General Anaesthesia Flashcards

1
Q

TXA how does it work

does it affect PT / VII

side effect post op

A

lysine derivative which is an antifibrinolytic

No effect on PT/VII
Benefit on TEG

Reduce seizure threshold

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2
Q

TXA in trauma

A

CRASH 2

9% relative risk reduction

From 16% to 14.5% with a NNT of 67.

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3
Q

restrictive respiratory defect.

A

FEV1/FVC ratio is greater than 70%

severity of a restrictive respiratory defect is based on the % reduction of the FVC compared with predicted value

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4
Q

calculating doses of local

A

The maximum safe amount of bupivacaine with adrenaline is variously quoted as 2-2.5 mg/kg. The addition of adrenaline is thought to slow absorption of the local anaesthetic.

The maximum safe dose of bupivacaine is 120 mg.

A 0.125% solution will contain 0.125g/100mL or 125mg/100 mL.

The maximum volume of local anaesthetic is approximately 100-120 mL.

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5
Q

TURP Syndrome

A

The most likely diagnosis is the TURP syndrome. TURP syndrome is associated with excessive systemic absorption of irrigation fluid. The syndrome is caused by acute changes in intravascular volume, changes in serum osmolarity and sodium level and the direct effects of the irrigation fluid.

Factors increasing the risk of TURP syndrome include:

Prolonged duration of surgery (>1 hour)
Inexperience of surgeon
Excessive bleeding, and
Low venous pressure (for example, hypovolaemic patient).
Clinical features include hypervolaemia with rise in blood pressure and bradycardia. Fluid overload may cause pulmonary oedema and desaturation. Hyponatraemia may cause dizziness, confusion, nausea and vomiting. Seizures and coma may develop.

Glycine is the most common irrigation fluid used. It is an inhibitory neurotransmitter and may cause transient visual disturbance.

The surgical team should be informed immediately and surgery stopped. Supportive treatment may include intubation and ventilation for respiratory support, benzodiazepines for seizure control. Fluid restriction, furosemide and hypertonic saline should be considered

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6
Q

Compartment pressure monitoring.

A

The key to diagnosis is early compartment pressure monitoring.

A normal tissue compartment pressure is between 0 and 8 mmHg. The clinical picture correlates with the degree to which tissue pressure within the affected compartment approaches systemic blood pressure.

Capillary blood flow becomes compromised when tissue pressure increases to within 25 to 30 mmHg of mean arterial pressure. Pain may develop as tissue pressures reach between 20 and 30 mmHg. Tissue ischaemia is probable when compartment pressures approach arterial diastolic pressure.

Peripheral Doppler arterial pressure measurements may be present even with late signs of ischaemia.

A spinal cord haematoma is unlikely to give rise to these neurological symptoms and signs. The patient is also likely to have back pain.

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7
Q

Compartment pressure monitoring.

A

The key to diagnosis is early compartment pressure monitoring.

A normal tissue compartment pressure is between 0 and 8 mmHg. The clinical picture correlates with the degree to which tissue pressure within the affected compartment approaches systemic blood pressure.

Capillary blood flow becomes compromised when tissue pressure increases to within 25 to 30 mmHg of mean arterial pressure. Pain may develop as tissue pressures reach between 20 and 30 mmHg. Tissue ischaemia is probable when compartment pressures approach arterial diastolic pressure.

Peripheral Doppler arterial pressure measurements may be present even with late signs of ischaemia.

A spinal cord haematoma is unlikely to give rise to these neurological symptoms and signs. The patient is also likely to have back pain.

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8
Q

Dibucaine number

A

A dibucaine number of 20 suggests that this patient has an acquired or genetic deficiency of butyrylcholinesterase (plasma cholinesterase).

The dibucaine number represents the percentage inhibition of the local anaesthetic dibucaine (cinchocaine) by butyrylcholinesterase.

A normal dibucaine number is 70-80 (homozygous typical with a genotype E1uE1u). Butyrylcholinesterase is responsible for the metabolism of suxamethonium and mivacurium.

The genotypes E1uE1a (heterozygous atypical) and E1aE1a (homozygous atypical) are associated with dibucaine numbers 50-60 and 20-30 respectively.

Butyrylcholinesterase normally hydrolyses suxamethonium to succinylmonocholine and eventually to succinic acid.

Mivacurium is a benzylisoquinolinium choline-like ester that also undergoes extensive hydrolysis to monoester and alcohol metabolites.

Reduced dibucaine numbers result in the prolongation of action of these two muscle relaxants. Cocaine and procaine are also substrates for butyrylcholinesterase.

Atracurium besylate and its 1R‐cis, 1R’‐cis isomer, cisatracurium, both undergo Hofmann elimination, a process dependent on pH and temperature. Both drugs have a secondary degradation pathway by non-specific esterases.

Rocuronium is metabolised to a less active metabolite, 17-desacetyl-rocuronium by the liver and excreted in bile, urine and faeces.

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9
Q

Hyperkalaemia
Sequelae

A

Hyperkalaemia causes electrocardiogram abnormalities, for example:

peaked T waves
prolongation of the PR interval
QRS widening
decreased P waves
heart block, and
arrhythmias.
Hyperkalaemia also causes muscle abnormalities, for example:

weakness
paraesthesias, and
hypoactive reflexes.
U waves on the electrocardiogram are seen in hypokalaemia.

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10
Q

venous air embolism (VAE)

A

The likely diagnosis in this case is venous air embolism (VAE) in a patient who is at risk due to surgical positioning with the operative site higher than the right atrium.

Other risk factors include:

Pressurised infusion
Central venous line insertion
Long bone surgery, and
Pressurised gas in operative field (for example, laparoscopic surgery).
Diagnosis is made with high index of clinical suspicion and may be confirmed by transoesophageal echocardiography and precordial Doppler. The classic “mill wheel murmur” on precordial stethoscope is insensitive.

VAE may present with:

Raised right heart pressure with raised CVP
Tachycardia
ECG changes (right heart strain)
Hypotension, and
Oxygen desaturation.

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11
Q

Vertebral canal haematoma

Timing of Anticoagulation

A

Following the third National Audit Project (NAP3) conducted on behalf of the Royal College of Anaesthetists, the incidence of vertebral canal haematoma after neuraxial blockade was 0.85 per 100 000 (95% CI 0-1.8 per 100 000). Whilst unquantifiable, the incidence of vertebral canal haematoma following neuraxial blockade in coagulopathic patients is likely to be higher. For that reason, a coagulopathy remains a relative contraindication for conducting a spinal or epidural and only performed by experienced personnel having weighed up the balance of risk.

An acceptable time after the last dose of rivaroxaban (in a patient with a creatinine clearance of greater than 30mL/minute) to perform a block is 18 hours.

An acceptable time after the last dose of subcutaneous LMWH as prophylaxis to perform a block is 12 hours.

An acceptable time after the last dose of subcutaneous UFH as prophylaxis to perform a block is 4 hours.

An acceptable time after the last dose of thrombolytic therapy (streptokinase or alteplase) to perform a block is 10 days.

It is common practice to stop clopidogrel 7 days prior to surgery, particularly if a central neuraxial procedure is considered.

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12
Q

Commonest bleeding diathesis

A

Not that much is given away by this history just the issue of a prolonged bleed after prior dental extraction.

The most likely diagnosis when considering this patient is von Willebrand’s disease which is an autosomal dominant condition and is one of the commonest bleeding disorders. Most cases are mild, with bleeding after only mild injury, particularly mucosal membrane injuries.

The condition is due to a reduction or structural abnormality of von Willebrand’s factor, which has the dual role of promoting normal platelet function and stabilising coagulation factor VIII.

von Willebrand’s disease can give normal results on screening tests and diagnosis may require specialist investigation.

Most patients with mild disease respond to desmopressin (DDAVP) but clotting factor concentrates are needed for a minority.

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13
Q

Mitral Regurg surgery

A

Mitral regurgitation leads to a proportion of blood ejected by the left ventricle flowing back into the left atrium, and therefore dilation of the left atrium and pulmonary hypertension.

Anaesthetic goals include:

Improve forward LV stroke volume
and decrease regurgitant fraction.

Vasodilatation can improve forward flow
especially if pulmonary hypertension is a feature.

Preload should be maintained or slightly increased.

Decrease in afterload is beneficial as
long as this is not suddenly reduced

Hypoxia, hypercarbia, and high inspiratory pressures can all worsen pulmonary hypertension,

and should be avoided.

A slightly increased heart rate is preferred, as this reduces time for regurgitation as well as reducing time for excessive left-ventricular filling.

High afterload would increase the degree of regurgitation.

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14
Q

Serotonin syndrome

is

sx

A

Serotonin syndrome is the result of over stimulation of serotonin (5-HT) receptors in the brain. Common symptoms include:

fever
confusion
clonus
hyperreflexia
tremor
rigidity
hyperhidrosis, and
shivering.

In addition, it can cause agitation, tachycardia, ataxia and mydriasis.

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15
Q

What is parkland formula

A

The Parkland formula for fluid resuscitation after burns is:

4 ml × % body surface area burnt (BSAB) × weight (kg) = fluid over initial 24 hours following the time at which the burn was sustained.

So, 4 ml × 20% × 80 = 6400 ml in first 24 hours.

Thus, half should be given in the first eight hours = 3200 ml.

He has already received 1000 ml and is one hour post-burn. So he should receive 2200 ml over the next seven hours. This is 314 ml/hr, or approximately 300 ml/hr.

The rule of nines can be used to estimate BSAB in adults or a Lund-Browder chart in children.

Either 0.9% saline or Hartmann’s solution would be appropriate.

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16
Q

Calculating DLCOs post pneumonectomy / lobectomy

A

Prior to pulmonary lobectomy or pneumonectomy a simple spirometry to establish the FEV1, FVC or diffusion capacity (DLCO) can determine the likelihood of postoperative pulmonary dysfunction and mortality. Low mortality can be predicted if these preoperative criteria are followed:

FEV1 >1.5 L for a lobectomy
FEV1 >2 L for a pneumonectomy.
Usually an FEV1 in comparison with predicted values (corrected for sex, age, height, etc) is more appropriate; for example, an FEV1 >80% would indicate suitability for a pneumonectomy.

Similary, predicted values for DLCO have also been used. DLCO <60% and <80% predicted is associated with increased mortality and the incidence of pulmonary complications respectively:

Male DLCO (STPD) 29-39 mL/min/mmHg
Female DLCO (STPD) 21-27 mL/min/mmHg.
The bronchopulmonary segments are well-defined areas of the lung, which are ventilated via segmental (tertiary) bronchi. There are three lobes and ten bronchopulmonary segments in the right lung:

Right upper lobe - 3 segments
Right middle lobe - 2 segments
Right lower lobe - 5 segments.
There are two lobes and nine bronchopulmonary segments in the left lung:

Left upper lobe - 5 segments (sometimes the apical and posterior segments are fused as one) including the the lingular lobe - 2 segments.
Left lower lobe - 4 segments. (with fusion of anterior basal and medial basal)
The predicted or estimated postoperative (ppo or epo) values for FEV1, FVC and DLCO can be calculated by quantifying the lung volume removed at surgery.

In this example, the ppo value will be:

The total number of bronchopulmonary segments is 19 minus the five in the left upper lobe that has been removed.

(19 − 5) / 19 = 0.74%

15 mL/min/mmHg × 0.74 = 11.1mL/min/mmHg.

This, however, assumes that preoperatively all the bronchopulmonary segments are contributing equally to DLCO.

17
Q

Afib and WPW

A

Wolff-Parkinson White syndrome (WPWS) is associated with an accessory pathway of electrical conduction between the atria and the ventricles. Unlike the atrioventricular (AV) node, this accessory pathway (bundle of Kent) does not have the capability of slowing down a rapid rate of atrial depolarisation. The AV node is, in other words, bypassed by a short circuit.

Patients are prone to atrial fibrillation or flutter with a rapid ventricular response or narrow complex AV re-entry tachycardia. If a patient with WPWS develops atrial fibrillation, digoxin can promote transmission of impulses through this accessory pathway as its action is by blocking the AV node. This may result in an extremely rapid ventricular rate, and even ventricular fibrillation. It is therefore contraindicated.

Other drugs that interfere with AV nodal conduction such as adenosine, beta-blockers and calcium channel blockers are also relatively contraindicated.

Drugs of choice are the class III antiarrhythmic drugs amiodarone and ibutilide (K+ channel block) and flecainide and procainamide (Na+ channel block

18
Q

SVR calculation

A

The analogy is Ohm’s law:

Potential difference (V) = Flow of current (I) x Resistance (Ω)
Therefore R = V/I

SVR = (MAP−CVP/CO) × 80:

(60 − 10/5) × 80 = 800 dynes·s·cm−5
Normal values range between 700 − 1600 dynes·s·cm−5