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

Critical Care: Shock (including septic shock) Flashcards

(55 cards)

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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

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

Approach to fluids in shock

Study These Flashcards
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
when to start vasoactive agents in treating shock pts
start AFTER fluid MAP is still < 65 ## Footnote required lines - arterial line if possible for monitoring - CVC for admin
26
vasopressors vs. inotropes
- chronotropy: rate of contraction - inotropy: contractile strength
27
NE MOA | KNOW
alpha adrenergic agonst (and a lil beta 1) ## Footnote increase peripheral vasoconstriction (alpha MOA)-> inrease MAP
28
beta 1 MOA
HR, stroke volume
29
beta 2 MOA
- contration strength - vasodilaton - bronchial relaxation
30
alpha 1 MOA
vasoconstriction -> increase MAP
31
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
32
epinephrine mOA
alpha (at high dose) and beta adrenergic agonist ## Footnote - Increase in HR and stroke volume (beta 1) - Increase in MAP (both secondary to the beta 1 effect and alpha 1 effect)
33
epinephrine use in shock
- secondary choice in sepsis - useful in anaphylactic shock dt beta 2 (bronchial relaxaton)
34
epinephrine ADR
aeroic lactate production -> makes it hard to see if pt's own lactate is going down
35
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
36
DA use in shock
- not really used dt ADR (**tachycarida and arrhythmias (KNOW)** ) - most effective in hypotensive pts with decreased cardiac function
37
phenylephrine MOA | KNOW
selective alpha 1 agonist ## Footnote peripheral vasoconstriction (can go overboard and induce **reflex bradycardia (KNOW)**)
38
phenylprine use in shock | KNOW
not recomended i shock unless CO is high and BP is persistenly low
39
vasopressin use in shock | antidiuretic hormone; KNOW
used with vasopressors (catecholamines) to reduce the dose required ## Footnote do NOT use alone in sepsis
40
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)**
41
dobutamine MOA | KNOW
produceds inotropic action via beta 1
42
dobutamine use in shock | KNOW
added to catecholinae treatment when CO, SVO2/SCVO2 goals have not been achieved
43
septic shock management
- correctoin of underlying caused (abx and source control) - fluid resuscitation - vasopressors - inotropes - CS
44
sepsis
life threatening organ dysfuction causd b a dysregulated host response to infection
45
septic shock
subset of sepsis with profound circulatory, cellular, and metabolic abnormaities
46
SIRS criteria | KNOW
at least 2 of the following - temp > 38C or < 36C - HR > 90 - RR > 20 - WBC > 12 or < 4
47
qSOFA score | KNOW
rapid bedside score - at least 2 of the following * SBP <100 mmHg * RR > 22 * Altered mentaton | like SIRS
48
sepsis shock - 1 hr bundle
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
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
50
when to use 2 gra neg agents for empiric septic shock cvoerage | KNOW
high risk for MDR (multi drug resistant bugs) ## Footnote - 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
goal of fluid admin in septic shock
- increase SV, CO, DO2 - rehydrate *intravascular* space (that’s what’s usually dehdyrated in sepsis)
52
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 ## Footnote starches NOT recommended dt inncreased risk of mortality, AKI, bleed
53
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)
54
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
55
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

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

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