Critical Care

Front 1

Front (Term)

Back 1

Plateau is lower than peak

Volume : of 500ml delivered, about 300mk not exhaled

- large leak: cuff rupture

Front 2

Ischemic stroke sbp <220

Hemorrhage sbp < 140

Back 2

Acute upper GI bleed

Common - peptic ulcer

Urea/creatinine ratio >100 - upper

Front 3

Variceal bleed : band ligation preferred over sclerotherapy

Back 3

Risk of recurrent bleed ulcer

Active arterial bleed - 90%

Non bleeding visible vessel - 50%

Front 4

Acute liver failure - cerebral edema is the common cause of death.

Cautious with Peep as it can worse brain edema

Back 4

Seizures- Phenytoin better

ICP: paco2 25-30, mannitol, barbiturates

Hepatic encephalopathy- lactulose is controversial. No change in outcomes

Front 5

TIPS - dec mortality in severe variceal bleeds

Back 5

Tips CI: severe TR, PH >45, chf, poly cystic liver disease, sepsis, unrelieved biliary obstruction

Front 6

Quantity massive hemoptysis

Back 6

Definitions vary-

1. >100 ml/hr

2. >150 ml single time

Front 7

Life threatening hemoptysis

Back 7

1. hemodynamic instability

2. significant gas exchange defect

3. significant airway obstruction

Front 8

When can TXA be used in hemoptysis

Back 8

1. non massive hemoptysis- neb TID x 5 days

2.

Front 9

Inferior MI, which vessel and EKG pattern?

Back 9

1. RCA

2. Elevation II III aVF, depression V1-3

Front 10

Left circumflex STEMI EKG?

Back 10

Elevation in 1, V5, V6

Front 11

Causes for abrupt loss of tidal volume on p-cmv

Back 11

1. obstruction- volume loss and flow loss w/prolonged expiratory time (mucous plugging, tube kinking, foreign body, blood clot in the tube, or bronchospasm)

2. abrupt compliance reduction: inspiratory and expiratory time are shortened (flash edema, pneumothorax, pleural bleeding, or mainstem bronchus intubation)

Front 12

RAP estimate from IVC measurement - spontaneously breathing pt

Back 12

IVC <1.5: 0-5

IVC 1.5-2.5 cm >50% collapse: 5-10

IVC 1.5-2.5 <50% collapse: 11-15

IVC >2.5 <50% collapse: 16-20

Front 13

How does transducer affect a-line BP reading?

Back 13

Should be at the level of the heart. If higher- lower BP read d/t gravity effect. As long as transducer at heart level, arm position doesn't matter.

Front 14

Pressor of choice in takotsubo CM?

Back 14

alpha agonist

- also don't volume deplete - can cause LV outflow tract obstruction

Front 15

Estrogen in pregnancy

Back 15

Upper airway issues - edema, nasal polyps. Difficult intubation

LAM - estrogen responsible for inflammation

Front 16

Progesterone in pregnancy

Back 16

Central resp stimulation causing ventilation changes

Front 17

what is this?

Back 17

breath stacking or double stacking

If on volume control > switching to pressure control will resolve the breath stacking but the delivered volume will be higher than the desired volume (but less the the increased volume that occurs with breath stacking).

Front 18

Can this patient get a VILI with these setting? (this is a brain bleed pt w/ nl CXR and ABG).

Back 18

Yes. This is SELF induced lung injury (SILI) due to excessive patient respiratory drive (likely bc of brain injury). What to do: address underlying causes of excessive patient respiratory drive (resp alk, liver dx, pain). Can consider suppressing resp drive

Front 19

what drugs are known to unmask or worsen myasthenia gravis symptoms

Back 19

macrolides, fluoroquinolones, aminoglycosides, magnesium, and β-blockers

Front 20

what is End-inspiratory transpulmonary pressure

Back 20

Pplat − end-inspiratory pleural (esophageal) pressure. Values >30 cm H2O are generally considered excessive.

Front 21

what is this?

Back 21

circuit leak

Front 22

what is rapidly reversible sedation-associated delirium (RRSAD)? and does it effect mortality like prolonged delirium does in the ICU?

Back 22

subtype of delirium with outcomes not different than that of patients never exhibiting delirium.

Front 23

acid/base problem and other symptoms that can hint at salicylates toxicity.

Back 23

HAGMA + respiratory alkalosis. If patient has tinnitus that can be a sign of ASA toxicity.

Expected CO2 (winters formula) = (1.5 x HCO2) + 8 +- 2

Front 24

formula for osmolar gap?

and what is formula for calculated osmolality?

Back 24

osmolar gap = measured - calculated

calculated Osm = 2xNa + BUN/2.8 + glucose/18

Front 25

how to measure respiratory system compliance on ventilator if not given?

Back 25

TV/inflating pressure

inflating pressure = Pplt - PEEP

Front 26

what drug is the only FDA approved reversal agent for NOAC dabigatran (directly inhibits thrombin)?

what about for rivaroxaban, apixaban, and edoxaban (factor Xa inhibitors)?

Back 26

Idarucizumab (binds to where dabigatran binds to thrombin - higher affinity then thrombin)

Andexanet alfa (looks similar to factor Xa - so it acts like a decoy and has factor Xa inhibitors bind to intself instead of real factor Xa)

Front 27

what happened in A, B, and C in a PRESSURE mode

Back 27

A: airway obstruction (bronchospasm, mucus plug, ETT kink, foreign body, clot on ETT). Drop in TV but SLOW expiratory flow pattern.

B: stiff lung/low compliance (flash pulm edema, PTX, pleural effusion, parenchymal lung injury). Low TV, same set pressure, FAST expiratory flow pattern bc of low compliance. If pulm edema happened in VOLUME mode -> same TV with INCREASE in pressures

C: TV is intact but expiratory vol is much less = circuit leak

Front 28

how to distinguish between sepsis fever/serotonin syndrome/neuroleptic malignant syndrome/and malignant hyperthermia

Back 28

look at reflexes vs rigidity vs GI disturbances to give clues

Front 29

difference between HIT 1 and 2

Back 29

Front 30

what vent changes do you make in an ARDS pt when they are placed on VV ECMO

Back 30

Decrease TV - even to the point of anatomical dead space (3-5ml/kg)

Decrease FiO2

Goal of above to decrease Pplt to 5-8 cm H20

Leave PEEP to prevent atelectal trauma

Front 31

Tx for GBS

Back 31

PLEX or IVIG

Front 32

Diagnosis and findings with heptatopulmonary syndrome (HPS)

Back 32

Triad: 1/ liver dx, 2/ increased A-a gradient on RA, 3/ intrapulm vascular dilatations (IPVD). Sx include: hypoxemia, platypnea, and orthodeoxia

IPVDs cause a V/Q mismatch where blood streaming through center of capillary might not have time to get oxygenated.

Dx: ECHO with bubble study (appearance of micro-bubbles in LA w/in 3-6 cycles).

Tx: no medical therapy. May resolve after liver tx (but also puts pt at higher risk for problems/mortality during liver tx)

Front 33

results of the study using intensivist vs palliative care to talk to family.

Back 33

No difference in anxiety/depression score between two groups.

Increased PTSD in palliative care group

No difference in mortality/HLOS

Front 34

what happens to the BP reading when the arterial line transducer is not at the level of the heart?

Back 34

if above level of heart > lower BP (and vica versa)

Front 35

what is and what are causes of:

High peak and plt presures?

High peak and lower plt pressures?

Back 35

High peak/plt = change in compliance/parenchymal issue (PTX, pleural effusion, RMS intubation [severe atelectasis], flash pulm edema, increase in extrathoracic pressures). Expiratory flow would be faster and shorter.

High peak/normal plt = airway resistance (mucus plug, bronchospasm, Kinked ETT). you ALSO will see reduced expiratory flow with prolonged expiration (you will ONLY see this if it is a pressure mode)

Front 36

which oral anticoagulation has been shows to be effective for VTE and malignancy

Back 36

edoxaban (Lixiana).

Front 37

what are some of the things that happen in ARDS when you do lung protective strategies

Back 37

1) decrease lung injury

2) decrease proinflammatory cytokines

3) decrease alveolar edema by active transport of Na/Cl across alveolar epithelium

Front 38

what is the leading cause of death for patients with neurofibromatosis

Back 38

The intrathoracic lesions are plexiform neuroblastomas, which can undergo malignant transformation. Any patient with neurofibromatosis type 1 (NF1) who develops new onset symptoms not otherwise explained, with a change in size of a neurofibroma, should be evaluated for malignancy. Malignant transformation of benign neurofibromas to malignant peripheral nerve sheath tumors (MPNSTs) is the leading cause of mortality.

FIRST prove it is malignant (w/ bx) THEN you can do surgical excision