shock states Flashcards
what is SIRS?
unchecked out of control systemic response of inflammatory/immune system- warning sign of what is to come
SIRS criteria
diagnosis: 2+ presentHR gt 90RR gt 20 -or- PaCO2 lt 32T lt 36 -or- gt 38leuk- WBC lt 4k -or- gt 12k- OR gt 10% immature neutrophilsin high risk pts that can’t be explained by other causes
SIRSinsult → pathophysiology x4
peripheral vasodilationcapillary permeabilitymicrovascular clottingcellular activation
what is shock?
broad categoryinitiated by insult → inadequate tissue perfusion comp to cell metabo reqs → cellular hypoxia + end organ dysfxn
what is compensated shock?
relatively stable may see early s/s shockcompensatory mechanisms: moderately effectivecause:- rapidly corrected = minimal residual effects- not corrected → uncompensated
what is MODS? x3
uncompensated shock worsens → MODSinvolves 2+ organ systems (that weren’t previously failing)altered organ function in acutely ill patientsorgan system homeostasis cannot be achieved without interventioncompensatory mechanisms from compensated shock NO LONGER ADEQUATE
geriatric population & shock
- progression rapid- reduced compensatory mechanisms- pre-existing comorbs (renal failure, lung disease, cardiomyopathy) INTERVENE STATE
present in every type of shock
inadequate tissue perfsuion & cellular hypoxia
hemodynamic goals of therapy for shock x7
- MAP gt 60- CVP 8-12- CI gt 2.1- UOP gt 0.5 mg/kg/hr- SaO2 gt 92%- SVO2 gt 70- serum lactate lt 2 mmol/L
hypovolemic shock causes
- ABL/ongoing hemorrhage- non-hemorrhage fluid depletion– GI (v/d)– burns– polyuria– aggressive pharm diuresis– insensible losses
can lose how much via insensible losses + how?
1L/day; diaphoresis, open burn wounds, vents
hypovolemic shock is
loss or redistribution of volume… (blood, plasma, or other body fluids) which result in decreased intravascular volume
obstructive shock is
mechanical obstruction impacting the cardiovascular system… that decreases ventricular filling and/or emptyingend result: ↓ CO, tissue perfusion, O2 delivery
obstructive shock causes
↓ ventricular filling =- cardiac tamponade- tension pneumothorax- vena cava compression/thrombus- atrial mass or thrombus↓ ventricular emptying- PE (saddle embolism = sitting across either/both arteries)
saddle embolism is
thrombus sitting across either/both arteriescauses ↓ ventricular emptying → obstructive shock
cardiogenic shock is
occurs when heart fails as a pump↓ contractility → ↓ SVwhich leads to ↓ CO, BP → ↓ tissue perfusion
cardiogenic shock causes
MI !!!!!!!!HFrEF exacerbation (ischemic v nonischemic)dysrhythmias (poor O2 at first, can exacerbate cardiogenic shock states)LV outflow tract obstruction (hypertrophic obstructive cardiomyopathy, muscle/tumor overgrowth is pretty uncommon)
1 cause of cardiogenic shock
MI
neurogenic shock is…
typically results from SCI w damaged symp pathways, usually seen in injuries T6 or higher- higher injury = greater symptoms- common in trauma or neuro patients↓ symp of organs distal to injury = stimulated by PS toneresults: bradycardia, massive vasodilation, inability to regulate body temp (hypothermia)EASIEST SHOCK TO SPOT
anaphylactic shock is…
life threatening allergic reaction resulting in IgE mediated response or mast cell (non-IgE degranulation)- occurs following reexposure to specific antigen- immediate response causing release of histamines, prostaglandins, vasoactive mediatorsresults: massive vasodilation, capillary permeability, constriction of non-vascular smooth muscle (RESPIRATORY!!)triggers: drugs, foods, other (see lecture)s/s: see lecture
*SEPSIS *
SIRS likely s/t infection; positive cultures add to validity but not required
SEVERE SEPSIS
sepsis + at least 1 sign of hypoperfusion or organ dysfunction (new, not explained by other etiology)
SEPTIC SHOCKmust know definition + pathophys/results
severe sepsis associated with refractory hypotension (BP lt 90/60) despite adequate fluid resus and/or serum lactate gt 4.0—release: endotoxins trigger overzealous release of inflammatory mediators (cytokines, interleukins, tumor necrosis factor, complement system)results: systemic vasodilation, widespread endothelial injury, activation of coagulation cascade
septic shock pathophys + results
release: endotoxins trigger overzealous release of inflammatory mediators (cytokines, interleukins, tumor necrosis factor, complement system)results: systemic vasodilation, widespread endothelial injury, activation of coagulation cascade
inflammatory response: goal of vasodilation
increase availability of - nutrients (O2, glucose)- neutrophils, macrophages, and their mediatorsto injured area
inflammatory response: goal of microvascular permeability
increase availability of - nutrients- cells- mediatorsto injured area
inflammatory response: goal of coagulation
- minimize blood loss- wall off injury
inflammatory response: goal of cellular activation
WBCs –>- phagocytosis foreign debris + cells- wound microdebridement
SIRS mediators: inflammatory cells
neutrophilsmacrophagesmast cellsendothelial cellsplatelets
SIRS mediators: biochemical mediators
- tumor necrosis factor (TNF)- interleukins- platelet activating factor- arachidonic acid metabolites prostaglandins, leukotrienes, thromboxanes- toxic oxygen radicals- proteases
SIRS mediators: plasma protein systems
- complement system- kinin- coagulation- fibrinolysis
organ dysfunction and SIRS
ORGAN DYSFUNCTION STARTS EARLY
SIRS mediators x3
biochemical mediatorsinflammatory cellsplasma protein systems
