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Y2 > Surgery: intensive care > Flashcards

Surgery: intensive care Flashcards

1
Q

How is an ICU note written?

A 
by system: 
neuro (GCS, MAE (moves all extremities), pain control)
pulmonary (vent settings)
CVS (pressors)
GI
heme (CBC)
FEN (fluids, electrolytes, nutrition)
renal (urine output, BUN, Cr)
ID (T max, WBC, antibiotics)
Assessmnet
Plan
(physical exam included in each section)
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2
Q

what is the best way to report urine output in the ICU

A

24 hours/last shift/last 3 hour rate

ex. urine output has been 2L over last 24 hours, 350 last shift, and 45, 35, 40 cc over last 3 hours

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3
Q

what are possible causes of fever n the ICU

A 
central line infection
pneumonia/atelectasis
UTI, urosepsis
intra-abdominal abscess
sinusitis
DVT
thrombophlebitis
drug fever
fungal infection, meningitis, wound infection
endocarditis
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4
Q

what is the most common bacteria in ICU pneumonia

A

gram negative rods

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5
Q

what is the acronym for basic ICU care checklist

A 
FAST HUG
feeding
analgesia
thromboembolic prophylaxis
head-of-bed elevation (pneumonia prevention)
ulcer prevention
glucose control
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6
Q

what is cardiac output

A

HR X stroke volume

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7
Q

what is normal cardiac output?

A

4-8 L/min

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8
Q

what is CI?

A

cardiac index: CO/body surface area (BSA)

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9
Q

what is normal CI?

A

2.5-3.5

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10
Q

what is normal stroke volume

A

60-100 cc

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11
Q

what is central venous pressure an indirect measurement of

A

intravascular volume status

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12
Q

what is normal CVP

A

4-11

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13
Q

What is pulmonary capillary wedge pressure an indirect measure of?

A

left atrial pressure which is an estimate of intravascular volume (LV filling pressure)

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14
Q

what is the normal PCWP

A

5-15

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15
Q

what is anion gap?

A

Na - (Cl + HCO3)

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16
Q

What are the normal values for anion gap?

A

10-14

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17
Q

why do you get an increased anion gap

A

unmeasured acids are unmeasured anions in the equation that are part of the counterbalance to the sodium cation

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18
Q

what are the causes of increased anion gap acidosis in surgical patients

A 
"SALUD"
starvation
alcohol
lactic acidosis
uremia (renal failure)
DKA
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19
Q

define MODS

A

multiple organ dysfunction syndrome

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20
Q

what is SVR

A

systemic vascular resistance (MAP-CVP)/C0 x 80

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21
Q

what is SVRI

A

systemic vascular resistance index

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22
Q

what is the normal SVRI

A

1,500- 2,400

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23
Q

what is MAP

A

mean arterial pressure: diastolic blood pressure + 1/3 (systolic -diastolic pressure)
(diastole lasts longer than systole)

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24
Q

what is PVR

A

pulmonary vascular resistance: PA - PCWP/CO x 80

PA = pulmonary artery pressure

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25
Q

what is normal PVR value

A

100 + or - 50

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26
Q

what is the formula for arterial oxygen content

A

hemoglobin x O2 saturation x 1.34

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27
Q

what is the basic formula for oxygen delivery

A

CO x oxygen content

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28
Q

what is the formula for oxygen delivery

A

CO x 1.34 x Hgb x SaO2 x 10

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29
Q

what factors can increase oxygen delivery

A

increased CO by increasing SV, HR, or both

increased O2 content by increasing the hemoglobin content, SaO2 or both

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30
Q

what is mixed venous oxygen saturation?

A

Svo2
the O2 saturation of the blood in the right ventricle or pulmonary artery
an indirect measure of peripheral oxygen supply and demand

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31
Q

which lab values help asses adequate oxygen delivery

A 
Svo2 (low = inadequate delivery)
lactic acid (elevated with inadequate delivery)
pH (acidosis with inadequate delivery)
base deficit
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32
Q

what is FENa

A

fraction excretion of sodium

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33
Q

how is FENa calculated

A

(urine sodium + plasma Cr)/(plasma Na x urine Cr) x 100

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34
Q

what is the prerenal FENa value

A

<1

renal failure from decreased renal blood flow: cardiogenic, hypovolemia, arterial obstruction, etc

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35
Q

compare BUN to Cr ratio in prerenal and renal ATN

A

prerenal >20:1

renal ATN <20:1

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36
Q

compare FENa in prerenal vs renal ATN

A

prerenal <1

renal ATN >1

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37
Q

compare urine osmolality in prerenal vs renal ATN

A

prerenal >500

renal ATN <350

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38
Q

compare urine Na in prerenal vs renal ATN

A

prerenal <20

renal ATN >40

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39
Q

what is urine specific gravity in prerenal acute renal failure

A

> 1.020

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40
Q

how long do lasix effects last?

A

lasix last 6 hours

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41
Q

what is the formula for renal flow/pressure/resistance

A

pressure = flow x resistance

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42
Q

what is the 10 for .08 rule of acid base?

A

for every increase of PaCO2 by 10 mmHg, the pH falls by .08

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43
Q

what is the 40, 50, 60 for 70, 80, 90 rule for O2 sats

A

PaO2 of 40, 50, 60 corresponds roughly to an O2 sat of 70, 80, 90 respectively

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44
Q

one liter of O2 via nasal cannula raises FiO2 by how mcuh

A

about 3%

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45
Q

what is pure respiratory alkalosis

A

high pH (alkalosis), increased PaCO2, normal bicarbonate

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46
Q

what is pure respiratory acidosis

A

low pH, increased PaCO2, and normal bicarb

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47
Q

what is pure metabolic acidosis

A

low pH, low bicarb, normal PaCO2

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48
Q

what is pure metabolic alkalosis

A

high pH, high bicarb, normal PaCO2

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49
Q

how does the body compensate for respiratory acidosis? respiratory alkalosis?

A

increase bicarb

decrease bicarb

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50
Q

how does the body compensate for metabolic acidosis? alkalosis?

A

decrease PaCO2

increased PaCO2

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51
Q

what does MOF stand for

A

multiple organ failure

52
Q

what does SIRS stand for

A

systemic inflammatory response syndrome

53
Q

what is the site of action and effect of dopamine at low does

A 
dopamine agonist
renal vasodilation (aka renal dose dopamine)
54
Q

what is the site of action and effect of dopamine at intermediate dose?

A

alpha 1 and Beta 1 agonist (more beta 1)

positive inotropy and some vasoconstriction

55
Q

what is the site of action and effect of dopamine at high dose?

A

alpha 2 agonist

marked afterload increase from arteriolar vasoconstriction

56
Q

has renal dose dopamine been shown to decrease renal failure?

A

no

57
Q

what is the site of action and effect of dobutamine

A

B1 and B2 agonist (more beta 1)
increased inotropy
increased chronotropy
decrease in systemic vascular resistance

58
Q

what is the site of action and effect of isoproterenol?

A

B1 and B2 agonist
increases ionotropy and chronotropy
vasodilation of skeletal and mesenteric vascular beds

59
Q

what is the site of action and effect of epinephrine? what is the effect at high doses?

A

B1>A1>A2, B2 agonist
increased inotropy and increased chronotropy
at high doses: vasoconstriction

60
Q

what is the site of action and effect of norepinephrine? what is the effect at high doses?

A

A1 and B1 > B2 and A2 agonist
increase inotropy, increased chronotropy, and increased in blood pressure
high doses: severe vasoconstriction

61
Q

what is the action and indications of vasopressin?

A

vasoconstriction (increases MAP and SVR)
Indications: hypotension (especially refractory to other vasopressors ) or as a bolus during ACLS (advanced cardiac life support)

62
Q

what is the site of action, effect, and major toxicity of sodium nitroprusside?

A

venodilation and arteriolar dilation
decreased preload and afterload allowing blood pressure titration
cyanide toxicity

63
Q

what factors influence mixed venous oxygen saturation

A 
oxygen delivery (hemoglobin concentration, arterial oxygen saturation, cardiac output)
oxygen extraction by the peripheral tissues
64
Q

what lab test for tissue ischemia is based on the shift from aerobic to anaerobic metabolism

A

serum lactic acid levels

65
Q

define dead space

A

the part of the inspired air that does not participate in gas exchange

66
Q

define shunt fraction

A

the fraction of pulmonary venous blood that does not participate in gas exchange

67
Q

what causes increased dead space

A

overventilation (emphysema, excessive PEEP) or underperfusion (pulmonary embolism, low cardiac output, pulmonary artery vasoconstriction)

68
Q

at high shunt fractions, what is the effect of increasing Fio2 on arterial PO2

A

(FiO2 = fraction of inspired oxygen)
at high shunt fractions (>50%), changes in FiO2 have almost no effect on arterial PO2 because the blood that does “see” the O2 is already at maximal O2 absorption; thus, increasing the FiO2 has no effect (FiO2 can be minimized to prevent oxygen toxicity)

69
Q

define ARDS

A

acute respiratory distress syndrome: lung inflammation causing respiratory failure

70
Q

what is the ARDS diagnostic triad

A

a “CXR”:
Capillary wedge pressure <18
Xray of chest with bilateral infiltrates
Ratio of PaO2 to FiO2 <300 (aka P/F ratio)

71
Q

define mild, moderate, and severe ARDS

A

mild: p/f ratio 200 to 300
moderate: 100 to 200
severe <100

72
Q

what does the classic chest xray look like with ARDS

A

bilateral fluffy infiltrates

73
Q

at what concentration does O2 toxicity occur

A

FiO2 >60% x 48 hours

thus, try to keep FiO2 less than 60% at all times

74
Q

what are the only ventilatory parameters that have been shown to decrease mortality in ARDS patients? what else has been shown to decrease mortality in severe ARDS patient?

A

low tidal volumes (< 6 cc/kg) and low plateau pressures less than 30

prone positioning

75
Q

what are the main causes of carbon dioxide retention

A

hypoventilation, increased dead space ventilation, and increased carbon dioxide production (as in hypermetabolic states)

76
Q

why are carbohydrates minimized in the diet/TPN of patients having difficulty with hypercapnia?

A

respiratory quotient is the ratio of CO2 production to O2 consumption and is highest for carbohydrates (1) and lowest for fats (.7)

77
Q

why are indwelling arterial lines used for blood pressure monitoring in critically ill patients

A

because of the need for frequent measurements, the inaccuracy of frequently repeated cuff measurements, the inaccuracy of cuff measurements in hypotension, and the need for frequent arterial blood sampling/labs

78
Q

what happens with a line tracing with hypovolemia

A

variation with arterial line tracing with inspiration

79
Q

what is the primary use of the pulmonary capillary wedge pressure

A

as an indirect measure of preload = intravascular volume

80
Q

what is ventilation

A

air through the lungs, monitored by PCO2

81
Q

what is oxygenation

A

oxygen delivery to the alveoli, monitored by O2 sats and PO2

82
Q

what can increase ventilation to decrease PCO2

A

increased respiratory rate (RR)

increased tidal volume (minute ventilation)

83
Q

what is minute ventilatione

A

volume of gas ventilated through the lungs (RR x tidal volume)

84
Q

what is tidal volume

A

volume delivered with each breath

should be 6-8 cc/kg on the ventilator

85
Q

are ventilation and oxygenation related

A

basically no, you can have an O2 sat of 100% and a PCO2 of 150
O2 sats do not tell you anything about the PCO2

86
Q

what can increase PO2 (oxygenation) in the ventilated patient

A

increased FiO2

increased PEEP

87
Q

what can decrease PCO2 in the ventilated patient

A

increased RR

increased tidal volume

88
Q

define IMV ventilation mode

A

intermittent mandatory ventilation: mode with intermittent mandatory ventilations at a predetermined rate
patients can also breathe on their own above the mandatory rate without help from the ventilator

89
Q

define SIMV ventilation mode

A

synchronous IMV: mode of IMV that delivers the mandatory breath synchronously with patient’s initiated effort
if no breath is initiated, the ventilator delivers the predetermined mandatory breath

90
Q

define A-C ventilation mode

A

assist-control ventilation: mode in which the ventilator delivers a breath when the patient initiates a breath or the ventilator assists the patient to breathe
if the patient does not initiate a breath, the ventilator takes control and delivers a breath at a predetermined rate

91
Q

define CPAP ventilation mode

A

continuous positive airway pressure: positive pressure delivered continuously (during expiration and inspiration)by ventilator, but no volume breaths (patient breathes on own)

92
Q

define pressure support ventilation mode

A

pressure is delivered only with an initiated breath

pressure support decreases the work of breathing by overcoming the resistance in the ventilator circuit

93
Q

define APRV ventilation mode

A

airway pressure release ventilation: high airway pressure intermittently released to a low airway pressure (shorter period of time)

94
Q

define HFV ventilation mode

A

high frequency ventilation: rapid rates of ventilation with small tidal volumes

95
Q

define PEEP ventilation mode

A

positive end expiratory pressure: positive pressure maintained at the end of a breath
keeps alveoli open

96
Q

what is physiologic PEEP

A

PEEP of 5 cm H2O

thought to approximate normal pressure in normal nonintubated people caused by the closed glottis

97
Q 
what are the typical initial ventilator settings for: 
mode
tidal volume
ventilator rate
FiO2
PEEP
A 
mode: synchronous intermittent mandatory
tidal volume: 6-8 mL/kg
ventilator rate: 10 breaths/min
FiO2: 100% and wean down
PEEP: 5 cm H2O
98
Q

what is the normal I:E (inspiratory-to-expiratory time)?

A

1:2

99
Q

when would you use an inverse I:E ratio?

A

to allow for longer inspiration in patients with poor compliance, to allow for alveolar recruitment

100
Q

what clinical situations cause increased airway resistance

A 
airway or endotracheal tube obstruction
bronchospasm
ARDS
mucous plug
CHF (pulmonary edema)
101
Q

when would you used a prolonged I:E ratio?

A

COPD to allow time for complete exhalation (prevents breath stacking)

102
Q

what are the presumed advantaged of PEEP?

A

prevention of alveolar collapse and atelectasis, improved gas exchange, increased pulmonary compliance, decreased shunt fraction

103
Q

what parameters must be evaluated in deciding if a patient is ready to be extubated?

A 
patient alert and able to protect airway, gas exchange, tidal volume, minute ventilation, negative inspiratory pressure, FiO2 < 40% 
PEEP 5 
pH >7.25
RR <35
tobin index <105
104
Q

what is the rapid-shallow breathing index?

A

aka tobin index
rate: tidal volume ratio
tobin index <105 is associated with successful extubation

105
Q

what is a possible source of fever in a patient with an NG or nasal endotracheal tube

A

sinusitis (diagnoses by sinus films/CT scan)

106
Q

what is the 35-45 rule of blood gas values

A

normal values:
pH 7.35-7.45
PCO2 35-45

107
Q

which medications can be delivered via an endotracheal tube

A 
NAVEL
narcan
atropine
vasopressin
epinephrine
lidocaine
108
Q

what conditions should you think of with increased peak airway pressure and decreased urine output?

A
  1. tension pneumothorax

2. abdominal compartment syndrome

109
Q

dx: 48 yr old male with pancreatitis is now with acute onset of respiratory failure, PaO2 to FiO2 ratio of 89, normal heart echo, bilateral pulmonary edema on CXR

A

severe ARDS

110
Q

dx: 67 yr old female with severe diverticulitis now with acute onset of respiratory failure, PaO2-to FiO2 ratio of 234, normal hear echo, bilateral pulmonary edema on CXR

A

mild ARDS

111
Q

dx: 22 yr old male s/p MCC (motor cycle crash) 48 year old now with bleeding through liver and pelvic packs
TEG reveals progressive narrowing of the TEG tracing over time (small tail)

A

hyperfibrinolysis

112
Q

dx: 22 yr old female s/p fall with severe TBI, urine output 30-50 cc/hr, CVP 15, sodium 128

A

SIADH

113
Q

dx: 45 yr old with severe pancreatitis, now with increasing peak airway pressures, decreased urine output, and hypotension

A

abdominal compartment syndrome

114
Q

dx: 70 yr old male with sever sepsis on three pressors (vassopressors), antibiotics, refractory to fluid bolus and progressively increasing doses of pressores

A

adrenal insufficiency

115
Q

dx: 44 yr old male with pulmonary contusions s/p several infusions of KCl for hypokalemia with no increase in postinfusion potassium level

A

hypomagnesemia

116
Q

dx: 44 yr old female with severe pancreatitis on ventilator ABG reveals pH of 7.2, PO2 of 100, PCO2 of 65, bicarb 26

A

respiratory acidosis (uncompensated)

117
Q

dx: 65 yr old male s/p pulmonary contusion on a ventilator, ABG reveals pH 7.35, PO2 80, PCO2 of 60, bicarb of 35

A

compensated respiratory acidosis

118
Q

dx: 34 yr old female s/p liver injury from an MVC on the ventilator, ABG reveals pH 7.23, PO2 105, PCO2 40, bicarb 17

A

metabolic acidosis

119
Q

dx: 76 yr old male with severe diverticulitis on ventilator, pH 7.35, PO2 76, PCO2 25, bicarbonate 16

A

metabolic acidosis with respiratory compensation

120
Q

dx: 45 yr old found down with pH of 7.17, PCO2 39, PO2 90, sodium 140, chloride 108, bicarbonate 26

A

normal anion gap metabolic acidosis

140-108-26=6

121
Q

dx: 56 yr old female found down with pH of 7.19, sodium 140, bicarbonate 18, chloride 100

A

increased anion gap acidosis

140-18-100=22

122
Q

tx: 34 yr old female s/p MVC with carotid dissection on CTA

A

antiplatelet (aspirin and/or plavix) or anticoagulation (enoxaparin or IV heparin or PO anticoagulation medication, classically Coumadin) therapy

123
Q

tx: 25 yr old male s/p crush injury with CK of 45,000, dark urine

A

myoglobinuria: IV fluid hydration

+ or - bicarb IV

124
Q

tx: DVT prophylaxis for 34 yr old trauma patient with acute renal failure

A

unfractionated heparin

125
Q

tx: 78 yr old male in ICU develops SVT and hypotensive 75/palp

A

synchronized cardioversion

126
Q

tx: 80 yr old male s/p Hartmann’s procedure for severe fecal diverticulitis, now with urine output of 10 ccs per hour, FENa <1%, creatinine 1.7, BUN to Cr ratio > 20, urine sodium of 8

A

prerenal acute renal failure

treat with IV volume

Y2 (2 decks)

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