Considerations For Specific Conditions: Specific Surgeries/Traumas

What is the motor nerve terminal

Large nerve from the spinal cord carries impulses to the skeletal muscle. There are multiple nerve branches stimulating a vast number of nerve fibres which must be activated simultaneously for muscle contraction.

Where would you find the motor end plate?

At the neuromuscular junction, the post synaptic membrane is highly folded

Where would you find the most nicotinic ACh receptors ?

These are most concentrated on the shoulders of the folded post-junctional membrane

 

What happens when an ACh neurotransmitter is triggered?

Once triggered (when the impulse reaches travel down the nerve and depolarises the nerve terminal), it’s release from vesicles in the pre-synaptic membrane and crosses the junction to stimulate receptors on the post-synaptic membrane where it sets off an sectional potential and the muscle fibre contracts.

What is the synaptic cleft?

The gap between the nerve terminal and the motor end plate.

What happens to the ACh once it’s activated the post-synaptic receptors?

The ACh is rapidly hydrolysed by a cholinesterase enzyme. Its constituent parts (acetyl and choline) are recycled and taken back to the pre-synaptic membrane to form more ACh.

What is the difference between the 2 types of acetylcholine receptors: muscarinic and nicotinic?

Muscarinic AChR are involved in physiological functions (HR, force, contraction of smooth muscles and release of neurotransmitters).

NAChR are involved in either neuronal or muscle-type physiological processes. Muscle-types are localised at NMJ. Each NAChR consists of 5 glycoproteins: 2 alpha, 1 beta, 1 delta and 1 gamma. They are arranged in a cylinder with a pore in the centre. One ACh molecule must bind to the two alpha subunits simultaneously for channel activation to occur and pore to open.

When would we want to perform a neuromuscular blockade?

To facilitate intubation
To aid muscle relaxation for surgery
To facilitate PPV
To create a central eye for ophthalmic surgery
As part of a balanced anaesthesia

Simply, how to neuromuscular blocking drugs work?

The block or antagonise, the binding of ACh to NAchR

What are the two main types of neuromuscular blocking drugs?

Depolarising (one drug group: suxanethonium or succuinylcholine) and Non-depolarising (two groups: aminosteroids and benzylisoquinoliniums)

 

Describe the succinylcholine drug molecule and its action

Two ACh molecules back to back. When they bind to ACh receptors, they cause widespread muscle fasciculations, they then stay bound to the receptor and the channel remains open until it’s ready to disengage so remains flaccidly paralysed. It causes no fade and is non-competitive- it’s an agonist of the ACh receptor. It stays there until it’s broken down- it cannot be antagonised.

 

What problems are associated with succinylcholine?

·  widespread muscle faciculations due to depolarising nature

·  reported muscle pain afterwards in humans

·  increases serum potassium (relaeased when muscle contracts)

·  possible malignant hyperthermia trigger

·  occasionally can cause histamine release

·  muscles faciculations can cause increase in IOP, ICP and IAP

Describe non-depolarising drug molecules and how they work?

Large polar molecules with a positive end (N+ atom) and a negative end.
The positive atom binds with the alpha subunit and prevents ACh molecules binding (so they are an antagonist of this receptor). It’s a competitive block - only 75% of receptors need to be blocked to create muscle relaxation. Fade is present.

What is the difference between the two classes of non-depolarising neuromuscular blocking drugs.

Aminosteroids are accurate- short sticky molecules. Metabolised in the liver and likely to produce active metabolites. Dont cause histamine release.

Benzylisoquinoliniums are leptocurare molecules and are long and spindly. Probe to degradation and broken down by hydrolysis and enterases. Prone to causing histamine release.

Describe the characteristics of Pancuronium

·  can cause tachycardia and hypertension

·  no histamine release IV

·  long half life

·  80% renal excretion- rest liver.

·  active metabolites produced

Describe the characteristics of vecuronium

·  dry powder reconsistitued with water

·  no histamine release IV

·  40% renal excretion- rest liver

Describe the characteristics of rocuronium

·  fast onset of action

·  more CVS effects Than other aminosteroids

 

Describe the characteristics of atracurium

·  contains 10 isomers

·  can cause histamine release IV

·  must be kept in the fridge

·  10% excreted in urine. 40% Hoffmann elimination. 50% plasma hydrolysis (broken down in the blood stream by non-specific enzymes)

Describe the characteristics of Cis-atracurium

·  one of the active isomers of atracurium

·  more potent than parent drug

·  much less histamine release that atracurium

·  mostly cleared by Hoffmanns elimination

 

Describe the characteristics of mivacurium

3 isomers (2active)
Wrong shape for hoffmans eliminations so broken down by hydrolysis and cholinesterase.
Histamine release IV
NO OTHER CARDIAC EFFECTS

What is hoffmans elimination

Spontaneous degradation in plasma and tissue at normal body oh and temperature

List the order of which skeletal muscles are blocked by NMblocking drugs in small animals

Facial expression muscles
Jaw muscles
Tail muscles
Neck and distal limbs
Proximal limbs
Swallowing
Abdominal muscles
Intercostal muscles
Diaphragm

How does the order of blocked skeletal muscles differ in horses and cows

 

Facial expression muscles are more resistant so further down the list

How does administration of a NMBlockade affect our anaesthetic?

Won’t be able to monitor Resp parameters (need manual ventilation)
Can’t monitor eye position or palpaebral reflex.
Can’t monitor jaw tone
Can’t see movement if patient light.

We need to use HR, BP, lacrimation and salivation.

How can we monitor a NMB itself?

Monitor for reflexes returning or ideally use a peripheral nerve stimulator

Where are the electrodes of a peripheral nerve stimulator placed?

There is a positive and negative electrode. The positive (often red) is placed proximal to the nerve.

What small animal peripheral nerves can we stimulate with a stimulator?

Facial, ulnar, peroneal

What horse peripheral nerves can we stimulate with a stimulator?

Facial and peroneal

What is fade

Fade is an unsustained tension in a muscle under non-dep NMB after a supramaximal stimulus. Usually seen as decreasing twitch heights.

 

What twitch patterns are available on a nerve stimulator

Single twitch (TW)
Tetanus stimulus (TET)
Double Burst Stimulus (DBS)
Train of four stimulus (TOF)

Why is a single twitch of limited use?

Wouldn’t see fade

How many twitches per second (Hz) in a tetanic stimulus?

50Hz

 

How many twitches in a double burst stimulus?

50 twitches per second, 750ms apart

How many twitches in a train of four?

2 twitches per second, over 2 seconds - most commonly used.

How can we check if a MNB is wearing off and what can we do to prolong it?

Should check twitches after 30mins has lapsed, every few minutes. If twitches return, the duration of the blockage can be prolonged same time again by administering half the original dose

 

How can we end NMB?

1.    Let it wear off naturally. Using the TOF ratio (the height of the fourth twitch compared to the full height of the first twitch). This ratio must be >0.9.
Or

2.    Give drugs. For depolarising NMB, give exogenous plasma cholinesterase. For non-dep NMB give anti-cholinesterase.

How does giving an anti-cholinesterase help reverse a NMB?

Stops the acetylcholinesterase working so ACh isn’t broken down and you increase the concentration in the synaptic cleft so it competes with the non-dep drugs for receptors and helps recover. Must wait for twitches to return before giving as need some receptors free.

Care: increasing ACh will act on the muscarinic receptors as well as the desired NAChR! So you’ll see physiological effects such as bradycardia and bronchoconstriction. Often administer an anticholinergic alongside e.g atropine, glyco.

 

Describe the characteristics of the 2 common used anti cholinersterases

Neostigme- ++ muscarinic effects, + pre/ synaptic effects, + acetylcholinesterase inhibitor, ++ plasma cholinesterase inhibitor. Best suited with glyco and slower onset of action.
Edrophonium: +/- muscarinic effects, ++ pre-synaptic effects, ++ acetylcholinesterase inhibitor, - plasma cholinesterase inhibitor. Best suited with atropine and faster onset of action.

What is suggamadex? When is it used?

A sugar ring molecule reversal agent for rocuronium and vecuronium. It encapsulates the molecule and doesn’t have any muscarinic effects. And you don’t have to wait until twitches return to give it.

What is peep?

Positive end expiratory pressure. It keeps 3-20cmh2o in the alveoli so it doesn’t allow the lungs to empty to atmospheric pressure at the end of ventilation. Helps recruiting closed alveoli also- improves oxygenation and prevents atelectasis.

 

What powers ventilators

Electrical power or gas supply

 

Describe a mechanical thumb ventilator

 

Mechanical principle of the thumb closing the valve to deliver a breath.

Describe a bag in a bottle ventilator

Bellows may be squeezed pneumatically by placing it in a canister and feeding a gas into the space between. Or squeezed mechanically by a motor

 

What is a minute volume divider?

Ventilators that have pressurised gas fed into a reservoir bag that is continually pressurised by a spring or its own eleastic recoil. The patients minute volume is calculated and the dialled up as fgf. The ventilator then divides up the MV into tidal volumes

 

What ventilator settings should we start with?

RR 10-20 bpm
Inspiratory TV 10-15mls/kg
Maximum peak inpiratory pressure (20 in dog, 12in cat)
I:E ratio of minumum 1:2

What effects does mechanical ventilation have on BP?

Causes hypotension due to positive pressure in thorax reduces venous return by compressing vena cava.
Reduces pre-load and therefore will reduce CO and BP. More likely to happen if patient is hypovoleamic.

What effects can mechanical ventilation have on the renal system?

Inappropriate ADH release.
Kidneys recognise theres a drop in CO abd lowered renal blood flow, so the kidneys release ADH in response so the body retains water and reduces UO.

What effects does mechanical ventilation have on carbon dioxide levels?

Overzealous ventilation can cause hypocapnia which may result in respiratory alkalosis or cerebral vasoconstriction.
Hypoventilation may result in hypercapnia and respiratory acidosis and cerebral vasodilation.

 

How can mechanical ventilation cause oxygen toxicity?

If on 100% (>60%) o2 for more than 12 hours, exhaust the free radical scavengers which usually mop up the free oxygen radicals. This damages the alveolar basement membrane.

What can oxygen toxicity cause in a ventilated patient and what can we do to avoid it?

Tracheobronchitis and absoprtive atelectasis to alveolar damage.
If patient ventilated long-term, get o2 % to less than 60 whilst maintaining an spo2 of 95%

What is the formula for oxygen delivery

 

O2 delivery = CO x content of o2 in blood

Define CO

 

Volume of blood ejected from the heart in a minute
= HR X SV

 

How is O2 carried in the body?

97% carried bound to haemoglobin (SaO2)
3% carried dissolved in blood (PaO2)

 

What is the formula for calculating oxygen content of the blood (CaO2)?

CaO2= (1.34 x Hb x SaO2) + (PaO2 x 0.003)

What is the formula for MABP?

 

CO X SVR

What is SVR affected by?

Changes in vessel diameter
Changes in blood viiscocity

If a patient is in heart failure, what happens to their blood flow?

Usually diverteed to central compartment decreasing peripheral perfusion.

What influence can drugs to treat heart diseases have on an anaesthetic?

Some drugs e.g. acce inhibitors, cause vasodilation which may cause hypotension under GA.
Frusemide may cause patients to have low potassium levels.

What special consideratios are there for anaesthetising patients with cardiac disease generally?

Oxygenate pre and post to maximise the oxygen content of blood

Ensure adequate analgesia to lower doses of induction agent and volatile agent which both may cause myocardial depression.

Avoid fluid overload and use lower sodium fluids as easier to cope with e.g. Hartmanns.

What should be included in a pre-GA clinical exam for a patient with suspected heart disease?

MM colour, moistness, CRT
Ausc of all 4 chambers, noting point of intensity of any murmurs.
Auscultate lung fields
Palpation of pulses when listenting to heart to identify any lung deficits.
Observation of respiratory rate and pattern
Peripheral pulse quality and rate.

Where can we auscultate the mitral, aortic, pulmonic and tricuspid valves?

Mitral - btw LA&LV. Heard at 5th Intercostal space on L side
Aortic - LV & body. Hears @ 4th ICS on L side
Pulmonic - btw RV & lungs. Heard 3rd ICS at sternal border
Tricuspid - Btw 3&4th ICP R side.

What are our anaesthetic aims in a patient with mitral valve disease?

·  Mild vasodilation (decrease resistance so blood takes easiesst path out of the heart)

·  Avoid bradycardia. Lets the heart have more time to fill with blood before contraction making regurgitation worse.

Descibe the changes and concerns with a hypertrophic cardiomyopathy?

Thickening of left ventricle, decreased volume of heart chamber and abnormal relaxation of heart muscle.

Causes:
- tachycardia
- decreased myocardial oxygenation
- development of arrythmias due to worsening function of heart.

 

What are our anaesthetic aims in a patient with HCM?

·  Decrease HR

·  Suppress ventricular arrythmias

·  Maintain fillling pressures

·  Maintain or slightly increase SVR by vasoconstriction

·  reduce outflow obstruction in cats (alpha 2s)

Use of medetomidine or dex will cause an increase in SVR and a decrease in HR so may be good for these patients.

What are the issues with the heart in a patient with pulmonic stenosis?

Narrowing of the pulmonary valve, limiting R ventricular outflow. This in turn will increase the R ventricular systolic pressure and render the tricuspid valve inefficient

What are our anaesthetic aims in a patient with pulmonic stenosis?

·  maintain contractility (use MAC sparing drugs to limit volatile agent and the effects on myocardial contractility)

·  maintain or slightly reduce HR. Avoid tachycardia

·  Maintain preload with fluid therapy

·  Avoid excessive IPPV pressures as can make it harder for blood to flow out of the R side of the heart into the lungs.

 

What is aortic stenosis?

There is a stenotic valve - narrwing of the aortic valve - which limits left ventricular outflow

What are our anaesthetic aims in a patient with aortic stenosis?

 

·  Avoid hypotension by maintaining SVR (try not to vasodilate or constrict)

·  Maintain HR within 20% of baseline

·  Avoid factors that reduce myocardial oxygenation

What is dilated cardiomyopathy (DCM)?

Happens as a result of heart muscle degeneration causing the heart muscle to become thinner. The thin stretched walls make the heart much larger.
Due to its large size, atrial fibrillation can occur. (Irregularly irregular HB where no p waves).

What are our anaesthetic aims in a patient with DCM?

Maintain myocardial contractility and oxygenation
- Avoid bradycardia and maintian the normla HR( patient will already likely be tachycardia to compensate for the poor stroke volume)
- Maintain preload with fluid therapy and avoid increases in afterload (e.g. vasocontriction).

What is the pleural space?

The space between the parietal layer (lying over the inside of the ribcage) and the visceral layer (lying over the outside of the lungs)

What should we monitor during thoracotomy and why?

Capnograph - tell us if things get disconnected, obstructions in ETT, reduced ETCO2 if lungs ‘ packed out way’ by vet.

Pulse ox - alerts poor o2 content in blood. Spo2 may drop if obstruction of large airways with debris or lungs packed away.

ECG - phrenic nerve, vagus nerve etc run through thorax - may see arrthmyias if tweaked or patient goes hypoxic or hypercapnic.

BP- drops from compression of vena cava.

Why is pain relief so important in thoracoctomy surgery?

Extremely painful surgery and patient may be reluctant to breath properly if sore.

 

What drugs can we give for thoracic surgery and why?

Opioids - may depress respiratory drive facilitating mechanical ventilation.
Ketamine - can be used on opening and closure as very good for somatic pain. Care in Cardio and onco patients.
NSAIDs - usual contraindications - wait until recovery. +/- paracetemol (dogs)
Alpha 2 adrenergic agonists - contribute to multi-modal analgesia
Others - including gabapaentin, maropitant, tramadol.
Local Anaesthetics - intercostal, interpleural blocks. Wound diffusion catheters and epidurals with morphine. Can use CRI of lidocaine in dogs also.

Why is nitrous oxide contraindicated in thoracic surgery?

Those with lung pathology require higher concentrations of oxygen inspired.
NO will expand a pneumothorax rapidly.

What would stabilisation of a patient about to have thoracic surgery entail?

·  Draining pericardial and pleural effusions

·  Oxygen therapy

·  Antibiotic therapy in some cases e.g. pyothorax

·  Cardiac medications

What steps should be taken if a patient presents for emergency thoracoctomy due to e.g. flail chest, punctured thorax or intrathoracic bleeding.

·  Pain relief! Opioids.

·  Oxygen therpay if doesnt cause stress

·  Blood loss calculations once in chest +/- fluid therapy

·  Gain control of ventilation once animal under GA (dont wait for chest to be opened)Contraindicated in tension pneumothorax - have equipment for thoracocentesis

What are the knock-on effects of lung contusions and cardiac contusions?

Pulmonary - bruising of lungs, blood and other fluid can gather in lungs. Excessive fluid interferes with gas exchange , potentially leading to hypoxia

Cardiac - Bruises of heart muscle can cause life-threatening arrythmias.

How shoudl we stabilise a diaphragmatic hernia patient?

Fluids, analgesia (non-emetic) and oxygen

What can we check in terms of other organs with a diaphragmatic hernia?

Any obstructed organs may have impaired function. Take bloods to check liver function etc.

What drug is contraindicated in diaphragmatic hernias if the spleen is in the thoracic cavity?

ACP - can cause splenic enlargement.

What ventilatory pattern should be used during diaphragmatic hernia repair and why?

Low volume high frequency.
Because of the presence of abdominal contents in the chest, the tidal volume is reduced, so minute volume is maintained by increasing the respiratory rate.
Also do this to prevent over-inflating atelectic lungs once repaired and cause pulmonary oedema.

 

What is atelectasis?

Collapse of lung or lobe pf lung due to deflation/compression or filling with fluid of the alveoli

Why should dorsal recumbency be minimised in diaphragmatic hernia repair surgery?

It may precipitate haemoglobin oxygen desaturation

 

What is a thymoma and what effects do they have on the patient?

Common tumour of the thoracic cavity
- Size compromises tidal volume, may compress trachea and caudal vena cava, can wrap about large blood vessels causeing blood loss on dissection.
Often cause myasthenia gravis (an autoimmune reaction to ACh receptors) - often treateed with anticholinesterase, however these drugs may alter the duration of action of opioids and response to NMB (so start at low doses).
Myaesthenia gravis can cause megaoesophagus so prone to regurge. So head up, pre-o2 and suction, secure airway.

What is a persistant right aortic arch (PRAA)?

A PRAA is a restrictive lesion around the oesophagus. Its caused by failure of the foetal vessel to regress and causes stricture of the oesophagus.

 

What are our anaesthetic aims in a patient with PRAA?

Uusally neonatal so consider this
Prone to regurge so head up induction and suction.
May also have aspiration pneumonia already so o2 therpay , monitoring spo2 and o2 in recovery.

What are our anaesthetic aims in a patient with pulmonary lesions (abscesses, tumours, foreign bodies etc.)

Oxygenation will be comprised so need o2 therapy. Surgeon may pack e including healthy lung out way so will see changes in bp, co2 and spo2.
Atmospheric contamination will happen so consider TIVA.
Can use bronchial blockers to prevent leakage of pus into airways.

 

When is a pericardectomy used?

Used to relieve pericardial effusion (fluid trapped between the pericardial sac and the heart muscle)

 

What is cardiac tamponade?

When there is so much fluid inside the pericardial sac that it interferes with the performance of the heart.

What are our anaesthetic aims in a patient with pericardectomy?

·  Fluid therapy to maintain venous return

·  Avoid myocardial depression (use MAC sparing drugs)

·  Avoid drugs which produce bradycardia (alpha 2s) as it will blunt the patient’s compensatory tachycardia.

·  arrythmias will happen when touch epicardium +/- lidocaine

·  may not use interpleural LAs as no pericardium to protect heart from cardiotoxic effects potentially.
Monitor blood loss

What is a patent ductus arteriosus?

A PDA is a connection between the aorta and pulmonic artery and represents a shunt between pulmonary and systemic circulation. It should close after birth.

 

What are our anaesthetic aims in a patient with PDA?

Paediatric considerations
May be ventricular enlargement
Diastolic pressure is often low (because of the connection to low pressure respiratory system) Aim to maintian BP - Avoid use of vasodilators.
Avoid vasoconstriction and dont use too high inflation pressures as can reverse the shunt.
When tying off the shunt may see a reflex bradycardia (Branham’s reflex) as a as a respomse to the increase in systemic BP.
+/- anticholinergic to correct.

What is Monroe-Kellie Doctrine?

The rule that the brain is made up of 3 parts: the brain parenchyma 84%, blood perfusing the brain 4% and the CSF 12%. If the volume of one component increases it has to be compensated by a decrease in another.

What are the clinical signs of increased intra-cranial prssure

·  altered mentation and changes in behaviour

·  cranial nerve deficits (deafness, dysphagia, dysphonia, visual disturbance.

·  blindness, changes in pupil size

·  seizures

·  circulatory and respiratory changes (including the cushings triad)

What is the cushings triad?

Its a CNS hypoxic response in which there is a massive sympathetic discharge which is a neurological emergency.
Includes: systolic hypertension, bradycardia, bradypnoea.

What may cause an increase in volume of brain parenchyma?

Oedema
Haemorrhage
Inflammation
Space-occupying lesions

What may cause an increase in volume of CSF?

increased production (e.g. due to a tumour)
Decreased drainage (e.g. due to space occupying lesions).

What may cause an increase in volume of blood in the brain?

Increased CVP
Increased Jugular pressure
Degree of vasodilation/vasoconstriction in the brain

What considerations should we have when anaesthetising a patient with ICP?

-Position of patient’s head should be kept raised at 30o to help drain blood out of the skull and into jugular vein.
- avoid occlusion of jugular vein.
- avoid valsalva manoeuvres (forced expiration against a closed glottis e.g. coughing, sneezing, gagging, v+)
- keep PIPs low during IPPV (as may increase CVP)
- Avoid changes in vasomotor tone
- avoid hypoxia (lowers PaO2)
- avoid hypercapnia (increases PaCO2)