LIVE VALLEY REVIEW DAY 1 Flashcards

1
Q

The only fused vertebrae is the

A

Sacral

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2
Q

C8 nerve runs under

A

T1

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3
Q

A Caudal block is an

A

Epidural

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4
Q

When you do caudal block the ligament you cross is the

A

Saccrococcygeal Ligament

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5
Q

Adults Spinal cord ends at

A

L1

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6
Q

Pediatric spinal cord ends at

A

L3

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7
Q

SIFEDSASP

A
Skin
Subcutaneous
Supraspinous ligament
Interspinous ligament
ligamentum Flavum
Epidural
Dura
Arachnoid
Subarachnoid
Pia
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8
Q

Other names spinal

A

SAB

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9
Q

Other names spinal

A

SAB, intrathecal

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10
Q

When does the infant SC ends at L1?

A

20-24 months

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11
Q

Toughest layer is the

A

Dura mater

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12
Q

Offer the most protection

A

Dura mater

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13
Q

Spinal web is the

A

Arachnoid mater

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14
Q

Spinal cord Layer that is tightly attached to the spinal cord

A

Pia

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15
Q

Delicate and highly vascular

A

Pia

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16
Q

At any time how much CSF in the body

A

100-150 ml

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17
Q

Per day how much CSF is produced

A

500 ml per day

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18
Q

Normal pressure of the CSF

A

10-20 cm H2O

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19
Q

Is the CSF high or low pressure

A

Low pressure (in healthy individuals)

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20
Q

Where is the CSF produced?

A

Choroid plexus third and fourth ventricle

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21
Q

Where is the CSF produced?

A

Choroid plexus third and fourth ventricles

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22
Q

***** Principle site of action of neuraxial blockade (SPINAL OR EPIDURAL) is the

A

Nerve root (Branch that sticks out of the picture)

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23
Q

Last ligament when you’re doing midline paramedian approach?

A

Ligamentum Flavum

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24
Q

Action of epinephrine with LA

A

Vasoconstriction, decreases absorption leading to a LONGER DURATION

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25
Q

Anatomical shape that can affect spinal/epidural?

A

Kyphosis or scoliosis

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26
Q

Angulation of needle can affect

A

Distribution

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27
Q

In a pregnancy , do you increase or decrease dose of LA

A

Decrease the dose

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28
Q

In a pregnant or morbidly obese, you decrease the dose why?

A

Increase abdominal mass which decreases the space.

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29
Q

If you don’t think the spinal is enough for a pregnant person, you think you underdose

A

Underdose redose can lead to TOTAL SPINAL

Do an epidural instead

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30
Q

To change density of the block you can change the

A

Change the concentration of the block

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31
Q

What can differentiate a Sensory vs motor block with choosing the local anesthetics?

A

Is the concentration .

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32
Q

SG of the CSF

A

1.004 - 1.009 (just remember 1.007)

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33
Q

Hyperbaric to CSF

A

Heavier than CSF (Sink)

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34
Q

Hypobaric to CSF

A

Lighter than CSF (Float)

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35
Q

To make hyperbaric mix with

A

Dextrose 5% to 8%

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36
Q

To make hypobaric mix with

A

STERILE water

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37
Q

To make isobaric mix with

A

CSF

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38
Q

Hypobaric laying down going

A

Cephalad

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39
Q

Hyperbaric laying down going

A

Caudal

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40
Q

If patient laying on affected side

A

use hyperbaric

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41
Q

Best for patient with hip fracture

A

HYPOBARIC

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42
Q

The most important factor affect SPINAL

A

Position

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43
Q

The most important fact for EPIDURAL

A

VOLUME

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44
Q

After spinal what do you get dilation vs constriction

A

Venous and arterial vasodilation

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45
Q

CV effect of sympathetic blockade

A
Massive vasodilation
Decrease preload
Decrease Venous return 
Decrease CO 
Decrease BP
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46
Q

CV effect of sympathetic blockade treatment necessary

A

BEST treatment with hypotension to spinal is PHYSIOLOGIC not pharmacological .

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47
Q

Maternal hypotension associated with

A

Late Decelerations

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48
Q

Late decelerations is associated with

A

maternal hypotension

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49
Q

If not normovolemic use

A

Fluids

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50
Q

If normovolemic use

A

EPHEDRINE

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51
Q

Before fluid loading, need to know

A

EF (heart pumping status)

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52
Q

If LV not functioning you will get

A

pulmonary edema

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53
Q

Cardiac changes occur to

A

Sick, very young, and elderly

THEY LACK RESERVE

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54
Q

Cardiac reserve decrease

A

1% every year after the age of 30.

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55
Q

High spinal vs Total spina

A

High spinal: Greater than T4

Total spinal :

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56
Q

High spinal vs Total spina

A

High spinal: Greater than T4

Total spinal : ALL THE WAY PAST T

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57
Q

Common reason of total spinal

A

Epidural dose for a spinal dose

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58
Q

Respiratory changes with neuraxial techniques

A

Severe chronic lung disease OR use of accessory muscles.

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59
Q

Interscalene block (ISB) for patients with respiratory issues?

A

No because of ISB possible adverse effects phrenic nerve palsy

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60
Q

High points

A

C3 and L3

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61
Q

Low points

A

T6 and S2

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62
Q

Widest level of spine

A

L2

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63
Q

Narrowest level of spine

A

C5

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64
Q

Cutting needle disadvantages

A

Bigger cut of dura

More at risk for PDPH

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65
Q

How long epidural set up

A

about 20 minutes

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66
Q

Spotte vs whitacre

A

Sprotte takes longer to setup

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67
Q

Cutting needle perpendicular to the fibers

A

Takes out lot of fibers.

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68
Q

Cutting needle bevel towards the

A

Flank

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69
Q

Aspirin and Neuraxial

A

NON issues

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70
Q

SC heparin or LMW, loo

A

ACT or PTT

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71
Q

Coumadin therapy

A

PT/INR

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72
Q

INR level for neuraxial

A

< 1.5 ok

>1.5 NO PROBLEM

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73
Q

Pulling a catheter , what to ask

A

Why is it in?

Anticoagulation reason

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74
Q

Fibrinolytics or thrombolytics therapy , about to have surgery, can they have neuraxial

A

NO , none for 10 days

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75
Q

Patient receive this should not receive neuraxial for 10 days

A

Fibrinolytics or thrombolytics therapy

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76
Q

Generic of plavix

A

Clopidogrel

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77
Q

Generic of eliquis

A

Apixaban

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78
Q

Generic of Pradaxa

A

Dabigatran

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79
Q

Aside from stopping AC , should know when to

A

Restart the medication

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80
Q

Xiphoid level

A

T6

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81
Q

L4 is the

A

illiac crest
Tuffiers line
intercristal lie

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82
Q

Absolute contraindications of neuraxialL: CHIP

A
CHIP
Coagulation
Hemodynamic instability
Infection at site
Patient refusal.
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83
Q

Assault vs battery

A

Verbal ASSAULT

Physical BATTERY

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84
Q

No absolute __________ for Neuraxial

A

Indications

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85
Q

Considerations that support using subarachnoid block- FATO

A

Full stomach
Anatomic distortions of the upper airway
TURP
Obstetrics.

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86
Q

Meningitis or increased ICP

A

Possible herniation , No neuraxial

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87
Q

Only aortic stenosis not to do neuraxial

A

Severe Aortic stenosis

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88
Q

Reason of the tight fitting styelet

A

27ga,

Enough body to bounce through tissue. Solid needle when stylet needle, and hollow without it

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89
Q

Predisposing factors to infections

A
3 AAAs CD
Advanced age]
Alcoholism
AIDS
Cancer
Diabeters
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90
Q

3 main signs of Meningitis

A

High fever
Nuchal rigidity
Headaches

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91
Q

Laying down, headaches gets better with

A

PDPH

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92
Q

Definitive symptoms that differentiate PDPH from meningitis

A

High fever

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93
Q

Risk factors to know for PDPH

A
Perpendicular needles
Large cutting needles
Female > men
Young > Elderly
Pregnant women
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94
Q

Epidural anesthesia can be done at

A

ANY LEVELS

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95
Q

Epidural anesthesia at the sacral

A

Caudal

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96
Q

Safest entry point into epidural space is the

A

Midline lumbar region

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97
Q

Binds the epidural space

A

dural posterior

and ligamentum flavum ANTERIOR

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98
Q

Why is epidural needle curve and noncutting?

A

A potential space

Loss of resistance -> thread the catheter

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99
Q

Crawford needle of the Epidural is the

A

STRAIGHT NEEDLE

and CUTTING

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100
Q

Tuohy needle of the epidural is

A

CURVE needle

non-cutting

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101
Q

Increase risk of epidural puncture is the

A

Crawford needle

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102
Q

Most epidural catheter is

A

Multi port or orifice

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103
Q

Agents for epidural ONSET FAST TO SLOW (2-2-2)

A
Chloroprocaine
Prilocaine
Lidocaine
Mepivacaine
Bupivacaine
Ropivacaine
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104
Q

WEISS has

A

WINGS

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105
Q

During an epidural if you get a blood return?

A

Remove and start it over.

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106
Q

Epidural air vs saline

A

use either .

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107
Q

How much catheter you want in the epidural space?

A

4 cm

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108
Q

How do you fix a one sided epidural )

A

Take tegaderm off
Withdraw catheter about 1 cm
inject extra medication .

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109
Q

Neuraxial acts on the

A

Nerve rootlets, nerve roots and spinal

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110
Q

Easiest to block : myelinated vs unmyelinated

A

Myelinated nerve

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111
Q

The order in which nerves are blocked following epidural

A

BC ADGBA

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112
Q

Sensory order: Myelinated and unmyelinated

A

Large myelinated
Small myelinated
Unmyelinated

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113
Q

Why do B fibers get blocked first.

A

B fibers gets blocked first because of their location

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114
Q

Sensitivity of LA vs order of Blockade

A

Page 400.

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115
Q

Sensory block most sensitive to

A

Alcohol swab to assess loss of temperature

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116
Q

Epidural hematoma most important issue

A

PARALYSIS

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117
Q

Incidence of epidural hematoma

A

1 : 150,000 blocks

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118
Q

Majority of epidural hematoma occur in patients with

A

ABNORMAL COAGULOPATHY

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119
Q

ABNORMAL COAGULOPATHY patients at risk for epidural hematoma

A
Disease state ( Factor VIII deficiency)
Pharmacological therapy
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120
Q

S/s of epidural hematoma

A

SHARP BACK and leg pain
Numbness
Motor weakness
SPHINCTER dysfunction .

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121
Q

Only way to diagnose EPIDURAL HEMATOMA

A

Imaging (CT, MRI) It ‘s an emergency you need it.

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122
Q

Definitive treatment is EPIDURAL HEMATOMA

A

Surgery

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123
Q

2 main complications of Epidural

A

Penetration of a blood vessel

Epidural hematoma

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124
Q

Signs and symptom of PDPH

A
Headches
Double vision (Diplopia) because of traction on the cranial nerve.
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125
Q

Headache with PDPH why

A

When the lay down medulla and brainstem to drop into the foramen magnum, stretching the menin

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126
Q

Differential diagnoses for PDPH:

A
SAH
Subdural hematoma
Meningitis
Anxiety 
Dehydration
Hypoglycemia
Lack of caffeine
Loss of resistance with air (pneumocephalus)
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127
Q

Definitive treatment for PDPH

A

Epidural blood patch

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128
Q

PDPH is

A

Self limiting

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129
Q

Epidural blood patch process

A

10-30 cc of aseptically drawn blood
blood is injected into epidural space until the patient can feel pressure in the back
After the epidural blood patch, bed rest 1-2 hours before ambulating

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130
Q

Caffeine is a ______in the cerebral bed

A

Vasoconstrictor

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131
Q

First blood patch injecting resolves : (success rate)

A

89-95% of headaches may repeat in 24 hours.

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132
Q

How much blood to inject

A

14-18 ml OR when patient say feel pressure

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133
Q

What does the blood do when injected?

A

Compressing SAH with the injected blood.

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134
Q

Most common regional anesthetic in children

A

Caudal

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135
Q

Caudal can be done

A

Awake or sleeping

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136
Q

You don’t want to get

A

CSF

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137
Q

Brachial plexus blocks

A

Interscalene
Supraclavicular
Infraclaviular
Axillary

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138
Q

Supraclavicular/ infraclavicular

A

Pneumothorax

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139
Q

Interscalene block best for

A

Shoulder

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140
Q

Nerve roots of Brachial Plexus

A

C5-T1

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141
Q

Branches of Brachial Plexus

A
MARMU
Musculocutaneous
Axillary
Radial
Median
Ulnar
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142
Q

Cords and divisions of brachial plexus.

A

3 cords

6 Divisions

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143
Q

Appears black of image

A

LIQUID (anechoic)

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144
Q

Appears white of image

A

BONE (hyperechoic)

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145
Q

Safer to work (in plane or out of plane)

A

In plane

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146
Q

Commit to memory pg.

A

409

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147
Q

Pain to pinky finger, what dermatome?

A

C8

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148
Q

Radial nerve stick gives you ______when stimulated everything else______

A

EXTENSION : FLEXION

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149
Q

Radial nerve stick gives you ______when stimulated everything else______

A

EXTENSION ; FLEXION

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150
Q

Cervical plexus block

A

Unilateral procedure of the neck

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151
Q

Complications of Cervical plexus block

A

Unilateral phrenic nerve paralysis (ONLY see with DEEP)
Horner’s syndrome
Hoarseness
Accidental subarachnoid or epidural injection .

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152
Q

Complication, Only seen with DEEP cervical block

A

Unilateral phrenic nerve paralysis

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153
Q

How much to inject for Cervical plexus block ?

A

4 ML (think C2-C4)

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154
Q

Interscalene is between

A

Between 2 scalene muscles

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155
Q

Level of C6

A

Cricoid Cartilage

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156
Q

Where it crosses interscalene groove

A

Level of C6

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157
Q

Best way to prevent intravascular injection

A

Aspirate first

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158
Q

Occurs in 100% patients undergoing interscalene block

A

Ipsilateral phrenic nerve block resulting in diaphragmatic paresis.

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159
Q

ISB is a ____volume block? how much ?

A

Large ; 40

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160
Q

Most inferior part of the interscalene groove

A

2 cm from MidPoint of clavicle on the medial side.

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161
Q

Landmarks to know Interscalene Groove

A

Anterior scalene
Middle scalene
Clavicle
1st rib

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162
Q

Complications of Supraclavicular

A

Pneumothorax. (hemothorax as well)
Horner’s syndrome
Phrenic nerve block

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163
Q

Supraclavicular volume

A

20-30 mL

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164
Q

Axillary bundle, nerve missing (muscle associated)

A

Musculocutaneous nerve (Costcobrachialis muscle)

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165
Q

Injection site for axillary block

A

Find axillary pulse as high as possible

Move to rope of muscle.

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166
Q

Most popular of the ISB

A

Axillary block

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167
Q

For axillary block, do this to the arm

A

90 deg out and 90 degrees up

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168
Q

Lies outside of axillary sheath

A

MCTN

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169
Q

For axillary block, what can cause incomplete spread.

A

Fascial septa result in INCOMPLETE SPREAD of LA

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170
Q

Median and radial nerve inject

A

3-4 cm

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171
Q

Radial where do you inject your LA.

A

Radial flexor muscle and extending to the dorsal surface of the ulna styloid

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172
Q

NO epi where with the elbow

A

Below elbow

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173
Q

NO epineprhine in 4 areas

A

Nose , toes, fingers, penis

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174
Q

Median and radial nerve blocks at elbows

A

Insert B bevel needle slighly medial to the brachial artery .

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175
Q

Radial nerve at elbow

A

Inject

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176
Q

Femoral nerve becomes the

A

Saphenous nerve

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177
Q

Lumbar plexus levels

A

L1 - L4 an some T12

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178
Q

Ulnar block of the elbow

A

Insert between the medial condyle of the humerus and the olecranon of the ulna

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179
Q

Ulnar block at the wrist

A

Insert B bevel needle slighly adjacent to the ulnar artery

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180
Q

Median nerve block at the wrist

A

Between long palmar muscle and the radial flexor muscle of the wrist.

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181
Q

Popliteal is a

A

Sciatic nerve block

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182
Q

Ankle block vs popliteal interchangeable

A

Saphenous is missing

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183
Q

Most difficult to block

A

Posterior tibialis

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184
Q

Superficial nerve of lumbar

A

All that starts with S

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185
Q

Radial nerve block at the wrist

A

Inject beginning at the radial flexor muscle and exendin to the dorsal surface of the ulnar styloid.

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186
Q

Webspace between 1st great toe and 2nd toe

A

DEEP peroneal nerve.

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187
Q

BLOCK REVIEW

A

421` 423

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188
Q

Retrobulbar

A

Up and away or down an dway s

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189
Q

Bier block , need to stay up for at least

A

20 minutes

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190
Q

Ilioinguinal and iliohypogastric nerve block

A

Inject 8-10 ccc

Most common complication

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191
Q

Most common complication of Ilioinguinal and iliohypogastric nerve block

A

Patient discomfort.

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192
Q

Maternal changes : lungs parameters unchanged

A

TLC, VC, IC unchanged

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193
Q

Maternal changes: decreased lung

A

Decreased FRC

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194
Q

What makes maternal desaturation fast?

A

Increase in Alveolar ventilation, and a decreased in FRC, desaturation quick

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195
Q

Makes maternal at risk for bleeding

A

Airway engogement

mucosal friable

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196
Q

Do not do this with maternal

A

no nasal instrumentation

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197
Q

Term changes of maternal : CO2 and PaO2

A

PaO2 increases

PaCo2 decreases

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198
Q

O2 consumption produces a

A

70% increase in alveolar ventilation at term.

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199
Q

Term and MAC

A

Decreased

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200
Q

Alveolar vs minute ventilation (difference between)

A

Dead space

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201
Q

Closing volume and capacity

A

Unchanged

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202
Q

Oxygen consumption at rest for maternal

A

20-30%

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203
Q

Oxygen consumption at Labor

A

2nd stage 100%

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204
Q

Uterine vasculature % of Co

A

10%

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205
Q

Blood volume and plasma volume

A

Dilutional anemia because plasma volume goes up greater than blood volume

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206
Q

Increase in Blood volume no increase in BP because

A

drop in SVR.

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207
Q

Increase in Blood volume no increase in BP because

A

drop in SVR and PVR

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208
Q

Maternal At risk for this because of an increase in blood volume

A

Thromboembolic events

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209
Q

CO =

A

HR x SV

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210
Q

Blood volume is

A

Up 25-40 %

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211
Q

Aortal caval compression aka

A

Maternal supine hypotensive syndrome

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212
Q

Best position for maternal

A

Left lateral tilt

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213
Q

Explains Aortal caval compression

A

Compression of IVC decrease VR and results in decrease SV and hypotension

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214
Q

What is the maternal response to Aortal caval compression?

A

TACHYCARDIA

VASOCONSTRICTION

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215
Q

CO increase in pregnant women is due to

A

Increase is SV

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216
Q

Stages of labor : First (four dermatomes)

A

Begins onset of contraction , result in complete dilation of the cervix

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217
Q

Stages of Labor: seconds (Sacral)

A

Sacral included.

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218
Q

Signs of fetal distress

A

Fetal scalp ph< 7.20
Meconium stained amniotic cluids
Oligohydramnios

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219
Q

Normal placental implantation

A

Top of the uterus

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220
Q

Placenta previa

A

Painless preterm bleeding
Plan
Pass on pushing (C-section needed)

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221
Q

Non-reassuring fetal heart rate pattern

A

Repetitive late decelerations
Late decelerations due to prolonged cord compression
Loss of beat-to beat variability associated with late or deep decelerations
Sustained fetal heart rate < 80bpm

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222
Q

Placenta previa ultimate goal

A

Keep fetus inside to as close to 37 weeks as possible

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223
Q

Expected management is terminated when

A

Active labor
documented lung maturity
Excessive bleeding
Gestational age reaches 37 weeks.

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224
Q

Most common cause of neonatal morbidity and mortality

A

Before 20 weeks

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225
Q

Incidence of accreta for normal

A

3%

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226
Q

Antibody serum

A

2- 4 hours for exact match blood

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227
Q

Emergency bleeding volume for labor and delivery

A

VOLUME, VOLUME, VOLUME

ACCESS

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228
Q

What to prepare for possible increase bleeding.

A

Large bore IV
4 PRBC
FLUID/BLOOD WARMERS (possible DIC)

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229
Q

Placental abruptio is the

A

loss of area for maternal fetal gas exchange

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230
Q

Known risk factors

A
HTN
Age
Parity
Tobacco
Trauma
History of
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231
Q

What to order for Placenta abruptio :

A

RBCs
Platelets
FFPs
Cryopreciptate

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232
Q

Any concenrst with volume or coagulation status

A

No epidural

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233
Q

Abnormal placental implantation, worst is

A

percreta

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234
Q

Placenta Accreta

A

Adheres to the

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235
Q

Placenta Increase

A

INvades and is confined the myometrium

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236
Q

Placental Percreta

A

PEN”etrate the myometrium

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237
Q

Hemabate don’t use with

A

ASTHMA

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238
Q

Methergine don’t use with

A

Hypertension (High blood pressure)

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239
Q

If mom has had a placenta previa, previous C-section or had uterine trauma she is at risk for

A

developing PLACENTA ACCRETA.

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240
Q

The more C section the greater the incidence of

A

ACCRETA

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241
Q

Amniotic Fluid embolism

A

High mortality rate 50% in the first hour

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242
Q

Amniotic fluid embolism (A- OK)

A

A OK
Atropine
Ondansetron
ketorolac

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243
Q

MAternal heart Group I

A

Regional ok

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244
Q

Maternal heart Group II

A

NO regional

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245
Q

DIC fibrinogen

A

< 150

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246
Q

DIC platelets

A

Decrease

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247
Q

DIC times all

A

increase

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248
Q

Pre-eclampsia DEFINITIVE TREATMENT

A

DELIVERY of the fetus.

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249
Q

Maternal Heart problems Group I

A

MVP, AI, L to R shunts

Everything else group 2

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250
Q

Hemodynamically Magnesium does the

A

OPPOSITE OF CALCIUM

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251
Q

Loss of DTRs, magnesium level mg/dL

A

7-12

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252
Q

During laryngoscope , see fluid, next action

A

Suction

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253
Q

Does the risk of preeclampsia ends with delivery

A

NO

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254
Q

Normal Mag mg/dl, mEq/L

A
  1. 8-2.5

1. 5-2.1

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255
Q

Treat which decelerations with priority

A

Late

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256
Q

Agent with lower pka

A

more ionized

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257
Q

Nonionized form is

A

Lipid soluble.

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258
Q

3% chlorprocaine does

A

Not follow the rule,

VERY HIGH CONCENTRATION

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259
Q

The lower pKA the

A

the faster the onset

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260
Q

Speed of onset is dependent on

A

Degree of ionization

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261
Q

Lipid solubility is a measure of

A

potency

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262
Q

Duration of action is more important for

A

Protein binding and LIPID SOLUBILITY

But MAINLY protein binding

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263
Q

Oil water partition coefficient

A

Highest potency

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264
Q

The higher the Oil water partition coefficient

A

The higher the potency and lipid solubility

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265
Q

Low albumin

A

Increase action of highly bound drug.

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266
Q

What determines blood cocentration

A

Wheter

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267
Q

The only vasoconstrictor LA

A

Cocaine

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268
Q

LA goes away from site from

A

Absorption

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269
Q

What form do you need to have an effect for a conduction

A

BOTH (one to cross one to bind)

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270
Q

2 forms of esters

A

Procaine

Chlorprocaine

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271
Q

Dibucaine is an

A

Amide local anesthetics

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272
Q

80% suppression with dibucaine

A

Normal

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273
Q

Dose of Lipid

A

1.5 mg/kg followed 0.25 ml/kg/min

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274
Q

Succinylcholine to vecuronium

A

Make sure you check twitches before giving NDNMB

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275
Q

No propofol in the

A

Context of cardiovascular instability

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276
Q

ECF Liter

A

14 L (1/3)

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277
Q

ICF Liter

A

28 L (2/3)

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278
Q

Other name for ICF

A

Cytosol and cytoplasm

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279
Q

Cell membrane has a

A

Phospholipid bilayer

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280
Q

What is the role of the phospholipid bilatery

A

prevent things from crossing

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281
Q

Cell membrane

A

50% proteins

50% of fatty acids.

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282
Q

For substance to cross you need

A

Channel

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283
Q

You need Amino acids to create

A

proteins

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284
Q

Amino acids are made from

A

DNA

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285
Q

Proteins 3 main functions

A
  1. receptor
  2. transporter
  3. enzymes
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286
Q

Receptor with 7 seven branches in and out of the cell

A

GPCR

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287
Q

Transporter receptor is a type of

A

bring products in an out depending on the concentration gradient

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288
Q

Major ions in extracellular and concentration

A

Sodium (135-145}
Chloride 98-108
Calcium (8-10.2)g/dL
Bicarbonate (22-27)

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289
Q

Major ions in INTRACELLULAR and level

A

K

135-150

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290
Q

All Major ions in INTRACELLULAR and level

A

K, Mag, and phosphate and PROTEINS

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291
Q

Phosphate INside is

A

100

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292
Q

Proteins levels inside the cell

A

65

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293
Q

Na+ inside the cell

A

10-15

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294
Q

Any ionized gets inside cell you get

A

Neurotransmitter release

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295
Q

BICARBONATE inside the cell is

A

18-22

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296
Q

K+ outside of cells level

A

3.5 - 5

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297
Q

Phosphate and Mag outside of the cell lvels

A

2 and 2

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298
Q

Protein outside of the cell level

A

16

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299
Q

Ficks law of diffusion

A

Concentration gradient
Size
thickness
Surface of the molecule

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300
Q

NA-K pump move Na+

A

Against concentration gradient, so OUT , 3 NA+

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301
Q

NA-K pump move K+

A

Against concentration gradient, soIN, 2 K+

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302
Q

ATP broken down to ADP

A

Releases a phosphate

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303
Q

Na-K ATPase uses

A

ENERGY

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304
Q

Calcium attaches to the

A

RECEPTOR*(which is a protein)

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305
Q

When calcium or ions attach to a receptor is.

A

A LIGAND-GATED ION CHANNEL._

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306
Q

Examples of ligand

A

Drugs, chemical , neurotransmitter, hormones

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307
Q

1st messenger is the

A

ligand

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308
Q

2nd messenger is the

A

GPCR

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309
Q

Signal transduction is

A

RELAY of message, (tweet , retweet).

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310
Q

G-Protein (i)

A

Inhibitory

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311
Q

G-Protein (s)

A

Stimulatory

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312
Q

Beta adrenergic agonist would be a

A

Stimulatory (Gs) (stimulates production of adenylate cyclase producing cAMP)

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313
Q

AcH binds to

A

Inhibitory muscarinic , prevent production of adenylate cyclase

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314
Q

2nd messengers are all

A

TISSUE SPECIFIC

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315
Q

Bronchial smooth muscle : Terbutaline”:

A

Ligand and first messenger

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316
Q

Terbutaline binds to

A

Beta -2 receptor, activate G protein

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317
Q

Enzymes are generally located on the

A

inside

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318
Q

Adenylate cyclase is an

A

Enzyme

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319
Q

Substrate is

A

ATP

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320
Q

The first messenger is where?

A

Outside the cell

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321
Q

The second messenger is where

A

inside

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322
Q

Cyclic AMP

A

active protein kinase (all kinase add a phosphate)

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323
Q

Calcium and bronchial

A

Bronchial constriction

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324
Q

ATP substrate create

A

Cyclic AMP

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325
Q

Signal transduction steps 1-6

A
  1. ligand
  2. activates recepot
  3. binds to protein
  4. Enzyme (adenylate cyclase)
  5. 2nd messenger cyclic AMP
  6. Physiological response
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326
Q

Nitric oxide is not a ____why?

A

LIGAND; Way to small travels in the body

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327
Q

Nitrous oxide is not a ligand but it is

A

STILL a 1st messenger

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328
Q

Nitrous oxide is still a first messenger because

A

It still sends a signal from outside to the inside of the cell

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329
Q

Nitric oxide inside the cell

A

Nitric oxide synthase (NOS) , convert the substrate GTP to cyclic GMP

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330
Q

cGMP works on

A

protein kinase G and we get physiological response–> BRONCHODILATION

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331
Q

Cyclic GMP PDE5

A

Cialis , viagra

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332
Q

PDE 3

A

milrinone

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333
Q

Sildenafil is

A

viagra which is a PDE5

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334
Q

Phospholipase C action

A

Phospholipase C remove the head of the phopholipids then it becomes IP3, cut head off.

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335
Q

IP3 acts on ER because calcium

A

2nd messenger

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336
Q

2nd messenger with IP3

A

2nd , second messenger is CALCIUM

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337
Q

Peripheral nervous system

A

Efferent NS (motor)

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338
Q

VEM mnemonic for

A

Ventral
Efferent (away central to peripheral)
MOTOR

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339
Q

Going in or towards

A

Afferent

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340
Q

The predominant neurotransmitter in the periphery is

A

AcH

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341
Q

Cell bodies –> Axons terminal then

A

Dendrites, Ganglion , organ

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342
Q

What is a ganglion?

A

Peripheral collection of nerve cell bodies

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343
Q

Neurotransmitters list

A
Ach
Histamine
Serotonin
Glutamate
GABA
Etc..
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344
Q

Neurotransmitters list

A
Ach
Histamine
Dopamine
Serotonin
Glutamate
GABA
Epinephrine
Norepinephrine
Glycine
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345
Q

A-alpha most of the work done with what neurotransmitter

A

Ach

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346
Q

Dopamine neurons are called

A

Dopaminergic neurons

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347
Q

Autonomic divisions

A

Visceral : heart , gut ,stomach,

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348
Q

Long pre-ganglionic and short post ganglionic neurons

A

parasympathetics neurons

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349
Q

Short pre-ganglionic and Long post ganglionic neurons

A

Sympathetic neurons

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350
Q

All preganglionic neurons release

A

ACH

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351
Q

Release of NE are called

A

Adrenergic nerve

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352
Q

Preganglionic neurons act on adrenal medulla

A

ACH

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353
Q

Because NE is release into the adrenal medulla it is a

A

HORMONE

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354
Q

Muscarinic is a

A

GPCR

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355
Q

Muscarinic is a _____receptor

A

GPCR

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356
Q

All Adrenergic receptors are

A

GPCR

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357
Q

SAME for remembering afferent vs efferetn

A

Sensory –> Afferent

Motor- EFFERENT

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358
Q

To know where you are look for the

A

Ganglion (it is the posterior)

359
Q

Where does the action potential start

A

Dendrites , send signal –> Dorsal root ganglion =–> goes to dorsal horn –> axon collaterals

360
Q

Axon collaterals stay on the same

A

Side (ipsilateral pathWAYS)

361
Q

90%

A

PSEUDOpolar

362
Q

SAD to remember

A

SENSORY
AFFERENT
DORSAL

363
Q

Dorsal horn has what ?

A

Bunch of layers called REXED LAMINAE

364
Q

A-delta travel ? which lamina

A

Travel pass dorsal root ganglion, will synapse as fast as they can REXED LAMINAE I or REXED LAMINA V

365
Q

How many rexed laminae

A

10 (I-X)

366
Q

Fast and sharp pain fibers go up to the brain using

A

LATERAL SPINOTHALAMIC PATHWAYS

367
Q

Slow and chronic pain travel using

A

VENTRAL spinothalamic pathways.

368
Q

Lamina for slow and chronic pain

A

Lamina II and III

369
Q

Slow and fast pain

A

Anterior and lateral pathway

370
Q

C fibers

A

Slower burning throbbing pain pathway

371
Q

Substantia Gelatinosa found in

A

Rexed lamina II and /or III

372
Q

Neurotransmitter release from A delta is

A

GLUTAMATE which binds to AMPA and NMDA receptors on the receptors on the postsynaptic membrane

373
Q

Neurotransmitter released from C fibers is

A

Substance P which binds to NK-1 neurokinin 1 receptors on the postsynaptic membrane.

374
Q

Anterolateral system

A

Lateral spinothalamic tract

Ventral spinothalamic tract

375
Q

Tracts looking lines are on the

A

DORSAL

376
Q

SSEPs

A

Dorsalateral fasciculus

377
Q

Slower pathway is the

A

Ventral Spinothalamic tract

378
Q

Crude touch and pressure

A

Ventral spinothalamic (spinal to thalamic)

379
Q

Where are pain impulses attenuated?

A

Susbstantia Gelatinosa

380
Q

Pain in the body

A

Endorphins
Enkaphelins
Dynorphins

381
Q

Opiods receptors

A

Mu-1
Mu-2
Kappa
Delta

382
Q

**The predominant opioid receptor is

A

Mu-2

383
Q

Mu-2 receptor action

A

Pain transmission/sensation is decreased

384
Q

Mu-2 creates ____Analgesis

A

SPINAL

385
Q

Supraspinal analgesia

A

you feel it but you dont care

386
Q

Spinal analgesia

A

Mu-1

387
Q

Spinal analgesia

A

Perception of pain is diminished

388
Q

Opioids acts on the

A

Periventricular gray or Periaqueductal gray ,

389
Q

Spinal analgesia results fromthe action of opioids in the

A

Substantia Gelatinosa or in the periventricular (after epidural or intrathecal administation) /periaqueductal gray (after IV admnistration )

390
Q

Nuclei

A

Central bodies collection

391
Q

Ganglia

A

Peripheral nerve bodies collection

392
Q

Key term for Vd is

A

Theoretical volume

393
Q

Elimination Half Life

A

TOTAL AMOUNT of the drug

394
Q

Elimination half time

A

T 1/2 beta

395
Q

Vd =

A

Quantity / plasma concentration (at time =0)

396
Q

Large volume of distribution

A

Induction agent like propofol

397
Q

Charged and ionized

A

Water soluble.

398
Q

Drugs with small Vd

A

Muscle relaxants

399
Q

MR are water soluble due to their

A

POLAR nature.

CHARGED NATURE>

400
Q

Induction agents are

A

Lipid soluble because NONPOLAR and UNCHARGED NATURE

401
Q

Neonates need more succinylcholine ____why?

A

MORE; IMMATURE NMJ

402
Q

Neonates and NDNMA

A

Less , immature NMJ

403
Q

Zero order kinetics aka

A

Michaelis Menses

404
Q

Linear order kinetics

A

Linear (constant)

405
Q

First order kinetics

A

LOG (constant FRACTION)

406
Q

Most drug eliminated through

A

FIRST ORDER KINETICS

407
Q

Distribution is

A

Alpha

408
Q

Elimination is

A

B”e”ta

409
Q

Contraindicated in patients receiving dandrolene therapy

A

CCBs

410
Q

Weak acids and weak bases important concept

A

pKa

411
Q

Weak bases LA when is pka/pH relevant

A

Patient is septic

412
Q

If pH < Pka for WA

A

Nonionized

413
Q

If pH > Pka for WA

A

Ionized

414
Q

If pH < Pka for WB

A

Ionized

415
Q

If pH > Pka for WB

A

Nonionized

416
Q

Follow 3 steps for acids bases questions

A
  • WA or WB
  • Look at pKa
  • pH of the target solution
417
Q

Renal effects of nitrous oxide include:

A

decreased renal blood flow secondary to increased renal vascular resistance

418
Q

Nitrous oxide appears to decrease renal blood flow by increasing renal vascular resistance. This results in

A

decreased glomerular filtration and decreased urine output.

419
Q

Most drugs are

A

Neither weak acids or weak bases

420
Q

Barbiturates are

A

Weak acids

421
Q

Weak acids is an

A

molecule that give up hydrogen ions incompletely

422
Q

HBarb examples of weak acids breakdown

A

[H+] + [Barb - ]

423
Q

SA node location

A

Posterior Right atrium

424
Q

Internodal pathway : Anterior

A

Bachmann RA to Left atriuj

425
Q

Internodal pathway : Middle

A

Wenckeback tract

426
Q

Internodal pathway: Posterior

A

Thorel tract

427
Q

AV node located on

A

Floor of the right atrium , near tricuspid valve.

428
Q

Triangle of Koch is in the

A

heart

429
Q

AV node delay allows

A

Proper conduction of action potential

allow the heart to be synchronous

430
Q

Right and Left bundle branches small branches called

A

Fascicle

431
Q

Action potential sequence of propagation

A

SA node, AV node,s Bundle of HIs, R+L BB , purkinje fibers.

432
Q

Nodal action vs ventricular myocytes action potential

A

No phase 1

No phase 2 in nodal

433
Q

RMP for the nodal is (stable vs unstable)

A

Not stable

434
Q

What ECG represents

A

Electrical activity

435
Q

P wave

A

Atrial depolarization

436
Q

QRS complex

A

Ventricular depolarization

437
Q

U wave may represents

A

hypokalemia

438
Q

RMP ventricular myocytes

A

-90 mV

439
Q

RMP SA nodal cells

A

-70 mV

440
Q

RMP is maintained by

A

Potassium Efflux (Leaky channels)

441
Q

Depolarization is caused what ions

A

sodium influx

442
Q

Ventricular myocytes Phase 0

A

Sodium influx

443
Q

Ventricular myocytes Phase 1

A
Transient repolarization (Chloride influx) 
Inactivation of the fast sodium channels
444
Q

Plateau phase is

A

Phase 2

445
Q

PHase 2 of ventricular myocytes

A

Calcium L-types channels open , and calcium influx

446
Q

Phase 3 of ventricular myocytes

A

Late/ delayed repolarization

Delayed rectifier potassium channels

447
Q

Phase 4 of ventricular myoctyes

A

Back to RMP

448
Q

Na-K pump only responsible for about

A

6 mV

449
Q

Helps maintain and restore RMP

A

Na-K- ATPase

450
Q

Ohm’s law states

A

Voltage = Current / Resistance

451
Q

V = (voltage)

A

IR (current x resistance)

452
Q

For nodal phase 4 , what channels are responsible to maintain

A

Funny sodium channels

453
Q

What type of Calcium channels for nodal phase 0

A

T-type calcium channels (transient)

454
Q

For phase 3 what is the channel working

A

L-type calcium channels

Delayed rectifier potassium efflux

455
Q

With release of ACH, it binds to

A

muscarinic receptor M2

456
Q

Excitatory M receptors are

A

M1, M3, M5

457
Q

Inhibitory M receptors are

A

M2, M4

458
Q

NE binds to

A

B1, GPCR

459
Q

Transplanted heart: parasympathetic innervation

A

no parasympathetic innervation

460
Q

SA node beating at

A

110 for transplanted heart because of a lack of parasympathetic stimulation .

461
Q

Potassium leaky channel is a

A

2 port

462
Q

Primary cause of negative charge is

A

Protein

463
Q

Phase 2 also has a

A

conformational change to sodium channels, shuts the H-gates

464
Q

The conformational changes that occurs to the sodium channels is responsible for the

A

Absolute Refractory period (plateau phase)

465
Q

Repolarization phase 3 , the

A

Relative Refractory period (strong enough stimulus can cause an action potential).

466
Q

SV will be determined

A

EDV- ESV

467
Q

EDV is primarily determined by

A

Preload (volume)

468
Q

Ejection fraction formula

A

EF = SV/ EDV x 100

469
Q

EF =

A

EF = EDV- ESV/ EDV

470
Q

Lusitropy meaning

A

myocardial relaxation

471
Q

Preload is dependent on

A

Compliance
venous tone
Venous return
Blood volume

472
Q

Extravascular volume determined by

A

Sodium

473
Q

3 types of reflex

A

Baroreceptors
Bain bridge
Bezold -Jarisch

474
Q

Angiotensinogen is made in the

A

LIVER

475
Q

ACE is in the

A

lung

476
Q

Precursor of angiotensin I

A

Angiotensinogen

477
Q

Force at end diastole, right before contraction is

A

Preload

478
Q

The more filling the more

A

Preload

479
Q

Contractility is determined by the

A

CHEMICAL environment of the cardiac cell

480
Q

Atrial kick

A

20-30%

481
Q

Frank Starling mechanism

A

Increase preload

482
Q

Decrease Venous return states all the hemodynamic changes

A
Decrease Preload
Decrease filling
Decrease EDV
Decrease SV
Sam
483
Q

After fluids administration , what parameter is increased?

A

Increased preload
EDV increase
ESV unchanged.

484
Q

When you give a loop diuretic, what parameter is increased?

A

Decreased preload
EDV increase
SV decrease
ESV unchanged.

485
Q

Cardiac tamponade : filling

A

Decrease ability to fill the heart.

486
Q

Afterload is associated with

A

pressure.

487
Q

Can increase SVR

A

Alpha 1 agonist

488
Q

If you increase afterload what happens to EDV, ESV, SV, BP and HR

A
EDV increase
ESV increase
SV decrease
BP increase
HR decrease due to reflex. (which reflex?)
489
Q

What happens after you give nitroprusside?

A
EDV decrease
ESV decrease
SV increase
BP decrease
HR increase due to reflex. (Baroreceptor? )
490
Q

After given a vasopressor, what happens to EDV, ESV, SV, BP and HR

A

Afterload increase
SV decreases
BP increase

491
Q

Phosphodiesterase Inhibitors OR DIGITALIS administration: EDV, ESV, SV, BP and HR

A
Increase in contractility 
Decrease EDV 
Decrease ESV
Increase SV
BP increase
HR decrease (BaroReflex) 
LV decrease
492
Q

CHF what happens ?

A
EDV increased
ESV increased
SV decreased
BP decrease 
and HR increase ( Baroreceptor reflex)
493
Q

Bezold Jarisch in response to

A

(hypotension) Low HR

494
Q

Concentric remodeling is associated with

A

Pressure overload. (AS)

495
Q

Eccentric remodeling is associated with

A

Volume Overload

496
Q

Wall stress / wall tension on questions think

A

LAPLACE’s law

497
Q

Hypertrophic cardiomyopathy is associated with

A

LV outflow tract obstruction .

498
Q

Hypertrophic cardiomyopathy is inherited in the

A

Autosomal dominant pattern

499
Q

Most common cause CARDIAC death for young adults and peds

A

Hypertrophic cardiomyopathy

500
Q

Hypertrophic cardiomyopathy is not a result of

A

HTN
CAD
Valvular disease
Pericardial disease.

501
Q

Hypertrophic cardiomyopathy dysfunction

A

Asymmetrical septal hypertrophy (ASH)

502
Q

Hypertrophic cardiomyopathy motion

A

Systolic anterior motion (SAM)

503
Q

Dilated LA associated with

A

Atrial fibrillation

504
Q

Hypertrophic cardiomyopathy may have atrium

A

LA enlargement

505
Q

Management of patient with Hypertrophic cardiomyopathy: HR

A

Maintain HR, not slow not fast

506
Q

Management of patient with Hypertrophic cardiomyopathy: RHYTHM

A

Keep it sinus

507
Q

Regurgitant management FFF

A

Fast, Full, forward

508
Q

Management of patient with Hypertrophic cardiomyopathy: Preload

A

Increase

509
Q

Management of patient with Hypertrophic cardiomyopathy: Afterload

A

iNcrease, Pure vasoconstrictor is the 2nd line of defense for hypotension

510
Q

***Management of patient with Hypertrophic cardiomyopathy: CONTRACTILITY you want

A

DECREASE

511
Q

Blood going trough LVOT is , what effect?

A

Venturi effect

512
Q

LVOT with Hypertrophic cardiomyopathy

A

Increased contract
Decrease preload
Decrease LV ventricular afterload (hypotension, vasodilation)

513
Q

Do not give with Hypertrophic cardiomyopathy

A

Lasix, NTG, PEEP nitroprusside.

514
Q

Medications to decrease contractility with Hypertrophic cardiomyopathy

A

Beta blockers

CCBs

515
Q

OLD CATs PEE Alot

A

Obstruction
Contractility
Preload
After loading

516
Q

Hypertrophic cardiomyopathy patient have this

A

AICD (if you disactivating you need the external defibrillator)

517
Q

Venturi effects draws the anterior leaflet of the mitral valve out as blood rushes by whose principles is this

A

Bernoulli’s principle.

518
Q

If the patient goes to a funny rhythm

A

Take the magnet off

519
Q

Magnet put pacemaker mode

A

Asynchronous mode ;

520
Q

Hypertrophic cardiomyopathy S/S (SAD)

A

Syncope
Angina
Dyspnea

521
Q

Notched P waves

A

Atrial enlargment

522
Q

Main.Goal intraoperative Hypertrophic cardiomyopathy

A

Prevent release of Catecholamines

523
Q

Hypertrophic cardiomyopathy prevents

A

Stimulation that can cause an increase in the HR and sympathetic stimulation

524
Q

No spinal or epidural with this condition

A

Hypertrophic cardiomyopathy

525
Q

A line with Hypertrophic cardiomyopathy shows

A

Biferiens pulse

526
Q

Vasopressor of choice for Hypertrophic cardiomyopathy

A

Phenylephrine

527
Q

If they ask about a valvular lesion in doubt pick

A

Rheumatic fever

528
Q

Severe Coronary artery disease

A

You want MORE TIME in diastole

Decrease HR

529
Q

Most prominent end point of severe cardiac issue

A

PULMONARY EDEMA

530
Q

Why fast HR with regurgitation?

A

Because diastole time you want lower for less regurgitation.

531
Q

Can cause regurgiation

A

Aortic annulus dilation

532
Q

Acute aortic regurgitation triad:

A

Severe dyspnea
Hypotension
weakness

533
Q

Acute AR LV has not

A

Compensate

534
Q

AR presents as

A

Sudden onset of pulmonary edema and HYPOTENSION

535
Q

Aortic regurgitation minimal vs severe

A

When regurgitnat volume remains < 40% SV

But severe if it > 60% SV

536
Q

Aortic regurgitation SPINAL and EPIDURAL

A

OK

537
Q

Aortic regurgitation Best vasopressor

A

EPHEDRINE

538
Q

RRRE

A

Regarding Regurgitation Reach Ephedrine.

539
Q

PCWP estimation of LV

A

Indirect

540
Q

Chronic MR is usually due to

A

Rheumatic fever

incompetent fever

541
Q

Acute MR cause

A

Acute MI ,

Papillary muscle rupture

542
Q

As much as ________% of the SV may be regurgitant with MR

A

50%

543
Q

LV compensates in MR by

A

Dilating and increasing EDV

544
Q

Filling to a greater volume emptying in the same

A

Frank Starling law

545
Q

In MR End Systolic volume remains

A

normal but eventually increases as the disease process progresses.

546
Q

In mild MR

A

regurgitant factors < 30 %

547
Q

Valvular lesion of MR radiates to the

A

Axilla

548
Q

In moderate MR

A

regurgitant factors 30-60 %

549
Q

In severe MR

A

> 60%

550
Q

Regurgitant disease is AR, and MR tolerates spinal or epidural

A

YES

551
Q

AS ventricles gets thicker what happens

A

There is subendocardial ischemia.

552
Q

Rhythm for AS wanted VERY IMPORTANT

A

NSR (b/c atrial kick)

553
Q

From least to most invasive to restore

A

Meds
EP labs
Atrial ablation

554
Q

Important to Aortic stenosis

A

NEED ATRIAL KICK (without it , 40% decrease in CO)

555
Q

Aortic Stenosis and afterload

A

maintain normal

556
Q

Aortic Stenosis and Contractility

A

Maintain

557
Q

Most common valvular disease in the US

A

AS

558
Q

Most common cause of AS

A

Calcification

559
Q

Aortic valve is a (bi/tricuspid)

A

TRICUSPID VALVE

560
Q

Normal size of Aortic Area

A

2.5 - 3.5 cm

561
Q

Severe stenosis , and surface area

A

75 % of decrease surface area

562
Q

Criticial AS

A

< 0.8 cm^2

563
Q

Concentric hypertrophy its because trying to decrease

A

WALL TENSION (La place law)

564
Q

La place law formula

A

(2 x Thickness x Tension)/Radius

565
Q

Epidural vs spinal for AS

A

Epidural, raise level of LA

566
Q

The higher the pressure gradient

A

The worst the patient

567
Q

Mean transvalvular pressure gradient : mild to mod

A

Mild to moderate , < 20

568
Q

Mean transvalvular pressure gradient : severe

A

20-50

569
Q

Mean transvalvular pressure gradient critical

A

> 50

570
Q

Peak transvalvular pressure gradient : mild to mod

A

< 36

571
Q

Peak transvalvular pressure gradient severe

A

> 50

572
Q

Peak transvalvular pressure gradient critical

A

> 80

573
Q

Aortic valve area, Mild to mod

A

1 - 1.5

574
Q

Aortic valve area, severe

A

0.8-1

575
Q

Aortic valve area,critical

A

<0.8

576
Q

Once angina from Aortic stenosis

A

Angina 5 years
Syncope 3 years
Dyspnea 2 years

577
Q

RV failure

A

Cor pulmonale

578
Q

The elimination half-time of a drug: related to clearance

A

is inversely proportional to the clearance

579
Q

The elimination half-timeof a drug is proportional to the v

A

Volume of distribution

580
Q

Delayed complication of rheumatic fever

A

mitral stenosis

581
Q

Mitral normal size

A

4-6 cm

582
Q

Most common cause of right side HR

A

Left side HF

583
Q

ARDS

A

Aortic regurgitation Diastolic sternal border

584
Q

MRSA

A

Mitral regurgitiaton systolic Apex

585
Q

MSDA

A

Mitral stenosis Diastolic Apex

586
Q

ASS ARCh

A

Aortic Stenosis systolic Aortic Arch

587
Q

Anesthesia Risks: GREATER DETERMINANT of postop complication

A

co- morbidities are the best prediction

588
Q

Surgical risk and outcome in patients 65 years and older primarily on 4 factors (APET)

A

Age
Patients status and coexisting
Emergency or elective
Type of procedure.

589
Q

Can decrease incidence of VAP

A

Subglottic suctioning

590
Q

Decline in organ function –>

A

1% decline per year in organ function after age 30 years . For example 70 year old has a 40% decline in general function

591
Q

DNA/RNA changes

A

Change in DNA/RNA replication, decrease in function.

592
Q

Elderly and thermoregulation

A

They shiver at 35C

593
Q

Young adults and thermoregulation

A

They shiver at 36.1

594
Q

Elderly and body fat

A

Increase body fat

595
Q

Elderly and total body water

A

Decrease body fat.

596
Q

Blood volume and Elderly

A

Decrease

597
Q

Collagen and skin elasticity is

A

Decrease

598
Q

Increase SVR in elderly cause

A

reduce arterial compliance

599
Q

Circulation time and elderly

A

Reduced myocardial pump function leads to reduced CO which prolong circulation time.

600
Q

Adrenergic receptors and elderly

A

A decrease in adrenergic receptor response.

601
Q

Decrease all drugs doses EXCEPT : why?

A

Atropine and beta agonist (like isoproterenol) because of a decrease adrenergic response.

602
Q

Increase risk of aspiration in elderly why?

A

Due to vocal cord stimulation being elevated.

603
Q

Sensitivity of need to clear secretion in the elderly is

A

Decreased

604
Q

FB close to carina , elderly response

A

Low stimulus to cough , more likely to aspirate

605
Q

Work of breathing in elderly is _____why?

A

Because of skeletal calcification and increased airway increase the work of breathing, predisposes them to ACUTE POSTOP VENTILATORY FAILURE

606
Q

What can put the elderly patient at risk for Acute postop ventilatory failure?

A

Increase WOB due to skeletal calcifications.

607
Q

Chest wall compliance for the elderly patient?Pulmonary compliance?

A

Decrease: Increase

608
Q

Respiratory changes in elderly mimics (obstructive/restricvie)

A

Restrictive

609
Q

Most sensitive indicator for renal function in the elderly

A

CrCl

610
Q

With decreased albumin

A

Give less

611
Q

MAC decrease is reduced by

A

4-6% decade of age over 40 years

612
Q

Summary box pg 507

A

507

613
Q

Elderly and Decrease vascular volume anesthetic consequence

A

Results in high initial plasma concentration

614
Q

Dose to stay the same for the elderly, 2 medications:

A

Neogstimine, Edrophonium

615
Q

Elderly and Decrease protein binding anesthetic consequence

A

increase availability of free drug

616
Q

Elderly and Increase body lipid storage sites

A

Prolonged action of lipid soluble drugs

617
Q

Decrease renal and hepatic blood flow

A

Prolonged actions of drugs dependent on kidneys and liver for elimination

618
Q

Pediatric larynx level

A

C2-C4

619
Q

Adult larynx level

A

C3-C6

620
Q

Narrowest function location for adult vs pediatric

A

Adult Vocal

Pediatric cricoid

621
Q

Pediatric emergency know when it is a

A

Medical vs surgical emergency

622
Q

V shaped epiglottis

A

Adult

623
Q

Omega shaped epiglottis

A

Pediatric

624
Q

ETT tube ID UNCUFFED

A

Age (years) / 4 + 4

625
Q

ETT tube ID for CUFFED

A

Uncuffed minus 3.5

626
Q

Defining hypotension in kids: at Term:

A

<60 mmHg

627
Q

Defining hypotension in kids: 1- 12 months

A

<70 mmHg

628
Q

Defining hypotension in kids:1-10 years

A

< 70 mmHg + (2x age in years)

629
Q

Ducturs arteriorsus shunt is

A

RIGHT to LEFT

630
Q

Syndrome think of –>

A

Craniofacial anomalies.

631
Q

Greatest risk of apnea

A

<46-60 weeks

632
Q

Diaphragmatic herniation highest occurrence on the

A

LEFT foramen of Bochdalek.

633
Q

CHD you can cause a

A

CONTRALETERAL PNEUMOTHORAX (small underdeveloped lung)

634
Q

First apgar in CHD

A

usually fine

635
Q

Between first and 2nd apgar, what happens to the baby

A

transitioning from high PVR, low SVR to low pVR high SVR

636
Q

CHD issues what preop information we need

A

ECHO, Heart disease, and conditions?

637
Q

CHD abdomen

A

SCAPHOID ABDOMEN ,

BOWEL IN THE THORAX

638
Q

CHD hallmark signs

A

Profound arterial hypoxia due to Right to left shunt
Barrel-shaped chest,
SEVERE RESTRATIONS

639
Q

CHD treatment goal

A

Preductal saturation over 85% using peak inspiratory pressure below 25 cm H2O and allowing PCo2 to rise to 45-55 mmHg

640
Q

CHD concern Respiratory

A

RIGHT SIDED PNEUMOTHORAX

641
Q

Increase PVR 3 things:

A

Hypothermia
Hypoxia
Acidosis

642
Q

Sings of TEF Feeding leads to

A

CCC
Choking
coughing
Cyanosis

643
Q

Most common variation is the form that ends in a

A

BLIND

644
Q

More likely for aspiration : TEF

A

TEF D

645
Q

Less likely for aspiration TEF

A

TEF A

646
Q

TEF is associated with what mnemonic

A
VACTERL
Vertebral defect
Anal atresia
CArdiac anomalies
TEF
Esophageal atresia
Renal dysplasia
Limb anomalies
647
Q

TEF anesthesia considerations: Key to successful anesthetic management

A

Correct positioning of the ETT

648
Q

TEF and PPV

A

Avoid PPV which will distend the stomach, thereby increasing the risk for reflux and ventilatory compromise.

649
Q

What should you avoid in a patient with TEF?

A

Avoid instrumentation of the esophagus.

650
Q

What should you avoid in a patient with TEF?

A

Avoid instrumentation of the esophagus increase the risk for reflux and ventilatory compromise.

651
Q

Describe the most common TEF

A

Noncommunicated blind pouch and a lower esophageal connection to the trachea

652
Q

How do you suction a patient with pyloric stenosis

A

Suction supine, left decubitus, and right decubitus

653
Q

CHD more at risk for pneumothorax

A

Lung is small can’t carry normal tidal volume.

654
Q

Most common cause of acute airway obstruction in otherwise healthy kids

A

CROUP

655
Q

With croup , what problem becomes evident and requires the patient to be intubated ?

A

Increase PaCO2.

656
Q

Treatment croup

A

2.25% epi in 3 ml of NS 0.05 ml.kg up to 0.5 ml/kg repet 1-4

657
Q

Edema of supraglottic structures (croup vs epiglottidis)

A

ACUTE EPIGLOTTIDIS

658
Q

Inspiratory stridor associated with

A

Epiglottidis

659
Q

Signs of Epiglottitis

A

Sitting forward and upright, , chin up, mouth open , drooling.

660
Q

Epiglottitis what vaccine to prevent?

A

Hemophillus influenza type B

661
Q

DO NOT ATTEMPT to do this with epiglottidis

A

Not attempt to visualize glottis

662
Q

Tube size with Epiglottidis

A

1-3 mm smaller

663
Q

Epiglottitis extubation usually

A

2-3 days

664
Q

Epiglottidis extubation, readiness?

A

Do an AIR leak
Use Glidescope.
Pediatric fiberscope

665
Q

Omphalocele covered?

A

Covered

666
Q

Gastrochisisis covered?

A

Sausage (not covered)

667
Q

Mortality Gastrochisis vs omphalocele

A

Mortalitiy related to cardiac and chromosomal abnormalities.

668
Q

Worst combination.

A

Macroglossia and MICROGNATHIA

669
Q

Survival omphalocele vs gastrochisis

A

Gastrochisis > 90 %

Omphalocele > 70-90

670
Q

Pierre Robin and treacher collins syndrome Anesthesi

A

Intubation very difficult
use awake technique
Fully awake before extubation

671
Q

Pierre Robin and treacher collins syndrome

A

ASD
VSD
PDA
Tetralogy of fallot.

672
Q

Pierre Robin and treacher collins syndrome : glottis

A

ASSOCIATED WITH SUBGLOTTIC STENOSIS

673
Q

Trisomy 21 most common issues.

A

Macroglossia and MICROGNATHIA

674
Q

Trisomy 21 associated anomalies

A

CHD

SUBGLOTTIC STENOSIS

675
Q

Right to left shunt you need to

A

NO AIR BUBBLES IN IV LINE

SHORT IV TUBING< WITH FEWEST CONNECTIONS>

676
Q

Malignant Hyperthermia triggers

A

All VA (halogenated) and succinylcholine

677
Q

Early MH signs

A

Masseter spasm
Tachypnea
Tachycardia

678
Q

Early MH SYMPTOMS

A

Masseter spasm
Tachypnea
Tachycardia

679
Q

Intermediate MH SYMPTOMS

A

CLASSIC MOTTLED CYANOSIS

680
Q

EARLY SIGNS of MH

A

Increased ETCO2

Peaked t waves

681
Q

Exhausted CO2

A

Not going back to baseline

682
Q

CO2 increase with MH is

A

Abrupt and very high

683
Q

Incidence of MH

A

1: 50,000

684
Q

MH increase in temperature

A

Increase 1C every 5 minutes

685
Q

MH is associated with increase

A

CO2

686
Q

Leading cause of death with MH

A

Vib
Renal failure
DIC

687
Q

Interventions:

A

Cooling pads

688
Q

Dandrolene will cause

A

Diuresis because of the mannitol

689
Q

Why do you need foley?

A

because dandrolene has mannitol

690
Q

Ryanodex mixing vs Dandrolene

A

Dandrolene: 20 mg in 60 ml; 3000mg manniotr
Ryanodex: 250mg in 5 ml . 125 mg mannitol each vial

691
Q

Testing for MH

A

Genetic

muscle biopsy: CAFFEINE (Caffeine Halothane contracutre test)

692
Q

First step in coagulation is

A

Endothelial damage

693
Q

Platelets: What promotes platelet adhesion

A

Von willebrand’s factor.

694
Q

Platelet binds to von willebrands via

A

Glycoprotein Ib (GP Ib)

695
Q

Problem with glycoprotein Ib

A

Platelet adhesion does not occur

696
Q

Most common inherited coagulation defect.

A

Von willebrand’s disease

697
Q

Type I von willebrand’ disease

A

insufficient amount of von willebrands production

698
Q

Most common von willebrand’s type is

A

Type I

699
Q

Increase in bleeding time with normal platelets and others

A

Von willebrand’s disease.

700
Q

Standard treatment for von willebrand’s disease

A

DDVAP (work 80% of the cases) if doesn’t work CRYOPRECIPITATE

701
Q

Platelet adhesion to VWF via GPIB now we need activation how?

A

Thrombin receptor –> located on the platelet, Precusor of thrombin is

702
Q

Platelet adhesion to VWF via GPIB now we need activation how?

A

Thrombin receptor –> located on the platelet, Precusor of thrombin is prothrombin, activated by thrombin (activate self)

703
Q

When platelet activated,

A

It changes shape, allows aggregation

704
Q

Thromboxane A2 and ADP

A

Signaling molecules that are released by platelets.

705
Q

Thromboxane A2 and ADP

A

Signaling molecules that are released by platelets,

Promotes Platelet aggregation

706
Q

2 that promotes platelet aggregation

A

Thromboxane A2 and ADP

707
Q

Thrombin role

A

thrombin activates self to promote more thrombin.

708
Q

Platelet aggregation feedback loop.

A

Positive feedback loop

709
Q

When platelet start aggregated , a platelet plug is formed, which is called

A

A white thrombus.

710
Q

How does the platelet plug formed? what is used

A

Fibrinogen is used.

711
Q

Prevent fibrinogen from sticking to platelets

A

Fibrinogen receptor GLYCOPROTEIN IIB/IIIa

712
Q

Fibrinogen receptor GLYCOPROTEIN IIB/IIIa is capped to prevent fibrinogen from sticking to it, which can remove the cap

A

ADP and Thromboxane A2.

713
Q

Most effective way to protect from coagulation

A

Intact endothelium

714
Q

Once platelets activated,we use

A

Phospholipase A2

715
Q

Phospholipase A2 (easy to remember)

A

Amputates leg (remove lipids)

716
Q

Phospholipase A2 after legs removes turns into

A

Arachidonic Acid

717
Q

The most common acquired blood clotting defect is due to

A

Inhibition of Cyclooxygenase production by ASA or NSAIDS.

718
Q

Common antiplatelet

A

ASA

719
Q

ASA is (reversible/irreversible)

A

Irrreversible for lifetime of the platelets.

720
Q

NSAIDS recommendation no more than

A

5 days

721
Q

3 antiplatelets other ASA or NSAIDS

A

Clopidogrel (Plavix)
Prasugrel (Effient)
Ticagrelor (Brillinta)

722
Q

Dipyridamole (persantine) increase

A

cAMP in platelets

723
Q

Dipyridamole (persantine) acts

A

by prevents aggregation of platelet via cyclic AMP (cAMP)

724
Q

Antifibrinogen receptor drugs are

A

GIIb and IIIa

CAP and BLOCK fibrinogen receptor.

725
Q

GIIb and IIIa drugs

A

Eptifibatide (intergrillin)
abciximab (Reopro)
Tirofiban (Aggrastat)

726
Q

Stimulates creation of platelets

A

Thrombopoietin.

727
Q

Tissue factor aka

A

Thromboplastin

728
Q

Fibrin what do you use

A

Intrinsic
Extrinsic
Final common pathways

729
Q

Fibrinogen to fibrin conversion done by

A

Thrombin

730
Q

Fibrin stabilizing factor (Factor XIII)

A

Secure clots

731
Q

Factor XIII bond is a

A

Covalent

732
Q

Activates factors XIII to XIIIa

A

Thrombin

733
Q

When in doubt think

A

Thombin for activation.

734
Q

Thombin impacts

A
Itself (Factor II) 
Helps activate factor XIII
Fibrinogen to fibrin
Factor V 
Factor VIII
Factor XI
735
Q

Final common pathway factors

A

1, 2, 5, 10, 13.

736
Q

Extrinsic pathway (extrinsic

A

3, 7

737
Q

Intrinsic pathway

A

Cant buy for 12 but for 11.98

738
Q

Glue
Fibrin
Activator

A

13
I
II

739
Q

Activated C is an

A

anticoagulant

740
Q

Activated protein S

A

stabilizes it.

741
Q

Direct thrombin inhibitors

A

Dabigatran
Argatroban
Bivalirudin

742
Q

Determinant of osmolality: Primarily

A

Sodium

743
Q

Concentration is

A

Amount/ volume

744
Q

Determinant of how much sodium we have

A

Aldosterone.

745
Q

Hormone that deal with water

A

ADH (vasopressin) arginine vasopresor. (AVP

746
Q

Volume determinant

A

ADH

747
Q

Normal Osmolality

A

270-310

748
Q

End products of metabolism is

A

Excreted

749
Q

End products of metabolism is

A

Excreted by kidneys

750
Q

OTher name for VITAMIN D

A

1,25 dihydroxycholecalciferol

751
Q

Calcium is involved in homeostasis

A

Vitamin D3

752
Q

Functional unit of nephron

A

nephron

753
Q

Kidney location

A

retroperitoneal space

754
Q

Nephron per kidney

A

about 1 Million

755
Q

Lose how much of nephron

A

65% of nephron before needing therapy

756
Q

Afferent arteriole

A

Toward the kidney

757
Q

Efferent arteriole

A

away from the kidney

758
Q

Efferent arteriole is associated

A

Peritubular capillaries

759
Q

Vasa recta is responsible for the

A

Hyperosmotic concentration

760
Q

Kidney receive CO

A

25%

761
Q

Pressure in the kidney

A

HIGH PRESSURE 80 mmHg

762
Q

Glomerular capillaries pressure is about

A

60 mmgh

763
Q

High pressure in glomerular capillaries and low pressure of bowman’s capsule favor

A

Filtration

764
Q

Fitration rate

A

125 ml/min then rest to efferent arteriole

765
Q

Filtration amount

A

180 L/ day

766
Q

Aldosterone acts on the

A

collecting duct

767
Q

Aldosterone acts on the

A

collecting duct (think AC)

768
Q

Reabsorbed most of the ions in

A

Proximal tubule

769
Q

Proximal tubule absorption of

A

Mag, Chloride, water, Glucose

770
Q

% of water absorbed in Proximal tubule

A

65%

771
Q

Majority of ions absorbed where?

A

Proximal tubule.

772
Q

Impermeable to sodium

A

Descending loop of Henle

773
Q

Thick ascending loop of henle

A

Sodium , Potassium - 2Chloride pump

774
Q

The juxtaglomerular apparatus

A

Juxtaglomerular apparatus

775
Q

In tubules, structure that sense fluid, sodium concentration

A

Macula densa

776
Q

Juxtaglomerular cells can communicate with

A

Macula densa

777
Q

Renin leads to the production on

A

Aldosterone

778
Q

Aldosterone role at the collecting tubule.

A

Sodium reabsorped

Potassium excretion

779
Q

PTH deals with

A

Calcium, Mag and Phosphate

780
Q

PTH acts on

A

Distal convoluted tubule.

781
Q

From distal nephron

A

Distal nephron–>Cortical collecting ducts –>

782
Q

Medullary nephron have

A

Aquaporin-2 channels.

783
Q

Aquaporin-2 channels need this hormone to function

A

ADH

784
Q

Aquaporin-2 helps with the

A

reabsorption of water

785
Q

Medications for blood pressure : HCTZ works where in the nephron ?

A

Early part of the distal tubule

786
Q

Loop diuretics work where do they work in nephron ?

A

Thick ASCENDING LOOP of HENLE

787
Q

Potassium sparing where do they work in nephron?

A

LATE PART OF THE DISTAL TUBULE

788
Q

Potassium sparing agents most common agent

A

Spironolactone

789
Q

Carbonic anhydrase inhibitors work where in the nephron?

A

Proximal tubule

790
Q

Osmotic diuretic(mannitol) work where in the nephron?

A

Proximal tubule or anywhere water is involved

791
Q

Ventricular Myocytes

A

Leaky K+ RMP

792
Q

-60MV set

A

Ca++ outside threshold

793
Q

RMP move from -90mV to -100mv cell is

A

HYPERPOLARIZED (further from threshold potential)

794
Q

Hyperpolarized K level

A

HypOkalemia

795
Q

When cell is hyperpolarized distance further from

A

RMP

796
Q

Hypokalemia cell is hyperpolarized, arrhythmia why

A

Reduction in potassium channel conduction, delay and increase in action potential duration. PURKINJE FIBERS MORE LIKELY TO FIRE> (Torsade, vtach)

797
Q

Threshold potential set by ____at __mV

A

Calcium ; -60 mV

798
Q

RMP becomes LESS negative (hypopolarized) what happens?

A

Due to HYPERkalemia

799
Q

Excitability with HYPERKALEMIA

A

VERY HIGH because RMP is close to threshold

800
Q

RMP close to threshold makes cell more

A

EXCITABLE (more likely for VFIB, Torsades)

801
Q

When the RMP is move UP past threshold ____what happens

A

(-40 for example) RMP move over the threshold

802
Q

Cardioplegia K level

A

15-40 K + mEq/L

803
Q

Cardioplegia puts the cardiac cells

A

Put in Absolute Refractory period( cannot fire)

804
Q

Threshold potential increase with

A

HyperCALCEMIA

805
Q

RMP Increase and Threshold potential increase

A

HyperKALEMIA and HYPERCALCEMIA (after treatment of hyperkalemia)
Cells is hyperpolarized, calcium stabilizes, LESS EXCITABLE , it raises the threshold potential level.

806
Q

RMP of nerve cell

A

normal at -70 mV

807
Q

Decrease threshold potential of nerve cell

A

HYPOCALCEMIA

808
Q

Hypocalcemia increases

A

Excitability

809
Q

Acute hyperkalemia treatment FIRST

A

Calcium chloride (works in 1-2 min)

810
Q

Acute hyperkalemia BICARB (work in how long)

A

Reduction in plasma concentration of K+ (3-5min)

811
Q

Hyperventilation and acute hyperkalemia (work in how long)

A

15 minutes

812
Q

Each 10 mmhg decrease in PaCo2 , serum K+

A

decrease 0.5 mEq

813
Q

Loop diuretics for hyperkalemia how does in

A

Work on distal nephron to increase K+ excretion

814
Q

Insulin, glucose and hyperkalemia

A

Acts on Na-K pump and drives potassium into the cells.

815
Q

Administer B2 agonist for hyperkalemia does what

A

Stimulates the Na-K pump

816
Q

The law of place states

A

For cylindrical shaped structures with an infinitely thin wall

817
Q

Law of Laplace formula

A

T= wall tension, P = pressure of liquid R= radius

818
Q

As structure expands, the radius _______, the tension in the wall of the structure ____. This law applies to

A

Increases; Increases; blood vessels and the left ventricle which also may be considered a cylinder.

819
Q

The law of Laplace has two applications to alveoli

A

Normal alveoli and alveoli deficient in normal surfactan.

820
Q

The smaller the radius of the bubble,

A

The greater the pressure inside of the bubble.

821
Q

No normal surfactant what happens to wall tension?

A

wall tension becomes constant and independent of the radius

822
Q

Smaller radius ____pressure

A

Higher pressure.

823
Q

Smaller alveoli empties into the

A

LARGER ALVEOLI.

824
Q

What causes atelectasis with ARDS?

A

Smaller alveoli empties into larger alveoli causing atelectasis.

825
Q

Flow 2 types

A

laminar / turbulent

826
Q

Flow is

A

Concentric ring of fluid.

827
Q

Flow is __________ to the fourth power of the radius

A

Directly proportional

828
Q

What has the most dramatic effect on floww?

A

Changing radius

829
Q

Flow is ____________to the hydrostatic pressure gradient

A

Directly proportional

830
Q

Flow and fluid viscosity

A

FLow is inversely proportional to fluid viscosity

831
Q

Property of a fluid that largely determines flow when flow is Laminar is

A

VISCOSITY .

832
Q

Trippling the radius increases flow to

A

81 times.

833
Q

What is more difficult when flow is turbulent

A

Ventilating patients.

834
Q

Resistance is _________to fluid viscosity

A

Directly proportional

835
Q

The greater the blood viscosity the greater the

A

Resistance.

836
Q

O2 dissociation curve x axis is

A

PO2

837
Q

O2 dissociation curve y axis is

A

Hgb Saturation.

838
Q

PaO2 clinical meaning of less than 60 mmhg

A

Hypoxemia

839
Q

CADET MS RIGHT

A
Increased Co2
Acidosis
2,3 DPG
Exercise 
Increase in temperature
Maternal hemoglobin
Sickle cell.
840
Q

BOhr effect deals with

A

Unloading and loading to O2 from tissues

841
Q

Bohr effect shifts curve to the

A

Rightt

842
Q

IN pulmonary capillary , BOhr effect

A

CO2 moves up and the dissociation curve shifts to the left and facilitates loading of O2.

843
Q

Total oxygen carrying capacity of the blood

A

(O2 Bound to hgb) + (O2 Dissolved in blood

844
Q

How to find how much Hgb bound to O2

A

1.34 x 15g / hg x100 ml of blood X % O2

845
Q

How to find O2 content that is DISSOLVED in blood?

A

0.003 x 90

846
Q

The solubility coefficient of O2 is

A

0.003

847
Q

The solubility coefficient of CO2

A

0.67

848
Q

Gas inversely related to

A

Temperature

849
Q

More gas will be given if patient is

A

Hypothermic , dissolves quicker/

850
Q

How much (%) of CO2 is transported in blood as HCO3- (bicarb) in WHOLE BLOOD

A

90% (whole blood)

851
Q

How much (%) of CO2 is transported in blood as HCO3- (bicarb) in WHOLE BLOOD

A

90% (whole blood) general accepted

852
Q

Hydrate CO2 you get

A

Carbonic Acid (H2CO3)

853
Q

CO+ H2O to get –

A

Carbonic acid

854
Q

Enzyme that convert the reaction of CO2 + H2O to carbonic acid

A

Carbonic anhydrase.

855
Q

Le Chatelier principle

A

Law of mass action

856
Q

More reactant will facilitate more reaction as per the law of

A

Mass action

857
Q

H2CO3 will lead to

A

HCO3 + H+

858
Q

O2 unloading is favored by an _______in Co2

A

Increase

859
Q

Major muscle for inspiration of

A

Diaphrgam

860
Q

Diaphragm is a

A

Skeletal muscle.

861
Q

Internal intercostal muscles from rib 1-7 help

A

INSPIRATION MOve ribs up and up

862
Q

Internal intercostal muscles from Ribs 8-12 they are located in a way that they help with

A

EXPIRATION

863
Q

VRG deal both with

A

Inspiration and expiration

864
Q

Everything originates in the

A

DORSAL RESP GROUP

865
Q

Everything originates in the

A

DORSAL RESP GROUP and goes to the DRG

866
Q

DRG is the

A

Inspiratory pacemaker.

867
Q

Apneustic Center + Pontine respiratory ROLE

A

Fine tune rate and depth of respiration

868
Q

Pneumatix center now known as the

A

Pontine respiratory group

869
Q

Pneumataxic center now known as the

A

Pontine respiratory group

870
Q

Hering Bruer reflex

A

Lung distention , stretch receptors

871
Q

Hering Bruer reflex more active in

A

Neonates.

872
Q

By when do people have adult number of alveoli

A

By 2 years of age.

873
Q

By when do people have adult number of alveoli

A

By 2 years of age. (though immature)

874
Q

Aortic arch we have

A

We have chemoreceptors

875
Q

Carotid bifurcation has

A

Peripheral chemoreceptors.

876
Q

Aortic sends message via

A

VAGUS NERVE

877
Q

Carotid send message via

A

GLOSSOPHARYNGEAL Nerve.

878
Q

What drives NORMAL Ventilation

A

CO2

879
Q

STRONGEST drive for ventilation

A

O2

880
Q

PaO2 less than 60, hypoxemia

A

Chemoreceptors will kick in

881
Q

When asked about dependent, vs nondependent.

A

Upright, normal TV quiet breathing

882
Q

FRC range

A

2-3L

883
Q

V/Q infinite

A

Extreme dead space

884
Q

Obstrcutive SLEEP APnea

A

KNOW EVERYTHING

885
Q

Obesity hyperventilation Syndrome

A

Know everything

886
Q

Know reversal of opioid

A

narcan Dose and infusion

887
Q

Know reversal of bnzo

A

Flumazenil Dose and infusion

888
Q

OHS worst than

A

OSA

889
Q

Alveoli are windows to the

A

Brain

890
Q

Lipid solubility is related to

A

Potency

891
Q

Pathophysiologic changes associated with metabolic alkalosis include: (Select 2)

A

hypokalemia, reduced tissue oxygen availability

892
Q

Metabolic alkalosis is associated with

A

hypokalemia, ionized hypocalcemia, secondary ventricular arrhythmias, increased digoxin toxicity, and compensatory hypoventilation (hypercarbia).

893
Q

Alkalemia may reduce tissue oxygen availability by

A

shifting the oxyhemoglobin dissociation curve to the left and by decreasing cardiac output.

894
Q

The use of long-acting beta-2 agonists without the concomitant use of ______ is associated with fatal and near fatal asthma attacks.

A

Inhaled Corticosteroids