Critical Care: Shock (including septic shock) Flashcards
Shock (definition)
cellular dyxoxia: diminished blood circulation -> anaerobic metabolism and hypoperfusion -> end organ dysfunction
CNS manifestation of end organ dysfunction
- encephalopathy
- cortical necrosis
Cardiac manifestation of end organ dysfunction
- tachycardia, bradycardia
- ventricular ectopy
- myocaridal ischemia/depression
Pulmonary manifestation of end organ dysfunction
- acute respiratory failure
- acute respiratory distress syndrome
what systems can experience end organ dysfunction shock
- CNS
- cardiac
- pulmonary
- renal
- GI
- hepatic
- hematologic
- metabolic
- immune system
Renal manifestation of end organ dysfunction
- Pre renal insult
- AKI
- ATN
GI manifestation of end organ dysfunction
- Erosive gasttritis
- ileus
- pancreatitis
Hepatic manifestation of end organ dysfunction
- Ischemic hepatitis
- cholestais
- “shock” liver
Hematologic manifestation of end organ dysfunction
- disseminated intravascular coagulation
- dilutional thrombocytopenia
Metaolic manifestation of end organ dysfunction
- Hyperglycemia (then hypo)
- glycogenolysis
- glyconeogeneis
- hypertriglyceridemia
immune sstem manifestation of end organ dysfunction
- gut barrier function
- cellular and humoral immunity depression
clincal presentation of shock (think labs)
- lactate > 2
- SVO2 < 60%
- SCVO2 < 65%
- SBP <90 (or 40 below baseline)
- MAP < 65
- urine output < 0.5 ml/kg/hr
MAP calculation
KNOW
(1/3 SBP) + (2/3 DBP)
Goals of shock treatment
labs
- MAP > 65
- lactate < 2
- SVO2 > 60%
- SCVO2 > 65%
- PCWP 12-15
PCWP
- pulmonary capillary wedge pressure
- correlates with preload
Hypovolemic shock as decribed by PCWP, CO, SVR, SVO2
- PCWP: decreased
- CO: decreased
- SVR: increased
- SVO2: decreased
Less volume in body -> decreased CO (CO = SVR * HR) -> compensatory increase in SVR
Cardiogenic shock as described by PCWP, CO, SVR, SVO2
KNOW
- PCWP: increased
- CO: decreased
- SVR: increased
- SVO2: decreased
failure of LV (pump) -> fluid backed up in left side of heart -> increased PCWP and decreased CO (CO = SVR * HR) -> compensatory increase in SVR
Distributive shock as described by PCWP, CO, SVR, SVO2
- PCWP: decreased
- CO: increased then decreased
- SVR: decreased
- SVO2: increased then decreased
vasodilation (KNOW) is a decrease in SVR (CO = SVR * HR) -> initial compensatory increase in CO and SVO2, however this is unstainable end
obstructive shock as described by PCWP, CO, SVR, SVO2
- PCWP: increased
- CO: decreased
- SVR: increased
- SVO2: decreased
Decrease in LV stroke volume (KNOW) or outflow obstruction (inability to pump bood for non-cardiogenic reason)
Causes of hypovolemic shock and general treatment
- hemorrhage - PRBC (KNOW)
- GI loss - fluids
- severe dehydration - fluids
- third spacing - fluids
- burns - fluids
Causes of cardiogenic shock and general treatment
- acute MI (KNOW) - revascularization/CABG
- arrhythmias - achieve sinus rhythm
- end stage HF
- valve failure/disease
- dilated cardiomyopathy
Causes of distribute shock
- SEPSIS (KNOW)
- anaphylaxis
- neurogenic
- thyroid insufficiency
- adrenal insufficiency
- hepatic insuffiency
Causes of obsturcive shock and general treatment
- PE (KNOW) - thrombolytic therapy (alteplase)
- severe pulonary HTN
- tension pneumothorax - needle decompression
- pericardial tamponade - drain fluid
Approach to fluids in shock
- fluids increase SV, CO, and DO2
- crystalloids preffered over colloids (LR)
-
30 ml/kg over 15-30 min then 10 ml/kg boluses
- if pt has cardiogenic shock: 100-200 mL boluses
when to start vasoactive agents in treating shock pts
start AFTER fluid MAP is still < 65
required lines
- arterial line if possible for monitoring
- CVC for admin
vasopressors vs. inotropes
- chronotropy: rate of contraction
- inotropy: contractile strength
NE MOA
KNOW
alpha adrenergic agonst (and a lil beta 1)
increase peripheral vasoconstriction (alpha MOA)-> inrease MAP
beta 1 MOA
HR, stroke volume
beta 2 MOA
- contration strength
- vasodilaton
- bronchial relaxation
alpha 1 MOA
vasoconstriction -> increase MAP
NE use in shock
- the golden child, our favorite in most cases dt beter side effect profile (however may vasoconstrict too much, so monitor)
- high dose may be neede din septic shock dt endogenous down regulation of alpha receptors
epinephrine mOA
alpha (at high dose) and beta adrenergic agonist
- Increase in HR and stroke volume (beta 1)
- Increase in MAP (both secondary to the beta 1 effect and alpha 1 effect)
epinephrine use in shock
- secondary choice in sepsis
- useful in anaphylactic shock dt beta 2 (bronchial relaxaton)
epinephrine ADR
aeroic lactate production -> makes it hard to see if pt’s own lactate is going down
DA MOA
dose dependent
- low dose: DA - vasodilation, icnrease in renal blood flow, GFR, and Na excretion
- medium dose: beta 1 - HR, stroke volume
- high dose: alpha 1 - vasoconstriciton
DA use in shock
- not really used dt ADR (tachycarida and arrhythmias (KNOW) )
- most effective in hypotensive pts with decreased cardiac function
phenylephrine MOA
KNOW
selective alpha 1 agonist
peripheral vasoconstriction (can go overboard and induce reflex bradycardia (KNOW))
phenylprine use in shock
KNOW
not recomended i shock unless CO is high and BP is persistenly low
vasopressin use in shock
antidiuretic hormone; KNOW
used with vasopressors (catecholamines) to reduce the dose required
do NOT use alone in sepsis
angiotensin II use in shock
- Added on after we’ve already tried one or two vasopressors; the idea is to redued catecholamine vasopressors
- risk for thromboembolism (KNOW)
dobutamine MOA
KNOW
produceds inotropic action via beta 1
dobutamine use in shock
KNOW
added to catecholinae treatment when CO, SVO2/SCVO2 goals have not been achieved
septic shock management
- correctoin of underlying caused (abx and source control)
- fluid resuscitation
- vasopressors
- inotropes
- CS
sepsis
life threatening organ dysfuction causd b a dysregulated host response to infection
septic shock
subset of sepsis with profound circulatory, cellular, and metabolic abnormaities
SIRS criteria
KNOW
at least 2 of the following
- temp > 38C or < 36C
- HR > 90
- RR > 20
- WBC > 12 or < 4
qSOFA score
KNOW
rapid bedside score - at least 2 of the following
* SBP <100 mmHg
* RR > 22
* Altered mentaton
like SIRS
sepsis shock - 1 hr bundle
- measure lactate level (remeasure if > 2)
- obtain blood cultures before admin of ABX
- admin broad spectrum ABX
- if hypotension or lactate > 4: admin 30ml/kg of crystallloid over 15-30 min followed by 10 ml/kg boluses prn (if pt potnetially has cardiogenic shock, avoid the prn, but still give the initial)
- consider vasopressors (goal MAP > 65mmHg; if MAP > 65 with serum lactate > 2mmol/L AND no hypovolemia → give vasopressors)
when to provide MRSA coverage for empiric septic shock
KNOW
- stuff that would make you thinnk mrsa (hx, recurrent infection)
- hospital: IV abx, recent hosptal admit
- more prone: invasive device, hemodilysis
- bad bad infection
when to use 2 gra neg agents for empiric septic shock cvoerage
KNOW
high risk for MDR (multi drug resistant bugs)
- proven infection or colonization of MDR in past year
- area: travel to highly endemic country in past 90 days; local prevalence resistant organisms
- hospital: hospital acquired; recent broad spectrum IV ABX in past 90 days
goal of fluid admin in septic shock
- increase SV, CO, DO2
- rehydrate intravascular space (that’s what’s usually dehdyrated in sepsis)
why type of fluid is preferred in septic shck
- crystalloids (LR and NS)
- albumin (colloid) can be added if pt requried substantial amounts of crystalloids
starches NOT recommended dt inncreased risk of mortality, AKI, bleed
how does cortisol improve psyioglogic response to stress
- regulation of pro-inflammatory state
- inhibition of inducible nitric oxide synthesis (iNOS)
- revereses adrenergic receptor desnsitiation
- incease Na and wate retetion(icrease intravascular volume)
when wouold you consider hydrocortisone in septic hock
- dded after poor response to fluids and vasopressors (refractory shock)
- improves time to shock resolution and increased in vasopressor days
- recommended when there is ongoing need for vasopressors
- though usually added when pt is hypotensive despite increasing NE dose and/or initiatoin of vasopressin
hydrocortisone dosing for septic shock
- 200mg IV QD 3-7D
- 50mg IV Q6H OR 200mg/day as continuous infusion
- taper off over 2-3 days wehn shock is resolved
