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SM MODS

Deleted user User has deleted their subject information English 57 cards

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  1. 1Definition of shockinadequate tissue perfusion
    resulting in cellular hypoxia and dysfunction
    manifestation of cardiovascular failure
    inability to supply adequate oxygen to match tissue demand
  2. 2Systemic clinical syndrom characterised byhypotension
    hypoperfusion
  3. 33 stages of shock1. compensatory
    2. progressive
    3. refractory
  4. 4Compensatory stagehomeostasis: maintanence of constant internal environemnt in the face of an ever changing external environment
    e.g. constant temp, bp, metabolic rare, blood chem
  5. 5Compensatory mechanismsnervous system response - sends impulses to organs
    endotherlial cells - potent vasocontrictors
    endocrine system - sustained response
  6. 6How do we diagnoses shock?age, history, polypharmacy, major organ tissue perfusion
    high index of suspicion
    Hypotension is sentinal clinical sign (but late sign)
    trends are more significant
  7. 7Sepsisneurogenic
    Distributive
    Obstructive
    Cardiogenic
    hypovolemic
  8. 8Cardiogenic shockmanifests are circulatory failure from cardiac dysfunction
    decrease in CO with evident tissue hypoxia in adequate presence of intravascular volume
    sustained hypotension longer than 30 mins
    commoncly seen by MI, arrthymias, tension pneumothorax
  9. 9Cariogenic shock can be:obstructive: inability of heart to fill adequately, outflow from heart is obstructed
    OR
    Distruptive: normovolemic shock, neurogenic decrease sympathetic tone of BV, anaphylactic, immune reaction, septic, infection associated (bacterial)
  10. 10AMImost common cause of cardiogenic shock
    typical anterior MI
  11. 11Mitral regurgitationtypically inferior MI 2-7days post infarct
    dramatic presentationL acute PO, hypotension, cardiogenic shock
  12. 12Ventricular septic defectanterior MI
    st elevation and pain, acute PO, hypotention, cardiogenic shock
  13. 13Subacute free wall rupture/tamponadeoften present sudden cardiac death
    occassionally preceded by subacute phase
    clinical features: pain, tachycardia, hypotension
  14. 14Reversible myocardial dysfunctionstunned myocardium - represents post-ischaemic dysfunction that persist despite restoration of normal blood flow
    hibernating myocaridum - impaired function due to persistent ischaemia
  15. 15How do we diagnose cardiogenic shock?extensive infarction
    hypotension
    signs of hypoperfusion
  16. 16Clinical features of cardiogenic shockrestless, foncused, hypotensive, diaphoretic, distended neck vains, mumurs, crackles on lung sounds, oluguira, resp alkalosis (hyperventilation), lactic acidosis
  17. 17Management of cardiogenic shockincrease myocardial oxygen supply
    decreased myocardial oxygen demand
    increase CO
    ventilation and intubation
    PVAD - percutaneoue ventricular assist device
    ECMO
    use of inotrope agents
  18. 18Revascularisationprimary PCI associated with lower mortality
    increased blood supply
    interventions:
    improve by reducing pre and after load, and reduce myocardial oxygen demands
  19. 19Hypovolaemic shockmanifests as circulatory failure from loss of circulating volume
    not adequate to fill vascular network
  20. 20MILD, MOD, SEVERE HYPOVOLEMIC SHOCKmild - min tachy, cool extremities, slight drop in BP
    mod - decrease pulse pressure, hypotension, sweating, oliguria
    severe - anuria, acidosis, mental stupor
  21. 21Hypovolaemic shock precipitating events1. trauma causes - Heart ruptures, pelvic fracture
    2. endocrine disorders - diabetes
    3. vascular disorders - anerysms
    4. GI bleeding
    5. pregnancy - related disorders
  22. 22Hypovolaemic shock treatmenetmaximise oxygen delivery
    control further blood loss
    resus
    prevent tissue hypoxia
  23. 23Complications of fluid resusacidosis, hyperkalaemia, infection, hypothermia, PO
  24. 24Neurogenic shockimbalance between parasympathetic and sympathestic stimulation of vascular smooth muscle
    blood pools in venour and capilary beds
    form of distributive shock
    manifests as circulatory failure
    'blood volume has not changed, but space contained fluid has increased'
  25. 25Neuroenic shock clinical manisfestationssevere autonomic dysfunction
    transection of spinal cord
    spinal shock - complete loss of neurologic functino, including reflexes and rectal tone
  26. 26Neurogenic shockhamodynamic triad of hypotension, bradycardia, peripheral vasodilation, resulting from autonomic dysfunction
  27. 27Clinical features and treatment of neurogenic shockABC, spine immobolisation
    aim for adequate tissue perfustion
    urine output more than 30ml/hr
    clinical features: hypotension, flaccid paralysis, bradycardia
  28. 28Distributive - septic shockmost common form of distributive shock
    manifests as circulatory failure sure to infection (sepsis with persistent hypotension)
  29. 29Septic shockmost common is MODS (multi organ dysfunction syndrome)
  30. 30Bacteraemiapresence of pathogens in circulating blood
  31. 31Sepsispresence of SIRS second degree to infection
  32. 32Severe sepsisbody's response to overwhelming infection
    intensified immune response with
    altered tissue perfusion and associated with organ dysfunction and hypoperfusion
  33. 33SIRSSystemic inflammatory response syndrome
    a sepsis like syndrome in which no infectiour process is present
    causes include multiple trauma
  34. 34MODSmultiple organ dysfunction syndrome
    may occur in both sepsis and SIRS
    presence of altered organ dysfunction where homeostasis cannot be maintained without intervention
  35. 35Septic shock2 or more changes in temp, hr, resp, WBC
    septic shock = SIRS + infection + inadequate perfusion
  36. 36Septic shock risk factorsage, malnutrition, age, neutropenia, invasive catheters, surgery
  37. 37Septic shock causes and precipitating eventsevents: factors that affect immune response, infections, bactereamia
    causes: gram + and -, virus, fungi, parasite
  38. 38Gram neg bacteriamost common cause of hospital infection and septic shock
    e.g. escheria coli
    bacteria cause released of endotoxins and other medications which precipitate a series of biochemial reactions
  39. 39Inflammatory medicatorsendotoxins
    TNF
    Interleukins
  40. 40Coagulation abnormalitiesrandom activation of clotting systems
    DIC
    systemic haemorrhage
  41. 41Abnormalities in oxygen requirements uptake and utilisation clinical manisfesationsin sepsis: increased o2 demand due to hypermetabolic state
    cellular hypoxia
    clinical manisfestations - fevers, hypotention, WBC increased, altered CNS
  42. 42Hyperdynamic phasewarm shock - without medical intervention, patient will remain in a warm state
    tachy, oedema, pyrexia, HIGH CO
  43. 43Hypodynamic phase and clinical manifestationscold shock - associated with myocardial failure to myocardial depressant factor
    cold to touch, poor gas exchange, BP unresponsive to inotropes
  44. 44Management of septic shockidentify and treat septic cause
    maintain adequate tissue perfusion
    oxygen demand and supply
    mechanical ventilation - oxygenations
    correct hypovolemia
    antibiotic therapy
    haemodynamic monitoring
    vasopressor - vasopressin
    dialysis
    steriors
  45. 45Sepsis management bundlelow dose steriods
    activated protein C
    glucose control
    inspiratory pressure maintained
  46. 46Early goal directed therapy1. commence ABX
    2. check lactate
    3. insert CVC if lactate high
    4. boluse of crystalloid every 30 minutes
    5. if MAP remains below 65 IV vasopressoes
    6. IF SCVO2 remains less than 70%, RBCs
    7. SVCO2 maintained for 6 hours, intubate and sedate if cannot be
  47. 47Prevention strategiesminimise risk of sepsis to septic shock
    care using invasive procedure
    monitor potential sites of infection
    identify risk patients
    alert early clinical manisfestations such as fever or confusion
  48. 48MODprogressive dysfunction of 2 or more organs caused by uncontrolled inflammatory response
    septic shock most common cause
  49. 49Multi organ failurecellular damage in organs, onset of local injury, activation of immune system
  50. 50Multiple organ dysfunctionresult from reduced cellular performance in shock states
    hypermetabolic response
    DIC
    electroyte imbalances
  51. 51Clinical manisfestations of MODresp - ARDS, dysponea,
    renal - hypoperfusion
    hepatic - increase liver enzymes
    neuro - confusion, fever
    cardio - decrease MAP, SV
    haem - increase bleeding, PT
  52. 52Meninggococcal septicicaemiaa haemorrhagic rash
    blanching macular and rash
    true rigors
    severe pain
    headache
    treat with benzylpenicliin and ceftriaxone
  53. 53management of meniniggoccaol septicaemiaABC, fluids, acid- base balance, treat infection, nutritional and metabolic needs
  54. 54ARDSacute respiratory distress syndrome
    scute diffuse inflammatory lung injury
    leading to increased pulmonary vascular permeabilityand lung weight
    increased dead space
  55. 55Patho and risk factors of ARDSrisk factors - pneumonia, lung contusion, near drowning, inhalation injury
    patho - alveolar capillary membrance disruption with inflammatory cell infiltrate and exudate
  56. 56Resolution of ARDS1. pulmonary oedema from damage to alveocapillary barrier
    2. inflammatory infiltrates
    3. surfactant dysfunction
  57. 57Clinical management of ARDSnutrition, ventilation, PEEP, oxygentation, antibiotics, resuscitate
    prone position improve oxygenation
    glucocorticoids

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User has deleted their subject information Flashcards on SM MODS, created by Deleted user on 29/08/2018.
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  • Created by Elizabeth Then · Aug 29, 2018
  • Copied by Elizabeth Then · Aug 29, 2018
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