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sept viva Flashcards

1
Q

intralipid contents

A

Intralipid, which is an emulsion of soy bean oil, egg phospholipids and glycerin,

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2
Q

LA tox risk

A

LA drug factors Pr B and affinity to NaCH and pregame’s, acid, renal, hep

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3
Q

prev LA tox

A

USS
monitor
awake
test dose

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4
Q

AFOI blcok

A

Glossopharyngeal not oropharyngeal.

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5
Q

LA tox ecg

A

sinus bradycardia, intracardiac conduction defects (prolonged PR & QRS complex), ventricular arrhythmias, cardiac arrest.

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6
Q

Desc pain

A

PAG–>RVM–>DH

LC–>DH

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7
Q

Rexed Laminae

A

The Rexed laminae comprise a system of ten layers of grey matter (I–X),

P+H

Adelta–>laminae 2,5
C fibers–>2

The substantia gelatinosa is one point (the nucleus proprius being the other) where first order neurons of the spinothalamic tract synapse. (laminae II)
Many μ and κ-opioid receptors, presynaptic and postsynaptic, are found on these nerve cells;

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8
Q

gate theory

A

Ab touch and desc inhib in SUBSTANTIAL GENATINOSA (lamina II of DH)

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9
Q

glucose uptake

A

Glut1 the 1 most important thing so brain
Glut 2 food panc and hep
Glut 4 is lock in door (insulin dep)

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10
Q

BMR measurement

A

heat or indirect calaromitery

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11
Q

atp production cellular respiration

A

google
atp production cellular respiration

RB pyruvate oxidation CO2 prod

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12
Q

fatty acid

A

Fats into fatty acids and glycerol

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13
Q

ketogen

A

Fatty acid–>acetylcoa (b oxidation)
aceytl coa–>acetone, acetoacetate and betahydroxybutyrate via 3 steps including HMG coa synthase

When the body has no free carbohydrates available, fat must be broken down into acetyl-CoA in order to get energy. Under these conditions, acetyl-CoA cannot be metabolized through the citric acid cycle because the citric acid cycle intermediates (mainly oxaloacetate) have been depleted to feed the gluconeogenesis pathway. The resulting accumulation of acetyl-CoA activates ketogenesis.

Ketone bodies are produced mainly in the mitochondria of liver cells,

The production of ketone bodies is then initiated to make available energy that is stored as fatty acids. Fatty acids are enzymatically broken down in β-oxidation to form acetyl-CoA. Under normal conditions, acetyl-CoA is further oxidized by the citric acid cycle (TCA/Krebs cycle) and then by the mitochondrial electron transport chain to release energy. However, if the amounts of acetyl-CoA generated in fatty-acid β-oxidation challenge the processing capacity of the TCA cycle; i.e. if activity in TCA cycle is low due to low amounts of intermediates such as oxaloacetate, acetyl-CoA is then used instead in biosynthesis of ketone bodies via acetoacetyl-CoA and β-hydroxy-β-methylglutaryl-CoA (HMG-CoA). Furthermore, since there is only a limited amount of coenzyme A in the liver, the production of ketogenesis allows some of the coenzyme to be freed to continue fatty-acid β-oxidation.[8] Depletion of glucose and oxaloacetate can be triggered by fasting, vigorous exercise, high-fat diets or other medical conditions, all of which enhance ketone production

The three ketone bodies, each synthesized from acetyl-CoA molecules, are:

Acetoacetate, which can be converted by the liver into β-hydroxybutyrate, or spontaneously turn into acetone. Most acetoacetate is reduced to beta-hydroxybutyrate, which serves to additionally ferry reducing electrons to the tissues, especially the brain, where they are stripped back off and used for metabolism.
Acetone, which is generated through the decarboxylation of acetoacetate, either spontaneously or through the enzyme acetoacetate decarboxylase. It can then be further metabolized either by CYP2E1 into hydroxyacetone (acetol) and then via propylene glycol to pyruvate, lactate and acetate (usable for energy) and propionaldehyde, or via methylglyoxal to pyruvate and lactate.[10][11][12]
β-hydroxybutyrate

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14
Q

R quotient

A

CO2/R=0
CO2/O2=R

fat is .7 pr .8
feed COPD fat
stomach consumes CO2

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15
Q

lattent heat of…

A

melting

lattent TB= hidden

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16
Q

nicotine

A 
Acute exposure to nicotine
–
HD effects last 1hr
Abstinence cigarettes 12hrs
–
10
-
20% increase in physical work capacity
T ½ COHb 4
-
6hrs so overnight abstinence helpful (10hrs
in men)
Peak benefit re: upper airway irritability at 10 days (effects start at 48hrs)
Autonomic ganglia
(N1 receptors)
–
blocked by hexamethonium
2.
NMJ
(N2 receptors)
–
blocked by tubocurarine
3.
CN

Initial stimulation then persistent depression of autonomic ganglia
CNS stimulant
–
tremor
Increased ventilation v
ia nicotine stimulating aortic/carotid body chemoreceptors
CVS: tachycardia, hypertension, increased SVR (via SNS increase)
Resp: initial stimulation of saliva/bronchial secretions then inhibition
GI: PNS activation causing vomiting, diarrhoea

ADrenal medulla ADr release

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17
Q

sweat glands ANS

A

In sweat glands the receptors are of the muscarinic type.

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18
Q

isometric isotonic

A

ismetric–>nil external work–>100% energyoutput as heat

isotonic–>some external work–>50% heat loss

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19
Q

brown fat

A

uncouples oxidative phosphorylation
not dep on consumption of ATP for ATP
heat produced through chemical reaction without ATP needing to be utilised

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20
Q

COX pathway

A

Sm muscle–>PG

cycloendoperoxidase

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21
Q

nerve twitch face

A

orbicularis occuli

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22
Q

nerve monitory placement

A

Typically smaller muscle groups are more sensitive
The positive (red) lead is placed proximal
Ulnar nerve
Electrodes are placed along the ulnar border of the wrist at the flexor crease, and thumb adduction is assessed.
Facial nerve
The positive electrode is placed at the outer canthus, and the negative electrode is placed anterior to the tragus. Eyebrow twitching is assessed. orbicularis occuli
Posterior tibial nerve
Electrodes are placed posterior to the medial malleolus, and plantar flexion is assessed. posterior tib

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23
Q

r vs s

A

rectus right clock

sirrius anticlock

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24
Q

levo vs dextro

A

A dextrorotatory compound is a compound that rotates the plane of polarized light clockwise as it approaches the observer (to the right)

Dr X

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25
Q

stereoisomer

A

diff 3d orientation same bonds

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26
Q

diastereioismer

A

non enantiomers

  • ->geo (cis)
  • ->configurational (cant rotate around single bond)
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27
Q

thio tautomerism

A

So, as demonstrated by the diagram I nabbed from the net above, the ketone form C=O* is lipid soluble and is favoured in acidic environments. The enol form is favoured in alkaline environments and is water soluble.

Enol forms for barbiturates are water-soluble at pH 10-11at 6% sodium carbonate

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28
Q

valsalva phase 3

A

BP drops as LV afterload worsened with release and prelead reduced

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29
Q

Valsalva quantification

A

highest HR in phase 4 over lowest in phase 4

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30
Q

ANS dx vasovagal

A

Figure 4.49 The Valsalva response in autonomic
dysfunction: excessive fall in blood pressure
in Phase II and absence of overshoot and
bradycardia in Phase IV.

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31
Q

NSAID SE

A

CCF and fluid and salt rention

NSAIDs promote sodium and water retention, and this has generally been explained by a reduction in prostaglandin-induced inhibition of both renal chloride reabsorption and the action of antidiuretic hormone

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32
Q

3 phases of heat loss

A

Rapid reduction
Core temperature falls by 1-1.5°C in the first 30 minutes.
Predominantly due to vasodilation, which is due to:
Reduction in SVR, with generalised vasodilation and increased skin blood flow
Heat redistribution is the major initial factor (rather than heat loss), as vasodilation leads to increased heat content of peripheries.
Impairs thermoregulatory vasoconstrictive responses
Inter-threshold range is widened to 4°C (up from 0.4°C)
Gradual reduction
Further drop in core temperature of 1°C over following 2-3 hours.

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33
Q

humidity

A

evernote

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34
Q

preg ABG

A

26-32mmHg CO2

pO2 → essentially unchanged 100-105mmHg

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35
Q

resp drive preg

A

Hyperventilation centrally stimulated by

progesterone

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36
Q

preg CO

A

O2 Flux
Measured as the product of blood O2 content and CO
- ↑CO (30%)

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37
Q

normal HCT

A

40%

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38
Q

CVS changes preg %s

A

all about 25% except CO=50% and BV=50%

https://primarysaqs.files.wordpress.com/2009/12/makeup-describe-the-cardiovascular-changes-that-occur-in-pregnancy.pdf

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39
Q

thyroid anatomy

A

inf to cricoid caritlage
ext branch of sup laryngeal
recurrent laryngeal

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40
Q

thyroid production

A

In follicular cells
Iodine from basement memebrane
Iodination of tyrosyl residue of thyroglobulin
Lysosomal enzymes cleave T4 from iodinated thyroglobulin
T4 cross into blood

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41
Q

thyroid effect

A

physiocal vs chemical

catachol and insulin sens due to B rec upreg

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42
Q

hypothyroidism and GA

A

Hypothyroidism may result in depression of myocardial function, decreased spontaneous ventilation, abnormal baroreceptor function, reduced plasma volume, anaemia,82 hypoglycaemia, hyponatraemia and impaired hepatic drug metabolism

Preventative measures should be adopted to protect against hypothermia. Because of an increased incidence of adrenocortical insufficiency and a reduced adrenocorticotropic hormone response to stress, hypothyroid patients should receive hydrocortisone cover during periods of increased surgical stress.

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43
Q

Hyperthyroidism

A

Of importance to the anaesthetist are the cardiovascular effects of hyperthyroidism including atrial fibrillation, congestive cardiac failure and ischaemic heart disease.4

In an attempt to prevent the dreaded complication of ‘thyroid storm’, patients should be euthyroid before surgery.4286 This is achieved by the use of antithyroid drugs, commonly carbimazole or propylthiouracil. These drugs block the synthesis of thyroxine but take 6–8 weeks to work. Beta‐blockers, particularly propranolol, are used to ameliorate the effects of thyrotoxicosis13 and are effective in the acute preoperative phase. Longer‐acting beta‐blockers such as atenolol or nadolol may achieve better control of symptoms.2736 Anaesthetic drugs may be affected by the hypermetabolic state of hyperthyroidism. For example, the clearance and distribution volume of propofol are increased in hyperthyroid patients. When total intravenous anaesthesia is used, propofol infusion rates should be increased to reach anaesthetic blood concentrations.9

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44
Q

Bohr effect

A

boring is stable #evernote and eqn

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45
Q

Bohr eqn

A

a-E/a

as a is higher than e

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46
Q

humidity

A

renaults!!!!!

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47
Q

propofol infusion rate and CSHT

A

6mg/kg/hr bristol final stage

onset 30s

CSHT at infinity is 10min MILLERS
CSHT 5hrs is 5min

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48
Q

THio presentaion

A

NaCO3
NaTP
2.5%
stable 24 hrs

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49
Q

thio doa

A

10min

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50
Q

thio CVS

CORE

A

neg ino with CO decrease 20%
some VD
compensatory tachy!!!!!!

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51
Q

thio resp

A

BC

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52
Q

thio hep

A

inducer of CYP450

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53
Q

thio other

A

arterial injection

porporia

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54
Q

porphyria

A

Porphyric crisis due to build up of porphyrins—>skin and nervous system effects

  • abdo and chest pain
  • vomiting fever
  • HTN tachy
  • Confusion
  • Blisteres

Complication

  • seziure
  • Paralysis
  • Fatal

Rx
* IV haem or glocuse—>decreased haem synth—>less precursor accumulating

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55
Q

intraarterial injection thio

A

alpha antag
anticoag
analgesia
block

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56
Q

alpha anatag

A

phenoxybenzamine non selctive for pheochromocytoma

phentolamine

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57
Q

neo vs edro vs other

A

evernote

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58
Q

muscurinic antag

A

eyedrop to dilate

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59
Q

SE of neostig

A

CLINICAL FEATURES

confusion
CNS depression
weakness
salivation
urinary and faecal incontinence
GI cramping
vomiting
sweating
muscle fasciculations
pulmonary oedema
miosis
brady or tachycardia
seizures
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60
Q

QT prolonged

A

1,3

sux, volatile, low K, low Mg

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61
Q

NO moa

A

Activates gyanalate cyclase

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62
Q

Oxytocin se

A

Phtn and coronary spasm ci in congenital hear tdx

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63
Q

Misoprostol

A

Pge1 analogue

Diarrhoea in the bum

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64
Q

Carbeprost

A

F2alpha
BC and pulm HTN
DIARHOEA VOMIT

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65
Q

central vs mixed venous

A

superior vena cava and proximal pulmonary artery,

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66
Q

reticulocytes

A

Like mature red blood cells, in mammals, reticulocytes do not have a cell nucleus. They are called reticulocytes because of a reticular (mesh-like) network of .

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67
Q

RBC production

A

google

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68
Q

rbc met

A

everntoe Bile secretion bilirubin

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69
Q

whole blood

A

Whole blood is typically stored under the same conditions as red blood cells and can be kept up to 35 days if collected with CPDA-1 storage solution or 21 days with other common storage solutions such as CPD.

double if PRBC

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70
Q

PRBC additives

A

CONTINUED PROF DEV
CPDA

SAGM

Sodium Chloride 0.92g
• Adenine 0.02g
• Dextrose Monohydrate 0.95g
• Mannitol 0.55g

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71
Q

storage lesion

A

Blood can be stored for up to 35 days, which corresponds to 70% survival

Hyponatraemia

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72
Q

oxy dose post infusion

A

> Prolonged use of oxytocin induces oxytocin receptor desensitisation and larger doses of
oxytocin may be required to prevent or treat uterine atony and PPH 3

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73
Q

levosimendine

A

sensitizes Ca

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74
Q

milronone

A

Milrinone, commonly known and marketed under the brand name Primacor, is a medication used in patients who have heart failure. It is a phosphodiesterase 3 inhibitor that works to increase the heart’s contractility and decrease pulmonary vascular resistance.

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75
Q

pulm HTN

A

Pulmonary Vasodilaters (generally referring to chronic Mx but some acute: http://www.rcjournal.com/contents/07.07/07.07.0885.pdf

  • O2—>reverse HPVC
  • CCB—>VD eg nifedipine and diltiazem
  • Nitric Oxide Gas
  • Low-dose intravenous sodium nitroprusside causes pulmonary vasodilation and reduces PAP, PVR, and right-ventricular afterload, but is not selective.
  • Nitroglycerin is another NO donor that has selective pulmonary vasodilation effects when delivered via aerosol
  • In vascular smooth-muscle cells, prostacyclins stimulate soluble adenylate cyclase and convert adenosine triphosphate to cyclic adenosine monophosphate (cAMP). In turn, protein kinases mediate a cAMP-induced decrease in intracellular calcium and produce relaxation and vasodilation (see Fig. 3).99,100 Prostaglandin I-2 and prostaglandin E-1 are both potent pulmonary vasodilators and inhibitors of platelet aggregation
  • -Epoprostenol, a short-acting prostaglandin I-2
  • -Aerosolized epoprostenol is an effective alternative to INO in the acute care setting
  • Sildenafil, a phosphodiesterase type 5 inhibitor, approved for the treatment of erectile dysfunction, has been shown to be an effective treatment for PAH in several randomized controlled trials in adult patients154 –156 and was approved by the FDA in June 2005 as an oral PAH therapy.
  • -Phosphodiesterases are enzymes that inactivate cGMP and cAMP. Use of phosphodiesterase inhibitors to prevent the breakdown of cGMP and cAMP in vascular smoothmuscle cells can augment or prolong the vasodilator signaling pathways of both NO and prostacyclin
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76
Q

23dpg weeks

A

consumed–>increased sats in pRBC

5% left at 4 weeks

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77
Q

storage lesion

A

K 28 at 28 days
ph 6.7
PRBC 75% at 28 days

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78
Q

dex CVS

A

BRADY–>DEATH

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79
Q

Dex CNS

A

less deleirum

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80
Q

Dex PK

A

high Prb

extensive hep with nil minimal renal dep vs clonidine 50% peed out unchanged

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81
Q

affect Pulm VR

A

Factors which influence pulmonary vascular resistance

Pulmonary blood flow:
Increased blood flow results in decreases pulmonary vascular resistance in order for pulmonary arterial pressure to remain stable
This is due to:
Distension of pulmonary capillaries (mainly), and
Recruitment of previously collapsed or narrowed capillaries
Lung volume:
Relationship between lung volume and PVR is “U”-shaped
Pulmonary vascular resistance is lowest at FRC
At low lung volumes, it increases due to the compression of larger vessels
At high lung volumes, it increases due to the compression of small vessels
Hypoxic pulmonary vasoconstriction
A biphasic process (rapid immediate vasoconstriction over minutes, then a gradual increase in resistance over hours)
Mainly due to the constriction of small distal pulmonary arteries
HPV is attenuated by:
Sepsis and pneumonia
hypothermia
iron infusion
Metabolic and endocrine factors:
Catecholamines, arachidonic acid metabolites (eg. thromboxane A2) and histamine increase PVR
Hypercapnia and (independently) acidaemia also increase pVR
Alkalaemia decreases PVR and suppresses hypoxic pulmonary vasoconstriction
Hypothermia increases PVR and suppresses hypoxic pulmonary vasoconstriction
Autonomic nervous system:
α1 receptors: vasoconstriction
β2 receptors: vasodilation
Muscarinic M3 receptors: vasodilation
Blood viscosity
PVR increases with increasing haematocrit
Drug effects:
Pulmonary vasoconstrictors: Adrenaline, noradrenaline and adenosine
Pulmonary vasodilators: Nitric oxide, milrinone, levosimendan, sildenafil, vasopressin, bosantan / ambrisantan, prostacycline and its analogs, calcium channel blockers and ACE-inhibitors.

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82
Q

Stomache secretion

A

Stomache secretion evernote

g cells enterochroffin like cells

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83
Q

H2 blockers

A

H2 blockers are available by prescription or over-the-counter, and include ranitidine, famotidine, cimetidine

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84
Q

Hypothal thermo reg parts

A

anterior hypothalamus is sensitive to
local warming of blood, which increases the ring rate, producing sweating and vasodilatation.
e posterior hypothalamus responds to cold
Cutaneous responses to heat 383
aerent impulses from the peripheral temperature
receptors and causes increased shivering thermogenesis.

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85
Q

layers of adrenal medulla

A

zona glomerulosa: The outermost layer of the adrenal cortex, responsible for producing mineralocorticoids such as aldosterone. zona fasciculata: The middle layer of the adrenal cortex, responsible for producing glucocorticoids such as cortisol.

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86
Q

magnesium level vs side effects

A

magnesium level vs side effects google

5 SA AV
10 weak
15 AV block and resp paralysis
20 Arrest

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87
Q

ANS strucutre

A

ANS

  • SNS-efferent cell bodies in lateral grey column and in peripheral ganglion of T1-L2
  • PSNS-efferent Brainstem CNs 3,7,9,10 and sacral primary rami—>pelvic splanchnic nerves
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88
Q

mass effect SNS

A

SNS-mass effect

  • exit lat grey column—>white rami communicans 3 options in the Sympathetic trunk
    1. Synapse at that ganglion in white rami communicans
    2. Travel upon down trunk to ganglions above # cervical ganglion
    3. Pass through and synapse with a more distal ganglion
  • therefore blocking or stimulating one white rami communicans segment—>wide effect on many organs at many levels above and below
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89
Q

eqipment class

A

Class I
Equipment that has an earth wire connected to its outer metal casing
This protects against shock in case a fault causes the active wire to contact the outer case
eg refrigerator, electric kettle

Class II
Double insulated equipment
Has a plastic outer case in addition to the normal internal insulation
An earth wire is not required as the outer casing is non-conductive
eg hair dryer

Class III
Extralow voltage (< 40V) or battery powered equipment
Doesn’t require an earth wire, even if it has a metal case because the voltage is low so that the risk of macroshock is negligible
eg mobile phone

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90
Q

avoid electricution

A

(i) general measures; (ii) equipment design; (iii)

equipotentiality; (iv) isolated circuits; and (v) circuit breakers.

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91
Q

warfarin MoA

A

inhibits reduction of vit K by inhibiting vit K epoxide reductase
recuded form required as a coenzyme for carboxylation of glutamic acid residue

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92
Q

sux arrhythmias

A

Bradycardia
 due to direct action on muscarinic ACh receptors in SA node
o sinus brady, junctional/ventricular escape rhythm, asystole
 worse if high vagal tone
o children,  blocked, hypoxic, laryngoscopy
 more commonly if repeat dose given
 can be offset by co-administration of atropine
Tachycardia / Hypertension
 “large” / second dose of sux can directly stimulate nicotinic ACh receptors in sympathetic ganglia
o  SNS nerve activity
o  catecholamines released from adrenals
 tachycardia, hypertension
 ventricular arrhythmias

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93
Q

o2 storage in blood calc

A

150.1X1.34=200g

so 1L of O2 in blood

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94
Q

preoxygenation

A

PAo2=110/176 ie 13%
13% of 2.1L is 275ml
3.5ml.70 is 245ml

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95
Q

fuel cell vs other

A

clarke

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96
Q

HME

A

During expiration, the HME picks up some of the moisture from the expired humid air.

These water droplets retain some of the heat from the gas which has carried them.

During inspiration, the incoming torrent of air collects these warm water droplets, and carries them as vapour into the lungs of your patient.

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97
Q

Laplace

A

T=p.r/2

Tension is equal to TMP.RADIUS IN heart

P=2T/R

Pressure to collapse alv=ST/r to collaps

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98
Q

Surfactant

A

1.compkiance
2.oedema
3 stabilises

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99
Q

Surfactant oedema

A

Less ST so less oedema

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100
Q

Hb structure

A

4 heam

4globin polypeptide chains 2a 2b

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101
Q

Methhb

A

Fe3+
Prilocaine nitrites
Less able to bind O2 and less able to offload
Treat with methelene blue and vit c

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102
Q

hep BF calc

A

Like CO AUC (ficks prinicple is more complex with a fixed infusion)

ICG has a known HER 0.74

AUC (measured)=x (known)/cl
AUC=x/(Q.0.74)

HER is 0.74 for ICG
Cl is vol cleared per min=Q.HER ie Q.0.74

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103
Q

renal BF calc

A

PAH is filtered at the glomerulus, and any remaining in the peritubular capillaries is secreted into the lumen by proximal tubules. When the PAH concentration is low, all the plasmaperfusing, -filtering and -secreting parts of the kidney (the effective renal plasma flow is 85%–90% of the total renal plasma flow) are completely cleared of PAH. The renal clearance of PAH is therefore equal to the effective renal plasma flow, from which the effective renal blood flow can be calculated: = − Effective renal blood flow Effective renal plasma flow 1 Blood haematocrit

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104
Q

PaO2 at altitide

A

0.21(380-47)-50

=19mmHg (5x worse)

105
Q

neuropathic pain def

A

x

106
Q

niceception def

A

x

107
Q

neuropathic pain mech peripher

A 
increased Na ch perm. microanatomical change-cross connection and sprouting
central 
-migroglial activation
-ca ch sens due to over expression
-loss of large fibre inhibition
-anamotical reorg (brain and SC)
108
Q

cross and SC

A

decussate

109
Q

paracetamol MOA

A

evernote

110
Q

paracetamol met

A

evernote

111
Q

NSAID flow chart

CORE

A

endoperoxidase

112
Q

NMDA coagonist

A

Glycine is NMDA coagonist

113
Q

NMDA rec

A

xenon NO2 ketamine methadone

114
Q

post pit

A

ADH oxytocin

115
Q

adrenaline secretion

A

enterochromafiin cells

116
Q

COMT effect

A

The enzyme introduces a methyl group to the catecholamine, which is donated by S-adenosyl methionine (SAM).

117
Q

phenylephrine dose

A

Initial dose: 50 to 250 mcg by intravenous bolus (most common doses: 50 to 100 mcg)
1ml is 100 microg

118
Q

hep BF calc

A

INDOCYNIN GREEN

119
Q

PLACENTA HORMONES

A

e placenta acts as an endocrine organ as it
produces both peptide (human chorionic gonadotrophin [HCG] and human placental lactogen
[HPL]) and steroid hormones (oestrogen and progesterone).

120
Q

uterus blood supply

A

uterine and ovarian–>arcuate–>radial–>basal and spiral

121
Q

uterine unit

A

chorionic villi

fetal villi with chorioic external 2 layers
-syncitiotrophoblast and cytotrophopblast (cyto near cytoplasm)

intervillous space-maternal blood (YES)

122
Q

MEAC

A

x fent is 3mcg/ml

123
Q

uterine BF determ

A

alpha stim and uterine artery pressure

124
Q

t.f in uterus

A

diff
facilitated-glut1
active-Fe vit C
endocytosis IgG

125
Q

Selegiline

A

PDx Selegiline acts as a monoamine oxidase inhibitor,

126
Q

nonobstetric anaesthetic

A

Neostigmine crosses the placenta and fetal bradycardia can occur, while glycopyrrolate does not. !!!!

Non-steroidal anti-inflammatory drugs in early pregnancy may be associated with increasing fetal loss12 and in the third trimester may cause the premature closure of the ductus arteriosus. Single doses are unlikely to be harmful. T

All volatile agents up to an MAC of 1.5 dilate uterine arteries and increase uterine blood flow, but at higher concentrations, this is offset by decreases in maternal arterial pressure and cardiac output. Volatile agents also reduce uterine tone. Nitrous oxide is avoided during the first trimester (see the Anaesthetic drugs and teratogenicity section). Light anaesthesia and pain are avoided to prevent maternal catecholamine release and consequent reduced uteroplacental perfusion.

127
Q

Droperidol PK

A

extensive liver met 1% renal unchanged

128
Q

acinus

A

The centre of the acinus is formed by the
portal triads consisting of portal vein, hepatic
artery and bile duct. The acinus is supplied by
terminal branches of the hepatic artery and portal veins, which drain into sinusoids. The blood
in the sinusoids drains into hepatic venules. The
hepatic acinus may be divided into three functional zones: (1) periportal, (2) mediolobular and
(3) centrilobular zones (Figure 6.1). Periportal
hepatocytes (zone 1) receive blood with the highest
oxygen content and have the highest metabolic rate
and are especially involved in protein synthesis.
Centrilobular hepatocytes (zone 3) receive the
least oxygen but contain high concentrations of
cytochrome P-450 and therefore are important
sites for drug biotransformation.

129
Q

NAPQI

A

phase I

glutathion mop–>cysteine

130
Q

Nociception

A

Nociception (also nocioception, from Latin nocere ‘to harm or hurt’) is the sensory nervous system’s process of encoding noxious stimuli.

131
Q

sevo SVP

A

20kpa
158mmHg
2% with 90% bipass

132
Q

artline MAP

A

AUC per cardiac cycle

133
Q

SE RE

A

SE max 91=awake

134
Q

Evoked potentials (EP)

A 
Evoked potentials (EP)
Evoked potential monitors measure electrical activity in certain areas of the brain in response to stimulation of specific sensory nerve pathways.
135
Q

entropy CI

A

patient-brain dead neonat
Surgical-MRI
Drug-ket, N20

136
Q

entropy

A

entropy, freq, time

137
Q

bis

A

freq, phase, duration

138
Q

doppler shift

A

shift=v/c x freq0. cos theta

139
Q

measure BF

A

tracer uniquely handled by organ and doesnt change BF itself

140
Q

innate vs adaptive

A

nonspec vs targetted protein triger

141
Q

Anaphylaxis def

A 
Anaphylaxis is an acute severe type I hypersensitivity reaction affecting multiple
organ systems (there is currently no consensus definition)
142
Q

adaptive immune

A

Over next 10 – 14 days produces IgE specific to the antigen

143
Q

late anaphylaxis

A

TNF-α with a cumulative mean difference of 22.81 ng/ml is also an inflammatory soluble mediator and is released as both pre-formed and late-phase mediator and has the ability to activate neutrophils, recruits other effector cells and enhances the synthesis of chemokine

144
Q

normal ICP

A

ICP is defined as 5 to 15 mm Hg

145
Q

MAP to CBF linear

A

TBI

146
Q

altered Ach at NMJ

A

sux, NDMR
producution blocked with Hemi
release blocked with Bot

LA blocks post synaptic
Volatile blocks positive feedback and Ca and Nach res and Na Ch
aminoglyco blocks presynaptic ca
frusemide blocks camp for less release.

147
Q

gibbs donan

A

uneven distribution of permiable charged ions on either side of SPM due to distribution of impermiable charged ions

“The Gibbs-Donnan effect describes the unequal distribution of permeant charged ions on either side of a semipermeable membrane which occurs in the presence of impermeant charged ions. “ derranged phys

148
Q

AFOI

A

internal of sup laryngeal is sens (inside)

149
Q

m. of larynx

A

intrinsic m-

CT is sole adductor ext sup lary n.

150
Q

laryngeal cartilage

A

evernote

151
Q

AP tissues

A

In physiology, an action potential occurs when the membrane potential of a specific cell location rapidly rises and falls:[1] this depolarization then causes adjacent locations to similarly depolarize. Action potentials occur in several types of animal cells, called excitable cells, which include neurons, muscle cells, endocrine cells, glomus cells, and in some plant cells.

152
Q

pain in elderly

A

evernote

153
Q

Conc effect

A

In the study ofinhaled anesthetics, theconcentration effectis the increase in the rate that the Fa (alveolar concentration)/Fi (inspired concentration) ratio rises as the alveolar concentration of that gas is increased. In simple terms, the higher the concentration of gas administered, the faster the alveolar concentration of that gas approaches the inspired concentration. In modern practice is only relevant fornitrous oxidesince other inhaled anesthetics are delivered at much lower concentrations due to their higher potency.

154
Q

remi pka onset t/2

A

7.1 so 68% unionized at 7.4
onset 90s
t/2 5min so doa 10min or so.
clearance ++ fast 5l/min

clearance remi>morp>fent>alfent !!

155
Q

why does morph have a longer t/2 vs fent

A

fent bolus offset is due to redistribution!!

156
Q

why does alfent have a smaller t/2 vs fent

A

t/2=vd/cl

as Vd is smaller t/2 is shorter

157
Q

why does remi have fast onset

A

pka 7.1

lipid sol

158
Q

why does remi have short doa

A

non spec plasma and tissue esterase hydrolysis

t/2=Vd/Cl
vd small and clearance large

159
Q

FGF req for T piece

A

2.5xMV

MV of 30kg=300mlx20=6L–>15L/min FGF

160
Q

he dilution

A

V1.C1=C2.(V1+V2)
V2=TLC!!!!!
then with TLC known spirometry can determine FRC

161
Q

mole

A

The mole (symbol: mol) is the unit of measurement for amount of substance in the International System of Units (SI). A mole of a substance[1] or a mole of particles[2] is defined as exactly 6.02214076×1023 particles, which may be atoms, molecules, ions, or electrons.[1] In short, for particles 1 mol = 6.02214076×1023

162
Q

Avogadro’s law

A

Avogadro’s law states that “equal volumes of all gases, at the same temperature and pressure, have the same number of molecules.”[1]

1mole=22L at STP

163
Q

gas cylinder size

A

E=emergency

J=juganaut

164
Q

vol in anaesthetic clinder

A

V1.P1=V2.p2
O2
4.7x137/1=629L from size E bottle

NOTE N20 is a vapour so not applicable
-it is stored at 44bar and produces 1800L (as liquid can produce a shit tone of gas)

137 bar for air, o2, entenox

165
Q

VIE figures

A

VIE figures BP=-180 Crit temp -118 VIE -150C

166
Q

psuedocrit temp

A

at 147 bar is -5.5

at 4 bar (ine pipeloine is-30C)

167
Q

partician coeff

A

x

168
Q

USS limitations errors

A

x

169
Q

APL pos

A

distal to Bag to avoid PTx!

170
Q

scavenging

A
  • Active or passive systems are incorporated to collect gas waste.
  • This method consists of a collecting and transfer system, a receiving system and a disposal system.
  • Both excessive positive and negative pressure variations in the system are limited.
  • Other methods are used to reduce theatre pollution: theatre ventilation, circle system, total intravenous and regional anaesthesia.
171
Q

sample line vol

A

120ml/min O2 consumption 3.5ml/kg/min= 250

hence 350ml min.

172
Q

la place

A

To appreciate the afterload on individual muscle fibers, afterload is often expressed as ventricular wall stress (σ), where AL=2.r.p/thickness
In alv P to collapse= T/r

173
Q

contractility factors

A

The Frank-Starling law holds that increased stretch on the myocytes (to a point) increases the force of their contraction.
(indep of preload-simple stretch in a lab)

174
Q

afterload

A

Afterload can be defined as the resistance to ventricular ejection - the “load” that the heart must eject blood against. It consists of two main sets of determinant factors:
Myocardial wall stress, which represents intracardiac factors
Input impedance, which represents extracardiac factors
Wall stress is described by the Law of Laplace ( P × r / T)
and therefore depends on:
P, the ventricular transmural pressure, which is the difference between the intrathoracic pressure and the ventricular cavity pressure.
Increased transmural pressure (negative intrathoracic pressure) increases afterload
Decreased transmural pressure (eg. positive pressure ventilation) decreases afterload
r, the radius of the ventricle
Increased LV diameter increases wall stress at any LV pressure
T, the thickness of the ventricular wall
A thicker wall decreases wall stress by distributing it among a larger number of working sarcomeres
Input impedance describes ventricular cavity pressure during systole and receives contributions from:
Arterial compliance
Aortic compliance influences the resistance to early ventricular systole (a stiff aorta increases afterload)
Peripheral compliance influences the speed of reflected pulse pressure waves (stiff peripheral vessels increase afterload)
Inertia of the blood column
Ventricular outflow tract resistance (increases afterload in HOCM and AS)
Arterial resistance
Length of the arterial tree (the longer the vessels, the greater the resistance)
Blood viscosity (the higher the viscosity, the greater the resistance)
Vessel radius (the smaller the radius, the greater the resistance)

175
Q

what changes contractility

A

homeometric-frank starling
heterometric-HR bowditch and Anrep (AL)

HR, preload, afterload

drugs, electoolytes, disease.

176
Q

anrep

A

AL

Sustained myocardial stretch activates tension dependent Na+/H+ exchangers, bringing Na+ ions into the sarcolemma. This increase in Na+ in the sarcolemma reduces the Na+ gradient exploited by sodium-calcium exchanger (NCX) and stops them from working effectively. Ca2+ ions accumulate inside the sarcolemma as a result and are uptaken by sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) pumps. Calcium induced calcium release (CICR) from the sarcoplasmic reticulum is increased upon stimulation of the cardiac myocyte by an action potential.

177
Q

bainbridge

A

The Bainbridge reflex, also called the atrial reflex, is an increase in heart rate due to an increase in central venous pressure. Increased blood volume is detected by stretch receptors (Cardiac Receptors) located in both sides of atria at the venoatrial junctions.

178
Q

bezold jarish

A

The Bezold–Jarisch reflex (also called the Bezold reflex, the Jarisch-Bezold reflex or Von Bezold–Jarisch reflex[1]) involves a variety of cardiovascular and neurological processes which cause hypopnea (excessively shallow breathing or an abnormally low respiratory rate), hypotension (abnormally low blood pressure) and bradycardia (abnormally low resting heart rate) in response to noxious stimuli detected in the cardiac ventricles

179
Q

CO autoregulation

Golden

A

heterometric-HR,AL–>contract. Pressure–>HR
homeometric-FS–>cont

40-180 CO indep of HR in vitro

180
Q

what makes prop good for TCI

A

t/2=vd/cl

relatively predictable vd, cleara,ce redistribution, and half time

181
Q

CVP information

A

ΔCVP = ΔV / Cv

end-expiration,
PEEP — PEEP of 10 cmH20 usually results in increase of CVP by ~3 cmH20

182
Q

swan ganz

A

evernote

183
Q

GABA rec

CORE AF

A

aa,bb,g
ab x2=GABA binding site
ag=modulatory allosteric BNZ binding site (increased activation)
b= propofol, volatile site, barbituates (increased duration)

Although benzodiazepines and barbiturates produce the same electrophysiological action (increase in chloride conductance) at the macroscopic level, studies of channel kinetics indicate that benzodiazepines act primarily by increasing channel activation/ reactivation whereas barbiturates act by increasing the duration

184
Q

allosteric

A

relating to or denoting the alteration of the activity of an enzyme by means of a conformational change induced by a different molecule.

185
Q

how do drugs works

CORE

A

1) PC
2) rec
a) LGIC
b) second messenger
- GPCR, TKR, GCyclase
c) steroid
3) enzymes
4) VGIC

186
Q

DV

A

UV–>IVC and liver the shunt is the DV

187
Q

umbi vein artery Po2

A

verin 28 artery 18

188
Q

max MV

A

30xnormal

cardiac output not even close

189
Q

Resp exchange ratio

A

CO2 EXPIRED/O2 CONSUMED. varies dep on metabolic and non metabolic facotrs.

RQ is fixed and simply reflects substrate.

In the body, the volume of CO2 expired and
the volume of O2 consumed vary with metabolic,
as well as non-metabolic, factors. During exercise, the RER approaches a value of 2 because a
greater volume of CO2 is expired due to hyperventilation. In metabolic acidosis, the RER increases
because the respiratory compensation for acidosis
causes the amount of CO2 expired to increase,
whereas, in contrast, the RER decreases in
metabolic alkalosis as the hypoventilatory compensatory response reduces the amount of CO2
expired.

190
Q

anaesrobic threshold

A

e workload above which the blood concentration of lactic acid rises is called the ‘anaerobic
threshold’.

191
Q

pasteurs point

A

The Pasteur point is the partial pressure of oxygen at which oxidative phosphorylation ceases, and is ~1mmHg

192
Q

measure CO2

A

ABG: Carbon dioxide tension is measured with a Severinghaus electrode, which is based on the pH electrode, as PaCO2 is related to [H+]. The Severinghaus electrode consists of:

expired IR
mass spec
ramand spec

193
Q

anaesthetic gas measurement

A

evernote

194
Q

phase capno

A

1,2,3,4

195
Q

beerlambert

A

absorpptoin=molarabcoeff.c.l

196
Q

NSAID SE

A

rash, allergic,

AKI–>heartfailure, hyperkalaemia, HTN

197
Q

double bohr

A

so easy to get wrong

mum gives freely
fetus clings

198
Q

metabolic role placenta

A

COMT, MAO, butylcholinesterase

199
Q

long term potentiation

A

In neuroscience, long-term potentiation is a persistent strengthening of synapses based on recent patterns of activity.

200
Q

central sens

A

glutamate, NO, glia
sensitization of wide dynamic range neurons
wind up is short term and progresses if sustained to long term potentiaion #sdney

Expansion of receptive field size
Increase in magnitude and duration of response to stimuli
Reduction in threshold of firing

201
Q

picco vs swancanz

A

Picco: if swan canz CI

PICO
insert a central line
place PiCCO into a large artery, usually the femoral (axillary is an alternative)
CO and pulse contour analysis

202
Q

RMP def

A

The resting membrane potential of a cell is defined as the electrical potential difference across the plasma membrane when the cell is in a non-excited state. Traditionally, the electrical potential difference across a cell membrane is expressed by its value inside the cell relative to the extracellular environment.

203
Q

Vapour pressure =fi.barometroc pressure

A

Vapour pressure

204
Q

CSHT definition

A

Context-sensitive half time is the time required for a 50% decrease in the central compartment drug concentration after drug administration has ceased; where the “context” is the duration of a “BET” (bolus, elimination, transfer) infusion that maintained a steady concentration in the central compartment.

205
Q

Ka

A 
Law of mass action:
Rate of reaction is proportional to conc of reactants
A+R—>AR
V1=V2 at equillibrium
V1=D.R.k1
V2=DR.k2
So DR/D.R=K1/K2=Dk
Kd=dissociation constant inverse of Ka
Ka= K2/K1=A.R/AR
KA=association constant and is reciprical (strenght of sticking on once bound)
206
Q

starling forces numbers and principle

A

MAP=60
PBC=15
oncCap=21

loosely 60-20-20=20

filtration coef=SA.p
reflection coef=1/proptein perm=glycocalyx function

207
Q

steroids dose potency

A

dex 4=pred 25=hydrocort 100

dex spec glucocort!!

208
Q

Moa Dex

A

increased enceph–>eat
decreased sub P
decreased 5HT
decreased PG

209
Q

getn

A

positive effect-conc dep, post Abx and small degree time above MIC
SE determined by time above crit level.

block ribosome s30–>mistranslate tNRA–.weak protein–>wall breaks –>cidal –>synergistic with b lactams

SE nephrotox ATN reversible, Dx ototoxicity
not met–>excreted unchanged kidneys +water sol.
muscle weakness

210
Q

prolonged block

A

Patient: PK, PD
drug: choice
Anaesthetic: intereactions

2006a(6): Explain the possible mechanisms for prolonged neuromuscular blockade after a 4hr procedure using a non-depolarising muscle relaxantGeneral: Non-depolarising muscle relaxants work by competitively antagonizing ACh at the nAChR on the motor endplate of the NMJ. Prolonged blockade after 4 hours can be due to:Pharmacokinetics- AbsorptionoRepeated administration of NMBD during the case oAccidental administration of long-acting NMBD during the case Drug error- DistributionoInfusion (eg of vec which is lipid soluble) would lead to accumulation in lipid rich tissue without monitoring level of blockadeoInappropriately large doses→ high conc in synaptic cleft- MetabolismoImpaired metabolism: Hepatic failure preventing the metabolism of active drug into less active/inactive metabolites (eg pancuronium)o↓T°C if Pt not adequately warmed during the case: slows down drug metabolism- EliminationoRenal failure:↑ amount of active drug remaining in the body PancuroniumoRenal failure: active metabolite (vec) not eliminated fast enoughoHepatic failure: ↑ active drug remaining Vecuronium, Rocuronium, pancuroniumPharmacodynamics - Electrolyte disturbances:o↓K+, ↑Mg2+(competes w Ca2+), ↓Ca2+- ↓pH: ↑affinity of non-depolarising NMBDs (except gallamine) for nAChRo↑risk during a long case- Drugs:oVolatiles (prolonged exposure during a long case)- ↓ACh release at NMJoLithium -↓Na+ transmission at NMJoAminoglycosides - ↓ACh releasedby ?competition w Ca2+oLA – may block Na+ channel at NMJ (variable)oDiuretics – may effect cAMP production (variable)oCa2+ blockers - ↓ACh releaseoMg- Neuromuscular abnormalityomyasthenia gravis→ defective nAChRoEaton-Lambert → impaired Ca reuptake

211
Q

Define the term “hepatic extraction ratio”

A

Define the term “hepatic extraction ratio”

“Hepatic extraction ratio … is the fraction of the drug entering the liver in the blood which is irreversibly removed (extracted) during one pass of the blood through the liver”.

212
Q

determinants of HER

A

BF, uptake, enzyme capacity

213
Q

HER drug types

A

high HER–>BF is relevant. Prb and HF not
low HER
->low Prb–>protein binding irrel
–>high Protein binding–>protein binding change–>toxicity

214
Q

nerve test palcement

A

Typically smaller muscle groups are more sensitive
The positive (red) lead is placed proximal
Ulnar nerve

Electrodes are placed along the ulnar border of the wrist at the flexor crease, and thumb adduction is assessed.

Facial nerve orbicularis occult

The positive electrode is placed at the outer canthus, and the negative electrode is placed anterior to the tragus. Eyebrow twitching is assessed.

Posterior tibial nerve

Electrodes are placed posterior to the medial malleolus, and plantar flexion is assessed. post-tibial nerve-flexor hallucis brevis
215
Q

onset of different muscle group block

A

onset is determined by BF
since larynx and diaphragm equal and larynx more sens order is L, D
adductor has poor BF and as a peripheral muscle group is most sensistive

offset is determined by resistance
D>L>Adductor

Orbicularis occuli corresponds well with larynx but depth of block can be underestimated by direct stim of muscle anddecause facial nerve is quite reistant

clinical imp: AD is safe indicateor of when to tube and extubate
diaphragm recovery is not equal to larynx recovery which is not equal to upper airway muscle tone. (wait for adductor)

216
Q

venous drainage brain

A

dural venous sinus–>IJV

217
Q

CSF foramen

A

foraemen of munroe
aqueduct of silvia

goes to arachnoid villi outpouches from dura in sagital sinus

218
Q

arachnoid villi

A

Arachnoid granulations (also arachnoid villi, and pacchionian granulations or bodies) are small protrusions of the arachnoid mater (the thin second layer covering the brain) into the outer membrane of the dura mater (the thick outer layer).

219
Q

coricoid plexus

A

in ventricles

ultrafiltration glucos facilitated Na actively transported Cl fo;llows

220
Q

hi HER

A

prop, GTN, ketamine #only IV or +++ dose

221
Q

low HER

A

methadone, roc, phenytoin, thio

222
Q

nerve fibre types

A 
A
alpha somatic motor
beta touch
delta cold sharp
B preganglion ANS
C post gang ANS and pain and temp
223
Q

resistance unit

A

dyne.s/cm^5
or mmHg.Min/Lx80

normal is 100

224
Q

muscle of artery

A

media=muscle

225
Q

PVR factors

A

luminal-r4
intraluminal-PAP
extraluminal-lung vol, PEEP

226
Q

PTC

A

It consists of applying a 50-Hz tetanic stimulus to the ulnar nerve for 5 s, followed by single twitch stimulation at 1 Hz. The number of twitches observed in the period of post-tetanic facilitation, the post-tetanic count, correlates inversely with the degree of neuro- muscular blockade.

227
Q

PTC to TOFC

A

TOFC 1=PTC of 9

PTC of 2–>10min until TOFC of 1

228
Q

rec occupancy for depression

A

75% NDMR, depol is only 20%

229
Q

placenta

A

IgG

230
Q

ketamine bidning site

A

Phencyclidine (PCP

231
Q

preg and prB

A

α1‐acid glycoprotein decreased during pregnancy with the lowest value around week 30

232
Q

changes in preg

A

peaks:
map 20
CO30

https://primarysaqs.files.wordpress.com/2009/12/makeup-describe-the-cardiovascular-changes-that-occur-in-pregnancy.pdf

233
Q

roc met

CORE

A

NIL!!!

234
Q

VEC

A

CVS SE: nil P+H (NIL BRADY)
active met with short half life peed out
also bile out

235
Q

panc

A

active met with half potency
unchanged peed
mets in bile

236
Q

Atrac met

A

hoffman hydrolysis–>lordenosine

nonspec esterases–>ludenosine

237
Q

Cisat met

A

hoff–>nonspec esterases

238
Q

miv

A

isomers

histamine release

239
Q

ED 95

CORE AF

A

In anaesthesia, the term ED95 is also used when referring to the pharmacology of neuromuscular blocking drugs. In this context, it is the dose which will cause 95% depression of the height of a single muscle twitch, in half of the population.

240
Q

secondary immune response

A

2nd time seen it ++ quick 1 vs 5 days

241
Q

opiate terms

A

phenanthrene
thebaine
phenylpiperadine

242
Q

opiate receptors

A

all act suprasinally, SC and peripherally
yet predominate at

mu-supraspinal #Morphine
delta-spinal
kappa-spinal
NOP-supra and spinal

243
Q

GqpCR

A

evernote

244
Q

CYP450

A

3A4 is midaz and alfent and warf

2D6 is codeine tramadol

245
Q

dabagat vs riva #evernote

A

Dabagatran Double DURATION +Double action + DIALYSIS proDRUG. Min prB
Thrombin inhibitor #coag cascade and PL agg

246
Q

ropivocaine strucutre

A

propyl group on its piperadine nitrogen
S enantiomer
less lipid sol–>more discriminatory block
elim half life 150min 2.5hrs

247
Q

AchEi

A

physiostigmine crossed BBB to treat central antichol Sx

neostig-reacts with amide site to cause conformational change alowing esteratice site to forma covalent bond #carbamylated

248
Q

micromacro

A

0.01ma ie 10microamp vs 100ma

249
Q

earthing

A

completes circuit when fault–>trip and path less resistant than through you.

in powerlines –>escape

250
Q

aladin caseete

A

electrical injection of liquid (doesnt change volume with temp much.)

251
Q

flow meteres viscosity density

A
  1. At low flow rates, the clearance is longer and narrower, thus acting as a tube. Under these circumstances, the flow is laminar and a function of gas viscosity (Poiseuille’s law).
  2. At high flow rates, the clearance is shorter and wider, thus acting as an orifice. Here, the flow is turbulent and a function of gas density.
252
Q

mannitol end point

A

should be discontinued if Na+ > 160 or osmolarity > 320mosmol/kg

253
Q

hypertonic salien end point

A

end point of therapy Na+ 145-155

254
Q

STP

A

NaCO3

255
Q

propofol contains

A

benzyl alcohol

NaOH ph 7.4

256
Q

TEG

A

What is r?
r = reaction time (normally <6 minutes)
Measured from sample placement until the amplitude reaches 2 mm
Represents activation of the coagulation cascade (intrinsic)
Prolonged with heparin, coagulation factor deficiency
If abnormal, consider FFP
Initiation

What is k?
k = clot formation time (normally <6 minutes)
Measured from r until the amplitude reaches 20 mm
Represents fibrin formation
Requires normal intrinsic clotting factors, fibrinogen and platelets
Amplification

What is the α angle?
Measured from the top of r to the k value
Normally 60 degrees
Represents the rate of clot propagation
If abnormal, consider fibrinogen = cryoprecipitate

What does the maximum amplitude represent?
Represents clot strength
Normally 60 mm
Significantly disturbed by platelet abnormalities

257
Q

midaz

A

0.5mg/kg PO 0.1mg/kg IV

258
Q

flumazenil

A

0.5mg ie 1ml

259
Q

naloxone

A

50-100mcg Q5min

Viva (7 decks)

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