SM MODS

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Flashcards on SM MODS, created by Elizabeth Then on 29/08/2018.
Elizabeth Then
Flashcards by Elizabeth Then, updated more than 1 year ago
Elizabeth Then
Created by Elizabeth Then over 5 years ago
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Question Answer
Definition of shock inadequate tissue perfusion resulting in cellular hypoxia and dysfunction manifestation of cardiovascular failure inability to supply adequate oxygen to match tissue demand
Systemic clinical syndrom characterised by hypotension hypoperfusion
3 stages of shock 1. compensatory 2. progressive 3. refractory
Compensatory stage homeostasis: maintanence of constant internal environemnt in the face of an ever changing external environment e.g. constant temp, bp, metabolic rare, blood chem
Compensatory mechanisms nervous system response - sends impulses to organs endotherlial cells - potent vasocontrictors endocrine system - sustained response
How 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
Sepsis neurogenic Distributive Obstructive Cardiogenic hypovolemic
Cardiogenic shock manifests 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
Cariogenic 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)
AMI most common cause of cardiogenic shock typical anterior MI
Mitral regurgitation typically inferior MI 2-7days post infarct dramatic presentationL acute PO, hypotension, cardiogenic shock
Ventricular septic defect anterior MI st elevation and pain, acute PO, hypotention, cardiogenic shock
Subacute free wall rupture/tamponade often present sudden cardiac death occassionally preceded by subacute phase clinical features: pain, tachycardia, hypotension
Reversible myocardial dysfunction stunned myocardium - represents post-ischaemic dysfunction that persist despite restoration of normal blood flow hibernating myocaridum - impaired function due to persistent ischaemia
How do we diagnose cardiogenic shock? extensive infarction hypotension signs of hypoperfusion
Clinical features of cardiogenic shock restless, foncused, hypotensive, diaphoretic, distended neck vains, mumurs, crackles on lung sounds, oluguira, resp alkalosis (hyperventilation), lactic acidosis
Management of cardiogenic shock increase myocardial oxygen supply decreased myocardial oxygen demand increase CO ventilation and intubation PVAD - percutaneoue ventricular assist device ECMO use of inotrope agents
Revascularisation primary PCI associated with lower mortality increased blood supply interventions: improve by reducing pre and after load, and reduce myocardial oxygen demands
Hypovolaemic shock manifests as circulatory failure from loss of circulating volume not adequate to fill vascular network
MILD, MOD, SEVERE HYPOVOLEMIC SHOCK mild - min tachy, cool extremities, slight drop in BP mod - decrease pulse pressure, hypotension, sweating, oliguria severe - anuria, acidosis, mental stupor
Hypovolaemic shock precipitating events 1. trauma causes - Heart ruptures, pelvic fracture 2. endocrine disorders - diabetes 3. vascular disorders - anerysms 4. GI bleeding 5. pregnancy - related disorders
Hypovolaemic shock treatmenet maximise oxygen delivery control further blood loss resus prevent tissue hypoxia
Complications of fluid resus acidosis, hyperkalaemia, infection, hypothermia, PO
Neurogenic shock imbalance 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'
Neuroenic shock clinical manisfestations severe autonomic dysfunction transection of spinal cord spinal shock - complete loss of neurologic functino, including reflexes and rectal tone
Neurogenic shock hamodynamic triad of hypotension, bradycardia, peripheral vasodilation, resulting from autonomic dysfunction
Clinical features and treatment of neurogenic shock ABC, spine immobolisation aim for adequate tissue perfustion urine output more than 30ml/hr clinical features: hypotension, flaccid paralysis, bradycardia
Distributive - septic shock most common form of distributive shock manifests as circulatory failure sure to infection (sepsis with persistent hypotension)
Septic shock most common is MODS (multi organ dysfunction syndrome)
Bacteraemia presence of pathogens in circulating blood
Sepsis presence of SIRS second degree to infection
Severe sepsis body's response to overwhelming infection intensified immune response with altered tissue perfusion and associated with organ dysfunction and hypoperfusion
SIRS Systemic inflammatory response syndrome a sepsis like syndrome in which no infectiour process is present causes include multiple trauma
MODS multiple organ dysfunction syndrome may occur in both sepsis and SIRS presence of altered organ dysfunction where homeostasis cannot be maintained without intervention
Septic shock 2 or more changes in temp, hr, resp, WBC septic shock = SIRS + infection + inadequate perfusion
Septic shock risk factors age, malnutrition, age, neutropenia, invasive catheters, surgery
Septic shock causes and precipitating events events: factors that affect immune response, infections, bactereamia causes: gram + and -, virus, fungi, parasite
Gram neg bacteria most 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
Inflammatory medicators endotoxins TNF Interleukins
Coagulation abnormalities random activation of clotting systems DIC systemic haemorrhage
Abnormalities in oxygen requirements uptake and utilisation clinical manisfesations in sepsis: increased o2 demand due to hypermetabolic state cellular hypoxia clinical manisfestations - fevers, hypotention, WBC increased, altered CNS
Hyperdynamic phase warm shock - without medical intervention, patient will remain in a warm state tachy, oedema, pyrexia, HIGH CO
Hypodynamic phase and clinical manifestations cold shock - associated with myocardial failure to myocardial depressant factor cold to touch, poor gas exchange, BP unresponsive to inotropes
Management of septic shock identify 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
Sepsis management bundle low dose steriods activated protein C glucose control inspiratory pressure maintained
Early goal directed therapy 1. 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
Prevention strategies minimise 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
MOD progressive dysfunction of 2 or more organs caused by uncontrolled inflammatory response septic shock most common cause
Multi organ failure cellular damage in organs, onset of local injury, activation of immune system
Multiple organ dysfunction result from reduced cellular performance in shock states hypermetabolic response DIC electroyte imbalances
Clinical manisfestations of MOD resp - ARDS, dysponea, renal - hypoperfusion hepatic - increase liver enzymes neuro - confusion, fever cardio - decrease MAP, SV haem - increase bleeding, PT
Meninggococcal septicicaemia a haemorrhagic rash blanching macular and rash true rigors severe pain headache treat with benzylpenicliin and ceftriaxone
management of meniniggoccaol septicaemia ABC, fluids, acid- base balance, treat infection, nutritional and metabolic needs
ARDS acute respiratory distress syndrome scute diffuse inflammatory lung injury leading to increased pulmonary vascular permeabilityand lung weight increased dead space
Patho and risk factors of ARDS risk factors - pneumonia, lung contusion, near drowning, inhalation injury patho - alveolar capillary membrance disruption with inflammatory cell infiltrate and exudate
Resolution of ARDS 1. pulmonary oedema from damage to alveocapillary barrier 2. inflammatory infiltrates 3. surfactant dysfunction
Clinical management of ARDS nutrition, ventilation, PEEP, oxygentation, antibiotics, resuscitate prone position improve oxygenation glucocorticoids
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