Pathopysiology of Shock

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

• State of cardiovascular dysfunction
• generalized inadequate tissue
  perfusion oxygenation
• relative to metabolic requirements

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Circulatory Shock

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

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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 or Cardiac Output filling
  pressure)

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Clinical Types of Circulatory Shock

• Neurogenic-spinal cord trauma
  peripheral vasodilatation
• Anaphylactic- allergic rxn
  peripheral vasodilatation

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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

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Aetiology of Cardiogenic Shock

• Myocardial Infarction (most common)
• Valve Failure
• Myocarditis
• Cardiomyopathy
• Cardiac Tamponade

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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

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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

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Pathogenesis

• Haemodynamic metabolic changes result from
• Low Cardiac Output
• Hypotension
• Stagnant Hypoxia

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Circulatory Effects

• Circulating Blood Volume
• CVP, PVP
• VR
• SV, CO
• aBP

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Compensatory Responses

• CVP aBP
• HR, myocardial contractility
• Generalized vaso/venoconstriction
• Flow skin, kidney, splanchnic organs
• Release adrenal catecholamines

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Physiological Circulations

• Vital Circulation
• Brain
• Heart
• Lungs
• Adrenals

• Standard Circulation
• Skin/Musculo-Skeletal
• Kidneys
• GIT

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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

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Renal Vasoconstriction

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

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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.

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Circulatory Shock

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

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Metabolic/Endocrine Changes

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

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Metabolic/Endocrine Changes

• Ishaemia/Impaired tissue perfusion
• Anaerobic Metab Lactic Acidosis
• ATP
• Failure Cell Membrane Na/K pump

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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.

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

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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

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Special Features of Cardiogenic Shock

• insufficient cardiac output i.e. CO
• despite
• adequate ventricular filling press i.e.
• CVP

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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)

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Treatment of Shock

• Resuscitation-A,B,Cs
• Early vigorous infusion fluids (crystalloids,
  colloids, plasma, blood)
• Monitoring- HR, BP, RR, UO, mental state, Temp,
  CVP (R ventricular preload), PCWP (LEDV)

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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)

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Prognosis Hypovolaemic Shock

• Depends on
• Underlying cause
• Severity
• Duration
• Patients age
• Pre-existing disease

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Prognosis Hypovolaemic Shock

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