Physiological Circulations • Vital Circulation • Brain • Heart • Lungs • Adrenals • Standard Circulation • Skin/Musculo-Skeletal • Kidneys • GIT

  14. Vascular Volume Tendency to restore Vascular Volume by: • Influx interstitial fluid bec intracapillary hydrostatic press • Activation Renin-angiotensin-aldosterone mechanism • Release ADH (post pituitary), renal tubular reabsorption of water

  15. Renal Vasoconstriction • GFR, Urine Output • Activation renin-angiotensin-aldosterone mechanism • Peripheral Vasoconstriction • Na+ tubular reabsorption

  16. Circulatory Shock • The above responses are compensatory & protective. • In severe & continued shock, decompensatory changes supervene, irreversibility & death. • Irreversibility mainly dependent on degree & duration hypotension, adequacy of treatment.

  17. Circulatory Shock • While the CV fluctuations, because of their urgency receive more attention, the metabolic/endocrine changes probably determine irreversibility

  18. Metabolic/Endocrine Changes Mainly result of: • generalized stagnant hypoxia & peripheral anaerobic metabolism • neuroendocrine activity (activation sympathoadrenal/ant. Pituitary-adrenal cortical systems)

  19. Metabolic/Endocrine Changes Ishaemia/Impaired tissue perfusion Anaerobic Metab Lactic Acidosis ATP Failure Cell Membrane Na+/K+ pump

  20. Metabolic/Endocrine Changes • Cytotoxic, vasodilator, vasoactive substances ( histamine, serotonin, kinins, lysosomal enzymes) released into circulation • Progressive vasodilation, myocardial depression, increased capillary permeability, intravascular coagulation, multi-organ failure & death.

  21. Possible Mechanism in Development Irreversible Shock Shock Stimulus Lysosomal Activation, Release Proteases Splitting of Plasma Proteins Vasoactive Peptides, Amines etc Hypotension, Fluid Loss IrreverisibleSHOCK

  22. Metabolic/Endocrine Changes • BMR, Body temp • Altered CHO Metab; blood glu (release Adr), later marked (hepatic failure) • Anaerobic glycolysis, blood lactate, pH, metabolic acidosis • Protein Catabolism, blood N2, NH4 • plasma catecholamines, 17 (OH) ketosteroids, plasma K+

  23. Clinical Features • Clinical History • Restless, confused, apathetic • Pallor skin/mm • Cold, sweaty • Rapid, weak, thready pulse (PR 140/min) • Low BP (85/40) • shell temp • Hyperventilation/Feeble respirations • Oliguria/ Anuria

  24. Special Features of Cardiogenic Shock • insufficient cardiac output i.e. CO despite • adequate ventricular filling press i.e. CVP

  25. Special Features of Septic Shock • Hyperdynamic state with • peripheral vasodilatation & PVR • usu N or Cardiac Output (CO) & filling pressure (CVP) • Pt flushed (vs pallor) & warm (vs cold, clamy)

  26. Treatment of Shock • Resuscitation-A,B,C’s • Early & vigorous infusion fluids (crystalloids, colloids, plasma, blood) • Monitoring- HR, BP, RR, UO, mental state, Temp, CVP (R ventricular preload), PCWP (LEDV)

  27. Specific Treatment Drugs • Alpha-vasoconstrictors eg meteraminol, methoxamine, noradr- (disadv further restrict peripheral tissue perfusion, increase cardiac afterload) • Inotropes eg adr, noradr, dobutamine, dopamine (if evidence myocardial involvement) Intra-aortic Balloon Counterpulsation (IABC)

  28. Prognosis Hypovolaemic Shock Depends on • Underlying cause • Severity • Duration • Patient’s age • Pre-existing disease

  29. Prognosis Hypovolaemic Shock • maintenance of a high cardiac output • adequate oxygen delivery • early, aggressive resuscitation • an underlying correctable cause are associated with improved survival

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