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ACCS > Anaesthetics notes > Flashcards

Anaesthetics notes Flashcards

1
Q

how do anticholinergics work?

give the main indication

give an example

A

inhibit the ACh transmitter in the vagus nerve (parasympathetic system)
therefore inhibit the vagus nerve (parasymp)
INCREASE HEART RATE
thus used to treat bradycardia, eg. when UA

atropine
glycopyrolate

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2
Q

how do B-adrenoreceptor agonists work?

give an indication

give some uses..

A

activate B-receptors on the myocardial cells
stimualte the myocardium

INCREASE HEART RATE / CONTRACTILITY

Dobutamine

uses - heart failure / ITU

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3
Q

give an example of a combined a+B agonist

A

Ephedrine

Noradrenaline - very potent, only used during arrests / ITU

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4
Q

how do a-agonists work?

example of peripheral and central a-agonists

A

stimulate the a-receptors found in smooth muscle of the peripheral vessels
vasoconstriction
increases BP by increasing systemic vascular resistance..

peripheral - phenylephrine / metaraminol
(phenyl-p for peripheral)

central - norad (combined a+B agonist..)

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5
Q

which fluid for:
vol replacement
blood loss
hypoglycaemia

A

vol replacement - hartmann’s / saline

blood loss - blood

hypoglycaemia - dextrose 10%

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6
Q

how do NSAIDs work?

how can they contribute to airway constriction in asthmatics?

where do nsaids work - and what are their main SEs at these areas…

A

inhibit the synthesis of prostaglandins from arachidonic acid by inhibiting the action of cyclooxygensase 1 and 2 enzymes.

Lipoxygenase converts arachidonic acid to leukotrienes -there is more spare arachidonic acid knocking about as less of it is being made into PGs

Stomach acid - peptic ulcers
Renal - AKI
Platelets - blood thinning

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7
Q

how does aspirin work

who can;’t have aspirin

A

aspirin is also a non-steroidal anti-inflammatory

Irreversibly inhibits COX to reduce production of the pro-inflammatory factor thomboxane from arachidonic acid

this reduces platelet aggregation
and the risk of arterial occlusion…

CIed in:
1. children under 16 - reye’s
aspirin hypersensitivity
thrid trimester of pregancy - may cause premature closure of the DA

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8
Q

list some SEs of opioids

A

think slowing down - parasympathetic

CNS - sedation / miosis
CVS - badycardia / hypotension
Resp - bradypnoea / apneoa

GI - n&V or constipation
Urinary retention
itching

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9
Q

what are a standard adult’s fluid, energy and Na+/K=/Cl- requirements

A

20-30 ml/kg/day of fluid up to about 2.5L
20kcal/kg/day
approx 1mmol/kg/day of Na+/K+/Cl-

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10
Q

why might it be good to use hartmanns instead of normal saline?

and when might it be best to not use hartmann’s?

A

if patients are renally impaired, the hypochloraemic acidosis caused by increased serum Cl-can increase renal impairment in some instances

in liver failure, the lactate in hartmann’s isn’t metabolised to bicarb..

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11
Q

what is the maximum amount of potassium that you can put in a 500ml bag of saline?

A

20mmol in 500ml

nb - if K+ keeps dropping, ask HDU for advice. they can give it stronger if needed…

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12
Q

fluid resuscitation?

A

1.5L/2L hartmanns - then call HDU for help

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13
Q

main clinical signs of HYPOVOLAEMIC shock?

A

long CRT / increased HR

give fluids
raise legs

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14
Q

what fluid for paeds?

A

Dex 5% and 0.45% NaCl

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15
Q

who is at risk of cerebral oedema from normal saline?

A

children

premeno women

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16
Q

outline the ATLS classification of hypovolaemic shock…

A

I - blood loss <750ml HR normal SBP normal UO normal
II - 750-1500ml HR>100 RR 20-30 SBP probs normal-ish
III - 1.5-2L RR 30-40 SBP decreased
IV - >2L (ie >40%) RR >35 SSBP decreased

17
Q

describe DIC

A

release of pro-coagulants into the circulation
cause widespread activation of the coagulation pathway
consumption of clotting factors and platelets
leads to an increased risk of bleeding

NB - fibrin strands also fill the small vessels - haemolysing passing RBCs and activating fibrinolysis

18
Q

how do you treat DIC - 2 principles

then the actual - what would you give for DIC

A
  1. treat the cause
  2. stabilise the patient by replacing whats lost

platelets if count <50x109

cryo to replace the fibrinogen (contains Factor VIII, von Willebrand factor and fibrinogen - concentrated the ones we really need)

FFP to replace the coagulation factors (contains all..)

Activated protein C - coag cascade regulator

19
Q

how much should 1 unit of blood raise the Hb by?

A

usually about 1g/dL

20
Q

what is the Glasgow-Blatchford score?

what are its components (easy to work out once you know what it is…)

A

Determines whether someone with UGI haemorrhage is likely to need OGD or can be managed outpatients

upper GI bleeding - big drinkers - glasgow

components
Hb
Blood urea levels
SBP
other components:
tachycardic / px with melaena / px with syncope / hepatic disease / cardiac failure
21
Q

what is the Rockall score

what are the criteria…

A

prognosis after upper GI bleed and OGD

crieria are ABCDE

Age, Blood pressure fall (shock), Co-morbidity, Diagnosis and Evidence of bleeding

22
Q

define massive hemorrhage

clinically…

A

Loss of more than one blood volume within 24 hours (around 70 mL/kg, >5 litres in a 70 kg adult)

50% of total blood volume lost in less than 3 hours

Bleeding in excess of 150 mL/minute.

OR CLINICALLY:
bleeding which leads to a systolic blood pressure of less than 90 mm Hg or a heart rate of more than 110 beats per minute.

23
Q

what is a pathological q waves and what do they usually indicate…

A

> 40 ms (1 mm) wide
2 mm deep
25% of depth of QRS complex
ANTERIOR LEADS - V1-3

mean current or previous MI

Q waves in leads III / AVR are a normal variant..

24
Q

how would you manage a warfarinised patient peri-operatively?

A
  1. stop his warfarin 5 days prior to the op
  2. Bridge with LMWH
  3. op can go ahead when INR <1.5
  4. resume warfarin about 24hrs after surgery?
25
Q

how long after major surgery would you check the Hb

below which level would you transfuse?

A

4hrs - allow haemostasis after blood loss

<8g/dL

26
Q

when is GTN CIed

A

patients with hypotension..

27
Q

what is your SpO2 target in ACS

A

94-98

28
Q

what is CPAP

why does it help so much in pulmonary oedema

A

greater level of positive pressure superimposed on top of a positive end-expiratory pressure

CPAP helps because it relieves breathlessness by:

increasing the pressure gradient between LV and extrathoracic arteries (almost like it’s helping to contract the LV…..)

which increases the stroke volume

reduced afterload and preload as increased intrathoracic pressure…

29
Q

what trop level would be suggestive of an MI?

what level would you want to repeat?

below which level would you be happy to say unlikely MI?

A

> 30 likely mi

14-30 unsure - repeat

do 3hr, 6hr and 12hr trops?

troponin <14 = unlikely to be MI

30
Q

how much insulin does someone need maintenance wiise if they are insulin dependant..?

A
  1. 1unit/kg/hour

ie. a 50kg lady needs 5units/hr

31
Q

what are the asa classification grades?

A

asa1 - a normal healthy patient, non smoking and minimal or no alcohol use

asa2 - a patient with mild systemic disease

asa3 - a patient with severe systemic disease (ie poorly controlled DM / ESRF etc…)

asa4 - a patient with severe systemic disease that’s a constant threat to life…. ie. recent MI / CVA etc. <3months /

asa5 - a patient who is moribund and not expected to survive without this operation… ie ruptured aneurysm etc.

asa6 - declared braindead

ACCS (2 decks)

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