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PHM 703: Crit Care/Heme/Onc > Critical Care: Shock (including septic shock) > Flashcards

Critical Care: Shock (including septic shock) Flashcards

1
Q

Shock (definition)

A

cellular dyxoxia: diminished blood circulation -> anaerobic metabolism and hypoperfusion -> end organ dysfunction

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2
Q

CNS manifestation of end organ dysfunction

A
  • encephalopathy
  • cortical necrosis
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3
Q

Cardiac manifestation of end organ dysfunction

A
  • tachycardia, bradycardia
  • ventricular ectopy
  • myocaridal ischemia/depression
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4
Q

Pulmonary manifestation of end organ dysfunction

A
  • acute respiratory failure
  • acute respiratory distress syndrome
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5
Q

what systems can experience end organ dysfunction shock

A
  • CNS
  • cardiac
  • pulmonary
  • renal
  • GI
  • hepatic
  • hematologic
  • metabolic
  • immune system
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6
Q

Renal manifestation of end organ dysfunction

A
  • Pre renal insult
  • AKI
  • ATN
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7
Q

GI manifestation of end organ dysfunction

A
  • Erosive gasttritis
  • ileus
  • pancreatitis
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8
Q

Hepatic manifestation of end organ dysfunction

A
  • Ischemic hepatitis
  • cholestais
  • “shock” liver
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9
Q

Hematologic manifestation of end organ dysfunction

A
  • disseminated intravascular coagulation
  • dilutional thrombocytopenia
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10
Q

Metaolic manifestation of end organ dysfunction

A
  • Hyperglycemia (then hypo)
  • glycogenolysis
  • glyconeogeneis
  • hypertriglyceridemia
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11
Q

immune sstem manifestation of end organ dysfunction

A
  • gut barrier function
  • cellular and humoral immunity depression
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12
Q

clincal presentation of shock (think labs)

A
  • lactate > 2
  • SVO2 < 60%
  • SCVO2 < 65%
  • SBP <90 (or 40 below baseline)
  • MAP < 65
  • urine output < 0.5 ml/kg/hr
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13
Q

MAP calculation

KNOW

A

(1/3 SBP) + (2/3 DBP)

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14
Q

Goals of shock treatment

labs

A
  • MAP > 65
  • lactate < 2
  • SVO2 > 60%
  • SCVO2 > 65%
  • PCWP 12-15
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15
Q

PCWP

A
  • pulmonary capillary wedge pressure
  • correlates with preload
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16
Q

Hypovolemic shock as decribed by PCWP, CO, SVR, SVO2

A
  • PCWP: decreased
  • CO: decreased
  • SVR: increased
  • SVO2: decreased

Less volume in body -> decreased CO (CO = SVR * HR) -> compensatory increase in SVR

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17
Q

Cardiogenic shock as described by PCWP, CO, SVR, SVO2

KNOW

A
  • 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

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18
Q

Distributive shock as described by PCWP, CO, SVR, SVO2

A
  • 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

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19
Q

obstructive shock as described by PCWP, CO, SVR, SVO2

A
  • 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)

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20
Q

Causes of hypovolemic shock and general treatment

A
  • hemorrhage - PRBC (KNOW)
  • GI loss - fluids
  • severe dehydration - fluids
  • third spacing - fluids
  • burns - fluids
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21
Q

Causes of cardiogenic shock and general treatment

A
  • acute MI (KNOW) - revascularization/CABG
  • arrhythmias - achieve sinus rhythm
  • end stage HF
  • valve failure/disease
  • dilated cardiomyopathy
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22
Q

Causes of distribute shock

A
  • SEPSIS (KNOW)
  • anaphylaxis
  • neurogenic
  • thyroid insufficiency
  • adrenal insufficiency
  • hepatic insuffiency
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23
Q

Causes of obsturcive shock and general treatment

A
  • PE (KNOW) - thrombolytic therapy (alteplase)
  • severe pulonary HTN
  • tension pneumothorax - needle decompression
  • pericardial tamponade - drain fluid
24
Q

Approach to fluids in shock

A
  • 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
25
Q

when to start vasoactive agents in treating shock pts

A

start AFTER fluid MAP is still < 65

required lines
- arterial line if possible for monitoring
- CVC for admin

26
Q

vasopressors vs. inotropes

A
  • chronotropy: rate of contraction
  • inotropy: contractile strength
27
Q

NE MOA

KNOW

A

alpha adrenergic agonst (and a lil beta 1)

increase peripheral vasoconstriction (alpha MOA)-> inrease MAP

28
Q

beta 1 MOA

A

HR, stroke volume

29
Q

beta 2 MOA

A
  • contration strength
  • vasodilaton
  • bronchial relaxation
30
Q

alpha 1 MOA

A

vasoconstriction -> increase MAP

31
Q

NE use in shock

A
  • 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
32
Q

epinephrine mOA

A

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)
33
Q

epinephrine use in shock

A
  • secondary choice in sepsis
  • useful in anaphylactic shock dt beta 2 (bronchial relaxaton)
34
Q

epinephrine ADR

A

aeroic lactate production -> makes it hard to see if pt’s own lactate is going down

35
Q

DA MOA

A

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

36
Q

DA use in shock

A
  • not really used dt ADR (tachycarida and arrhythmias (KNOW) )
  • most effective in hypotensive pts with decreased cardiac function
37
Q

phenylephrine MOA

KNOW

A

selective alpha 1 agonist

peripheral vasoconstriction (can go overboard and induce reflex bradycardia (KNOW))

38
Q

phenylprine use in shock

KNOW

A

not recomended i shock unless CO is high and BP is persistenly low

39
Q

vasopressin use in shock

antidiuretic hormone; KNOW

A

used with vasopressors (catecholamines) to reduce the dose required

do NOT use alone in sepsis

40
Q

angiotensin II use in shock

A
  • Added on after we’ve already tried one or two vasopressors; the idea is to redued catecholamine vasopressors
  • risk for thromboembolism (KNOW)
41
Q

dobutamine MOA

KNOW

A

produceds inotropic action via beta 1

42
Q

dobutamine use in shock

KNOW

A

added to catecholinae treatment when CO, SVO2/SCVO2 goals have not been achieved

43
Q

septic shock management

A
  • correctoin of underlying caused (abx and source control)
  • fluid resuscitation
  • vasopressors
  • inotropes
  • CS
44
Q

sepsis

A

life threatening organ dysfuction causd b a dysregulated host response to infection

45
Q

septic shock

A

subset of sepsis with profound circulatory, cellular, and metabolic abnormaities

46
Q

SIRS criteria

KNOW

A

at least 2 of the following
- temp > 38C or < 36C
- HR > 90
- RR > 20
- WBC > 12 or < 4

47
Q

qSOFA score

KNOW

A

rapid bedside score - at least 2 of the following
* SBP <100 mmHg
* RR > 22
* Altered mentaton

like SIRS

48
Q

sepsis shock - 1 hr bundle

A
  1. measure lactate level (remeasure if > 2)
  2. obtain blood cultures before admin of ABX
  3. admin broad spectrum ABX
  4. 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)
  5. consider vasopressors (goal MAP > 65mmHg; if MAP > 65 with serum lactate > 2mmol/L AND no hypovolemia → give vasopressors)
49
Q

when to provide MRSA coverage for empiric septic shock

KNOW

A
  • stuff that would make you thinnk mrsa (hx, recurrent infection)
  • hospital: IV abx, recent hosptal admit
  • more prone: invasive device, hemodilysis
  • bad bad infection
50
Q

when to use 2 gra neg agents for empiric septic shock cvoerage

KNOW

A

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
51
Q

goal of fluid admin in septic shock

A
  • increase SV, CO, DO2
  • rehydrate intravascular space (that’s what’s usually dehdyrated in sepsis)
52
Q

why type of fluid is preferred in septic shck

A
  • 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

53
Q

how does cortisol improve psyioglogic response to stress

A
  • regulation of pro-inflammatory state
  • inhibition of inducible nitric oxide synthesis (iNOS)
  • revereses adrenergic receptor desnsitiation
  • incease Na and wate retetion(icrease intravascular volume)
54
Q

when wouold you consider hydrocortisone in septic hock

A
  • 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
55
Q

hydrocortisone dosing for septic shock

A
  • 200mg IV QD 3-7D
    • 50mg IV Q6H OR 200mg/day as continuous infusion
    • taper off over 2-3 days wehn shock is resolved

PHM 703: Crit Care/Heme/Onc (16 decks)

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