Fluids & Monitoring Flashcards

1
Q

Extracellular ⅓ 20%

A

sodium, ca, chloride, hco3

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2
Q

Intracellular ⅔ 40%

A

potassium phosphate and magnesium

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3
Q

Extracellular compartments are composed of

A

80% interstitial fluid 11L
20% plasma 3L

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4
Q

Hormone system that regulates blood pressure & fluid balance

A

RAAS

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5
Q

effect of aldosterone from adrenals in RAAS

A

causes kidneys to reabsorb Na and H2O

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6
Q

how RAAS regulates BP

A

Hypotension
Increased tubular chloride
Sympathetic stimulation

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7
Q

posterior pituitary releases

A

ADH

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8
Q

ADH effect on V1 and V2

A

V1: vasoconstriction
V2: decrease UO by causing reabsorption in distal tubules.

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9
Q

PH of 3 cryalloids

A

NS: 5.5
LR: 6.5
Plasmalyte: 7.5

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10
Q

The oSMolality of 3 crystalloids
Standard: 280-295

A

NaCl: 310

LR: 275

Plasmalyte: 298

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11
Q

benefits of LR

A

helps maintain electrical neutrality

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12
Q

Contraindications of LR (mildly hypotonic)

A

TBI, neurovascular insult (cerebral edema), blood transfusion,

Theoretical insult to renal patients due to lactate to bicarb

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13
Q

Plamalyte effect on renal function

A

the most isotonic. preserve pH and renal perfusion best.

compatible with blood

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14
Q

What is a colloid

A

High MW molecules in electrolytes solution. doesn’t pass intact glycocalyx (hyperglycemia)

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15
Q

Dextrans side effects

A

1 renal failure
2 impairs vWF and plt aggregation
3 no longer used in clinical practice.

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16
Q

Albumin in endothelial injuries

A

Pulmonary edema in patients with hyperglycemia/diabetics

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17
Q

How does anesthesia impact MV flow and organ perfusion?

A
  1. Opioid and dex decrease HPA stress response
  2. Neuralaxia anesthesia decreases SNS stim
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18
Q

3 Goal-directed fluid therapy (GDFT)

A
  1. supports O2 balance
  2. suports neuroendocrine response
  3. euvolemia preserves glycocalyx and MV flow
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19
Q

What activates HPA

A

autonomic and somatic stimulation

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20
Q

CNS activation causes the release of hormones

A

corticotropin-releasing hormone –>
anterior pituitary releases ACTH –>
cortisol from adrenals –> increase energy

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21
Q

sympathetic stimulation release of catecholamines from adrenals

A

increase SVR, HR, MV vasoconstriction = increased metabolic rate and O2 consumption

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22
Q

Tissue injury causes the endothelium to release

A

cytokines and inflammatory cells = hyperthermia, increase O2 demand, alters MV circulation

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23
Q

Prolonged tissue injury may cause

A

vasodilation, endothelial damage, edema, insulin resistance, vascular loss, hypotension, DECREASED ORGAN PERFUSION

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24
Q

angiotensin 2 causes:

A
  1. vessel vasoconstriction
  2. kidneys reabsorb NaCl and H2O
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25
ANP pathway
atrial stretch --> ANP release by cardiac myocytes --> increase GFR --> drop renin and ADH release --> increase UO
26
Hydrostatic vs oNCotic pressure
Starling Forces --> dilute blood stops Na reabsoption
27
blood flow through capillaries depends on 4 things
1 BP in capillaries 2 hydrostatic pressure in interstitium 3 oncotic pressure 4 subglycocalyx
28
Atrial Natriuretic Peptide
Released by atrium in response to increased stretch
29
advantages of crystalloid
replacement ratio 3:1 Expands the ECF Restores 3rd space loss
30
disadvantages of crystalloid
-->Limited ability to expand plasma volume (lasts 20-30min) -->edema --> Large volume of NaCL --> hyperchloremic metabbolic acidosis -->dilutes albumin (decrease cap onc pressure) -->dilutes coags
31
Colloid Advanatges
replacement 1:1 increases plasma vol 3-6 hours small vol less edema anti-inflammatory dextran 40 decreases blood viscosity & improves microcirculatory flow in vascular surgery
32
Dextran
no longer used in clinical practice due to renal failure, impairing vWF and platelet aggregation
33
females
45 % solids, 55% fluids
34
males
40% solids 60% fluids
35
Fluid exchange between extracellular compartments is dependent on
Starling Forces
36
daily fluid volume required to maintain TBW
25-35 ml/kg per day
37
intravasuclar blood pressure driven by CO and impacted by vascular tone
capaillary hydrostatic pressure Pc
38
hydrostatic pressure of the interstitial space
interstital fluid pressure Pif
39
osmotic force of colloidal proteins within the vascular space
plasma oncotic pressure
40
3 effects of RAAS system
1 ADH release from posterior pituitary 2 Aldosterone release adrenal cortex 3 Renal efferent arteriolar vasoconstriction increases GFR
41
Atrial Natriuretic Peptide
Released by atrium in response to increased stretch
42
5 effects of ANP
1 Increase GFR (Kidneys release Na and Water) 2 Systemic vasodilation 3 Inhibit renin release 4 Opposed production & action of angiotensin 2 5 Decreases aldosterone secretion
43
Historical Fluid Management 4 Steps
1. 4 2 1 rule 2. NPO time hours x maintenance rate 3. surgical loss 4. Blood Loss
44
HPA --> cortiocoreleasing hormone -->
--> ant pit releases ACTH --> cortisol from adrenals
45
4 effects of cortisol from adrenals
1. protein breakdown 2. hepatic release of glucose 3. Glycogenolysis 4. anti-inflammatory ultimately increase energy levels and preserve intravascular volume
46
Increase catecholamine from adrenal medulla -->
Increased HR, SVR, and microcirculatory vasoconstriction (bad). Causes increased metabolic rate and O2 consumption
47
Anesthetic Considerations of GDFT
dex/opiods/neuralaxia supports O2 balance, neuroendocrine response, and euvolemia preserves glycocalyx and MV flow
48
CI <2.5 after 250cc bolus
inotrope
49
MAP <65 after 250cc bolus
vasopressor
50
what relationship does the frank starling law describe
LVEDP and SV. Increase in preload will increase contractility until a point that it cannot generate more force.
51
CVP a wave
atrial contraction
52
CVP c wave
tricuspid closure; buldging
53
CVP v wave
RV systole/ RA passive filling
54
2 reasons for the loss of CVP a waveform
a fib v pace no RA contraction
55
Giant a wave or cannon wave Teddys heart disease challenge
Junctional rhythm Complete AV block V pace T or M stenosis MIschemia Ventricular hypertrophy
56
large v waves on CVP
tricuspid mitral regurg acute increase in intravascular volume
57
High CVP
fluid volume overload tricuspid stenosis/regurg tamponade R heart failure L heart failure pulmonary hypertension constrictive pericarditis
58
distance from IJ to RA
15 cm
59
distance from IJ to RV
25-35cm
60
distance from IJ to PA
35-45cm
61
distance from IJ to PAOP
40-50cm
62
subclavian to RA length
10cm
63
L IJ to RA
20 cm
64
femoral vein to RA
40 cm
65
Allen test 3 steps
1 depress ulna and radial open and close fist 2 release the ulnar artery 3 blood should return --> positive fallen test
66
PA catheter dicrotic notch
closure of pulmonic valve
67
High PAP
pulmonary hypertension LV failure mitral stenosis/regurg volume overload ASD/VSD L to R shunt catheter whip
68
High PAOP
ischemia LV failure mitral stenosis or regurg volume overload cardiac tamponade constrictive pericarditis
69
PVRI Pulmonary Vascular Resistance Index
(mPAP - PAOP)/CI x 80 45-225 dynes * sec/cm5 * m2
70
SVRI Systemic Vascular Resistance Index
(MAP-RAP)/CI x 80 1760-2600 dynes * sec/cm5 * m2
71
CI
CO / BSA CI = 2.8-3.6 L/min * m2
72
area under time temperature curve
inversely proportional to CO
73
thermodilution
d5w in proximal swan port --> thermistor at trip of swam
74
Thermodilution and CO overestimated: 4
Falsly high CO low injection volume injection too warm thrombus on thermistor partial wedge Small warm wedged thrombus
75
Thermodilution and CO underestimated 2
Falsely low CO excess injection volume too cold injection
76
unpredictable thermodilution readings
shunts (L-->R & R-->L) tricuspid regurg
77
normal MVO2
60-80
78
what is mvo2
o2 left after delivering to tissues, indirect monitor of O2 delivery (decreasing CO)
79
increased O2 Need
fever, shivering, pain, stress, anxiety
80
decreased O2 Need
analgesia sedation mechanical ventilation hypothermia
81
decreased O2 supply
decrease CO hemodilution hypoxia anemia heart disease
82
increase O2 supply
increase CO early sepsis cyanide poisoning AV shunt
83
ET CO2 compared to ABG
2-5 torr lower than ABG with cardiopulmonary abnormalities and larger with dead space
84
ET CO2 (infared analysis) diverting monitor
Most common (the ones we use) . it measures gas from a sample tube, NOT the breathing system
85
CO2 end of inspiration, begins expiration
first phase of capnography
86
CO2 capno expiratory upstoke
second phase
87
CO2 capno plateau & alveolar emptying
third phase
88
co2 capno rapid decrease of CO2 due to inspiration
fourth phase
89
increased dead space (increased VQ mismatch) on ETCO2
decreases ETCO2
90
LOW co2 production
Decreased CO2 production/delivery Hyperventilation Equipment problems
91
High CO2
high CO2 production/delivery hypoventilation equipment problems:
92
Flow Volume Loops provide info on
pulmonary resistance Flow vs Volume
93
Pressure-Volume Loop provides info on
compliance v/p = compliance
94
Left Shift Oxyhemo
hypothermia hypocapnia alkalosis decreased 2,3 dgp carboxyhemoglobin met hemoglobin hgb f
95
What is the oxyhemoglobin curve telling us
relationship between saturation of hemoglobin at a given PO2 in plasma
96
Pulse oximetry deviancy
2% when 80-100% 5% when <80%
97
Deoxygenated hbg absorbs light at what wavelength
650-750 nm red
98
4 limitations of pulse ox Smic
1 methemoglobin (underestimates SPO2 when > 85%) 2 carboxyhemoglobin 3 sickle cell 4 injected dyes (methyl blue and indigo carmen)
99
6 risks associated with hypothermia
1 wound infection 2 increased O2 consumption (shivering) 3 increased r/o CV events 4 sickling in sickle cell 5 decreased drug metabolism 6 coagulation impaired
100
ANNA recommendation
temp monitoring for all peds patients recieveing GA and any other time when indicated (using a warmer or case >30m long)
101
ASPN definition of hypothermia
<36 c
102
forced air warmer is what kind of warming
convective warming
103
1u of blood or 1L crystalloid decreases body temp by how much
0.25 c
104
What is the gold standard of temp management?>
PA blood temp
105
what 3 other temp sites correlate with PA blood temp?
1 tympanic membrane 2 distal esophagus 3 nasopharyngeal
106
how to measure nasopharyngeal temp length
nose to ear
107
esophageal monitoring
45 cm from nose yes in GA with ETT No in LMA
108
thermoregulation afferent nerves a delta vs c
c fibers = warm a delta = cold
109
General anesthesia drops temp by how much
0.5 to 1.5 in first 30 m, then slowly declined 0.3 until plateau
110
why does regional anesthesia cause hypothermia
blocking ANS causes vasodilation
111
combining GA and regional causes that effect on temperature
plateau never comes, temperature will continue to drop
112
4 MOA of heat loss
1 radiation - from patient to environment 2 conductive - from patient to OR table 3 convective - moving air currents 4 evaporation - vaporization of liquid from body
113
5 effects of mild hypothermia on the body
1. shivering (increased O2 consumption) 2. coagulation issues 3. wound infection 4. decreased drug metabolism 5. 3x increase in morbid myocardial outcomes
114
3 reasons for hyperthermia in OR
1 iatrogenic over warming 2 MH 3 infection (less common)
115
the device that monitors anesthesia depth
BIS Bispectral Index
116
Where do you want your BIS?
40-60
117
limitations of BIS
Unreliable ketamine and nitrous oxide hypothermia cautery bare bugger baby <6m
118
<40 BIS?
deep hypnotic = oversedated = hemodynamic change
119
the upstroke of pulmonic PA catheter waveform
opening of pulmonic valve
120
wedge pressure a wave
LA systole
121
wedge pressure c wave
mitral closure (hard to see)
122
wedge pressure v wave
La filling