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PGY-2 > Critical Care, Ventilation, Etc > Flashcards

Critical Care, Ventilation, Etc Flashcards

1
Q

Inotropy

A

increased cardiac output

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2
Q

Hypovolemic Shock

A

<p>**low preload**
low CO
high SVR</p>

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3
Q

<p>Cardiogenic Shock</p>

A

<p>high preload
**LOW CO**
high SVR</p>

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4
Q

<p>Causes of Cardiogenic Shock</p>

A 
<p>Cardiomyopathy/SHF
acute MR or AS
Arrthythmia (V fib or complete heart block)
Brady or tachy
</p>
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5
Q

<p>Distributive Shock</p>

A

<p>decreased preload
increased CO
decreased SVR</p>

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6
Q

<p>Causes of Distributive Shock</p>

A 
<p>Septic
Anaphylaxis
Neurogenic
Endocrine
Drugs</p>
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7
Q

<p>Obstructive Shock</p>

A

<p>decreased preload
**decreased CO**
increased SVR</p>

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8
Q

<p>Causes of Obstructive Shock</p>

A

<p>PE or severe RHF
Tension pTx
pericardial tampaonade
restrictive/constriction</p>

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9
Q

<p>Respiratory Acidosis =</p>

A

<p>increased PCO2

| compensation is increasing bicarb</p>

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10
Q

Respiratory Alkalosis =

A

decreased PCO2

compensate by decreasing hco3

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11
Q

Metabolic Acidosis =

A

decreased bicarb

copenensate by decreasing Co2

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12
Q

Metabolic Alkalosis=

A

increased bicarb

compensate by increasing co23

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13
Q

Delta Gap

A

AG-12/24-Bicarb;
<1 NGMA;
>1 met alkalosis

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14
Q

Winter’s formula

A

pco2= 1.5xbicarb + 8 +/-2

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15
Q

Metabolic Alkalosis with hypochloriduria/fluid responsive

A

vomiting
NG suction
over diuresis
post hypercapnia

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16
Q

<p>ARDS- Berlin Definition</p>

A 
<p>Timing w/in 1 week of symptoms/insult
Bilateral opacities
Edema (resp failure not fully explained by cardiac failure or volume overload)
Poor Oxygenation 
</p>
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17
Q

<p>Oxygenation Criteria for ARDS - Mild</p>

A

<p>200-300 PaO2/FiO2 w/ PEEP or CPAP >5</p>

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18
Q

<p>Oxygenation Criteria for ARDS- Moderate</p>

A

<p>100-200 PaO2/FiO2 w/ PEEP >5</p>

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19
Q

<p>Oxygenation Criteria for ARDS- Severe</p>

A

<p>Pao2/fio2 <100 w/ peep>5</p>

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20
Q

<p>Stages of ARDS</p>

A

<p>Exudative
Fibroproliferative
Recovery</p>

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21
Q

<p>Exudative Phase of ARDS</p>

A

<p>fluid, protein, and inflamm cells leave alveolar capillaries and accumulate in airspace resulting in decreased pulmonary compliance and VQ mismatch (both physiologic shunting and dead space)</p>

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22
Q

<p>Fibroproliferative Phase of ARDS</p>

A

<p>Chronic inflammation causes connective tissue to proliferates in response to initial injury causing fibrosis. Pulmonary HTN may develop as a result</p>

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23
Q

<p>Recovery Phase of ARDS</p>

A

<p>Lung reorganizes as the aveloar epithelila barrier is restored. Gradual improvement of lung function over 6-12 months</p>

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24
Q

<p>TV in ARDS</p>

A

<p>ideal is 6ml/kg </p>

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25
Q

<p>PEEP in ARDS</p>

A

<p>no difference in outcomes in low vs high PEEP, recommend only using high PEEP in severe ARDS</p>

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26
Q

<p>Steroids in ARDS</p>

A

<p>no clear evidence

| increased mortality if given after 14+ days (fibroliferative phase)</p>

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27
Q

<p>HFNC in ARDS</p>

A

<p>decreases intubation </p>

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28
Q

<p>Cisatricurium in ARDS</p>

A

<p>given in severe ARDS that presented within 48 hours </p>

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29
Q

<p>Agitation in ICU- first line</p>

A

<p>propofol

| dexmedetomadine</p>

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30
Q

<p>Propofol AE</p>

A

<p>hyperTG --> pancreatitis
Infusion syndrome w/ lactic acidosis, liver and renal failure, GREEN URINE
</p>

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31
Q

<p>Vascular tone=</p>

A

<p>resistance</p>

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32
Q

<p>alpha 1&amp;amp;2</p>

A

<p>blood vessels

| VASOCONSTRICT</p>

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33
Q

<p>beta one</p>

A

<p>myocardium

| inotropy/chronotropy</p>

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34
Q

<p>Beta two</p>

A

<p>blood vessels

| vasodilation</p>

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35
Q

<p>V1</p>

A

<p>blood vessels

| vasoconstriction</p>

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36
Q

<p>NE- what receptors</p>

A

<p>alpha > beta 1

| Increase SVR w/ slight increase in CO</p>

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37
Q

<p>NE- adverse effects</p>

A

<p>arrhythmias</p>

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38
Q

<p>Ne- use</p>

A

<p>first line septic shock</p>

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39
Q

<p>Phenylephirne</p>

A

<p>alpha one (increase SVR)</p>

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40
Q

<p>Epi</p>

A

<p>b1 / b2 --> alpha one

| increased SVR w/ higher dose</p>

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41
Q

<p>Phenylephinephrine use</p>

A

<p>use if arrhythmias w/ NE or as adjunct</p>

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42
Q

<p>Dopamine</p>

A

<p>D --> B1 --> alpha one</p>

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43
Q

<p>Vasopressin</p>

A

<p>V1, vasoconstriction
adjunct
high doses decrease UOP</p>

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44
Q

Dobutamine receptors

A

B1 and B2
increase inotropy, chronotropy
vasodilation and afterload reduce

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45
Q

<p>Dobutamine AE</p>

A

<p>dysrhythmia, hypotension</p>

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46
Q

Dobutamine indications

A

<p>cardiogenic shock and HTN

| better w/ RF patients</p>

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47
Q

Milirinone

A

PD3 inhibitor
inotropy, profound systemic and pulmonary vasodilation
use if PAH/RHF

48
Q

<p>First line for anaphylaxis shock</p>

A

<p>EPI</p>

49
Q

<p>Compliance =</p>

A

<p>Volume/Pressure</p>

50
Q

<p>Alveolar Ventilation=</p>

A

<p>(TV-dead space) x RR</p>

51
Q

<p>BiPaP- how it works</p>

A

<p>Inspiratory pressure / PEEP (IPAP and EPAP)

| backup respiratory rate</p>

52
Q

<p>Peak Inspiratory Pressure</p>

A

<p>pressure required to deliver TV</p>

53
Q

<p>Plataea Pressure</p>

A

<p>pressure required to distend the lung
measured during inspiratory phase
measure of compliance!</p>

54
Q

<p>PEEP</p>

A

<p>pressure applied during exhalation

| increases recruitment of collapsed alveoli </p>

55
Q

<p>Assist Control</p>

A

<p>breaths triggered by preset machine rate or negative pressure/patient effort
preset rate acts as a backup
overbreathing, CO2 is high, can develop mild resp alk
</p>

56
Q

<p>SIMV</p>

A

<p>combines spontaneous breaths with ACV breaths
mandatory minimum resp rate is set
Set rate gives you TV for those, for generated breathes you determine TV</p>

57
Q

<p>Problems when increasing PEEP</p>

A

<p>decrease venous return
increase PIP
increase risk for barotrauma</p>

58
Q

<p>Urine Anion Gap</p>

A

<p>greater then 0 --> RTA type 1 and 4
excretion of ammonium chloride impaired
RTA, reanl failure, HYPOaldosteronism</p>

59
Q

<p>Mechanism behind Urine Anion Gap</p>

A

<p>Acidosis causes secretion of NH4+
then Cl- is secreted for balance
use Cl- for measurement of acid excretion
Urine NA + K - Cl</p>

60
Q

<p>Differential for Elevated Osmolar Gap</p>

A 
<p>greater than calculated, consider
methanol
ethylene glycol
isopropyal alcohol
toluene 
</p>
61
Q

<p>paO2 should be</p>

A

<p>greater than 60</p>

62
Q

inspiration and thoracic pressure

A

inspiration –> decrease thoracic pressure

increases venous return to the heart

63
Q

<p>IVC as measure of hydration</p>

A

<p>collapse = dehydration; correlate to CVP
less than 1.5 cm = CVP of 0-5
respiratory= total collapse</p>

64
Q

<p>Acid/Base: Timeline for respiratory vs metabolic compensation</p>

A

<p>hours for respiratory

| 2-5 days for metabolic</p>

65
Q

Acid/Base: Disorders where pH can normalize?

A

classically: chronic resp alkalosis

some evidence for chronic resp acidosis

66
Q

AGMA: Why does the gap increase physiologically?

A

Bicarb decreases (have more cations)

67
Q

AGMA: Why does albumin matter?

A

weak acid

68
Q

AGMA + Normal Lactate, consider…..

A

alcoholic ketoacidosis

ketonuria measures acetoacetate NOT B-hydroxyl which is predominate in alcohlid

69
Q

AGMA: D-lactic acidosis

A

short bowel syndrome

70
Q

Physiology behind NAGMA

A

decrease in bicarb with increase in chloride ions

= hyperchloremic metabolic acidosis

71
Q

NAGMA loss of bicarb due to

A

GI losses: diarrhea, utereal diversion

Renal loss: RTA, early renal failure

72
Q

ACIDOSIS: GOLD

A

Glycols-ethylene, proplene
5-Oxoproline
L-lactate, D-Lactate

73
Q

ACIDOSIS: MARRK

A 
Methanol
Aspirin
Renal Failure
Rhabdo
Ketoacidosis
74
Q

Metabolic Alkalosis: Chloride Responsive Mechanism

A

blood volume reduced –> RAAS activated –> reabsorb Na, Cl, Bicarb

75
Q

<p>Intubation- preinduction agents</p>

A

<p>fentanyl (pain)

| lidocaine (prevent bronchospasm, ICP)</p>

76
Q

<p>Intubation- induction agent</p>

A

<p>ketamine, etomidate, versed, propofol</p>

77
Q

<p>Intubation- paralytic</p>

A

<p>roc or succ</p>

78
Q

<p>Internal Jugular Vein VASCULAR anatomy</p>

A

<p>IJV + subclavian --> brachiocephalic --> SVC --> RA</p>

79
Q

<p>Internal Jugular Vein anatomy for central line placement</p>

A

<p>- between two heads of SCM and clavical

| - lateral and anterior to carotid a</p>

80
Q

<p>IJV Central Line Pros and Cons</p>

A

<p>lower risk of PTX, infection

| however can puncture carotid, CI in CEA</p>

81
Q

<p>Subclavian Central Line Pros and Cons</p>

A

<p>more comfortable and lower infection risk

| highest PTX risk</p>

82
Q

<p>Subclavian Line Contraindications</p>

A

<p>coagulopathy
SVC thrombosis
upper thoracic trauma</p>

83
Q

<p>Subclavian Line Insertion Anatomy</p>

A

<p>Intraclavicular

| seprated from subclavian a by scaline muscle</p>

84
Q

<p>Femoral Line Pros and Cons</p>

A

<p>good for coagulopathics

| no neeed for CXR</p>

85
Q

<p>Femoral Line contraindications</p>

A

<p>DVTs, IVC filter, local infection </p>

86
Q

<p>Indications of low cardiac output in shock</p>

A

<p>narrow pulse pressure
cool extremities
delayed cap refill</p>

87
Q

<p>Indications of high cardiac output in shock</p>

A

<p>wide pulse pressure +/- low diastolic pressure
warm extremities
bounding pulses
</p>

88
Q

<p>Initial CPAP settings</p>

A

<p>5-10</p>

89
Q

Initial BiPAP settings

A

10/5

90
Q

<p>GCS - Basics</p>

A

<p>Eye - 4
Verbal - 5
Motor - 6
</p>

91
Q

<p>GCS: Eyes</p>

A 
<p>none -1 
pain - 2
verbal -3 
spontaneous -4
</p>
92
Q

<p>GCS: Verbal</p>

A 
<p>Intubated/no response -1
Incomprehsnible sounds 2
Inappropriate owrds 3
COnfused 4
Oriented 5
</p>
93
Q

<p>GCS: Motor</p>

A 
<p>none-1
extension to pain-2
flexion to pain-3
withdrawal-4
localize-5
commands-6</p>
94
Q

<p>Ground Glass Opacity Differential</p>

A

<p>- inflamm

- edema
- neoplasm
- interstitial thickening
- fibrosis </p>

95
Q

<p>Nodular Pattern on CXR Ddx</p>

A

<p>Granulomatous Disease
Pneumococosis
Malignancy</p>

96
Q

<p>Air Bronchogram =</p>

A

<p>Airspace disease</p>

97
Q

<p>Airspace Disease DDx</p>

A 
<p>Water/Pulm Edema
Pus: Infectious or inflammation
Blood: Diffuse alveolar hemorrhage
Cells: carcinoma, lymphoma
Lipoprotein: pulmonary alveolar proteinosis</p>
98
Q

<p>Reticular Pattern Ddx</p>

A 
<p>Interstitial pulm edema
IPF
Granulomas
Interstitial PNA
Collagen Vascular Disease
Pneumoconiosis</p>
99
Q

<p>Navigating the vent problems- how to use peak and plateau</p>

A

<p>increased peak and plateau = compliance issue

| increased peak w/ normal/decreased plateau= airway problem</p>

100
Q

<p>Plateau pressure=</p>

A

<p>pressure in alveoli at end of inspiration

| measure w/ inspiratory hold</p>

101
Q

<p>RSBI</p>

A

<p>RR/TV(L)
less than 105 to extubate
</p>

102
Q

<p>NIF and weaning</p>

A

<p>less than 20 </p>

103
Q

<p>ABCs of ventilator weaning</p>

A

<p>patient is AWAKE
patient is BREATHING
patient can gag/COUGH
</p>

104
Q

<p>Status epilepticus- what to give initially</p>

A

<p>4mg lorazepam

| load with pheny or fospheny at 20mg/kg </p>

105
Q

<p>Goal ICU Blood Glucose</p>

A

<p>140-180</p>

106
Q

<p>Trophic Feeds</p>

A

<p>if on pressors

| 10-20cc/hr</p>

107
Q

<p>Altered mental status mmnemoic</p>

A

<p>DONT
Dextrose, Oxygen, Narcan 0.4, Thiamine 100mg IV
</p>

108
Q

<p>Oxygen content of room air</p>

A

<p>21%</p>

109
Q

<p>Nasal Canula- Oxygen Delivery</p>

A

<p>roughly 4% per L

| 1-6L; 24-44%</p>

110
Q

<p>Venturi Mask</p>

A

<p>FiO2 0.24-0.5, Variable LPM</p>

111
Q

<p>Non-Rebreather</p>

A

<p>10-15L (flow has to keep bag from deflating), FiO2 .7-1.0 (85-95%)</p>

112
Q

<p>Goals of High Flow Nasal Oxygen</p>

A

<p>Eliminate dead space

| Reservoir of FiO2 in nasal cavity</p>

113
Q

<p>LPM w/ High Flow Nasal Oxygen</p>

A

<p>8L in pediatrics

| 60L in adults</p>

114
Q

<p>Warm Shock =</p>

A

<p>Cap Refill <2 Secs, warm, flushed
Bounding pulse, tachycardia
Normotension w/ wide pulse pressure</p>

115
Q

<p>Cold Shock =</p>

A

<p>Cap Refill >2 seconds, cold clammy
tachy or brady
hypotension </p>

PGY-2 (21 decks)

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