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SM MODS
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- 1Definition of shockinadequate tissue perfusion
resulting in cellular hypoxia and dysfunction
manifestation of cardiovascular failure
inability to supply adequate oxygen to match tissue demand - 2Systemic clinical syndrom characterised byhypotension
hypoperfusion - 33 stages of shock1. compensatory
2. progressive
3. refractory - 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 - 5Compensatory mechanismsnervous system response - sends impulses to organs
endotherlial cells - potent vasocontrictors
endocrine system - sustained response - 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 - 7Sepsisneurogenic
Distributive
Obstructive
Cardiogenic
hypovolemic - 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 - 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) - 10AMImost common cause of cardiogenic shock
typical anterior MI - 11Mitral regurgitationtypically inferior MI 2-7days post infarct
dramatic presentationL acute PO, hypotension, cardiogenic shock - 12Ventricular septic defectanterior MI
st elevation and pain, acute PO, hypotention, cardiogenic shock - 13Subacute free wall rupture/tamponadeoften present sudden cardiac death
occassionally preceded by subacute phase
clinical features: pain, tachycardia, hypotension - 14Reversible myocardial dysfunctionstunned myocardium - represents post-ischaemic dysfunction that persist despite restoration of normal blood flow
hibernating myocaridum - impaired function due to persistent ischaemia - 15How do we diagnose cardiogenic shock?extensive infarction
hypotension
signs of hypoperfusion - 16Clinical features of cardiogenic shockrestless, foncused, hypotensive, diaphoretic, distended neck vains, mumurs, crackles on lung sounds, oluguira, resp alkalosis (hyperventilation), lactic acidosis
- 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 - 18Revascularisationprimary PCI associated with lower mortality
increased blood supply
interventions:
improve by reducing pre and after load, and reduce myocardial oxygen demands - 19Hypovolaemic shockmanifests as circulatory failure from loss of circulating volume
not adequate to fill vascular network - 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 - 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 - 22Hypovolaemic shock treatmenetmaximise oxygen delivery
control further blood loss
resus
prevent tissue hypoxia - 23Complications of fluid resusacidosis, hyperkalaemia, infection, hypothermia, PO
- 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' - 25Neuroenic shock clinical manisfestationssevere autonomic dysfunction
transection of spinal cord
spinal shock - complete loss of neurologic functino, including reflexes and rectal tone - 26Neurogenic shockhamodynamic triad of hypotension, bradycardia, peripheral vasodilation, resulting from autonomic dysfunction
- 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 - 28Distributive - septic shockmost common form of distributive shock
manifests as circulatory failure sure to infection (sepsis with persistent hypotension) - 29Septic shockmost common is MODS (multi organ dysfunction syndrome)
- 30Bacteraemiapresence of pathogens in circulating blood
- 31Sepsispresence of SIRS second degree to infection
- 32Severe sepsisbody's response to overwhelming infection
intensified immune response with
altered tissue perfusion and associated with organ dysfunction and hypoperfusion - 33SIRSSystemic inflammatory response syndrome
a sepsis like syndrome in which no infectiour process is present
causes include multiple trauma - 34MODSmultiple organ dysfunction syndrome
may occur in both sepsis and SIRS
presence of altered organ dysfunction where homeostasis cannot be maintained without intervention - 35Septic shock2 or more changes in temp, hr, resp, WBC
septic shock = SIRS + infection + inadequate perfusion - 36Septic shock risk factorsage, malnutrition, age, neutropenia, invasive catheters, surgery
- 37Septic shock causes and precipitating eventsevents: factors that affect immune response, infections, bactereamia
causes: gram + and -, virus, fungi, parasite - 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 - 39Inflammatory medicatorsendotoxins
TNF
Interleukins - 40Coagulation abnormalitiesrandom activation of clotting systems
DIC
systemic haemorrhage - 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 - 42Hyperdynamic phasewarm shock - without medical intervention, patient will remain in a warm state
tachy, oedema, pyrexia, HIGH CO - 43Hypodynamic phase and clinical manifestationscold shock - associated with myocardial failure to myocardial depressant factor
cold to touch, poor gas exchange, BP unresponsive to inotropes - 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 - 45Sepsis management bundlelow dose steriods
activated protein C
glucose control
inspiratory pressure maintained - 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 - 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 - 48MODprogressive dysfunction of 2 or more organs caused by uncontrolled inflammatory response
septic shock most common cause - 49Multi organ failurecellular damage in organs, onset of local injury, activation of immune system
- 50Multiple organ dysfunctionresult from reduced cellular performance in shock states
hypermetabolic response
DIC
electroyte imbalances - 51Clinical manisfestations of MODresp - ARDS, dysponea,
renal - hypoperfusion
hepatic - increase liver enzymes
neuro - confusion, fever
cardio - decrease MAP, SV
haem - increase bleeding, PT - 52Meninggococcal septicicaemiaa haemorrhagic rash
blanching macular and rash
true rigors
severe pain
headache
treat with benzylpenicliin and ceftriaxone - 53management of meniniggoccaol septicaemiaABC, fluids, acid- base balance, treat infection, nutritional and metabolic needs
- 54ARDSacute respiratory distress syndrome
scute diffuse inflammatory lung injury
leading to increased pulmonary vascular permeabilityand lung weight
increased dead space - 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 - 56Resolution of ARDS1. pulmonary oedema from damage to alveocapillary barrier
2. inflammatory infiltrates
3. surfactant dysfunction - 57Clinical management of ARDSnutrition, ventilation, PEEP, oxygentation, antibiotics, resuscitate
prone position improve oxygenation
glucocorticoids
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- El usuario ha eliminado su información de asignaturas Fichas sobre SM MODS, creado por Usuario eliminado el 29/08/2018.
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- Creado por Elizabeth Then · 29 ago 2018
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