Critical Care Flashcards

1
Q

How can PEEP and Pplat differ in patients receiving APRV?

A

Pplat should be the same as the set inspiratory pressure, but PEEP may be higher if the patient is auto-PEEPing, may need to perform expiratory pause to see.

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2
Q

How can a circuit leak affect the patient’s ventilation?

A

Can falsely trigger more breaths as the drops in pressure are interpreted as patient effort. Can be due to partial circuit disconnect, ruptures cuff, or large BP fistula

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3
Q

What conditions need to be met for IVC/SVC variation or pulse pressure variation to have adequate predictive value for volume responsiveness?

A

Patient must be passive, in sinus rhythm, VT 8ml/kg IBW, abdominal pressure less than 12, HR/RR ratio >3.6.

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4
Q

When is Pplat measured?

A

During an inspiratory pause, and a no-flow state

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5
Q

How is right ventricular pressure overload distinguished from volume overload on POCUS?

A

The timing of septal flattening. If during systole and diastole, then pressure overload. If only on diastole, then volume overload.

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6
Q

What is one measure seen to reduce delerium in intubated patients?

A

PT/OT started at the time of intubation for patients that can tolerate it. No data to support day-night time routines.

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7
Q

What would you see on ultrasound for a pneumothorax?

A

Absence of lung sliding, sometimes a lung point, A lines

Presence of B lines rules out PTX

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8
Q

What are the features of EVALI?

A

Features: diffuse lung injury, can see tetrahydrocannabinol and vit E acetate in BAL, vaping in the last 90 days
Imaging: diffuse GGO, organizing PNA
Dx: rule out other causes, eosinophilia in BAL/peripheral blood rare
Tx: steroids, supportive treatment

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9
Q

What causes autocycling?

A

Sawtooth pattern on vent on expiration, which signals pressure fluctuation in the airway to alter flow but not trigger the vent.

Can be due to cardiac contraction, mechanical ventricular assist devices, bubbling of a chest tube suction device, oscillations of water in ventilator tubing.

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10
Q

What are the benefits to APRV vent settings?

A

Generally less sedation/paralysis as patients are encouraged to breathe on top of the settings. But end point such as vent free days and survival have not been seen, and in some cases may worsen barotrauma in ARDS patients.

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11
Q

What is the estimated RAP on TTE evaluation of the IVC?

A

0-5cm: IVC collapses entirely and is <1.5cm
5-10cm: IVC collapses >50% and is 1.5-2.5cm
11-15cm: IVC collapses <50% and is 1.5-2.5cm
16-20cm: IVC collapses <50% and is >2.5cm

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12
Q

How does one determine candidacy for decannulation from tracheostomy?

A

Spontaneous breathing with continuous flow oxygen for 12+hrs on two consecutive days, not requiring suctioning more than 2x in 8 hr period over 24hrs (better criteria than 24hr capping and with less PNA and short LOS)

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13
Q

What vent changes can be made for ARDS patients who are then cannulated?

A

Decrease FiO2, decrease TV. Maintain PEEP to prevent collapse-reopening injury.

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14
Q

What risk factors are there for developing methemoglobinemia?

A

Change from oxygen binding ferrous state to non-binding ferric state in Hgb.

Meds: chloroquine, dapsone, bactrim, lido, nitrates, reglan

Treat with methylene blue

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15
Q

How does a difference in arterial line transducer level correlate with the difference in pressure?

A

10cm- 7.6mmHg
When the transducer is above the level of the heart, the tracing is a falsely low BP

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16
Q

How long would one treat amiodarone toxicity with steroids?

A

40-60mg/day with a slow taper over 4-12 months

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17
Q

What change in VTI predicts volume responsiveness?

A

10% or more

18
Q

Describe the differences between serotonin syndrome, NMS, and malignant hypertension

A

SS- mental status change, hyperactive GI disturbance, neuromuscular abnormalities, and autonomic dysfunction (pupillary dilation/mydriasis with BP changes and diaphoresis). 2hrs-24hrs after ingestion of culprit.

NMS- often rapid increase in antipsychotic meds. AMS, rigidity, pyrexia, elevated CK, autonomic dysfunction. Don’t see the shivering/hyperreflexia/myoclonus/ataxia/GI symptoms of SS

MH- usually anesthesia related. Abrupt elevation in end-tidal CO2. hyperthermia, rigidity, dysautonomia like NMS, but is more abrupt.

19
Q

What is electrical impedance tomography?

A

Uses analysis of electrical impedance signals across the chest to depict regional lung ventilation, may be helpful in avoiding overdistention

20
Q

When does one start to worry about self-induced lung injury on the ventilator?

A

VT More than 15mL/kg despite low pressure support

21
Q

Recall the regions affected by their corresponding coronary artery on short axis POCUS

A
22
Q

What are some causes of sudden volume loss on pressure control ventilation?

A

Obstruction- will see reduction in inspiratory flow, expiratory flow and expiratory time is prolonged. Caused by plugging, kinking of tubes, foreign body, blood clot in ETT, bronchospasm

Abrupt compliance reduction- inspiratory/expiratory flow reduced but also times are short. Caused by flash edema, PTX, pleural bleeding, mainstem bronchus intubation

Circuit leak- discrepancy between inspired volume and expired volume (expired much less)

23
Q

What causes increases in peak and/or plateau pressures in volume control?

A

Both increased- compliance worsening

Peak increased but not plateau- resistance worsening

24
Q

How do you calculate stroke volume from VTI?

A

SV= cross-sectional area X VTI
VTI need LVOT diameter to the square the radius X pi

25
Q

What ultrasound sign can you see in infiltrative cardiomyopathy?

A

“starry night” appearance of myocardium, such as in amyloidosis

26
Q

What factors place patients at risk for developing CAUTI?

A

Duration of catheterization, bacterial colonization of the drainage bag, older age, female gender, DM, breach of sterile technique, disruption of closed system

27
Q

How can one determine the intrinsic PEEP on the vent?

A

Expiratory hold

28
Q
A
29
Q

How can pulsus paradoxus be seen on ultrasound?

A

During inspiration when intrathoracic pressure is increased, LV preload increased and LV afterload decreases resulting in increased LVOT velocities. Opposite on exhalation.

30
Q

What strategy can be used to eliminate double triggering on the ventilator?

A

Adding 1s inspiratory hold is it will cut off the circuit from registering any inspiratory effort during that time

31
Q

What is a lung pulse seen on ultrasound?

A

A still but inflated lung is in contact with pleural space and pulsating from heart movement, no PTX present at that spot

32
Q

What are POCUS findings for PTX?

A

Absent lung sliding with A lines, lung point (specific but not sensitive)

33
Q

What is abdominal rounding consistent with?

A

During expiration, the lateral walls of the abdomen go inward, and the periumbilical region moves outward. Sign of volume overload as the body is trying to create intrinsic PEEP to reduce afterload on the left ventricle

34
Q

How do you manage drug coagulopathies for ICH?

A

Those receiving vit K- prothrombin complex over fresh frozen plasma

Antiplatelet- don’t give platelets unless going in to surgery

35
Q

Review a chart for vasopressors

A
36
Q

How does albumin+diuretic affect ARDS patients with hypoproteinemia?

A

Better oxygenation, more effective fluid removal, better hemodynamic tolerance

37
Q

Solutions to ventilator asynchronies

A

Ineffective trigger: decrease trigger threshold on vent
Double trigger: increase inspiratory time
Flow asynchrony: increase flow
Delayed termination: decrease inspiratory time
Premature termination: increase inspiratory time
Intrinsic PEEP: measure with expiratory hold, decrease rate/TV, deep sedation

38
Q

What are some things you’ll need to watch for in cooling and rewarming of TTM management?

A

Cooling: cold diuresis, coagulopathy, insulin resistance (hyperglycemia), bradycardia, increased lactate, reduced drug clearance

Rewarming: hyperkalemia (shift to extracellular), seizures
Rewarm at 0.25C/hr

39
Q

After TTM (72hrs out), what factors are associated with poor neuro outcomes?

A

2+ of the following:
No pupillary/corneal reflexes
Bilaterally absent N20 SSEP wave
Highly malignant EEG after 24hr
NSE >60ug/L at 48h and/or 72h
Status myoclonus
Diffuse and extensive anoxic injury on CT/MRI

40
Q

How do you calculate brain perfusion pressure?

A

MAP-ICP
Normal 60-80