Aba Basic Exam Questions

Front 1

Things that cause arterial pressure waveform dampening

Back 1

Arterial obstruction. Catheter occlusion or clot. Kinking of pressure tubing. Air in tubing. Loss of flush pressure in tubing. Transducer failure.

Front 2

If a-line transducer below level of heart what does it do to BP

Back 2

Overestimates. Remember - BP moves along WITH THE BED!!

Front 3

A-line transducer above level of the heart

Back 3

Underestimates BP. Remember - BP moves with bed!

Front 4

Does moving the arm up or down (lateral position) change arterial BP measurement?

Back 4

No

Front 5

Does lateral positioning change noninvasive BP measurement?

Back 5

Yes. Dependent arm has higher BP.

Front 6

Transducer height and BP change: conversion factor. 1 mmHg =

Back 6

1.36cm

Front 7

Narrow cuff

Back 7

Overestimates BP

Front 8

Large Cuff

Back 8

Underestimates BP

Front 9

Things that cause Acquired QT prolongation

Back 9

Antiarrhythmics class I:
-Quinidine
-Procainamide.
-Disopyramide.

Anti arrhythmic class III:
-Amiodarone.
-Sotalol.
-Ibutilide.
-Dofetilide.
-Dronedarone.

Hypomagnesemia.

Hypokalemia.

Tricyclic antidepressants:
-Amitryptiline.
-Doxepin.
-Imipramine.
-Clomipramine.

Non sedating antihistamines.

Erythromycin.

Pentamidine.

Azole antifungal agents.

Hypothyroidism.

CVA.

Liquid protein diets

Front 10

Which form of local anesthetic allows penetration of nerve membrane

Back 10

Uncharged form (unionized)

Front 11

Which form of local anesthetic blocks the sodium channel

Back 11

The charged form

Front 12

What does a low pKa mean about a local anesthetic

Back 12

It has a great(er) percentage of unionized drug (uncharged molecules) at a given pH

Front 13

What is the primary determinant of local anesthetic POTENCY

Back 13

Lipid solubility

Front 14

What determines speed of onset of action for local anesthetics

Back 14

PKa. LOWER pKa will have FASTER onset of action.

Front 15

What has faster onset of action: local with high pKa or low pKa?

Back 15

Low

Front 16

List the Ester Local anesthetics

Back 16

Procaine. Chlorprocaine. Tetracaine.

Front 17

How are ester local anesthetics eliminated

Back 17

Bio transformed by hydrolysis

Front 18

Order of blood levels based on site of administration

Back 18

IV. Tracheal. Intercostal. Caudal. Epidural. Brachial Plexus. Sciatic Femoral.

Front 19

How are ester local anesthetics eliminated

Back 19

Bio transformed by hydrolysis

Front 20

How are amide local anesthetics eliminated?

Back 20

Metabolized by hepatic microsomal enzymes.

Front 21

What genetic predisposition can delay metabolism/increase toxicity of ester local anesthetics?

Back 21

Pts with atypical or low plasma cholinesterase may have delayed metabolism, potentially increasing risk of toxicity

Front 22

What can increase risk of toxicity of amide local anesthetics?

Back 22

Decreased hepatic blood flow, ie hepatic disease or heart failure

Front 23

Cauda Equina Syndrome

Back 23

Severe back pain, saddle anesthesia, bowel/bladder dysfxn, sciatica, leg weakness
Associated w intrathecal lidocaine.
Associated w neurotoxic concentrations of drug.

Front 24

Contributing Factors of TNS (ONLY contributing factors)

Back 24

Lithotomy. Knee scope. Outpatient status.

Front 25

Resolution of TNS

Back 25

Within 3 days, rarely 7. Symptoms show up within 12-24 hrs. Treat w NSAIDS.

Front 26

Which has the least vasodilation, mepivicaine or lidocaine?

Back 26

Mepivicaine

Front 27

Prilocaine unique factor

Back 27

High doses can result in accumulation of metabolite ortho-toluidine which can produce methemoglobinemia.

Front 28

Bupivicaine consists of

Back 28

Racemic mixture of isomers

Front 29

Bupivicaine toxicity

Back 29

Cardio toxicity!!!! Bupivicaine tends to remain in Na channel ("fast in/slow out") Favors unidirectional block which can result in re-entry. Disrupts conduction thru AV node. Decreased myocardial contractility.

Front 30

Ropivicaine conformation

Back 30

S - enantiomer of Bupivicaine.

Front 31

Why is ropivicaine thought to be less toxic than Bupivicaine

Back 31

More vasoconstriction thus slower uptake. Less fast in/slow out. PS (drug is less potent). Not really relevant here though.

Front 32

Methemoglobinemia occurs in association with

Back 32

Benzocaine or EMLA cream

Front 33

What percentage of allergic reactions are associated with NMBs?

Back 33

33+%

Front 34

What causes proliferation of extrajunctional receptors

Back 34

Prolonged inactivity. Denervation. Trauma/Burns. Sepsis.

Front 35

Extrajunctional receptors bad effects (2):

Back 35

(1). Remain open longer --> more ion flow. Contributes to HYPERKALEMIA WITH SUCCINYLCHOLINE. (2). Proliferation accounts for resistance to non depolarizing muscle relaxants.

Front 36

Phase II Block

Back 36

Achieved by repeated dosing of sux. Resembles block achieved by non depolarizing drugs. Not reliably reversed by reversal agents.

Front 37

Side Effects of Succinylcholine

Back 37

Cardiac Dysrhythmias:
-Sinus bradycardia.
-Junctional rhythm.
-Sinus arrest.

Fasciculations.
Hyperkalemia.
Myalgia.
Myoglobinuria.
Increased intraocular pressure.
Increased intra gastric pressure.
Trismus.

Front 38

Sux is metabolized by

Back 38

Plasma cholinesterase

Front 39

How much sux reaches NMJ after injection

Back 39

Small fraction

Front 40

Is plasma cholinesterase present at the NMJ

Back 40

NO.

Front 41

What terminates the action of sux?

Back 41

Diffusion away from NMJ

Front 42

Things that cause decreased levels of pseudo cholinesterase

Back 42

Drugs:
-Nitrogen mustard.
-Cyclophosphamide.
-Anticholinesterase.

Liver disease.
Renal failure.
Cancer.

Front 43

Plasma cholinesterase wild type dibucaine #, duration of action, incidence

Back 43

80, 5-10 min, normal

Front 44

Plasma cholinesterase heterozygous atypical dibucaine #, duration of action, incidence

Back 44

50-60, 20 min. 1/480.

Front 45

Plasma cholinesterase homozygous atypical dibucaine #, duration of action, incidence

Back 45

20-30, 1-3 HOURS, 1/3200

Front 46

Molecular characteristics if NDMB

Back 46

Highly ionized, water soluble, poor lipid solubility (can't cross bbb or placenta)

Front 47

Things that prolong duration of action of NDMB

Back 47

*Aminoglycoside antibiotics. *Dantrolene. *Magnesium Local anesthetics. Antiarrythmics. Lithium. Tamoxifen.

Front 48

Clearance of Rocuronium

Back 48

Unchanged in bile. Up to 30% by the kidneys.

Front 49

Vecuronium metabolism/excretion

Back 49

Hepatic metabolism. **one metabolite, 3-something, is 50-70% as effective as Vec. Excreted in bile. Renal failure --> slight prolongation of duration of action.

Front 50

Which sodium channel conformational states do local anesthetics bind to the best, and what effect is this responsible for

Back 50

Bind to activated and inactivated states much better than resting state. Thus repeated depolarization produces more effective anesthetic binding. This is called USE DEPENDENT OR FREQUENCY DEPENDENT BLOCK. May relate to which nerves are blocked more quickly.

Front 51

Relationship between lipid solubility and time to onset (latency) of local anesthetic block

Back 51

The higher the lipid solubility the faster the time to onset of block.

Front 52

Things that correlate with duration of action of local anesthetic

Back 52

Protein binding. Lipid solubility (inverse correlation)

Front 53

A alpha nerve fiber: Myelinated? Relative conduction velocity? Function?

Back 53

Myelinated. Fastest. Proprioception, large motor.

Front 54

A beta nerve fiber: Myelinated? Relative conduction velocity? Function?

Back 54

myelinated. second fastest. small motor, touch, pressure

Front 55

A gamma nerve fiber: Myelinated? Relative conduction velocity? Function?

Back 55

myelinated. 3rd fastest. muscle tone.

Front 56

A delta nerve fiber: Myelinated? Relative conduction velocity? Function?

Back 56

myelinated, but slower conduction. 4th fastest. pain, temperature, touch.

Front 57

B nerve fiber: Myelinated? Relative conduction velocity? Function?

Back 57

myelinated. 2nd to slowest. preganglionic autonomic

Front 58

C nerve fiber: Myelinated? Relative conduction velocity? Function?

Back 58

UNmyelinated. slowest. dull pain, temperature, touch.

Front 59

chemical factors that delay local anesthetic uptake

Back 59

high lipophilicity, high protein binding.

Front 60

Mechanism of local anesthetic CNS toxicity

Back 60

Selective depression of cortical inhibitory neurons leaving excitatory pathways unopposed ( local anesthetics are neuronal depressants)

Front 61

EKG changes in local anesthetic toxicity

Back 61

Prolongation of PR interval
Widening of QRS complex

Front 62

Type of local anesthetic most likely to produce allergic reaction and why

Back 62

Esters- Produce metabolites related to PABA . Allergic reactions also can Be caused by Preservatives like methyl paraben

Front 63

Unique side effects of procaine

Back 63

Nausea
Hypersensitivity
Also can cause TNS

Front 64

Unique Characteristics of tetraCaine

Back 64

fairly long duration of action
high risk of TNS when used w/ Vasoconstrictor
slow onset
profound motor blockade
potential toxicity
slow metabolism

Front 65

Unique characteristics of Mepivicaine

Back 65

Similar to lidocaine but:
- Less vasodilation
-Slightly longer duration of action
-Ineffective as topical anesthetic

Front 66

How does Prilocaine induced methemoglobinemia resolve

Back 66

-Spontaneously subsides
- Can be reversed by methylene blue l-2mg per kg over 5 min

Front 67

Which enantiomer of bvpivicaine has less cardio toxicity

Back 67

S-

Front 68

Benefits of ropivicaine

Back 68

Be+ter than bupivicaine with Cardiac Sodium channels
Produces more Vasoconstriction
Motor blockade less pronounced
C fibers preferentially blocked ?

Front 69

Drawbacks of ropivicaine

Back 69

Less potent meaning more must be given to get same effect (potentially negating belter risk profile w/ cardiac toxicity)

More expensive

Front 70

what is the first ion change when action potential arrives at the NMJ ?

Back 70

Influx of calcium ions causes release of Ach

Front 71

What subunits do the NMBS bind to on the postjunctional receptor ?

Back 71

The two alpha subunits

Front 72

Chemical structure of NMDB that allows it to bind to alpha subunit

Back 72

Quaternary ammonium , positively charged nitrogen atom binds to alpha Subunit

Front 73

List the amino steroid NMDBS

Back 73

PANCVRONIUM
VECURONIUM
ROCURONIUM

Front 74

list the BENZYLISOQUINOLlNlUM NMDBS

Back 74

AtraCurium
cisatraCurium
Mivacurium

Front 75

Which NMBDs most likely to evoke the release of histamine & why

Back 75

atrawrivm
cisatracurium - doesnt really do it
MiVacurium

related to fast infusion of high doses

Front 76

Elimination of roCuronivm

Back 76

Liver

Front 77

Elimination of mivacurium

Back 77

metabolism by plasma cholinesterase

Front 78

Elimination of atracurium or cisatracurium

Back 78

Hoffman elimination

Front 79

What diminishes the effect of NMBDs

Back 79

calcium
corticosteroids
phenytoin & anticonvulsants

Front 80

What can cause resistance to NMBD

Back 80

Burn injury
CVA'S

Front 81

Cardiac effect of Pancuronium

Back 81

modest blockade of cardiac postganglionic mUscarinic receptors

Front 82

Pancuronium % renal excretion

Back 82

80 %

Front 83

% Renal excretion of Vecuronium

Back 83

15-25%

Front 84

Rocuronivm % renal excretion

Back 84

10-25%

Front 85

PanCuronium % hepatic degradation

Back 85

10%

Front 86

VecuroniUm % hepatic degradation

Back 86

20-30%

Front 87

RocuroniUm % hepatic degradation

Back 87

10-20%

Front 88

Pancuronium % Biliary excretion

Back 88

5-10%

Front 89

Vecuronium % Biliary Excretion

Back 89

40-75%

Front 90

Rocuronium % Biliary Excretion

Back 90

50-70%

Front 91

Pancuronium lntubating Dose

Back 91

0.1 mg/Kg

Front 92

Vecuronium lntubating Dose

Back 92

0.08 - 0.1%

Front 93

Rocuronium Intubating Dose

Back 93

0.3 mg/kg

Front 94

Atracurium intubating dose

Back 94

0.5mg/kg

Front 95

Cisatracurium Intubating Dose

Back 95

0.1 mg/kg

Front 96

Mivacurium lntubating Dose

Back 96

0.25 mg/kg

Front 97

Pancuronium- Duration to return to greater than or equal to 25%

Back 97

60-90 min

Front 98

Mivacurium - Duration to return to greater than or equal to 25%

Back 98

12-20 min

Front 99

Vecuronivm, Rocuronium, Atracurium, Cisatracurium - Duration to return to greater than or equal to 25%

Back 99

20-35 min

Front 100

What increases duration of action of pancuronium

Back 100

Renal failure

Front 101

What NMBD has a potent metabolite

Back 101

Pancuronium - 50 percent as potent

Front 102

Cardiac effects of pancuronium

Back 102

modest 10-15% increase in HR, MAP t CO

Front 103

How does pancuronium produce cardiac effects

Back 103

Selective blockade of cardiac muscarinic receptors principally in SA node - more likely to occur in pts with AV conduction issues already

Front 104

Clearance of Atracurium

Back 104

Hoffman elimination
Ester hydrolysis by nonspecific esterases

Front 105

Metabolite of NMB that can cause CNS stimulation and what NMB

Back 105

Laudanosine is metabolite
Atracurium
Much less produced by cisatracurium

Front 106

Clearance of ciSatracurium

Back 106

Hoffman elimination to Laudanosine- don't really see Laudanosine toxicity because cis is so potent

Front 107

What could theoretically slow the hydrolysis of mivacurium and why

Back 107

Neostigmine because it decreases plasma cholinesterase (pseudo cholinesterase activity)

Front 108

List Major Criteria for perioperative Beta Blockade

Back 108

Ischemic Heart Disease :
History of MI
Use of Nitrates
Q waves on ECG
Current history of angina
+ Stress test
Abdominal, thoracic, vascular surgery planned
Any history of congestive heart failure
Insulin dependent diabetes
Any history of CVA
Sewm Cr> 2.0
Arterial vascular disease

Front 109

Minor Criteria for perioperative Beta Blockade

Back 109

Age > 70
Hypertension
Total cholesterol > 240
Non Insulin Dependent Diabetes
Current Smoker

Front 110

perioperative beta blockade -
3+ major criteria and any minor criteria -elective surgery

Back 110

1. Beta blocker indicated but patient needs further Cardiac workup
2. Refer to preop clinic 5-7 days before surgery

Front 111

Perioperative beta blockade
3+ major criteria and any minor criteria - emergent surgery

Back 111

1. Beta blocker therapy probably indicated
2. Consult cardiology or medicine

Front 112

Peri operative Beta Blockade
l-2 major criteria plus 2 or More minor criteria -elective surgery

Back 112

1. Beta blocker therapy indicated
2. Refer to preop clinic 2-5 days before surgery

Front 113

Peri operative Beta Blockade
no major criteria plus 0-1 minor criteria -elective surgery

Back 113

1. Beta blocker not indicated
2. Refer to preop clinic for routine eval 2-3 days before surgery

Front 114

Peri operative Beta Blockade
l-2 major criteria plus 2 or More minor criteria -emergent surgery

Back 114

l. Beta blocker indicated

Consult cards or medicine

Front 115

Contraindications to periop beta blocker

Back 115

1. current symptoms of CHF or EF<30
2. sick sinus syndrome or 2nd or 3rd degree AV block without pacemaker
3. heart rate <55 without pacemaker
4. S3, rales, wheezing on exam
5. known intolerance
6. poorly controlled asthma or copd
7. sbp less than 100
8. same day or outpatient surgery

Front 116

Cardiac complication rate by risk factor - O, l, 2, 3 plus

Back 116

0.4%, 0.9%, 7%, 11%

Front 117

Independent Risk Factors for Cardiac Events (6)

Back 117

l. High Risk Surgery
2. History of ischemic heart disease
3. Congestive heart failure
4. Cercbwvaswlar disease
S. Insulin dependent diabetes
6. Cr>2.0

Front 118

Prophylaxis for anesthesia for people with chronic atopy or having Procedures associated with allergic reactions like dye studies

Back 118

Benadryl 25-50 mg
Cimetidine 300mg
occupy peripheral sites responsive to histamine

Front 119

Central Anti cholinergic Syndrome and treatment

Back 119

Delirium or Somnolence with Scopolamine or atropine
treatment - physostigmine up to 2mg IV

Front 120

H 2 blocker method of action

Back 120

competitive inhibitor of histamine at parietal cells which help increase ph of fluid
names - ranitidine, cimetidine, etc

Front 121

What is the partial pressure of 60 % Nitrous at Sea level?

Back 121

760 x 0.6 = 456 mmHg

760 = barometric pressure

Front 122

What amount of total airway resistance occurs in nasal passages

Back 122

2/3

Front 123

What innervates the nasal mucosa

Back 123

Trigeminal nerve - V1 and V2 opthalmic and maxillary .

Called anterior ethmoidal, nas0palatine, & spheNopalatine

Front 124

What provides sensation to anterior 2/3 of tongue

Back 124

Mandibular division of trigeminal -V3
Called Lingual Nerve

Front 125

What provides innervation to posterior third of tongue, soft palate and oropharynx

Back 125

glossopharyngeal nerve - cranial nerve IX

Front 126

What provides sensation to the hypopharynx

Back 126

Internal branches of SUPERIOR laryngeal nerve - branch of Vagus

Front 127

Independent predictors of difficult mask

Back 127

1. Age over 55 years
2. BMI over 26
3. Beard
4. Lack of teeth
s. History of snoring

Front 128

Superior Laryngeal Nerve Block - internal branch anatomy

Back 128

Between greater cornu of hyoid bone and superior cornU of thyroid cartilage as they traverse the thywhyoid membrane to the Sub mucosa of the piriform sinus

Front 129

Superior Laryngeal Nerve Block - internal branch approach

Back 129

Needle walked off cephalad edge of thyroid cartilage or caudal edge of hyoid bone

Front 130

Differences between infant and adult airway (7)

Back 130

1. larynx at c3-4 in infants vs c4-5 in adults
2. tongue larger relative to mouth size in infants
3. epiglottis in infants larger, stiffer, and angled more posteriorly
4. head and occiput larger relative to body size
5. short neck
6. narrow nares
7. cricoid ring is the narrowest region

Front 131

how many cervical vertebrae are there

Back 131

7

Front 132

how many thoracic vertebrae are there

Back 132

12

Front 133

how many lumbar vertebrae are there

Back 133

5

Front 134

Level of iliac crests

Back 134

L4

Front 135

Most outlying point of lower neck

Back 135

C7

Front 136

Level of the lower border of the scapulae

Back 136

T7-8 interspace

Front 137

What vertebral body does the 12th rib intersect

Back 137

L2

Front 138

Level of posterior iliac spine - what is special about this level

Back 138

S2 - caudal limit of dural sac in most adults

Front 139

What level does the spinal cord end in infants

Back 139

L3

Front 140

What level does the spinal cord end in adults

Back 140

L1

Front 141

At what level does the dura terminate

Back 141

Between S1 and S4

Front 142

What prevents migration of drug from epidural to subarachnoid space

Back 142

the arachnoid mater

Front 143

How does an epidural block spread

Back 143

Rostrally and caudally (up and down)

Front 144

What and where is maximal depth of epidural space

Back 144

6mm at midline L2

Front 145

Anterior spinal artery syndrome

Back 145

bilateral lower extremity motor loss. can be associated with surgery near aorta (AAA resection) or by stray epidural needle

Front 146

Name the dermatomes

Back 146

Front 147

Where does the artery of Adamkiewicz enter

Back 147

through L1 intervertebral foramen

Front 148

Posterior spinal artery - how many, where does it originate, what does it supply

Back 148

Two.
emerge from cranial vault.
supply dorsal (sensory) part of spinal cord
have rich collaterals.

Front 149

Anterior spinal artery - how many, where does it originate, what does it supply

Back 149

One.
originates from vertebral artery.
Supplies ventral (motor) part of spinal cord

Front 150

Effect of increased intra-abdominal pressure or tumors/masses compressing the vena cava on epidural anesthesia

Back 150

Blood is diverted from IVC and engorges veins in epidural space:
Increases likelihood of accidental vascular cannulation
Greater longitudinal spread of local due to effective reduction of epidural space

Front 151

Contraindications to neuraxial block: Absolute & Relative

Back 151

Absolute:
Patient refusal
Infection at planned needle site
Elevated lCP
Coaguiopathy

Relative:
Multiple sclerosis or other neurologic disease
Mitral stenosis
Idiopathic hypertrophic subaortic stenosis
Aortic stenosis

Front 152

Level and Significance of Sensory Block
Cutaneous level : Fifth digit
Segmental level , Significance :

Back 152

Segmental level: c8
Significance: All cardioaccelerator fibers blocked

Front 153

Level and Significance of Sensory Block
Cutaneous level : Inner aspect of arm and forearm
Segmental level , Significance :

Back 153

Segmental level: T1- 2
Significance: Some degree of cardioaccelerator block

Front 154

Level and Significance of Sensory Block
Cutaneous level : Apex of the axilla
Segmental level , Significance :

Back 154

Segmental level: T3
Significance: Easily determined landmark

Front 155

Level and Significance of Sensory Block
Cutaneous level : Nipple
Segmental level , Significance :

Back 155

Segmental level: T4-5
Significance: Possibility of cardio accelerator block

Front 156

Level and Significance of Sensory Block
Cutaneous level : Tip of the xiphoid
Segmental level , Significance :

Back 156

Segmental level: T7
Significance: Splanchnics (T5-L1) may be blocked

Front 157

Level and Significance of Sensory Block
Cutaneous level : Umbilicus
Segmental level , Significance :

Back 157

Segmental level: T10
Significance: Sympathetic nervous System block limited to the legs

Front 158

Level and Significance of Sensory Block
Cutaneous level : Inguinal Ligament
Segmental level , Significance :

Back 158

Segmental level: T12
Significance: No sympathetic nervous system block

Front 159

Level and Significance of Sensory Block
Cutaneous level : Outer side of foot
Segmental level , Significance :

Back 159

Segmental level: S 1
significance: Confirms block of root most difficult to anesthetize

Front 160

Site of action for intrathecal opioids

Back 160

Dorsal horn of spinal cord where Opioids mimic enkephalins

Front 161

neuroleptic malignant syndrome - etiology

Back 161

Related to dopamine blockade in the basal ganglia and hypothalamus due to long term administration of psychoactive drugs

Front 162

Respiratory changes of Old age

Back 162

Increased residual volume
Increased closing capacity
Increased chest wall stiffness
Decreased alveolar surface area , decreased Pao2
Blunted response to hypercapnia and hypoxia

Front 163

Epidural & spinal changes with old age

Back 163

Higher cephalad spread but shorter duration of analgesia and motor block- etiology unknown

spinals have longer duration of action

Front 164

Pharmacokinetic changes of old age

Back 164

Decreased VD for water soluble drugs
Increased VD for lipid soluble drugs

Decreased albumin binding of acidic drugs (opioids, BZD, barbiturates)

Increased alpha protein binding of basic drugs (LA)

Decreased Clearance of drugs

Front 165

What is produced by burning PVC ETT

Back 165

HCl -a pulmonary toxin

Front 166

What nerve roots supply LES tone

Back 166

T6 -T1O
Vagus & sympathetics

Front 167

Drugs that increase LES tone
Drugs that decrease LES tone

Back 167

Increase: Antacids (bicitra), reglan, sux, beta blockers - metoprolol. , anticholinesterases
Decrease: Benzodiazepines, narcotics (most sedatives but not propofol or etomidate at low doses), volatiles, anticholinergics

Front 168

NIOSH limit for N2O amount in OR (1977)

NIOSH limit for N2O + volatile amount in OR

NIOSH limit for volatile alone amount in OR

Back 168

1. 25 ppm
2. 0.5 ppm
3. 2 ppm

Front 169

Periop wrist drop - nerve injured

Back 169

radial

Front 170

Manifestations of citrate toxicity

Back 170

Narrow pulse pressure
Hypocalcemia --> prolonged QT

Front 171

What is mixed venous O2 in cyanide toxicity?

Back 171

High. cyanide toxicity blocks cytochrome oxidase in tissues and wont allow tissue use of O2 in blood.

Front 172

What determines the duration of conduction block of local anesthetic

Back 172

Protein binding