WEEK 6 (SHOCK)

• What is SHOCK?

  • imbalance between demand and supply of glucose + O2
  • impair ability to metabolise normally
  • normal = AEROBIC
  • abnormal = ANAEROBIC
• What is inadequate cardiac output?

  PUMP:

  • inadequate preload
  • contractility
  • HR
  • excessive afterload

  BLOOD VESSELS:

  • dilation without fluid change
  • inadequate SVR (diastole)

  FLUID:

  • hypovolaemia
  • fluid imbalance
• What is AEROBIC METABOLISM?

  stage 1:

  • glucose converted to pyruvic acid
  • no O2 needed, produces 2 ATP

  stage 2:

  • pyruvic acid undergoes oxidation via Kreb's cycle
  • requires O2, produces 36 ATP
  • byproducts of H2O and CO2
• What is ANAEROBIC METABOLISM?

  • cellular demand for O2 is more than supply
  • only stage 1 occurs
  • pyruvate acid concerted to lactic acid
  • can lead to acidosis
  • sodium accumulates inside cell and H2O follows = cell ruptures and snowball effect
• How to measure PERFUSION STATUS?

  • HR
  • RR
  • BP + PP + MAP
  • Skin
  • Temp
  • GCS
• What is CARDIAC OUTPUT?

  the volume of blood ejected from the heart per min. CO = HR x SV
• What is BLOOD PRESSURE?

  • pressure inside the arteries
  • BP = CO x SVR
  • SYSTOLIC = max pressure inside the arteries during contraction of the heart (SV)
  • DIASTOLE = max pressure inside the arteries during relaxation of the heart (SVR)
• What is PULSE PRESSURE?

  • SBP - DBP = PP (30-40mmHg)
  • increased DBP = vasoconstriction
  • decreased DBP = vasodilationNARROW PP = caused by shock. Less blood returning to the heart = decreased SV (decreased SBP)

  NARROW PP:

  • caused by shock = less blood returning to heart = decreased SV (decreased SBP)
  • sympathetic compensation = vasoconstriction = increased SVR (increased DBP)
  • decreased SBP + increased DBP = narrow PP

  WIDE PP:

  • vasodilation from distributive shock = decreased SVR (decreased DBP)
  • sympathetic activation = increase HR = maintaining SBP
  • same SBP + decreased DBP = wide PP
• What is MAP?

  • the average arterial pressure throughout the body during the cardiac cycle
  • MAP = DBP + (SBP - DBP)/3 = 70-100mmHG
  • end-organ perfusion requires >60mmHg otherwise they die
• How to recognise severity?

  • age + weight
  • MOI
  • comorbidities
  • medications
  • injuries
  • perfusion status
• What happens during COMPENSATED SHOCK?

  • activation of compensatory mechanisms = attempt to increase perfusion + ATP
  • normal or 'near normal' vital signs
  • requires more energy to maintain = peripheral vasoconstriction
• What happens during DECOMPENSATED SHOCK?

  • unable to produce enough energy to maintain compensatory mechanisms
  • pathological processes + complications progress too far to maintain CO
  • hypoperfusion worsens
  • abnormal vital signs = HoTN, ALOC (from decreased cerebral perfusion), increased tachy or brady
  • increased HR + RR until they drop
  • decreased BP, PP narrows
  • slow CRT
• What happens during IRREVERSIBLE SHOCK?

  • profound organ dysfunction (even if you correct shock they will die)
  • no clear vital signs to differentiate
• What are the components of COMPENSATED SHOCk?

  1. increase blood flow to major organs = prevent irreversible damage
  2. progressive vasoconstriction = shunt flow to important organs
  3. increase HR + strength of contractions = attempt to increase SV
  4. increased RR + bronchodilation = increase O2 for perfusion + ATP, prevent acidosis
  5. decreased urine output = decrease energy use, RAAS (increase fluid retention = increase circulating volume)
  6. influenced by CO + SVR

  • neuronal = increase sympathetic pathways (fast + less sustained)
  • endocrine = HPA Axis + RAAS (slow + profound)
• What are FEEDBACK MECHANISMS?

  • CO + SVR are maintained via the baroreceptor and chemoreceptor reflexes

  BARORECEPTORS:

  • located in carotid sinus + aortic arch
  • sensitive to pressure changes
  • sympathetic increases occur with decreased pressure

  CHEMORECEPTORS:

  • located within carotid and aortic bodies
  • sensitive to O2, CO2 + pH changes
  • sympathetic increase occurs with decreased O2, increased CO2 and/or low pH
  • hypoxia, hypercapnia or acidosis
• What are NEURONAL MECHANISMS?

  • hypothalamus initiates stimulation of adrenal medulla to secrete adrenaline and noradrenaline.
  • adrenaline binds to target organs and tissues

  A1 = systemic vasoconstriction, gluconeogenesis + glycogenolysis

  B1 = increase HR, contraction and conduction

  B2 = bronchodilation, mast cell stabilisation, gluconeogenesis + glycogenolysis
• What are HORMAL MECHANISMS - HPA AXIS?

  • In states of stress the hypothalamus releases CRH and ADH (vasopressin)
  • CRH instructs pituitary gland to release ATCH = promotes release of cortisol via adrenal cortex

  CORTISOL:

  • increases supply of energy to cells = increases metabolic demands
  • stimulates gluconeogenesis, glycogenolysis and lipolysis
  • increase Na+ reabsorption at kidneys
  • ADH = vasopressin = increase reabsorption of H2O = increase blood volume = increase SVR + SV = increase CO
• What are HORMONAL MECHANISMS - RAAS?

  Renin converts angiotensinogen (found in liver) into angiotensin-1. When angiotensin-1 interacts with ACE it is converted to angiotensin-2 (found in lungs)

  This increases vasoconstriction, Na+ reabsorption, aldosterone secretion and release of vasopressin.
• What is ARDS?

  • occurs 12-24hr after the onset of severe shock
  • lethal form of pulmonary injury
  • fluids + plasma leak into alveoli
  • reduced gas exchange
  • lung stiffness
  • alveolar collapse
  • acidosis + hypoperfusion leads to destruction of pulmonary epithelial cells + walls = increased permeability + break down of structures
  • severe dyspnoea
  • if proteins leave the blood into the alveoli this causes an osmotic gradient = increase alveolar pressure = fluid moves into alveoli = pulmonary oedema
• What happens if shock continues?

  • metabolites increase = increase acidosis
  • pre-capillary sphincters dilate (post = constrict) = fluid accumulation
  • increase capillary hydrostatic pressure
  • fluid loss from intravascular to interstitial
  • decrease vascular volume, decrease preload, decrease CO
  • cellular necrosis
  • death
• What is DIC?

  • clotting disorder + hormonal coagulation factor imbalance
  • wide spread clotting + bleeding = petechiae + purpura
  • systemic coagulation + occlusion of midsize vessels
  • clotting factors become exhausted = major bleeding
  • meningococcal septicaemia + septic shock
• What is MODS?

  • progressive dysfunction of 2+ organ systems
  • progresses to organ failure + death
  • occurs during severe sepsis