Revision Notes in

Anaesthesia and ICU

SAQs from NI School of Anaesthesia

For nal EDAIC, FRCA and FCAI

Ahmed Salahuddin
 Revision Notes in
Anaesthesia and ICU
 Revision Notes in
Anaesthesia and ICU

Clinical Science as Applied to Anaesthesia,

Intensive Therapy and Chronic Pain
A Guide to SAQs for EDAIC, FRCA and FCAI
From NI School of Anaesthesia

Ahmed Salahuddin
Saudi German Hospital
Jeddah, KSA
 This work is dedicated to

My parents Salahuddin and E. Tawfik may god bless their souls

My sincerely supporting wife S. Nasr who gifted me

Raghda, Yousef, and Mostafa hopping you the best in life

El-Pop
Chapter 1

Neuroanaesthesia
 Neuroanaesthesia

__________________________________________________________________________________________________

The field of Anaesthesia for neurosurgery, neuroradiology and neuro critical care requires the anaesthesiologist to
concentrate on special areas that are of utmost importance, namely the impact of patient positioning, the anatomy of the
lesion and the site of surgery, blood loss, the intracranial pressure (ICP) variations, the proximity of surgery to specific
brain and brainstem centres, and the impact of the later on haemodymanic and respiratory functions.
The above implies the necessity of getting instant numerical values expressing the rapid variations that may be due to
surgical manipulations, blood loss or fluid and electrolytes imbalance. That's why understanding the concept of
moment­to­moment monitoring is crucial. Also the pharmacological effect of anaesthetic drugs, drugs that affect the
volume status and those which affect the cardiac and circulatory functions are all of top importance.
__________________________________________________________________________________________________

1. Posterior fossa craniectomy 2. Venous air embolism, site of surgery above the level
of the heart entraining air.
A 34 year old man is scheduled for a posterior fossa 3. Pneumocephalus, particularly after closure of
tumour excision cranium, causing raised ICP.

A. List patient positions that might be employed for this C. The monitoring techniques that can specifically
operation. detect the presence of venous air embolism during
B. What potential intraoperative problems are associated surgery and method used, and the features that would
with posterior fossa craniotomy? indicate the diagnosis.
C. What monitoring techniques can specifically detect 1. Precordial doppler, most sensitive, non­invasive
the presence of venous air embolism during surgery device, change in audio of doppler
and for each method used, give the features that 2. Transoesophogeal echocardiography is the most
would indicate the diagnosis? sensitive invasive device → appearance on echo
3. End tidal CO2 → set tight alarm limits, a sudden
A. Patient positions that might be employed for this decrease in ETCO2
operation 4. End tidal Nitrogen → sudden increase in ETN2
1. Supine 5. Pulmonary artery catheter to measure pulmonary
2. Prone artery pressure → sudden rise in pressure
3. Sitting 6. Right atrial pressure → increase
4. Lateral 7. Oesopgeal stethoscope → mill wheel murmur
5. Park bench 8. ECG → arrythmias, RV strain, ST depression

2. Traumatic brain injury

A 54 year­old patient is admitted to the Emergency
Department following a traumatic brain injury. A CT
scan reveals only cerebral oedema.

A. What is secondary brain injury and when is it likely

Fig. 1. Park bench position to occur?
B. Outline the main physiological and cellular changes
B. The potential intraoperative problems associated associated with secondary brain injury.
with posterior fossa craniotomy C. How can secondary brain injury be minimised in this
1. Cardiovascular instability related to: patient?
a. Sitting position
b. Venous pooling in the legs A. Secondary brain injury and its onset
c. Direct surgical stimulation of lower pons, Inflammation and release of neurochemical mediators
upper medulla, floor of 4th ventricle, result in vasogenic oedema, contributing to raised ICP,
causing tachy/brady arrhythmia, hypoperfusion and ischaemia. It occurs over hours to days
associated hypo/hyper tensions. from the initial brain injury.

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 Neuroanaesthesia

B. The main physiological and cellular changes 2. Respiratory

associated with secondary brain injury a. Avoid hypoxia pO2 > 11 kPa
b. Maintain pCO2 4.5­5.0 kPa
1. Physiological c. Hyperventilation 4­4.5 kPa for impeding
a. Vasogenic oedema causes ongoing herniation, short term option due to
hypoperfusion and ischaemia normalisation of pH through bicarbonate
b. Disruption of blood­brain barrier with buffering
impaired vasomotor autoregulation 3. CVS
leading to dilation of cerebral blood a. Avoid hypotension by maintaining
vessels MAP > 90 mmHg
c. Hydrocephalus due to obstruction in flow b. Replace intravascular volume but avoid
and absorption of CSF due to blood in hypotonic and glucose containing
subarachnoid space solution
2. Cellular c. Use blood products as necessary →
a. Excitatory amino acids e.g. glutamate are reverse existing coagulopathy
significantly elevated post TBI d. Vasopressors to maintain
i. Cause cell swelling and CPP > 60 mmHg
neuronal death 4. Neuro
ii. Cause influx of sodium and a. ICP monitoring → aim < 20mmHg
chloride into the cell, causing b. Maintain CPP > 60 mmHg
acute neuronal swelling c. Adequate sedation, analgesia and muscle
b. Increased metabolism in injured brain relaxation
stimulated by increase in circulating i. Propofol, midazolam
catecholamines ii. Opioid infusion
c. TBI induced stimulation of iii. Cisatracurium infusion in
sympathoadrenomedullary axis and refractory increased ICP
serotonergic system d. Hyperosmolar therap
d. Increase in extracellular potassium i. keep Na < 155 mmol­1
leading to oedema ii. Mannitol or hypertonic saline
e. Increase cytokines contributing to iii. Posm < 320 mmol­1
inflammation e. CSF drainage (Extraventricular drainage)
f. Decrease in intracellular magnesium f. Treatment of seizures e.g. Phenytoin
contributing to calcium influx g. Barbituate coma in refractory raised ICP
g. Linked to delayed damage associated with cardiovascular instability
h. Head of bed elevated to improve venous
C. How to minimised secondary brain injury in this drainage
patient i. Endotracheal tube taped, to limit venous
congestion
Targeted resuscitation and early specialist management 5. Metabolic
beginning in the pre­hospital setting and continuing in a. Strict blood glucose control 6­10 mmol­1
tertiary hospital. b. Avoid hyperthermia
1. Prehospital c. Hypothermia for refractory raised ICP
a. Avoid hypotension and hypoxia
b. Airway 6. DVT prophylaxis
c. Early tracheal intubation if GCS <8,
hypoxic on supplementary oxygen, 7. Surgical
hypo/hypercarbic a. Decompressive craniectomy

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3. Raised intracranial pressure, 2. The normal ICP waveform is triphasic. In normal

normal and abnormal waveforms physiology the first peak is greater in amplitude
than the second and third. These peaks are known
as P1, P2 and P3. P1 reflects arterial pressure
A. What is a normal intracranial pressure (ICP)? which is transmitted through the choroid plexus,
B. Describe the normal ICP waveform?
P2 reflects cerebral compliance and because of
C. How does the waveform change with increased ICP?
this is variable, P3 reflects venous pressure.
D. What are the anatomical results of a raised ICP?
3. The waveform itself is plotted on a graph with x
E. What are the symptoms and signs of a raised ICP?
axis time (secs) and y axis pressure (mmHg, e.g.)
A. Normal intracranial pressure (ICP)
1. Intracranial pressure is the pressure within the
fixed volume of the skull, and is a balance of
relationship between brain tissue, blood and CSF.
2. The normal range estimated at being 7­13 mmHg.
3. An ICP above 20 mmHg is generally considered
as being raised.
4. There are slight variations in ICP with systolic
and diastolic pressures and with respiratory
patterns.
5. There are also variations with posture (slight
increase when supine) and on coughing, straining Fig. 2. Normal and abnormal noncompliant ICP waveform,
(P1) Percussion wave represents arterial pulsation, (P2)
Tidal wave represents brain tissue compliance, (P3)
B. The normal ICP waveform (Lundberg waves)
Dicrotic wave is due to closure of aortic valve. Under
1. Normal ICP waveform pulsatile and reflects
normal conditions. P1> P2, indicative of normal
cardiac and respiratory cycles compliant brain. In ABI brain compliance starts decreasing
resulting in reversal of Pl: P2 ratio (i.e., P2 > P1) which is
a sensitive predictor of poor brain compliance.

Reduced compliance

Plateau waves

Fig. 3. ICP monitoring system showing normal, moderately elevated and significantly elevated ICP

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.
C. Waveform change with increased ICP 5. Pressure transmitted along optic nerve causing
1. A raised ICP we have stated as being greater than papilloedema
20 mmHg therefore this will be reflected on the 6. Herniation of brain tissue at extremes of ICP
amplitude of the waveform a. Subfalcin or cingulate herniation:
2. The second and third peaks become greater in cingulate gyrus of frontal lobe herniates
amplitude in an elevated ICP across midline, across falx cerebri. May
3. P2 reflects cerebral compliance. If ICP is raised, occlude anterior cerebral artery
cerebral compliance is reduced and the second b. Central herniation: occurs when there is
peak becomes the most prominent downward pressure centrally and can
4. When observed over a period of time, a result in bilateral uncal herniation
pathological ICP trace may show pathological A c. Uncal herniation: temporal lobe
waves (A waves sustained < 20 mins) herniates below tentorium cerebelli. This
5. These are also what is known as plateau waves inturn may compress oculomotor cranial
because of the shape of the waveform seen at very nerve
high ICP values (e.g. 50­200 mmHg) indicating d. Cerebellotonsillar herniation: cerebellar
severe raised ICP and patient will often show tonsil herniates through foramen magnum
neurological signs of raised ICP e. Upward cerebellar herniation: if primary
lesion in posterior fossa
f. Transcalvarial herniation: where the
D. The anatomical results of a raised ICP brain squeezes through a fracture or a
surgical site in the skull. Also called
Monro­Kellie doctrine "external herniation", this type of
The pressure­volume relationship between ICP, volume of herniation may occur during
CSF, blood, and brain tissue, and cerebral perfusion craniectomy, surgery in which a flap of
pressure (CPP). The Monro–Kellie hypothesis states that skull is removed, the protruding brain
region preventing the piece of skull from
the cranial compartment is incompressible and that the being replaced during the operation.
volume inside the cranium is fixed.

The cranium and its constituents (blood, CSF, and brain

tissue) create a state of volume equilibrium, such that any
increase in volume of one of the cranial constituents must
be compensated by a decrease in volume of another

1. Based on Monroe Kellie doctrine, if the volume of

one of the cranium constituents rises, then the
other 2 must compensate to maintain a fixed
volume and pressure
2. Vascular anatomical changes include
vasodilatation to maintain CPP, reduction in
cranial blood volume
3. CSF moves out of cranial vault into thecal sac
4. Cerebral oedema, causing loss of sulci, reduction
in size of ventricles, from a number of causes;
cytotoxic, in cell death; vasogenic, vasodilatation,
raised BP; transependymal, outflow obstruction of
CSF Fig. 4. Types of brain herniation

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E. Symptoms and signs of a raised ICP ipsilateral mydriasis and

1. May vary depending on rate of onset, i.e. insidious movement of eye down and out.
(e.g. in brain tumour) vs acute (acute bleed, v. Papilloedema on fundoscopy
traumatic brain injury)
b. Cardiovascular signs
2. If insidious, or GCS not impaired, symptoms may i. Hypertension, physiological
include headache, particularly postural in nature response to maintain CPP
(worse supine, on straining etc.), visual ii. Hypertension and bradycardia,
disturbance (e.g. in cranial nerve involvement) or “cushing’s reflex” seen in
brainstem compression in
3. Signs, in significantly high ICP and acute onset tonsillar herniation also known
include: as coning
a. Neurological findings iii. Arrhythmias, again due to
i. Reduced GCS involvement of brainstem
ii. Focal neurology and motor
posturing c. Respiratory signs:
iii. Seizure activity i. Abnormal respiratory patterns in
iv. Cranial nerve lesions, e.g. 3rd brainstem herniation, e.g.
cranial nerve compression in cheyne stokes respiration
uncal herniation causing

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4. Acromegaly and pituitary surgery required for laryngeal obstruction.

A. What challenges does a patient with acromegaly b. Obstructive sleep apnea (OSA)
present to the anaesthetist?
B. What are the advantages and disadvantages of the c. Nasal CPAP can not be applied with
transphenoidal approach to the pituitary gland? nasal packs in postoperative period.
C. Why might the surgeon request a lumbar drain
insertion? 3. Cardiac
D. Describe the possible complications of pituitary a. Cor­pulmonale
surgery? b. Refractory HTN
c. Cardiomyopathy
d. IHD
e. Bi­ventricular dysfunction heart block

4. Endocrine:
a. 25% are diabetics
b. Secretion of ACTH, TSH also (as well as
GH) or alternatively compression of
tissue and reduced hormone secretion;
hypoadrenalism results in that situation
c. Hormonal and antihypertensive therapy
should be continued pre­operatively
5. Other
a. Excess peripheral soft tissue deposition
may make venous cannulation difficult
and increases the risk­nerve entrapment
syndromes; meticulous attention to
theatre positioning is therefore required

6. High dependency unit (HDU) care

post­operatively

7. Short acting agents such as remifentanil are ideal,

Fig. 5. Typical acromegaly facial characters
allowing intraoperative haemodynamic control
and facilitating rapid recovery; enables
A. Challenges that a patient with acromegaly present to neurological assessment
the anaesthetist
1. Airway: 8. NSAIDs linked with post op haematoma
a. Nasal polyps
b. Macroglossia 9. Steroid replacement therapy needed
c. Mandibular hypertrophy
d. Difficult bag mask ventilation (BMV)
B. Advantages and disadvantages of the transph­
e. Hypertrophy of aryepiglottic folds, soft
enoidal approach to the pituitary gland
palate and epiglottis
1. Advantages (extracranial approach)
f. Difficult intubation
a. Safest approach
g. Tracheal compression (1/3) secondary to
b. Shorter hospital stay
enlarged thyroid
c. Macro and microadenoma
h. Subglottic stenosis
d. minimal surgical trauma
i. Recurrent laryngeal nerve palsy
e. minimal blood loss
j. May need AFOI.
f. direct access to the gland
g. avoidance of the generic hazards of a
2. Respiratory:
craniotomy
a. Upper airway obstruction in acromegaly
2. Disadvantages
is usually regarded as being due to
a. Bifrontal craniotomy will be needed for
macroglossia and pharyngeal soft tissue
giant pituitary tumours or failed
hypertrophy. Tracheostomy my be

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transphenoidal approach 5. Postoperative neuroendocrine abnormalities can occur

b. Persistent CSF rhinorrhoea and the after pituitary surgery.
associated risk of postoperative a. DI (50%) usually develops within the
meningitis first 24 h, and resolves spontaneously in
c. Panhypopituitarism about a week. (Polyuria with a urine
d. Transient diabetes incipidus (DI) specific gravity of < 1.005 and low
e. Vascular damage osmolarity of < 300 mosm)
f. Cranial nerve injury b. Hyponatremia can be caused by excess
g. Cerebral ischaemia, and stroke as a result desmopressin admin
of vasospasm or thromboembolism. c. SIADH (20% occurs 1/52 post op); fluid
h. Deliberate nasal septum fracture is restriction to 500–1000 ml/ day
required for transsphenoidal transnasal d. Hormone replacement therapy HRT will
approach; to minimize nasal bleeding, be required in all patients after operation
mucosal vasoconstriction is achieved by e.g. steroids
using a topical anaesthetic and a e. Venous air embolism (VAE) 10%
vasoconstrictor
i. Co­phenylcaine (5% lidocaine 0.5%
phenylephrine) causes less of a
hypertensive response than adrenaline in
patients with Cushings.

C. Lumbar drain insertion may be requested

1. To allow descent of tumour into surgical field by
injecting small amounts of saline into
subarachnoid space
2. The same effect can also be achieved by
controlled hypercapnoea.
3. To control post op CSF leak

Fig. 7. Pituitary gland surrounding structures

D. Possible complications of pituitary surgery
1. Venous or arterial bleeding especially in larger
tumours
2. CSF leak, menigitis
3. Airway obstruction
4. CN II ­VI damage as the have close proximity to
surgical

Fig. 6. Relation between pituitary gland and CN II

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5. Scoliosis surgery and spinal cord A. Principles of preoperative assessment in scoliosis

surgery
monitoring
1. History: Type of scoliosis; idiopathic or
secondary
a. Idiopathic usually in fit, healthy patients
with no cardiorespiratory complications.
Standard assessment and history of good
exercise tolerance usually sufficient.
b. Secondary → elicit primary cause, any
other organ dysfunction that may be
present eg;
i. Muscular dystrophy
ii. Cardiomyopathy
iii. Restrictive lung defects
2. Tests:
a. Bloods: including coagulation screen,
calcium, phosphate and cross match
b. CXR and spirometry
c. If non­idiopathic, ABG if pulmonary
function tests (PFTs) not possible
d. ECG and Echo for cardiac function, if
exercise impossible pharmacological
stress Echo can be useful.

Fig. 8. Scoliosis deformity

A. Describe the principles of preoperative assessment in

scoliosis surgery.
B. What are the potential complications of the prone
position ­ how can these be avoided?
Fig. 9. Scoliosis is a twisting and sideways
C. How is the spinal cord monitored during the
curvature of the spine which makes the spine
procedure?
appear more like an “S” or a “C” than a straight
D. What are the options for postoperative analgesia after
a spinal procedure? line.

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B. Complications of the prone position and how to 4. Respiratory system (RS)

avoid a. Abdominal compression
i. Higher airway pressures
 Reduce abdominal pressure with pelvic and chest
wedges
5. Gastrointestinal (GI)
a. Visceral ischaemia
i. Mesenteric vascular occlusion
ii. Pancreatitis infarction
iii. Hepatic infarction
 Montreal mattress (hole for abdomen), pelvic and
chest wedges

C. Spinal cord monitoring during the procedure

Fig. 10. Prone positioning in a pediatric patient with
paddin, tapping, head turning and pelvic and chest wedges Continuous intraoperative motor and somatosensory
evoked potentials.
1. Dislodge of: 1. Somatosensory: lower limb nerve stimulated and
a. ETT spinal cord or cortical response monitored.
b. Monitoring cables a. Not affected by anaesthetic agents
c. Catheter (except local)
d. Cannulae b. May be affected by hypothermia
 Sufficient staff (6 recommended)
 Recheck all lines after turn 2. Motor: cortex stimulated and spinal cord or distal
 Reinforced (Armoured) ETT response monitored.
a. Sensitive to volatiles so less useful
2. Pressure damage: b. Nerve injury indicated by increased
a. Eyes (direct and reduced venous latency or reduced amplitude of response.
drainage), Joints
b. Peripheral nerves 3. Wake­up test
c. Indirect injury (chest wall, impaired a. If sudden deterioration
visceral blood flow) i. Stop relaxants and volatiles
 Turn head to side ii. Ask patient to move hands and
 Padding and tapping feet
 Frequently check iii. Remifentanil useful in case this
is necessary (responsive without
 Care if head down
pain).
 Nothing tight around neck
 Ascertain the range of motion (ROM) prior to
surgery and do not exceed it D. Options for postoperative analgesia after a spinal
 Avoid direct abdominal pressure (especially in procedure
obese)
1. Systemic:
3. Cardiovascular system (CVS) a. Simple analgesics and opioids
a. IVC compression b. NSAIDs usually avoided for 24 hours to
i. Reduced venous return avoid bleeding problems and reduced
ii. Reduced preload bone healing.
iii. Reduced stoke volume and COP
b. Chest wall weakness compressing RV 2. Regional:
with subsequent reduced RV filling a. Surgically placed paravertebral or
 Adequate fluid loading epidural catheters.
 Reduce abdominal pressure with pelvic and chest
wedges Usually a combination is used e.g. simple analgesia,
continuous epidural infusion of local anaesthetic and
continuous or patient controlled analgesia (PCA) infusion
of morphine.

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6. Aneurysmal subarachnoid
haemorrhage and anaesthesia

Fig. 12. Aneurysmal dilation in left middle cerebral artery

A. Symptoms and signs of subarachnoid haemorrhage

(including extra­cranial)

1. Sudden onset severe headache

2. Loss of consciousness (transient or prolonged)
3. Nausea and vomiting
4. Seizures
5. Focal neurological signs
6. Neck stiffness
7. Photophobia
8. Papilloedema
9. Pyrexia
10. Reactive hypertension
11. Cardiac arrest

B. Complications of subarachnoid haemorrhage (SAH)

1. Rebleeding
Fig. 11. Cerebral circulation
2. Raised ICP
3. Seizures
A. What are the symptoms and signs of subarachnoid 4. Hydrocephalus
haemorrhage (including extra­cranial)? 5. Hyponatraemia
B. What are the complications of SAH? 6. Delayed cerebral ischaemia and vasospasm
C. Describe specific measures for cerebral protection 7. Fever
following a SAH? 8. Hyperglycaemia
D. What are the goals of anaesthetic management for 9. Cardiac complications – neurogenic stunned
neurovascular surgery? myocardium syndrome
10. Pulmonary complications
E. What are the methods of minimising hypertension
a. Aspiration pneumonitis,
during induction of anaesthesia?
b. Acute lung injury (ALI)
c. Acute respiratory distress syndrome
(ARDS)
d. Pulmonary oedema

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2. The Triple H therapy is now not recommended it

included
a. Haemodilution
b. Hypertension
c. Hypervolaemia

3. New recommendations are aimed for:

a. Euvolaemia (avoid hyper/hypovolaemia)
b. Avoid hypotension
c. Normal Hct.

4. Control of arterial BP
a. Aim for a systolic BP < 160 mmHg
b. MAP < 110 mmHg
c. Avoid hypotension by keeping systolic
BP > 100 mmHg)

5. Endovascular treatment
a. In the situation of a new neurological
deficit where medical therapy fails
consider aggressive endovascular
treatment e.g. angioplasty

6. Treat fevers with antipyretics and cooling

7. Maintain serum blood glucose between 4.5­11

mmol.l­1

D. The goals of anaesthetic management for

neurovascular surgery

Management centres on:

1. Providing optimum operating conditions for
surgeon

2. Preventing increase in transmural pressure which

may cause rupture of aneurysm

3. Maintaining adequate cerebral perfusion pressure

and cerebral oxygenation

4. Prevent rise in MAP especially at laryngoscopy,

during placement of head pins and after skull is
open

5. Uncontrolled hypotension should also be avoided

because this may cause cerebral ischaemia
Fig. 13. CT images of subarachnoid haemorrhage
6. Maintain normothermia
C. Specific measures for cerebral protection following
a SAH 7. Ensure venous drainage is unobstructed by:
a. Good head position
1. Nimodipine a calcium channel antagonist that b. Head up tilt
reduces incidence of cerebral infarction c. Avoid tube ties
a. To be given prophylactically after SAH d. Avoid internal jugular lines
for 21 days (60 mg PO 4 hourly)

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8. Avoid acute drops in ICP as this may risk rupture

of aneurysm by increasing transmural pressure
gradient across aneurysm wall
9. Normalise MAP and PaCO2 prior to closure to
reveal any bleeding points
10. Smooth and rapid emergence and extubation
without coughing/gagging on ETT
11. Use short acting anaesthetic agents and opioids to
allow rapid return to consciousness to assess GCS
post op (unless poor grade SAH and requires
continued ventilation on ICU)

a) Methods of minimising hypertension during

induction of anaesthesia

1. Insert arterial line prior to induction to enable fine

control of BP
2. Pre­operative beta­blockade
3. Captopril 2­3 mg.kg­1 as premed
4. Adequate dose of alfentanil or remifentanil
5. Adequate induction dose of thiopental or propofol
6. Bolus dose of induction agent immediately prior
to stimulus (incisions)
7. IV lignocaine 1.5 mg.kg­1
8. Vasoactive drugs to reduce MAP (trimetaphan,
phentolamine)
9. Use of nerve stimulator to confirm muscle
paralysis
10. Careful intubation technique Fig. 14. Manifestation of subarachnoid haemorrhage

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7. Spinal cord injury ­ physiology and C. The principles of management of the airway in a
patient with an acute cervical spine injury
effects 1. The initial management of the polytrauma patient
A 27 year old man is admitted with a suspected spinal follows the Advanced Trauma Life Support
fracture following a fall into water. There are no other (ATLS) practice of airway and cervical spine
injuries. control, breathing and circulation.
2. (MILS or MILI) Manual in­line stabilisation or
A. Describe the respiratory effects at the different levels immobilisation to prevent further spinal cord
of spinal cord injury? trauma during laryngoscopy (download full text
B. Describe the physiology of spinal shock? from Manual in­line stabilization
C. What would be the principles of your management of 3. Intubation aids (boigie) and The McCoy is an
the airway in a patient with an acute cervical spine
alternative to the Macintosh for those experienced
injury?
D. What are the complications of hard and semi­rigid in its use
collars? 4. Rapid sequence induction (RSI) with adequate pre
E. Why and when may suxamethonium be oxygenation
contraindicated in a patient with spinal injury? 5. LMA or intubating laryngeal mask in the failed or
difficult intubation. The forces applied during
A. The respiratory effects at the different levels insertion can cause posterior displacement of the
of spinal cord injury cervical spine but the movement is less than that
1. C3 and above, denervation of diaphragm, seen in direct laryngoscopy
respiratory failure. 6. In the ‘can’t intubate, can’t ventilate’ scenario
2. C3­C5 partial diaphragm paralysis, usually need there should be early consideration of:
assisted ventilation
a. The surgical airway or cricothyroi­
3. C5­C8 complete intercostals paralysis, diaphragm
dotomy.
intact resulting in paradoxical ventilation,
ineffective cough b. These techniques can produce posterior
4. T1­T7, variable intercostals muscles involvement displacement of the cervical spine but
resulting in poor chest wall movement and poor this should not prevent the use of this
cough life­saving procedure
5. Above T7, Neurogenic cardiovascular 7. Nasal intubation has been superseded by oral
complication due to traumatic disruption of intubation for the low success rate and high
sympathetic system incidence of epistaxis and layngospasm
6. T1­T4, cardiac sympathetic supply, damage at this 8. Awake fibreoptic intubation : least amount of
level affects chronotropic and inotrpic responses
movement of the cervical spine, in the acute
of heart
trauma setting, blood or vomit in the airway may
B. Physiology of spinal shock make the technique impossible. Further
1. Spinal shock describes the initial phase after disadvantages include a relatively prolonged time
spinal cord trauma and defined as temporary to intubation,
interruption of spinal cord function.
2. All reflexes are lost and the cord below the level D. The complications of hard and semi­rigid collars
of the lesion becomes isolated from centre.( 1. Total immobilisation is not achieved
2. Increases the chance of difficult laryngoscopy
Flaccid paralysis)If there is an evidence of
3. Can exacerbate cervical spinal injuries
neurological sparing below the level of lesion it
4. Can cause airway obstruction
might recover. 5. Can increase intracranial pressure (ICP)
3. Autonomic and reflex activity gradually returns to 6. Increases risk of aspiration
an injured cord. Loss of descending inhibitory 7. Increases risk of deep vein thrombosis (DVT)
control causes autonomic hyperreflexia and 8. May cause significant decubitus ulcers
spasticity.

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E. Contraindications of suxamethonium in a patient Diffuse axonal injury

with spinal injury
1. Suxamethonium is safe to use in the first 72 hours e. Loss of grey­white matter differentiation
and after 9 months following the injury.
2. In the intervening period there is a risk of
suxamethonium­induced hyperkalaemia due to
denervation hypersensitivity and therefore should
be avoided.
3. After 24 Hours up to a year post burn

8. Head injury and sodium disorders

A. Differentiate between the CT findings of cerebral
contusions, diffuse axonal injury, SAH and
extra­/sub­dural haematomas?
B. Define primary and secondary brain injury?
C. What are the key principles dictating management of
the head injured patient on ICU?
D. Describe the fluid and electrolyte differences in Fig. 16. CT of diffuse axonal injury
SIADH, CSWS and CDI?
2. Subarachnoid haemorrhage (SAH)
a. Hyperdense substance filling normally
A. Differences between the CT findings of cerebral
dark CSF filled subarachnoid spaces
contusions, diffuse axonal injury, SAH and (fissures, sulci, lateral and third ventricle)
extra/sub­dural haematomas
1. Cerebral contusions
a. Early; foci of hyperdensity involving
grey matter and subcortical white matter.
b. Later; with surrounding oedema.
c. Gradually fade to areas of gliosis.
d. Can occur anywhere but predilection for
anterior cranial fossa, temporal pole and
coup/contrecoup pattern.

Fig. 17. CT of Subarachnoid haemorrhage

Fig. 15. CT of cerebral contusions

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 Neuroanaesthesia

3. Extradural haemorrhage (EDH) B. Definitions of primary and secondary brain injury

a. Biconvex/lentiform shaped hyperdense 1. Primary brain injury; Damage that occurs at the
extra­axial collection. Sharply time of initial insult and may be result of trauma,
demarcated. mechanical forces applied to the brain (diffuse
b. Does not cross sutures. axonal injury), haemorrhage or tumour
c. Often beneath temporal bone.
d. Often causes mass effect. 2. Secondary brain injury; Additional injurious
processes after the primary injury including

a. Ionic
b. Metabolic
c. Inflammatory processes

Hypoxaemia, hypercapnia, hypotension, raised

intracranial pressure, cerebral arterial spasm and
hypoglycaemia worsen secondary brain injury.

C. Key principles dictating management of the head

injured patient on ICU
1. Normotension
a. Strenuous attempts to maintain blood
pressure in normal range.
b. Hypotension has negative effect on the
outcome.
c. There is impaired cerebral autoregulation
Fig. 18. CT of Extradural haemorrhage in brain injury.
d. Cerebral perfusion pressure
4. Subdural haemorrhage (SDH) (CPP) = (MAP) ­ (ICP).
a. Acute; Crescent/sickle shaped e. Evidence unclear but aim to maintain
hyperdense extraaxial collection, crosses MAP of at least 70 mmHg and to achieve
sutures spreading diffusely over CPP target of over 70 mmHg (Rosner
hemisphere. protocol) or over 50 mmHg (Lund
b. Subacute; Isodense with cortex protocol)
c. Chronic; Hypodense with cortex f. Start initially with fluid resuscitation and
then vasopressors

2. Normoxia
a. Hypoxia associated with worse outcome
b. Cerebral blood flow (CBF) increases
when PaO2 falls below 8 kPa (60 mmHg)
c. Maintain PaO2 >13 kPa (97.5 mmHg)
d. PEEP to maintain oxygenation in the
range of (12­15 cmH2O) as exceeding
this will increase ICP affecting the
targeted CPP

3. Normocapnia
a. Aim for PaCO2 4.5­5.0 kPa
(33­37.5 mmHg)
b. CBF increases as PaCO2 increases
c. Hyperventilation reduces PaCO2 causing
vasoconstriction so hypocapnia should be
avoided as it worsens ischaemia
Fig. 19. CT of Subdural haemorrhage

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 Neuroanaesthesia

4. Normothermia 6. ICP management

a. Avoid hyperthermia which causes a. Aim ICP < 20mmHg with
increase in CBF and cerebral metabolic sedation/analgesia, maintain CPP,
oxygen requirement and increases ICP. osmotic therapy if required (mannitol or
hypertonic saline)
5. Normoglycaemia b. Avoid surges in ICP
a. Hyperglycaemia causes increase in
cerebral metabolism and in situation of 7. General ICU care
reduced CBF in trauma this results in a. Sedation
anaerobic metabolism b. Analgesia
b. Aim for tight blood glucose control c. Nutritional support
4.0­8.0 mmol.l­1 (72­144 mg.dl­1)with d. Venous thromboembolism prophylaxis
insulin e. Sodium homeostasis
c. Avoid dextrose

Fig. 20. Causes and diagnostic algorithm for hyponatremia

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 Neuroanaesthesia

D. Fluid and electrolyte differences in SIADH, CSWS 2. Diabetes insipidus (DI)

and CDI a. Lowered plasma volume
b. Equal sodium balance
1. Syndrome of inappropriate antidiuretic c. Negative water balance
hormone secretion (SIADH) d. High serum sodium
a. Raised plasma volume e. High serum osmolality
b. Positive/equal sodium balance f. Normal urine sodium
c. Positive water balance g. Reduced urine osmolality
d. Low serum sodium
e. Lowered serum osmolality
f. High urine sodium
g. High urine osmolality

Fig. 23. Pathophysiology of DI

Fig. 21. Pathophysiology of SIADH 9. Preassessment/intraoperative

Cerebral salt wasting syndrome (CSWS)
management of posterior fossa surgery
h. Lowered plasma volume
A. What are the anaesthetic goals in surgery for patients
i. Negative sodium balance with intracranial pathology?
j. Negative water balance B. What are the important features in pre­anaesthetic
k. Low serum sodium assessment of a patient listed for surgery for a large
l. High/normal serum osmolality glioma?
m. High urine sodium C. Describe the intraoperative anaesthetic management
n. Normal/high urine osmolality of a craniotomy?
D. What are the complications of posterior fossa
surgery?
E. Why is surgery in the posterior fossa of particular
concern?

A. Anaesthetic goals in surgery for patients with

intracranial pathology
An understanding of the multiple interactions between the
circulatory and respiratory systems and the cerebral
circulation is also required but, again, is not sufficient.
The anesthesiologist must consider several explicit thera­
peutic goals that sometime compete to successfully
optimize care.
Fig. 22. Pathophysiology of CSW

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 Neuroanaesthesia

These goals include: 2. Provide optimal operating conditions

a. May require osmotherapy if excessive
Optimization of surgical exposure while brain swelling
minimizing brain injury
Maximizing patient safety while providing 3. Avoid secondary injury
patient comfort a. Maintain cerebral perfusion and
oxygenation
b. With intracranial pathology attention to
1. The processes of neuroanesthesia and the management of ICP and maintenance
neurosurgery may both lead to brain injury. of adequate MAP to maintain CPP is
a. Surgeons must sometimes exert paramount
mechanical pressure on brain tissue to c. Avoid increasing venous pressure. A 30
expose a lesion. degrees head up reduces central venous
b. That pressure may cause injury by pressure.
tearing axons and synapses d. MAP can be manipulated with fluids,
c. Increasing tissue pressure, preventing vasopressors and inotropes as clinically
blood from traversing capillaries. indicated.
d. Anesthetics may also reduce systemic e. Avoid hypercarbia and hyperthermia.
blood pressure below the critical cerebral ICP can be reduced with osmotic
perfusion pressure (CPP) or may increase diruetics.
ICP, which also reduces CPP to a critical f. Keep patient comfortable and safe:
value. Padding of eyes and other pressure
e. Anesthesiologists can also be therapeutic, points; monitoring for venous air
reducing the bulk of the brain so less embolism
surgical retraction is needed to obtain the
required exposure. B. The important features in pre­anaesthetic
f. Anesthesiologists can select an anesthetic assessment of a patient listed for surgery for a large
and monitoring plan that use less in the glioma
way of vasodilatory drugs yet maintain
good blood pressure control. In addition to the normal preoperative assessment specific
g. Occasionally, the anatomic site of a issues include:
neoplasm is adjacent to, or intermixed 1. Drug history
with, the eloquent cortex. a. Diuretic therapy; affects electrolytes and
i. This portion of the brain that is intravascular volume
critical for a behavior such as b. Seroids; affects glucose levels
speech or somatic motor control. c. Antiepileptic drugs; affects QT interval
ii. To minimize the removal of
such vital tissue from the brain, 2. Neurology
a neurosurgeon may need to a. GCS
map the functional areas in real b. Focal motor deficits
time during surgery. c. Higher cortical function
iii. If the tumor is near the primary d. Seizures
motor cortex, the patient cannot
be paralyzed during mapping 3. Imaging
iv. If the tumor is near a language a. Size and location
center, the patient must be b. Midline shift >10 mm = severe
conscious, coop­ erative, and compromise
able to speak during the surgery. c. Vascularity or proximity to a major sinus
v. These requirements add an extra with potential risk of bleeding or venous
burden to the anesthesiologist to air embolism (VAE).
customize the anesthetic plan to
meet both the surgeon’s and the
patient’s needs

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 Neuroanaesthesia

4. Postoperative plan D. The complications of posterior fossa surgery, special

a. Level of care required will depend on concerns in posterior fossa surgery
extent of surgery
b. Likely complications and potential for 1. Surgery in the posterior fossa usually requires
airway or respiratory compromise from prone positioning and the lesion can be located in
reduced GCS or other deficit close proximity to vital brainstem centres.
2. Significant bleeding can occur without warning.
C. The intraoperative anaesthetic management of a 3. Intraoperative
craniotomy a. Bleeding
b. VAE
1. Positioning c. Cardiovascular disturbance
a. Avoid extreme neck flexion or rotation, d. Postoperative
ensure eyes and other pressure points are e. Raised ICP
protected. f. Cranial nerve palsies
g. Injury to respiratory centre
2. Monitoring h. Cerebellar mutism (children)
a. Arterial line i. Late
b. CVP j. CSF leak
c. Urinary catheter. k. Infection
d. Some units may use transcranial doppler, l. Pseudomeningoocele
jugular bulb oximetry and brain tissue m. Obstructive hydrocephalus
oxygenation probes. n. Tumour recurrance

3. Maintenance
a. Avoid N2O and maintain anaesthesia 10. Awareness ­ depth of anaesthesia
using volatile or target control infusion
(TCI) propofol. monitoring
b. Remifentanil is also used.
c. Application of a fixator is highly A. What are some of the causes of anaesthetic
stimulating and requires bolus analgesia awareness?
B. What is bispectral analysis (BIS)?
or anaesthetic.
C. What is the suggested interpretation of BIS values?
D. What other type of depth of anaesthesia monitoring
4. Cerebral oedema
are there?
a. Treatment with diuretics and mild E. What steps would you take if you were informed by
hypocapnia the midwives that a patient who had undergone a GA
the previous day was complaining of awareness
5. Fluids under anaesthetic?
a. Hypotonic fluids are absolutely F. Are you aware of any major studies going on at the
contraindicated moment into awareness?
b. Normal saline or Hartmann’s are the
crystalloids of choice.

6. Preparing for emergence

a. Closure of the dura
b. Bone flap and scalp takes half an hour
c. Analgesia should be added at this point if
remifentanil is used
d. Prepare to treat hypertension with
labetalol.

Fig. 24. Depth of anaesthesia monitor

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 Neuroanaesthesia

A. Some of the causes of anaesthetic awareness 2. Monitoring end tidal inhalational agent
3. Isolated forearm technique, refer to Anaesthesia
Type of surgery, GA caesarean section, cardiac surgery, UK Isolated forearm technique
trauma surgery, rigid bronchoscopy other factors include 4. Forehead galvanometry
5. Oesophageal motility
1. Patient Factors 6. EEG
a. Haemodynamically unstable patient e.g. 7. Auditory evoked potentials
major haemorrhage
b. Difficult airway C. Steps to be taken if you were informed that a
c. Drugs blunting hypertensive and patient who had undergone a GA the previous day was
tachycardic responses e.g. beta blockers, complaining of awareness under anaesthetic
calcium channel blockers
d. Chronic opioid or benzodiazepines use 1. Read patient’s notes, establish details of
anaesthetic and circumstances, find out who the
2. Anaesthetic Factors anaesthetist was
a. Use of neuromuscular blockers 2. Inform the anaesthetist who was involved and the
b. Failure of patient monitoring equipment consultant responsible if the patient was
c. Malfunctioning vaporizer anaesthetised by a trainee
d. Empty vaporizer 3. Arrange a discussion with the patient with a
e. Failure of TIVA pump witness present
f. Unrecognized tissued IV cannula with 4. Sympathetic approach to the patient
TIVA 5. Take a detailed history from the patient
g. Drug errors (e.g. mixing up thiopentone establishing what she remembers
and co­amoxiclav) 6. Ask if she felt any pain during surgery
h. Misjudgment of anaesthetic doses 7. Apologize to the patient
required 8. Explanation of awareness and why it sometimes
occurs
B. The bispectral analysis (BIS) 9. Document the discussion in the notes
10. Write to patient’s GP
BIS uses EEG monitoring. 11. Refer to psychologist if patient wants further
The machine uses an algorithm to interpret EEG waves and support
gives a numerical value from 0 to 100.
E. Major studies going on at the moment into
a) Interpretation of BIS values awareness
The target BIS value for general anaesthesia is 40 to 60.
1. NAP5 Report The National Institute of Academic
b) Other type of depth of anaesthesia monitoring Anaesthesia ­ National Audit Projects NAPs

1. Clinical assessment for signs of sympathetic 2. National audit project undertaken by the Royal
activity including College of Anaesthetists and AAGBI
a. Heart rate
b. Blood pressure
c. Sweating
d. Lacrimation

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 Neuroanaesthesia

11. ICP monitoring and management of C. Two methods of intracranial pressure (ICP)
measurement in detail
raised ICP 1. Intraventricular: gold standard, a catheter
inserted into the ventricle connected to a column
A. Which patients with severe head injury should have of fluid and a pressure transducer. Wheatstone
intracranial pressure (ICP) monitoring? bridge principle is applied for zeroing. Change in
B. List the methods by which the intracranial pressure pressure causing change in the resistance of the
(ICP) can be measured in intensive care?
transducer system, causing change in electrical
C. Describe two of these in greater detail?
current translates to change in intracranial
D. What methods are used to manage or prevent acute
rises in the ICP? pressure. Can be used for therapeutic CSF
E. Describe the mechanism of action of mannitol in drainage. There ìs high risk of infection, it can be
head injury? used for administration of antibiotics and can get
blocked.
A. Patients with severe head injury who should have
2. Intraparenchymal: Camino transducer uses
intracranial pressure (ICP) monitoring
fibreoptic cable with displaceable mirror at the
1. Severe head injury with GCS 3­8 with abnormal catheter tip, placed in the brain tissue. Change in
admission CT (ie haematoma, contusion, oedema, ICP distorts the mirror and reflected light intensity
or compressed basal cisterns) transduced into pressure. No saline filled column
of fluid and manometer in needed.
2. Severe head injury and normal CT but ≥ 2 of:
a. Age > 40 yrs
b. Unilateral or bilateral motor posturing
c. Systolic BP < 90 mm Hg
d. At risk of raised ICP requiring general
analgesia

3. Monitoring is not routinely indicated in patients

with mild/moderate head injury however may be
appropriate in certain conscious patients with
traumatic mass lesions

B. Methods of intracranial pressure (ICP)

measurement in intensive care
By pressure transduction of:
a) Intraventricular
b) Intraparenchymal
c) Subarachnoid
d) Subdural
e) Epidural

Fig. 26. Camino transducer

Accuracy comparable to intraventricular catheter but may

only reflect local change in ICP. Cannot be calibrated in
vivo. Prone to drift over time. Cannot be used for
therapeutic CSF drainage.

Fig. 25. Methods of ICP monitoring

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 Neuroanaesthesia

D. Methods used to manage or prevent acute rises in A. Indications for an awake craniotomy
the ICP
1. Anatomical
1. Physiological a. Space occupying lesions in or adjacent to
a. Head up > 30 degrees, avoid excessive eloquent areas of the cortex.
rotation of head b. Excision of tumours in the sensory and
b. Loose collar/ ET tube neck tie motor speech areas in the dominant
c. Avoid hypoxaemia, hypercarbia, hemisphere and sensorimotor cortex in
hyperthermia, vasodilatory drugs, either hemisphere following cortical
hypotension stimulation mapping.
d. Avoid PEEP
e. Avoid central line in neck. 2. Physiological
a. Stimulation or lesion generation of deep
2. Pharmacological brain nuclei (e.g. the subthalamic
a. Hypertonic saline 30% up to 20 ml nucleus) for intractable movement
b. Mannitol 1g.kg­1 disorders such as Parkinson’s disease and
c. Barbiturate coma dystonias.
d. Hypothermic therapy
e. Hyperventilation 3. Pharmacological
f. Steroid a. Epilepsy surgery when intraoperative
g. Insertion of external ventricular drain or electrocorticography (ECoG) is required
ventriculoperitoneal shunt to define the resection margins.
h. Surgical, decompressive craniectomy
B. The anaesthetic goals of management of OPCAB
surgery
E. Mechanism of action of mannitol in head injury
1. Confused patient
1. Immediate: Osmotically active sugar alcohol, 2. Communication difficulties
expands intravascular volume, increase flow, 3. Extreme anxiety
reduces viscosity, increase cardiac output, 4. Low occipital tumour (prone position)
increase cerebral perfusion, increase 5. Significant dural involvement (painful)
microvascular oxygenation. Compensatory 6. Inability to lie still for many hours
regional vasoconstriction where autoregulation is 7. Inexperienced surgeon
intact causing reduction ICP.

2. Delayed: Establish osmotic gradient between C. Local anaesthetic techniques that must be employed
plasma and brain cells. Draws out extracellular
to provide analgesia/anaesthesia
water into vascular compartment provided blood
brain barrier is intact reducing oedema.
1. If a Mayfield head fixator is used, adequate local
anaesthesia should be applied prior to application
of the pins.
12. Anaesthesia for awake craniotomy
2. Brain biopsy/mini­craniotomy
A. What are the indications for an awake craniotomy?
a. Infiltration of local anaesthetic into the
B. What are the contraindications for an awake
relevant area of scalp and pericranium,
craniotomy?
C. What local anaesthetic techniques must the and later onto the dura, is all that is
surgeon/anaesthetist employ to provide required.
analgesia/anaesthesia?
D. What is the asleep­awake­asleep technique? 3. Formal craniotomy
E. What complications may be encountered in an awake a. The neurosurgeon must perform field
craniotomy? blocks of the scalp, using combinations
of lidocaine and bupivacaine with
epinephrine.

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 Neuroanaesthesia

Fig. 24. Cutaneous nerves of head and neck

Fig. 27. Cutaneous nerves of head and neck

c. The skin, scalp, pericranium and

b. Six nerves need to be blocked bilaterally periosteum of the outer table of the skull
to completely anaesthetise the scalp: are all innervated by cutaneous nerves
i. Supratrochlear nerve arising from branches of the trigeminal
ii. Supraorbital nerve nerve. Subcutaneous infiltration with
iii. Zygomaticotemporal nerve local anaesthesia in the manner of a field
iv. Auriculotemporal nerve block or over specific sensory nerve
v. Lesser and greater occipital branches, blocks afferent input from all
nerves. layers of the scalp.

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 Neuroanaesthesia

d. The skull can be drilled and opened 2. The introduction of propofol improved the safety
without discomfort to the patient (no profile of the asleep–awake–asleep technique and
sensory innervation) provided more predictable intraoperative wake­up.
e. The dura is innervated by branches from
all three divisions of the trigeminal nerve, 3. A combination of propofol and remifentanil
the recurrent meningeal branch of the infusion is now the technique of choice because it
vagus, and by branches of the upper allows titratable levels of anaesthesia and fast and
cervical roots. It must therefore be reliable wake up.
adequately anaesthetized with a local
anaesthetic nerve block around the nerve 4. Bispectral index monitoring can be used to guide
trunk running with the middle meningeal target­controlled infusions.
artery, and also by a field block around
the edges of thte craniotomy.
E. Complications may be encountered in an awake
craniotomy
Techniques
1. Seizures
1. The supraorbital nerve is blocked just above the 2. Nausea and vomiting
supraorbital notch and local anaesthetic is 3. Dysphoric reactions
deposited just superficial to the periosteum. 4. Respiratory depression
5. Airway obstruction
2. The temporal branch of the auriculotemporal 6. Air embolism
7. Pulmonary aspiration
nerve is blocked immediately posterior to the
8. Conversion to general anaesthesia
superficial temporal artery at the level of the
auditory meatus.

3. The main branch of the zygomaticotemporal nerve

emerges from the temporalis fascia near the lateral 13. Sitting position and air embolism
border of the orbit, although many smaller deep
branches ramify within the temporalis muscle. A. For what types of neurosurgery is the patient
These small branches are especially important to positioned sitting?
block so as to cover temporally based flap B. What are the advantages and disadvantages of the
incisions. Field infiltration above the zygoma sitting or deckchair position?
through the temporalis muscle and almost down to C. Describe the pathophysiological effects of air
embolism?
the periosteum of the temporal bone will give a
D. How may an air embolism be detected?
good result, without causing a facial nerve block.
E. What is the management of a suspected venous air
embolism during a craniotomy?
4. The lesser occipital nerve can be blocked either
deep or superficial to the fascia at the upper, A. Types of neurosurgery where is the patient
posterior border of sternocleidomastoid. positioned sitting
5. The greater occipital nerve is blocked 1. Posterior cervical procedures
subcutaneously by injecting along the middle third 2. Posterior cranial fossa craniotomies
of a line between the mastoid process and the
external occipital protuberance along the superior
nuchal ridge. This injection will also reinforce the B. Advantages and disadvantages of the sitting or
lesser occipital nerve block as it becomes deckchair position
subcutaneous.
Advantages:
1. Better access to the airway
D. The asleep­awake­asleep technique 2. Reduced facial swelling
1. Some patients are not able to tolerate craniotomy 3. Improved hemodynamic stability
with sedation alone and general anaesthesia with 4. Reduced blood pooling in the operative field
intraoperative wake­up is an alternative.

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 Neuroanaesthesia

Fig. 28. Different settings of sitting position

C. Pathophysiological effects of air embolism

5. Disadvantages:
1. Venous air embolism
1. Air enters right atrium then right ventricle that
2. Hypotension secondary to venous pooling
may lead to CVS
3. Excessive neck flexion
4. Cord ischemia
2. Compressive air causes obstruction to right
ventricular ejections “AIR LOCK” or Pulmonary
outflow Tract.

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 Neuroanaesthesia

3. Slow ejection of air trapped at pulmonary f. Increased PA pressure (50%)

arterioles can lead to pulmonary arterial g. ABG may reveal hypoxaemia and, less
hypertension and right ventricular failure. commonly, hypercarbia
h. Chest X­ray is initially normal but signs
4. Micro­emboluses may obstruct flow of non­cardiogenic pulmonary oedema
may develop later
5. Neutrophils attracted to fibrin network of RBCs, i. ECG
fat globules and platelets that build around the i. Tachyarrythmias
bubbles ii. AV block
iii. Signs of RV strain
6. Ultrastructural damage of the basement membrane iv. Raised oe depressed ST
would affect the permeability and may lead to v. Non­specific T wave change
pulmonary edema.
8. Detector devices:
7. Paradoxical air embolus: a. ETCO2
a. Via patent foramen oval (PFO) or b. Precordial Doppler
transpulmonary gas shunting c. TOE gold standard
b. End arteriolar obstruction leads to distal d. CVP/PAC
ischaemia. e. ETN2
f. Oesophgeal steothoscope
D. Detecting air embolism
9. Differential diagnosis when respiratory symptoms
1. The presentation of VAE is dependent upon the and signs predominate includes:
rate and volume of air entrained. a. Pulmonary embolism
b. Pneumothorax
2. VAE can range from being clinically undetectable c. Bronchospasm
to potentially fatal. d. Pulmonary oedema.

3. Rapid entrainment of large volumes of air will E. Management of a suspected venous air embolism
result in apnoea, hypoxia and cardiovascular during a craniotomy
collapse.
1. ABCDE approach
4. Slower rates of entrainment may result in the 2. Discontinue N2O
patient complaining of light­headedness, breathing 3. Administer 100% O2
difficulties, shortness of breath, chest pain and a 4. Flood surgical field with Saline
sense of impending death. 5. Aspirate air from right atrium via CV catheter
6. Left lateral decubitus position (Durant Maneuver)/
5. A 10% obstruction to the pulmonary circulation Trendelenburg position
can cause a gasp reflex which, in itself, reduces 7. Inotropic agents
right atrial pressure (RAP) further increasing air 8. Cardiopulmonary bypass
entrainment. 9. Thoracotomy

6. Significant embolism leads to tachypnoea, Durant’s maneuver

tachycardia, and hypotension. This may be Consists of placing the patient in the left lateral
accompanied by altered mental status, decreased decubitus position in order to prevent a venous air
conscious level or focal neurological deficits. embolism from lodging in the lungs.
The air will rise and stay in the right heart until it
7. Signs: slowly absorbs.
a. Auscultation of the heart might reveal the Similarly, placing a patient in the Trendelenburg
classical ‘mill wheel’ murmur. position (head down) helps prevent arterial air
b. Pulmonary oedema may develop later. embolism from traveling to the brain causing a
c. End­tidal carbon dioxide falls as a conse­ stroke.
quence of an increase in physiological
dead­space and intrapulmonary shunting.
d. Arterial oxygen saturation falls.
e. Increased CVP (25%)

26 Revision Notes in Anaesthesia and ICU

Send any notes or comments to:

[email protected]
Chapter 2

Cardiac anaesthesia
 Cardiac anaesthesia

__________________________________________________________________________________________________

Cardiac surgery is a dangerous and complex field of medicine with significant morbidity and mortality. Quality
anaesthetic care with specific attention to details can greatly enhance patient safety and outcome. Details that are ignored
can lead to disaster.
Anesthetic evaluation is crucial, it must include attention to cardiac history, catheter reports, thallium, echo, and ECG.
Critical information includes left main disease or equivalent, poor distal targets, low ejection fraction, LVEDP, presence
of aneurysm, pulmonary hypertension, valvular lesions and congenital lesions.
Each of these points requires a modification of anaesthetic technique and specific information is required. How is their
angina manifest? You need to be able to understand their verbal reports. If a patient's angina is experienced as shortness of
breath, or nausea, or heart burn, or whatever, you need to be able to link that symptom to possible myocardial ischemia.
Past medical history including history of COPD, TIA, stroke, cerebral vascular disease, renal disease (CRI is an
independent risk factor), hepatic insufficiency will change anesthetic management. The above pictures the necessity of
developing an anaesthetic plan that individually suits each patients.
__________________________________________________________________________________________________

1. Aortic stenosis and open aortic valve A. The pathophysiology of worsening aortic stenosis
replacement Causes:
1. Degenerative calcification
A 70­year­ old woman with aortic stenosis presents for a. In degenerative calcific aortic stenosis
an open aortic valve replacement (AVR). there is initially sclerosis due to
mechanical stress causing fibrosis and
A. What is the pathophysiology of worsening aortic
calcification. Risk factors are as for
stenosis?
coronary artery disease.
B. Which specific cardiac investigations may be used
in assessing the severity of this woman's disease?
2. Congenital bicuspid valve (2%)
C. Give values for the peak aortic flow velocity,
a. In congenital bicuspid valve, the
mean pressure gradient and valve area that would
tendency toward turbulent flow through
indicate that this woman has severe aortic
the valve causes trauma resulting in
stenosis.
calcification and fibrosis.
D. What would be your haemodynamic goals for the
perioperative management of this patient
3. Rarely due to rheumatic disease

4. The normal aortic valve area (AVA) is 2.6­3.5

cm2 in adults. In a stenotic aortic valve there is
usually an asymptomatic latent period of 10­20
years, significant obstruction occurs gradually as
the aortic valve area approaches 1.0 cm2, then
sever haemodynamic instability becomes
manifeste as the COP becomes fixed with the
classical triad of symptoms:
a. Angina
b. Dyspnoea
c. Syncope. There can be sudden death.

5. There will be an initial LV hypertrophy to

maintain a pressure gradient across the stenosed
resistive valve.

6. Diastolic dysfunction: Later the LV becomes stiff

and less compliant. Compliance is the physical
relation between pressure and volume, less
compliant LV means that it will hardly fill during
diastole resulting in less LV end diastolic volume
Fig. 1. Healthy and stenosed aortic valve
and diastolic dysfunction

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 Cardiac anaesthesia

7. LV filling increasingly becomes dependent on D. Haemodynamic goals for the perioperative

atrial contraction (20 ­ 40%) management of this patient

8. Left atria then becomes then hypertrophied 1. Maintain normal (low) heart rate
2. Maintain sinus rhythm – Atrial filling is
9. Adequate filling and maintenance of CO increasingly important with LV hypertrophy due
dependent on sinus rhythm to decreased compliance and relaxation
3. Avoid tachycardia
10. Disturbance of LV supply/demand occur oxygen 4. Maintain preload ­ careful fluid balance, guided
requirements increase relevant to increased LV by invasive monitoring e.g. transoesophageal
muscle mass and LV systolic pressure i.e. LV echocardiography (TOE)
strock work increase. Supply is reduced due to 5. Maintain high­normal SVR using α­agonist to
relatively low aortic pressure and increases maintain coronary perfusion with extreme caution
diastolic pressures if central neuraxial blockade is used e.g. in LSCS
6. Maintenance of contractility
11. Demand and supply mismatch causes angina 7. Maintain K+ concentration within normal range
despite (occasionally) normal coronary arteries

12. The ventricle is sensitive to changes in preload,

dependent on the maintenance of sinus rhythm and
susceptible to ischaemia, especially when arterial
pressure is reduced.

B. Specific cardiac investigations used in assessing the

severity of this woman's disease

1. ECG
2. ECHO
3. Cardiac catheterisation +/­ angiography

Fig. 2. Left ventricular hypertrophy

Fig. 3. Echocardiography normal rages for measures of
systolic and diastolic function
C. The values for the peak aortic flow velocity, mean
pressure gradient and valve area that would indicate
that this woman has severe aortic stenosis.

1. Aortic flow velocity > 4 ms­1

2. Mean pressure gradient 40–50 mmHg Fig. 4. Echocardiography comparing data in mild and
3. Valve area < 1 cm2 severe aortic stenosis

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 Cardiac anaesthesia

2. Neurological complications of CABG B. The risk factors for central neurological

complications
a) What are the central and peripheral neurological
complications of coronary artery bypass surgery? Patient factors
b) What are the risk factors for central neurological 1. Advanced age
complications? 2. Male gender
c) How can the incidence of central neurological 3. LV systolic dysfunction
complications be reduced? 4. LV thrombus
5. Previous stroke
A. The central and peripheral neurological 6. Carotid stenosis
complications of coronary artery bypass surgery 7. Diabetes mellitus
8. AF
Central 9. Renal failure
1. Intraoperative stroke due to hypoperfusion and/or
embolisation. Procedural factors
2. Postoperative stroke related to postoperative AF 1. Long cardiopulmonary by­pass (CPB) time
or pre­existing cardiac disease. 2. Macro/micro embolus
3. Intracranial haemorrhage secondary to 3. Valve surgery
haemorrhagic extension of ischaemic stroke. 4. Hyperglycaemia
4. Delirium 5. Poor temperature control
5. Seizures 6. Cerebral hypoperfusion
6. Cognitive dysfunction due to global anoxic brain
injury, stroke, intracranial haemorrhage
7. Ischaemic optic neuropathy C. Reducing the incidence of central neurological
complications in CABG
Peripheral
1. Brachial plexus injury leading to upper limb 1. Anticoagulation by heparinisation aiming for ACT
neuropathy. This can occur due to traction or level >400 sec
compression during eternal retraction, 2. Use of high quality arterial filters and membrane
hypothermia and haemodynamic changes. oxygenators to reduce microembolic load
2. Phrenic nerve palsy associated with the ice flush 3. Minimise CPB time, ideally less than 2 hours.
used to cool the heart. 4. Utilising off pump techniques reducing risk of
3. Anterior intercostal nerve injury occurring during cerebral complications
harvesting of internal thoracic artery 5. Temperature control; mild hypothermia and
avoiding hyperthermia on rewarming
6. Optimisation of co­morbidities including BP
control and glycaemic control
7. Acid base control
8. Controlling the systemic inflammatory response to
surgery

Fig. 5. Retraction during cardiac surgery

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 Cardiac anaesthesia

3. Anticoagulation and cardiac surgery 3. High dose thrombin time

Advantages:
A 67 year­old patient is to undergo coronary artery  Less susceptible to artefact on CPB
surgery on cardiopulmonary bypass (CPB). Disadvantages:
 Expensive, not as familiar
a) What dose of heparin is used to achieve full
anticoagulation for CPB and how is it given? 4. Heparin Management Test
b) Which laboratory and “point­of­care” tests Advantages
determine the effectiveness of heparin  Less susceptible to artefact on CPB, able
anticoagulation in CPB patients? Give the to calculate individual doses of heparin
advantages and/or disadvantages of each test? and protamine for each patient
c) What are the causes of inadequate anticoagulation Disadvantages:
in a patient whom it is believed has already  Expensive, not as familiar
received heparin?
d) Describe the possible adverse reactions to
protamine? C. Causes of inadequate anticoagulation in a patient
whom it is believed has already received heparin

A. Heparin use to achieve full anticoagulation for CPB Inherited

and how is it gven 1. Antithrombin III deficiency

300­400 IU.kg­1 Intravenously post sternotomy and Acquired

pre­insertion of aortic and atrial venous lines 1. Previous heparin use
2. Reduced synthesis as in liver cirrhosis
3. Increased consumption as in DIC, sepsis
B. Laboratory and “point­of­care” tests determine the 4. Dilutional as in CPB
effectiveness of heparin anticoagulation in CPB 5. Increased excretion as in protein losing
patients, advantages and disadvantages of each test states

1. Activated Clotting time (ACT)

Advantages: D. Possible adverse reactions to protamine
 Familiar, cheap, easy to do, quick
Disadvantages: 1. Hypotenion
 Unreliable with hypothermia, 2. Pulmonary hypertension
haemodilution, antiplatelet agents. 3. Anaphylaxis
4. Reduced cardiac output
2. Activated Partial Thromboplastin time 5. Inhibiting platelet activity
Advantages:
 Sensitive
Disadvantages:
 Takes longer than other tests

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 Cardiac anaesthesia

4. Cardioplegia and hypothermic B. Routes through which solutions of cardioplegia can

be administered
circulatory bypass
Antegrade
a) What are the purposes, typical composition and Administered in the direction of blood flow into the aortic
physiological actions of cardioplegia solutions? root or coronary ostium to flow down the coronary arteries.
b) By which routes can solutions of cardioplegia be
administered? Retrograde
c) What are the possible complications of Through the right coronary sinus, this is used if there is
cardioplegia solution administration?
occlusion of the coronary circulation or aortic valve
d) What are the advantages and disadvantages of
incompetence however this may not give adequate
hypothermic cardiopulmonary bypass?
protection of the right ventricle.
e) Describe the differences between the utilisation of
alpha­stat and pH­stat?
C. Possible complications of cardioplegia solution
A. Purposes, typical composition and physiological
administration
actions of cardioplegia solutions
1. Under dosage; Avoided by using pre­made
1. Creates a diastolic electro­mechanical arrest
solutions or ampoules.
allowing the surgeon to work with a motionless,
2. Complications include those that are involved
bloodless heart.
with open heart surgery; MI, dysrhythmias,
including VF
2. Reduced the myocardial consumption of oxygen
to allow the tissue to withstand a period of
ischaemia
D. Advantages and disadvantages of hypothermic
cardiopulmonary bypass
3. Cardioplegia is a hyperkalaemic solution which
requires at least 20 mmol.l­1 of KCL. The ideal Advantages
solution is still under research. It should be: 1. Reduces cerebral oxygen consumption so
a. Hyperosmotic to prevent oedema providing cerebral protection
b. Alkalotic to attenuate subsequent pH 2. Reduces the incidence of cerebral ischaemia due
changes and low concentration of to microembolism
calcium 3. Systemic oxygen requirements decrease including
c. It may also contain aspartate and myocardial oxygen consumption.
glutamine to promote oxidative 4. Decreases the rate of release of excitatory amino
metabolism in energy­depleted hearts. acids and neurotransmitters that are associated
with axonal death
4. Esmolol may be an alternative as this may reduce 5. Reduces the inflammatory response
myocardial oxygen consumption, or nicorandil as 6. Reduces blood brain barrier permeability
this may cause arrest close the heart resting
potential. Disadvantages
1. Increased blood viscosity so increases the risk of
5. Cardioplegia can be in crystalloid or blood, warm embolism
or cold. 2. Increased rate of infection
a. Blood cardioplegia is potassium in blood 3. Decreased wound healing
and offers the advantage of having 4. Peripheral Vasoconstriction
increased oxygen carring capacity with 5. Moves oxygen­HB dissociation curve to the left
the presence of haemoglobin. so oxygen is not liberated as easily
b. Cold blood cardioplegia will move the
oxygen haemoglobin dissociation curve
to the left.

6. It works by inactivating fast inward sodium

channels preventing the upstroke of myocardial
cell action potentials, causing the myocardium to
become unexcitable in diastolic arrest.

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E. Differences between the utilisation of alpha­stat and Disadvantages:

pH­stat 1. May result in inadequate, nonhomogeneous brain
cooling before circulatory arrest
2. Might “steal” blood from cerebral to pulmonary
circulation in congenital heart surgery (pulmonary
circulation derived from arterial system)
3. May result in cerebral dysfunction in children
after cardiac surgery

pH stat
1. pH is corrected for temperature at 37°C and pH is
kept constant.
2. This allows pCO2 content during cooling that
causes cerebral vessels to vasodilate
3. Cerebral blood flow looses it autoregulation and
Fig. 6. pH changes with temperatures
becomes pressure dependent.
4. This may improve cooling and oxygen delivery to
the brain.
Alpha stat
5. Blood gas analysis performed at 37℃
1. Blood gas levels are uncorrected for temperature
6. Mathematically temperature corrected using a
and alkalosis is permitted during cooling.
nomogram
2. Currently it's the most widely accepted approach
7. CO2 added to oxygen passing the oxygenator
for acid­base management during CPB in adults.
8. Total CO2 stores elevated
3. It's achieved by maintaining normal pH at 7.40
9. Marked respiratory acidosis at 37℃
and pCO2 at 40 mmHg measured at 37℃.
4. Keeping these parameters uncorrected for actual
Advantages:
arterial blood temperature:
1. Previously thought to be beneficial for cerebral
a. Allows the pH to rise and pCO2 to fall
vasodilation and maintenance of cerebral blood
naturally with cooling
flow
b. Relative (respiratory) alkalosis at the
2. Increased cerebral blood flow leads to quick and
patient’s actual body temperature
homogeneous brain cooling during the cooling
c. No CO2 added to the circuit
phase of DHCA
3. Oxyhemoglobin dissociation curve shiftets to the
right improving peripheral O2 delivery
4. Offers protection in neonatal and infant cardiac
surgery
At 37°C
5. might inhibit cellular metabolism
Normal intracellular pH 6.8
6. Possibly better neurobehavioral development after
alpha ≅ 0.55 which is optimal for intracellular
DHCA in children
enzyme structure and function
7. Particularly beneficial in cyanotic neonates and
infants
Advantages:
8. Shifts more CPB flow toward the cerebral
1. Maintains and preserves cerebral autoregulation
circulation
during moderate hypothermia
9. Improving cerebral cooling and oxygen supply
2. Extends the lower limit of autoregulation to a
mean arterial pressure of 30 mmHg
Disadvantages:
3. Offers better control of cerebral blood flow
1. Slightly greater complexity compared to alpha­stat
4. Avoidance of “luxurious” perfusion
strategy
5. Reduced cerebral blood flow (CBF)
2. Loss of cerebral autoregulation
6. Decreased risk of microemboli
3. Cerebral blood flow becomes pressure passive
7. Preferable on cellular level while enzymatic
4. “Luxury brain perfusion”: mismatch of CBF and
function is well maintained
CRMO2
8. Possibly preferable in adults
5. Increased risk of cerebral embolization and
9. May result in better neurocognitive outcome
cerebral edema
compared to pH­stat (adults)

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 Cardiac anaesthesia

Blood gas management during hypothermic CPB Circulatory

1. Systemic inflammatory response
1. More important in children: 2. Ongoing vasoplegia
a. Greater degrees of hypothermia used, 3. Hypovolaemia
thereby 4. Massive bleeding
b. More profound differences in blood CO2 5. Sepsis
levels 6. Respiratory –
2. Paediatric vs. adult cardiac surgery: differences in 7. Tension pneumothorax
a. Brain neuroplasticity 8. Pharmacological –
b. Presence of atheromatous aorta and 9. Excessive sedation
cerebral embolic load 10. Excessive nitrates
c. Presence of multiple co­morbidities 11. Inotropes stopped inadvertently

Conclusion II. Hypertension

1. Both alpha­stat and pH­stat management seems to 1. Inadequate sedation
work well 2. Inadequate analgesia
2. Physiologic differences appear to be subtle 3. Awareness with residual muscle relaxant onboard
3. alpha­stat may be preferable for adults (protection 4. Persistent hypothermia ­> increased SVR
from microemboli) 5. Hypoxia
4. pH­stat may be preferable for children (enhanced 6. Hypercarbia
brain protection) 7. Sympathetic vasoconstriction
5. Evt. crossover­strategy during DHCA in adults 8. LVH
a. 10 min. cooling with pH­stat 9. Raised ICP (intracranial haemorrhage or infarct)
b. Followed by cooling with alpha­stat 10. Inadvertent bolus of inotrope
c. Rewarming with alpha­stat 11. Bladder distension

B. The causes of low cardiac output following cardiac

surgery
5. Cardiac failure post cardiac surgery
1. Reduced preload
A. What are the causes of hypotension and
a. Hypovolaemia
hypertension following cardiac surgery?
b. Cardiac tamponade
B. What are the causes of low cardiac output
following cardiac surgery? c. Increased intrathoracic pressure (High
C. What are the goals of inotrope and vasopressor airway pressures, tension pneumothorax)
use post­cardiac surgery? d. RV dysfunction (Pulmonary
D. Describe the mechanism of action of milrinone hypertension, RV infarction)
and similar drugs
E. What are the differences in cardiopulmonary 2. Decreased contractility
resuscitation in post­cardiac surgery patients? a. Myocardial stunning
b. Pre­existing poor LV function
c. Graft kinking
A. The causes of hypotension and hypertension d. Incomplete revascularisation
following cardiac surgery e. Acid/base disturbance
f. Arrhythmias
I. Hypotension
Cardiac 3. Increased afterload
1. MI a. Vasoconstriction
2. Kinking of bypass graft b. LV outflow tract obstruction
3. Poor myocardial protection c. Fluid overload ­> ventricular distension
4. Left ventricular dysfunction d. Diastolic dysfunction
5. Right ventricular dysfunction
6. Valvular failure – native or artificial 4. Co­existing condition
7. Arrhythmias a. SIRS/Sepsis
8. Cardiac tamponade b. Anaphylaxis
c. Adrenal insufficiency

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 Cardiac anaesthesia

C. Goals of inotrope and vasopressor use post­cardiac 6. Off pump coronary artery bypass
surgery
grafting
1. Increased cardiac output
2. Improved myocardial contractility
A. What are the theoretical advantages of off pump
3. Improved end­organ perfusion
CABG (OPCAB) compared to on pump?
4. Reduced ventricular diameter (in enlarged hearts) B. What are the disadvantages of OPCAB compared
5. Decreased myocardial oxygen demand to on pump cardiac surgery?
6. Decreased PVR leading to increased right heart C. What causes haemodynamic instability during
output OPCAB?
D. Which strategies help to minimise haemodynamic
instability during OPCAB?
D. Mechanism of action of milrinone and similar drugs E. What is ischaemic preconditioning?
F. What are the anaesthetic goals of management of
Milrinone OPCAB surgery?
1. Is a Phosphodiesterase inhibitor it works by
competitive inhibition of phosphodiesterase
isoenzymes (PDE) resulting in increased cAMP A. The theoretical advantages of off pump CABG
and positive inotropy (OPCAB) compared to on pump
2. Improved diastolic relaxation (lusitropy)
3. Also, potent vasodilator causing decreased 1. Reduced risk of CVA
preload, afterload and PVR 2. Less disruption of normal coagulation system and
4. Sensitises myocardium to β­agonists reduced requirement for blood products
5. Inhibit platelet aggregation 3. Lower heparin dosage can be used
6. Reduce post­ischaemic reperfusion injury 4. Earlier extubation
7. Dilate coronary arteries and grafts 5. Reduced length of stay
6. Reduced stress response
7. Isolated LAD grafting does not require a
E. Differences in cardiopulmonary resuscitation in sternotomy, surgery can be performed through a
post­cardiac surgery patients small thoracotomy

Immediately identifiable in highly monitored patient

For pulsless electrical activity (PEA) B. Disadvantages of OPCAB compared to on pump
1. Commence BLS cardiac surgery
2. If no immediately reversible cause is identified
resternotomy should be done. 1. More difficult operating conditions
2. Risk of myocardial ischaemia
For VF/VT 3. Mortality rate may be higher
1. 3 shocks before BLS as External chest 4. Not suitable for all patients, it's contraindicated in:
compressions can cause injury a. Small diameter vessels
2. If unsuccessful; BLS and emergency resternotomy b. Diffuse disease
3. While waiting for resternotomy follow standard c. Severe calcification
ALS algorithm d. Intramyocardial vessels
a. 30:2 compressions
b. Shock every 2 mins
c. Amiodarone 300 mg after 3rd shock C. Causes of haemodynamic instability during OPCAB
4. On re­sternotomy, commence internal cardiac
massage and defibrillation 1. Lifting of the heart out of the pericardial sac to
5. If unsuccessful; commence CPB work on the posterior and lateral sides of the heart
causing compression on the right side of the heart
Severe Bradycardia/Asystole and reduced venous return
1. Immediate pacing (DDD 90­100 bpm at max 2. External compression from retractors
amplitude) 3. Verticalisation of the heart causing mitral and
2. Atropine if epicardial pacing is unavailable or tricuspid regurgitation
unsuccessful
3. Use vasopressors with caution

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 Cardiac anaesthesia

D. Strategies that help to minimise haemodynamic A. Pathophysiology of aortic stenosis

instability during OPCAB
1. Stenosed aortic valve results in fixed obstruction
1. Maintain high perfusion pressure with a to ejection of blood from LV
MAP > 70 mmHg 2. Increased LV systolic pressure due to overload of
2. Avoid tachycardias to keep myocardial oxygen LV
consumption low 3. Compensatory LV hypertrophy results in:
3. Treat bradycardias a. Increased myocardial O2 demand
4. Fluid b. Reduced myocardial O2 supply leading to
5. Vasopressors subendocardial ischaemia
6. Trendelenburg position 4. Diastolic dysfunction occurs and results in:
7. Conversion to on pump surgery if haemodynamic a. Reduced compliance and increased
instability not corrected with the above reliance on atrial contraction for LV
filling that will be:
i. Preload dependent
E. Ischaemic preconditioning ii. Sinus rhythm dependent
iii. Can lead to pulmonary
1. The ischaemia that results from occlusion of the congestion
coronary artey is better tolerated if the technique 5. Systolic function is maintained
of ischaemic preconditioning is used. 6. End stage LV dilatation with reduced EF
2. This involves occlusion of the target vessel for 5 7. These changes can lead to symptoms of:
min, with subsequent reperfusion for 3 min before a. Angina
occlusion for suturing. b. Breathlessness
3. Preconditioning significantly preserves muscle c. Syncope
adenosine triphosphate (ATP) concentrations. d. Sudden death.

B. Classification of aortic stenosis according to valve

F. The anaesthetic goals of management of OPCAB area and LV­aortic gradient
surgery
Class Valve area (cm2) Peak gradient (mmHg)
1. Safe induction and maintenance of anaesthesia Normal 3­4 < 10
with cardiac protection
Mild > 1.5 < 40
2. Maintenance of haemodynamic stability
Moderate 1.0 ­1.5 40 ­65
3. Early emergence and ambulation
Severe < 1.0 > 65
4. Post operative analgesia

C. The principles of anaesthesia for non­cardiac

surgery in patients with aortic stenosis (important)
7. Aortic stenosis and transcatheter
aortic valve implantation Preoperative
1. Full preoperative assessment.
A. Describe the pathophysiology of aortic stenosis?
B. Classify aortic stenosis according to valve area 2. Even if it means delaying a non­urgent surgery,
and LV­aortic gradient? patients should have a preoperative ECHO to
C. What are the principles of anaesthesia for assess stenosis severity and LV function.
non­cardiac surgery in patients with AS and State 3. If not possible, a patient should be managed as if
the haemodynamic goals? having moderate AS.
D. What are the different types of intervention 4. If required, consultation with primary surgical
possible for treating AS? team, cardiologists and cardiac surgeons to
E. What are the principles of anaesthesia for determine if AVR, balloon valvuloplasty or valve
transcatheter aortic valve implantation (TAVI)? commissurotomy is required.
5. If AVR not required before non­cardiac surgery,
anaesthetist can assess risk from ECHO and
discuss risks with patient, family and surgical
team as to whether to consent and proceed.

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 Cardiac anaesthesia

Intraoperative
1. Careful haemodynamic monitoring including D. The different types of intervention possible for
arterial line. treating aortic stenosis
2. Central venous access provides a route for fluids
and vasoconstrictor therapy. 3 interventional options include:
3. Intra­op transoesophageal echo (TOE) may be 1. Surgical aortic valve replacement (AVR)
appropriate to assess LV filling and contractility. 2. Transcatheter aortic valve implantation (TAVI)
4. Appropriate antibiotic prophylaxis should be 3. Balloon valvuloplasty of the aortic valve (BAV)
given and strict aseptic precautions adhered to.
5. Potential surgical causes of haemodynamic E. The principles of anaesthesia for transcatheter
instability should be considered and modified aortic valve implantation (TAVI)
wherever possible.
6. Avoid systemic hypotension TAVI may be performed under:
a. Hypotension leads to myocardial  GA in transapical approach.
ischemia and a downward spiral of  Local anaesthesia with sedation may be possible
reduced contractility causing further falls in tansvascular approach.
in BP and coronary perfusion.
b. Aim to maintain BP at normal Preoperative visit:
pre­anaesthetic values 1. Quantify patient’s perioperative risk, optimise
c. Use neuroaxial techniques with caution it co­existing morbidity and provide informed
may require drugs to maintain systemic consent.
vascular tone e.g. noradrenaline, 2. Give information on invasive monitoring, ECHO
phenylephrine, metaraminol. and postoperative care on ICU.
7. Maintain a sinus rhythm as: 3. Careful premedication to reduce anxiety­induced
a. Atrial contraction is important for LV sympathetic response.
filling. 4. Monitoring, vascular access and haemodynamic
b. AF and nodal rhythms are poorly principles:
tolerated. a. When general anaesthesia is used
8. Avoid tachycardia with a rate of 60­80 bpm as: tracheal intubation is routine, single
a. Tachycardia reduces diastolic filling time lumen ETT for transapical TAVI.
therefore reduced time for coronary b. Basic standard monitoring plus an arterial
perfusion. line before induction.
b. Increases O2 demand. c. Large bore peripheral cannula, central
9. Avoid bradycardia with a rate of 60­80 bpm as: venous catheter, urometer and
a. Bradycardia results in a reduced cardiac temperature monitor is routine.
output as the stiff ventricle cannot d. Use of pulmonary artery catheter is less
increase stroke volume to compensate. common.
b. Increase in ventricular filling due to
longer diastole also increases ventricular Haemodynamic goals include:
wall tension further reducing coronary 1. Maintaining myocardial O2 delivery via adequate
perfusion. systemic pressure and diastolic time
10. Maintain high/normal preload to enable adequate 2. Maintenance of contractility
filling of LV. 3. Optimise preload for a non­compliant left
ventricle
Postoperative 4. Sinus rhythm with an ideal rate 60­80 beats/min.
1. Maintain appropriate IV fluids and arterial BP. 5. Opioid based technique may be favoured for
2. Minimise additional demands on the heart induction/maintenance of anaesthesia to minimise
incurred with inadequate analgesia. vasodilation and negative inotropy.
3. Regional anaesthetic techniques have a potential 6. Haemodynamic support with alpha­agonists and
role but require close monitoring because of fluids and inotropic support may be required in a
potential toxicity resulting in hypotension. poorly functioning LV.
4. Vasoconstrictor infusion may be required to offset 7. Defibrillation pads are essential.
any deleterious haemodynamic consequence of 8. If TAVI is performed under GA, TOE should be
central neuraxial block. used.
5. Avoid NSAIDS that can trigger the risk of 9. If TAVI is performed without GA, TTE should be
postoperative renal dysfunction. used.

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Postoperative C. The minimum standards of monitoring which apply

1. Majority of patients extubated at end of procedure. for electrophysiological procedures
2. Patient controlled analgesia (PCA), intercostal
blocks and paracetamol provide satisfactory 1. For sedation; at least pulse oximetry, usually ECG
analgesia after transapical TAVI. and NIBP. Propofol sedation requires
3. Most patients able to return to cardiac ward or capnography.
HDU. 2. For GA; pulse oximetry, ECG and NIBP; if
4. Care must include identification and management inhalational agents are given, end tidal oxygen,
of arrhythmias and pacing, chest drains, surgical CO2 and volatile agent monitoring. Invasive BP
incisions, and large vascular access devices. often used but not required.

D. The anaesthetic challenges in the cardiac

catheterisation laboratory
8. Anaesthesia for electrophysiological 1. Patient population: ranging from young, fit and
procedures healthy to elderly with multiple co­morbidities
requiring invasive devices such as intra­aortic
A. What groups of patients may require anaesthesia balloon pump to maintain circulation.
for electrophysiological procedures? 2. Environment: remote location, unfamiliar
B. What are the principles of anaesthesia for equipment, staff unused to unconscious patients,
electrophysiological procedures? difficulty obtaining advanced airway equipment,
C. What the minimum standards of monitoring which blood products, dim lighting.
apply? 3. Limited access to patient head, arms, airway and
D. What are the anaesthetic challenges of IV access.
anaesthetising in the cardiac catheterisation
laboratory? E. The potential complications of catheter ablation
E. What are the potential complications of catheter procedures
ablation procedures?
1. Vascular damage: bleeding, pseudoaneurysm
2. Arrhythmias: any including bundle branch and
A. The groups of patients that may require anaesthesia
complete heart block
for electrophysiological procedures
3. Oesophageal damage: thermal, fistula formation
4. Complications of trans­septal puncture: atrial,
1. Patients requiring ablation of arrhythmogenic
aortic perforation, pericardial effusion and
pathways
tamponade
2. Placement of pacemakers or implantable
5. Atrial stunning
defibrillators
6. Embolic damage: thrombus or air leading to TIA
3. Patients for diagnostic studies
or stroke
B. Principles of anaesthesia for electrophysiological 7. Infection: endocarditis
procedures 8. Burns: from skin electrodes

1. Range of anaesthesia from anxiolysis to GA with

muscle relaxation. 9. Angina, dual antiplatelet therapy and
2. General principles of cardiac stability and troponin
maintenance of physiological parameters.
3. Smooth emergence to prevent haematomas from A. How may angina be categorised?
access sites. B. What are the criteria necessary for the diagnosis of
4. Specifically, use of muscle relaxants may be acute and established myocardial infarction (MI)?
required for accurate mapping of intracardiac C. List the mechanisms by which troponin may be
structures raised in conditions other than myocardial
5. For ablation of re­entrant tachycardia phrenic infarction?
nerve stimulation is used and no relaxant is D. Describe the modes of action of aspirin and
permitted. clopidogrel and for which groups of patients is
6. Volatiles may suppress this arrhythmia so TIVA is dual therapy with these agents recommended?
often used. E. What are the indications for prolonged or
permanent dual antiplatelet therapy? (These are
also the risk factors for stent thrombosis)

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 Cardiac anaesthesia

A. Categories of angina Established myocardial infarction

Angina is a commonly a dull, heavy retrosternal pain which Development of pathological Q waves
commonly radiates to the neck, arm or jaw, which may be OR… pathological findings of healing or healed MI
exacerbated by exercise, stress or cold weather.
C. The mechanisms by which troponin may be raised in
Categories conditions other than myocardial infarction
1. Chronic stable angina; usually caused by fixed 1. Troponin is a regulatory protein, along with
stenosis, often with a significant stenosis of LAD tropomyosin which is found on actin.
or epicardial arteries. Typical pattern of pain and 2. It is necessary for cardiac and skeletal muscle
triggers contraction and is released in myocardial necrosis.
2. Unstable angina ; new onset angina, increased 3. However a number of conditions in which there is
severity or frequency or duration from previous myocardial damage but not AMI/ACS, including:
stable symptoms, often due to plaque rupture, part a. Demand ischaemia; e.g. tachycardia,
of spectrum of ACS increased myocardial O2 demand but
3. Nocturnal angina; most commonly at night, decreased diastolic time and therefore
secondary to changes in respiratory patterns, e.g. myocardial perfusion time. Another
OSA, which result in hypoxia and myocardial example LV hypertrophy, increased mass
ischaemia of myocardium therefore endocardial
4. Decubitus angina; occurs in supine position, ischaemia more likely in high oxygen
increased filling pressures causes increased consumption
strain/tension on chamber walls b. Ischaemia without coronary artery
5. Microvascular angina; triad of anginal pain, disease; e.g vasospasm as discussed
normal angiography but positive EST. Most previously. Also CNS events such as
commonly females and diabetics subarachnoid haemorrhage or CVA
6. Prinzmetal's or vasospastic angina; at rest or on associated with troponin rise and ECG
exertion, vasospasm of epicardial arteries, changes, thought to be secondary to
commonly associated with illicit drug use, more increased sympathetic outflow.
common in males, and hyperinsulinaemia c. Direct cardiac injury; that may be
7. Chronic refractory angina; not controlled by i. Mechanical e.g. cardiac
maximal medical therapy or interventions surgery, contusions, and CPR
8. Non­cardiac chest pain ii. Electrical e.g. DC cardioversion
iii. Chemical e.g. cardiotoxic
Also can be classified on severity, using the Canadian chemotherapy
Cardiovascular Society Classification, which grades iv. Inflammatory e.g. pericarditis
angina based on symptoms from class I with no limitations, and myocarditis
to class IV with a debilitating disease d. Strain; pathological stretching of
myocardial units and chamber walls
results in ischaemia, e.g. in:
B. The criteria necessary for the diagnosis of acute and i. Congestive cardiac failure
established myocardial infarction (MI) ii. Right ventricular strain as in a
large pulmonary embolism
This has been derived from European Society of e. Chronic kidney disease; at risk of silent
Cardiologists and American College Cardiologists necrosis, but also a reduced clearance of
plasma troponin
Acute myocardial infarction f. Inflammatory; inflammatory mediators
1. Increase in troponin causing direct injury e.g. in sepsis, septic
2. Ischaemic symptoms emboli causing obstruction of coronary
3. Pathological Q waves arteries
4. Ischaemia on ECG
5. Coronary artery intervention e.g. PCI
6. Pathological findings of acute MI

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 Cardiac anaesthesia

D. The modes of action of aspirin and clopidogrel, and

the groups of patients where dual therapy is
recommended
Aspirin and Clopidogrel are both antiplatelet agent, they
are similar in that they both cause irreversible platelet
inhibit but their mechanisms of action differ

Aspirin
1. Irreversible COX 1 inhibitor so reducing conve­
rsion of arachidonic acid to Thromboxane A2,
which promotes platelet aggregation
2. Favours production of prostaglandins which
inhibit platelet aggregation
3. Effects platelet for their entire life span therefore
takes 7­10 days for affected platelet to be
destroyed and its effects to diminish

Fig. 8. Clopidogrel mechanism of action on platelets

E. The indications for prolonged or permanent dual

antiplatelet therapy
Fig. 7. Asprin mechanism of action on platelets (These are also the risk factors for stent thrombosis)
1. Patients who have had a bare metal stent placed
may only require dual therapy for 4 weeks after
Clopidogrel PCI.
1. A thienopyridine, along with ticlopidine. 2. This is increased from 3 – 12 months if a drug
2. Selectively an irreversibly inhibits P2Y12 ADP eluting stent is used, this is because the regrowth
receptor on the surface of the platelet; it has no of epithelium around stent is much delayed and
effect on arachidonic acid. this is the period of time when risk of thrombosis
3. It is a pro drug meaning that it must be is greates.
metabolised by the liver in order for the drug to be 3. Prolonged therapy recommended in patients who
active. remain high risk for MI despite treatment.
4. Similar to aspirin in that it takes 7­10 days for 4. Also indicated in patients with cerebrovascular
platelet turnover for effects to be reversed. disease who are at high risk of CVA, and in
certain patients with peripheral vascular disease.
The dual therapy is recommended for certain patients as
drugs are having synergistic effect. It is recommended in
management of None­ST elevation MI, in patients with
known coronary artery disease but at risk of MI, and in
patients undergoing PCI.

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10. Complications of cardiac surgery Coagulopathy

1. Heparin Induced thrombocytopaenia
A. What are the potential cardiac complications 2. Hypoperfusion or thromboembolic related liver
immediately following cardiac surgery? and GIT complications
B. What are the potential non­cardiac complications
(excluding CNS) immediately following cardiac Other
surgery? 1. Protamine related:
C. What are the potential neurological complications a. Bronchospasm
immediately following cardiac surgery? b. Non cardiogenic pulmonary oedema
D. What are the recent advances in CPB aimed at c. anaphylaxis
minimising complications to do with CPB circuit?
2. Leg wound due to saphenous vien graft (SVG)
A. The potential cardiac complications immediately harvest:
following cardiac surgery a. Bleeding
b. Infection.
Mechanical
1. Spasm or occlusion of a coronary artery graft 3. Acid base and electrolytes imbalance:
2. Prosthetic valve paravalvular regurgitation a. Hyperkalaemia
3. Cardiac tamponade due to hematoma. b. Hypocalcaemia
4. Systolic anterior motion of the mitral valve with
left ventricular outflow tract obstruction. C. The potential neurological complications
immediately following cardiac surgery
Physiological
1. Myocardial stunning, low output state Central
cardioplegia related, low inotropic state. 1. Stroke: haemorrhagic or embolic
2. Inadequate preload due to poor relaxation of the 2. Delirium
diastolic dysfunction. 3. Neurocognitive impairment
3. Vasoplegia or vasodilatory shock resulting in low 4. Neuropsychiatric impairment
SVR 5. Seizure
4. Conduction abnormality with tachy/brady 6. Coma
arrhythmias, AF, ventricular arrythmias.
5. Myocardial infarction Peripheral
1. Phrenic nerve palsy
B. The potential non­cardiac complications (excluding 2. Intercostal nerve damage
CNS) immediately following cardiac surgery 3. Upper limb: brachial plexus, ulnar nerve injury
4. Lower limb: common peroneal, tibial nerve injury
Pulmonary
1. Atelectasis D. The recent advances in CPB aimed at minimising
2. Consolidation complications to do with CPB circuit
3. Pneumonia
4. Decreased compliance Centrifugal pump versus roller pump
5. Failure to wean 1. Less damage to RBC, platelets, plasma proteins.
6. ALI, ARDS 2. Non occlusive nature alters flow rate, prevents
7. Pulmonary oedema high pressure build up and prevents circuit
8. ulmonary embolism rupture.
9. Pneumothorax 3. Mini extracorporeal circulation – heparin bonded /
10. Plural effusion (left), early bloody, late serous phosphorycholine–reduces systemic inflammatory
fluid response syndrome (SIRS)
4. Haemofiltration, reduces the prime volume and
Renal haemodilution.
1. Acute kidney injury 5. Continuous in line acid base and electrolytes
monitoring.
Haematology 6. Leukocytes filter or ultrafiltration
1. Bleeding 7. Cell salvage
2. Transfusion related complications

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11. Cardiopulmonary bypass 10. Separate circuit for cardioplegia suction solution
to enters back into circuit
A. List the components of the cardiopulmonary
bypass (CPB) circuit? B. assessing adequacy of perfusion on CPB
B. How may perfusion on CPB be assessed as
adequate? Difficult to assess but aim to match blood flow with the
C. What methods of myocardial protection are organs oxygen demand.
employed during cardiopulmonary bypass?
D. Describe the process of weaning from 1. Factors related to:
cardiopulmonary bypass? a. CPB machine ­ blood flow per minute or
E. What factors may indicate failure to wean from prime viscosity
bypass? b. Patient factors ­ vascular resistance, total
body weight or temperature
2. MAP is aimed to be at 65 mmHg not less.
3. Arterial blood gases can assess lactate and acid
base balance these are reliable measures of
aerobic respiration (oxygenation), tissue perfusion
and CO2 elimination.
4. Venous oxygen saturation reflects the peripheral
O2 usage.
5. Neurological physiologic monitoring used to
estimate the degree of brain perfusion and CBF
tools are:
a. EEG.
b. Evoked potential.
c. Cerebral oximetry by near infrared
spectroscopy.
d. Transcranial doppler.
Fig. 9. Cardiopulmonary bypass machine
C. Methods of myocardial protection employed during
A. The components of the cardiopulmonary bypass
cardiopulmonary bypass
(CPB) circuit
1. Monitoring ECG to assess if any electrical activity
A circuit to direct blood from right atrium, uperior vena
when on bypass can be either through:
cava or inferior vena cava to oxygenate it, remove CO2 and
a. Endocardial transvenous approach
return it to aorta.
b. Epicardial surgical approach
1. Heparin or phosphorylcholine coated tubing and
components.
2. Venous line: large bore to drain under gravity.
3. Reservoir: venous from venous line, surgical
suction.
4. Cardiotomy: low volume cannula placed in left
ventricle to prevent accumulation of blood.
5. Filter ­ remove gas and particulate emboli,
leukocyte depleters
6. Oxygenator:
a. Membrane ­ large surface area of fine Fig. 10. ECG monitoring during CPB
capillary tubes allows gas flow. The FiO2
deterimines PaO2.
2. Cardioplegia solution: once the cross clamp is
b. Bubble ­ not used as often due direct
applied, anterograde and/or retrograde injections
contact of blood with air surfaces which
of cardioplegic solution can be given respectively
damage blood constituents.
into the aortic root or directly into the coronary
7. Heat exchanger: allows manipulation of
ostia. St Thomas or harfield solution with K+
temperature
20­80 mmol.l­1, Mg2+, Ca2+, Cl­ and procaine.
8. Pump: roller or centrifugal
3. Cooling with ice or icy slush to heart directly.
9. Arterial line: into aorta

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 Cardiac anaesthesia

Fig. 11. Icy slush

4. Cooling of patient to reduce core temperature

5. Ischaemic preconditioning (see page 37)

D. The process of weaning from cardiopulmonary

bypass

In order to make weaning possible (i.e. travelling safely

from CPB station to cardiac work station) a sequence of
events must be perfectly balanced to (TRAVVEL)
1. T Temperature: the nasopharyngeal temperature
should be normally adjusted at 36­37 C° Fig. 12. Different cardiac cannulations, cross clamping
2. R Rate: Sinus rhythm resumed and the rate and venting in CPB
controlled by an epicardial pacing system.
3. A Air: Transoesophageal echocardiography used
to confirm good intra­cardiac de­airing E. Factors that indicate failure to wean from bypass
4. V Ventilation: Mechanical ventilation and alarm 1. Low systemic BP, low SVR or poor CO
settings restarted with visual observation. 2. Cardiac filling pressures: increased right atrial
5. V Venting: Aortic root venting should be removed pressure and signs of a failing right or left
or reduced and matched by the arterial pump ventricle
(see Fig 12). 3. Arrhythmias
6. E Electrolytes and haemoglobin: resumed to a 4. Anaemia
normal physiological levels. 5. Acid­base disturbances, specifically severe
7. L Level: Zeroing the operating table acidosis
6. Hypovolaemia
7. Air embolism

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12. Cardiac transplantation, prednisolone. Long term treament with these

anaesthesia and the transplanted heart drugs is accosiated with infection, increased
incidence of malignancy, musculoskeletal
A. What are the intraoperative anaesthetic principles problems and chronic renal impairment
governing heart transplantation? 4. Associated diseases Patients may have required
B. What are the complications of cardiac transplantation for a systemic disease, the
transplantation? complications of which may have anaesthetic
C. What are the physiological differences of the implications. For example:
transplanted heart? 5. Ischaemic cardiomyopathy generalised
D. What is the pharmacological relevance of this to atherosclerosis.
anaesthesia? 6. Diabetes secondary to steroid immunosuppre­
ssion.
7. Sarcoid and amyloid cardiomyopathy.
A. The intraoperative anaesthetic principles governing
8. Epilepsy is common post­cardaic transplantation.
heart transplantation
9. Hypertension is common after cardiac transplan­
tation and may be related to cyclosporin therapy
1. Assess right ventricle function and pulmonary
resistance.
2. Blood products should be made available. C. The physiological differences of the transplanted
3. Deactivate implantable cardioverter defibrillator. heart
4. External defibrillator pads are required if it's a
re­do surgery. 1. The transplanted heart has no autonomic
5. Transoesophageal echocardiography (TOE). innervation.
6. Administration of immunosuppressants and 2. The resting heart rate is typically 90 ­100 bpm due
prophylactic antibiotics, and meticulous attention the loss of vagal tone.
to sterility. 3. The normal reflex heart rate changes that occur in
7. Monitoring: multi­lead ECG, oxygen saturation, response to laryngoscopy, visceral traction or
arterial blood pressure, central venous pressure, fluctuations in blood pressure are lost.
pulmonary artery pressure. 4. The lack of rapid homeostatic adjustments in heart
8. Large bore venous access, central venous access, rate to sudden drug­induced changes in vascular
8Fr central venous sheath, Foley catheter resistance can produce wide swings in blood
9. Balanced general anaesthetic with haemodynamic pressure which can be troublesome during
stability anaesthesia, therefore an adequate preload must be
10. Antifibrinolytics (e.g. transexamic acid) maintained.
11. TOE to provide information about donor heart 5. A blunted response to exercise is also seen with a
function gradual rise to a reduced maximal heart rate then a
12. Left atrial pressure line can be sited gradual decline following cessation of exercise.
intraoperatively for estimation of left ventricular 6. Dependence on endogenous catecholamines in
end­diastolic pressure order to mount a chronotropic response rather than
13. Inotropic support is nearly always used, agent then normal mechanism of vagal withdrawal
varies by institution together with an increase in cardiac sympathetic
14. Reduction of pulmonary vascular resistance e.g. nerve activity.
inhaled nitric oxide up to 20ppm or epoprostenol,
sildenafil
15. Pressure areas padded to avoid nerve compression D. The pharmacological relevance of this to anaesthesia
16. Maintenance of normal body temperature
following makes postoperative extubation feasible 1. Denervation alters the pharmacological response
to certain drugs.
B. The complications of cardiac transplantation 2. Cardiac vagolytic effect of drugs such as atropine
and glycopyrrolate are lost and denervation
1. Donor coronary artery disease commonest cause supersensitivity to other drugs is seen: Adenosine,
of death beyond the first year after transplantation Adrenaline, Noradrenaline.
2. Rejection important clinical problem but 3. Digoxin controls the ventricular response rate in
infrequent in longer­term patients on stable atrial fibrillation by increasing vagal tone and
immunosuppressive treatment therefore cease to be effective as an
3. Immunosuppression usually achieved with triple anti­arrhythmic in the transplanted heart.
therapy based on azathioprine, cyclosporin and

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13. Paediatric congenital heart disease 4. Excessive pulmonary blood flow results in pulmonary
oedema and poor systemic perfusion.
A. Describe the normal (or series) circulation 5. Conversely insufficient pulmonary blood flow
physiology, contrast this with the parallel and causes profound cyanosis.
single ventricle or Fontan circulation 6. Children with large unrepaired AVSD’s or VSD’s
pathophysiology of congenital heart disease? lesions can exhibit a balanced circulation
B. How may congenital heart disease in children be physiology.
physiologically classified?
C. How may children with heart disease undergoing Single ventricle circulation:
non­cardiac surgery be stratified according to 1. Some forms of CHD are not amenable to full
risk? correction to a series circulation.
D. Describe the basic principles of management of a
3 month old with a large VSD presenting for
2. Children with these conditions will have palliation
emergency surgery for scrotal swelling?
by creating a single ventricle circulation.
E. Describe the basic principles of management of a
6 year old with a repaired TOF presenting for
dental extraction? 3. This occurs as a staged process.
F. Describe the basic principles of management of a a. The first stage at 3­5 months is known as
12 year old with Fontan circulation presenting for a Glenn Shunt and involves the superior
emergency ORIF of fracture? vena cava being connected directly to the
right pulmonary artery.
b. The second stage connects the inferior
A. The normal (or series) circulation physiology, vena cava to the right pulmonary artery,
contrasting with the parallel and single ventricle or this separates the systemic and
Fontan circulation pathophysiology of congenital heart pulmonary circulation and returns arterial
disease oxygenation to normal. This stage occurs
at around age 3­5 years.
Normal (series) circulation:
1. Consists of a pulmonary and systemic circulation 4. A single ventricle pumps blood to the systemic
working together in series. circulation and the pulmonary circulation relies on
2. Blood flows from the right atrium to right blood flowing passively to the lungs and down a
ventricle, to the lungs where it is oxygenated and pressure gradient from the pulmonary artery to the
reaches the systemic circulation via the left atrium left atrium. The pressure gradient in the sole
and left ventricle. determinant for pulmonary blood flow.
3. Some CHD conditions e.g. ASD behaves as the
normal series circulation but with mixing of
deoxygenated and oxygenated blood through one
or more ‘holes’. B. Physiologically classification of paediatric congenital
4. The direction of blood flow through the lesion heart disease
depends on the pressure gradient across it.
Accordingly the degree of shunt depends on the Congenital heart disease can be classified in a number of
size of the defect and the relative pressure ways.
gradients.
Firstly, as cyanotic and non­cyanotic.
Balanced (parallel) circulation:
1. Instead of the circulation being in series they are Cyanotic heart disease include conditions with:
in parallel. 1. Obstruction to pulmonary flow e.g;
2. Some CHD conditions involving large a. Tretralogy of Fallot.
intra/extra­cardiac communications meaning that b. Pulmonary atresia.
blood flow to the systemic and pulmonary
circulation varies depending on the relative 2. Mixing in a common chamber e.g;
resistance in each circuit. a. truncus ateriosus.
3. Therefore blood flow to the lungs or the body
depends on the balance between pulmonary 3. Separation of the pulmonary and systemic
vascular resistance and systemic vascular circulations e.g;
resistence. a. Transposition of the great arteries.

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 Cardiac anaesthesia

Non Cyanotic heart disease include conditions with: c. Type of surgery.

1. Pressure overload conditions e.g; d. Young age.
a. Coarctation of the aorta. e. The most important factors are the
b. Aortic stenosis. physiological status and complexity of
heart disease.
2. Volume overload conditions e.g;
a. Atrial septal defect. 4. High risk children for non­cardiac surgery
b. Patent ducts ateriosus (PDA). include:
c. Hypoplastic left heart syndrome. a. Physiologically poorly compensated
and/or the presence of the following
major complications:
Another physiological classification divides conditions i. Cardiac failure
depending on the direction of blood flow through the ii. Pulmonary hypertension
lesion. iii. Arrhythmias
Simple left to right shunts which cause an increase in iv. Cyanosis
pulmonary blood flow e.g; b. Complex lesions e.g;
a. Atrial septal defect (ASD). i. Single­ventricle
b. Ventricular septal defects (VSD). ii. Balanced circulation physiology
c. Atrioventricular Septal Defect (AVSD). iii. Cardiomyopathy
d. Patent ducts ateriosus (PDA). iv. Aortic stenosis
c. Major surgery e.g;
Simple right to left shunts, which cause a reduction in i. Intraperitoneal
pulmonary blood flow (PBF) and cyanosis e.g; ii. Intrathoracic
a. Tretalogy of Fallot iii. Anticipated major blood loss
b. Pulmonary atresia requiring transfusion
c. Tricuspid atresia d. Under 2 years old
d. Obstein’s anomaly. e. Emergency surgery
f. Preoperative hospital stay more than 10
Complex shunts, these cause mixing of pulmonary blood days
flow and systemic blood flow. Amongst others these g. ASA physical status IV or V
include:
Hypoplastic left heart syndrome. 5. Intermediate risk includes:
Transposition of the great arteries. a. Physiologically normal or well
Truncus ateriosus. compensated
b. Simple lesions
c. Major surgery (intraperitoneal,
C. Risk stratification in children with heart disease intrathoracic, anticipated major blood
undergoing non­cardiac surgery loss requiring transfusion)
d. Under 2 years old
1. Generally, children with CHD undergoing e. Emergency surgery
non­cardiac surgery have: f. Preoperative hospital stay more than 10
a. Increased risk of morbidity. days
b. Perioperative cardiac arrest. g. ASA physical status IV or V
c. Higher 30 day mortality.
6. Low risk includes:
2. However, the complexity of cardiac defects and a. Physiologically normal or well
the variety of non­cardiac surgery means some are compensated
at an increased risk compared to others. b. Simple lesions
c. Minor (or body surface) surgery
3. Different studies identify a variety of factors d. Over 2 yr old
associated with a high risk of perioperative e. Elective surgery
complications, such as: f. Preoperative hospital stay less than 10
a. Disease complexity. days
b. Physiological status. g. ASA physical status I – III

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 Cardiac anaesthesia

Fig. 13. Tetralogy of Fallot (TOF) Fig. 14. Pulmonary atresia

Fig. 15. Truncus ateriosus Fig. 16. Transposition of the great arteries

Fig. 17. Coarctation of the aorta Fig. 18. Congenital aortic valve stenosis

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 Cardiac anaesthesia

Fig. 19. Ventricular septal defect Fig. 20. Atrial septal defect

Fig. 21. Patent ducts ateriosus Fig. 22. Hypoplastic left heart syndrome

Fig. 23. Atrioventricular Septal Defect Fig. 24. Tricuspid atresia

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 Cardiac anaesthesia

order to minimize left to right shunt and maximize

systemic perfusion.

7. They may require higher ventilator pressures than

expected because of pulmonary oedema.

8. Avoid air bubbles in venous lines because of the

risk of paradoxical embolus.

9. Endocarditis prophylaxis unnecessary

E. The basic principles of management of a 6 year old

with a repaired TOF presenting for dental extraction

1. If the TOF is repaired then the lesion is likely to

be small and well compensated for
physiologically. Therefore the patient is most
likely low risk. The surgery could be performed in
Fig. 25. Ebstein's anomaly their local hospital without the need for specialist
input.
2. However if there is evidence of ventricular
D. The basic principles of management of a 3 month ectopics on ECG then advice from cardiology is
old with a large VSD presenting for emergency surgery needed as this can sometime be an ominous sign.
for scrotal swelling
F. The basic principles of management of a 12 year old
This depends on a number of factors. with Fontan circulation presenting for emergency ORIF
1. Firstly the anaesthetist needs to assess the severity of fracture
of the CHD and if any VSD symptoms are
present, for example: 1. As this is a single ventricle circulation, the patient
a. Poor weight gain has a very complex condition and would be
b. Poor feeding deemed high risk.
c. Signs of cardiac failure
d. Pulmonary oedema 2. As this fracture may be an emergency there may
e. Arrhythmias not be time for transfer to a specialist hospital
where this patient should ideally be managed. If
2. If none if these signs are present and it is a simple transfer is not possible then advice should be
VSD for which the child has compensated well, sought from the specialist centre.
then he/she can be classified as intermediate risk.

3. If the operation is an emergency then: 3. Induction should be either a slow gas induction or
a. If hospital in question is used to dealing slow IV induction.
with children under the age of 2 then they
can proceed with the operation. 4. Spontaneous ventilation may be more beneficial
b. If needed liaise with a specialist hospital as this aids pulmonary blood flow but hypoxia,
for advice should commence. hypercarbia and basal collapse must be avoided,
c. If however, the hospital does not preform which will all increase pulmonary vascular
paediatric surgery routinely, the child resistence and reduce blood flow.
should be transferred to a specialist
hospital. 5. If using positive pressure ventilation, then high
pressure, high PEEP and long inspiratory times
4. Induction of anaesthesia should be a slow cautious should be avoided as these too compromise PBF.
gas or intravenous induction.
6. Slight head up position aids venous return and
5. Beware of the possibility of poor cardiac reserve. pulmonary blood flow, as does raising the legs.
6. Avoid high inspired oxygen concentrations in

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14. Cardiomyopathies and ventricular 4. High filling pressures required and high normal
assist devices SVR with maintenance of normal contractility and
sinus rhythm.
A. What are the distinguishing pathological features
between the different cardiomyopathies? How do B. The indications and contraindications for
these affect anaesthetic management aims? ventricular assist device (VAD) insertion
B. What are the indications and contraindications for
ventricular assist device (VAD) insertion? 1. Acute heart failure as a bridge to recovery i.e.
C. What are the principles of anaesthesia for VAD cardiogenic shock post MI or cardiotomy
insertion? 2. Chronic heart failure as a bridge to transplant i.e.
D. What postoperative complications may be secondary to IHD, HTN or other cardiomyopathy
encountered? 3. Destination (permanent) therapy when recovery is
unlikely and transplant is contraindicated. Not a
routine practice in the UK.
A. The distinguishing pathological features between the
different cardiomyopathies and how do these affect
anaesthetic management aims
C. The principles of anaesthesia for VAD insertion
There are three types of cardiomyopathy
Dilated: 1. Preoperative: Multi­comorbidities are usual;
1. An enlarged poorly contractile ventricle with cerebrovascular disease; COPD; renal impairment;
impaired systolic function although diastolic hepatic congestion; diabetes; anticoagulated;
dysfunction results in raised LVEDP in extreme potential PVC / CVC sepsis. Premed can cause
cases. hypoventilation with disturbed PVR.
2. Ensure medical therapy optimised and possible 2. Perioperative: Meticulous asepsis for new
need for cardiac resynchronisation addressed vascular catheters; IABP may be needed; attention
electively. to potential disturbance of PVR with hypoxia or
3. Aim for normal heart rate, rhythm, adequate hypercarbia during induction using RSI. Minimal
preload and avoid negative inotropy or increases monitoring plus CVC, IABP, 5lead ECG,+/­ PAC
in afterload. and TOE. CPB may not be required.
4. Potassium and magnesium should be corrected. 3. Postoperative: VAD in fixed mode for 24hours to
avoid excess emptying and collapse; managed on
Hypertrophic: CSICU; TOE left insitu to monitor.
1. Pressure overloaded left ventricle with normal or
reduced chamber size.
2. CPP is reduced secondary to increased LVEDP
and the hypertrophied ventricle has a greater D. Postoperative complications that may be
oxygen demand resulting in high risk for encountered
ischaemia.
3. Adequate volume loading also important with 1. Bleeding
increased LVEDP. 2. PFO: unmasked by left atrial decompression on
4. Significant interventricular septal hypertrophy ­ VAD activation with consequent right to left shunt
dynamic LVOT obstruction can occur. This can and hypoxia
cause complete LVOT obstruction if associated 3. Right heart failure: from increased PVR or
with systolic anterior motion of the anterior leaflet inadequate preload
of the mitral valve. 4. Hypotension: haemorrhage, aortic dissection;
5. Aim for sinus rhythm (very important), high tamponade; septic; adrenal insufficiency and low
normal afterload and avoid inotropy and VAD flows
chronotropy. 5. Arrhythmias: although VADs protect from lethal
arrhythmia they will affect native function and
Restrictive: reduce output
1. Characterised by reduced ventricular compliance 6. CNS: from thromboembolic or haemorrhagic
2. (Idiopathic then amyloidosis, haemachromatosis phenomena
and sarcoidosis). 7. Infection: strict measures taken to avoid device /
3. Anaesthesia can precipitate cardiac arrest due to line infection
reduced myocardial contractility, venous return
(esp. if IPPV), and reduced SVR.

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15. Coagulation issues in cardiac 1. Heparin 4­5 mg.kg­1 (500 IU.kg­1) is a negatively
charged molecule that potentiates the action of
surgery antithrombin III.
2. Arterial blood sample for ACT after 3–5 min
3. Ensure ACT above 3–4 times of baseline ACT (>
A. Describe the normal process of haemostasis?
480 s) before initiating CPB
B. Describe the agents which may be employed for
4. 5000 IU unfractionated heparin in CPB prime
anticoagulation and reversal of anticoagulation for
solution.
cardiopulmonary bypass?
C. Describe the monitoring of anticoagulation 5. Monitor ACT at least every 30 min during CPB
throughout the procedure? 6. In cases of HIT, alternative anticoagulants can be
D. What is thromboelastography, draw a normal TEG used e.g. bivalirudin , Low molecular weight
trace? heparin (LMWH), Danaparoid, Lepirudin.
7. Reversal of heparinisation is by protamine 1mg
A. The normal process of haemostasis per 100 units of heparin administered.

The mechanism by which bleeding ceases following C. The monitoring of anticoagulation throughout the
vascular disruption has 3 key components: procedure
1. Primary haemostasis; vascular endothelium
disruption leading to vasoconstriction, platelet 1. Activated clotting time (ACT) is monitored every
adhesion as exposed to collagen and vWF bind to 30 min, it must be maintained > 480 sec.
GPIa and GPIb platelet receptors respectively. 2. APTT and PT are lab. tests only useful in the
2. Secondary haemostasis; ctivation of the perioperative period.
coagulation cascade to produce thrombin and then 3. Thromboelastography (TEG) measure whole
fibrin from fibrinogen. blood viscoelastic changes, a quick test taking
3. Fibrin strengthening and stabilization of the about 10 min.
platelet plug.

D. Thromboelastography
1. Thromboelastography (TEG) measures whole
blood viscoelastic changes associated with fibrin
polymerization.
2. Information about coagulation factor activity and
platelet function within 10–20 min.
3. A pin, attached to a torsion wire, is suspended into
a blood sample contained in an oscillating cuvette.
4. Clot forms gradually in the blood sample creating
increasing displacement of the pin.
5. This is translated into a graphical representation
6. Graph represents sheer elasticity vs time.
Fig. 26. The clotting pathways 7. The magnitude of the output represents the
strength of the fibrin­platelet bonds and gives a
B. The agents which may be employed for wide TEG
anticoagulation and reversal of anticoagulation for
cardiopulmonary bypass

Fig. 27. Heparin accelerates inactivation of

coagulation factors by antithrombin.
Fig. 28. Thromboelastography

52
 Cardiac anaesthesia

16. Pacemakers and implantable 8. HOCM with sustained VT/VF in the absence of
reversible causes or with a family history of
defibrillators sudden cardiac death (SCD)

A. What are the indications for permanent pacing? C. Key information should be obtained about the
B. What are the indications of placement of a patient or device prior to anaesthesia and surgery
permanent defibrillator?
C. What key information should be obtained about 1. Ask for the patient's registration card for the
the patient/device prior to anaesthesia and device.
surgery? 2. Device manufacturer, model number, serial
D. What preoperative precautions should be taken number.
with regard to a patient with a pacemaker/ICD? 3. Anatomical position.
E. Describe the considerations in a patient with a 4. Indication
pacemaker that has not been switched off due to 5. Date of insertion.
emergent surgery?
6. Details of recent check­up and battery condition.
7. Mode of action.
8. Rate modulator function (should be de­activated
A. The indications for permanent pacing
prior to anaesthesia).
1. Acquired 3rd degree heart block. 9. Any dizziness, syncope or heart failure
2. Symptomatic acquired 2nd degree heart block. 10. Any recent deterioration in underlying medical
3. Chronic bifascicular and trifascicular block may condition
be the indications if 3rd degree block or 2nd 11. ECG – rhythm, pacemaker activity, electrical
degree (type II) occurs. capture.
4. Post­MI infranodal AV block and associated BBB 12. CXR – position of box leads electrode and cardiac
or persistent and symptomatic 2nd or 3rd degree failure.
block 13. Electrolytes – abnormalities affect capturing
5. Sinus node dysfunction with symptomatic
bradycardia and frequent sinus pauses or
D. Preoperative precautions should be taken with
symptomatic chronotropic pauses
regard to a patient with a pacemaker or ICD
6. Sustained VT
7. Hypertensive carotid sinus syndrome
1. Careful pre­op visit and review of notes.
8. Hypertrophic or dilated cardiomyopathy with
2. Rate modulator function (should be de­activated
sinus node dysfunction or AV block
prior to anaesthesia).
9. After cardiac transplantation, if symptomatic
3. Organise an interrogation or check­up of the
bradyarrhythmias
device in the elective scenario
10. Chronic AF with associated bradycardia
4. Reprogramming of the device as is appropriate for
the patient and the type of surgery (e.g. devices
B. The indications of placement of a permanent
with minute ventilation sensors for rate
defibrillator
modulation)
5. Anti­tachycardia therapy should be disabled
1. VF or sudden cardiac death (SCD) survivors.
6. If there is high risk of Electro­Magnetic
2. VT causing syncope not related to acute MI or
Interference (EMI) then precautions include the
other correctable causes.
use of magnets if appropriate.
3. Minimally symptomatic VT with LVEF of < 35%.
7. For ICD patients they should be connected to an
4. Patients with previous MI with LVEF < 35%,
external defrillator and continuously monitored.
asymptomatic spontaneous non­sustained VT with
8. Decide the method of diathermy and arrange for a
sustained VT/VF
telemetric programmer to be present if extensive
5. Long QT syndrome with recurrent syncope or
close­proximity electrocautery is required.
family history of SCD.
9. Arrange post­operative reprogramming/check­up.
6. Brugada syndrome presenting with VT/VF or
10. Arrange post­operative care level e.g. may require
syncope with inducible VT
high dependency unit (HDU) care.
7. Arrhythmogenic right ventricular dysplasia with
documented sustained VT/VF or those with a
family history of SCD.

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 Cardiac anaesthesia

E. The considerations in a patient with a pacemaker A. The basic physics of ultrasound and the doppler
that has not been switched off due to emergent surgery principle

1. Careful standard monitoring +/­ invasive blood 1. Ultrasound is defined as sound with a frequency
pressure monitoring and careful placement of any greater than 20 kHz.
central venous access (avoid vessels with leads) 2. Echocardiography machines typically emit
2. Diathermy – use bipolar if possible and if not ultrasound at a frequency of 210 MHz. The speed
position as far away from device as possible, at of ultrasound is determined solely by the medium
lowest amplitude and use in short bursts through which the wave travels.
3. Patient positioning, shivering, alteration in heart 3. The speed of sound in the heart is approximately
size and positive pressure ventilation may all 1540 m.s­1.
cause lead displacement which can result in loss 4. Ultra sound waves produce by using piezoelectric
of capture or increase in the pacing threshold effect in quartz crystals.
4. Shivering and fasciculation can confuse rate 5. Doppler: frequency of sound wave reflected from
modulators a moving object is different form the emitted
5. Peripheral nerve stimulators may interfere with frequency.
function
6. Defibrillation may cause damage B. The indications for transoesophageal
7. Have facilities for CPR, emergency defibrillation echocardiography
and temporary pacing available
8. Consider using a clinical magnet Specific indications for TOE:
9. Check function as soon after surgery as possible 1. Prolonged Imaging( Peri operative imaging)
2. Interest in posterior structures: LA,
3. High resolution required: Dx of Endocarditid
especially in Obese or Emphysematous pt
17. Ultrasound and transoesophageal
American college of cardiology 2011
echocardiography 1. Dx of Endocarditis
2. To evaluate suspected aortic pathology e.g.
A. Describe the basic physics of ultrasound. What is dissection
the Doppler principle? 3. To evaluate cardiac source of thrombus
B. What are the indications for transoesophageal 4. To evaluate for cardiac pathology when
echocardiography? transthoracic echo (TTE) is non diagnostic.
C. What are the contraindications for TOE ­ relative 5. To facilitate clinical decision making e.g.
and absolute?
cardioversion, ablation of pt with AF, atrial flutter
D. What are the complications of TOE?
6. To assist with non coronary percutaneus cardiac
E. What haemodynamic variables can be measured
interventions e.g. percutaneous valve placement
or derived from TOE?
of closure devices, valvuloplasty.
7. In ICU to assess pt with:
a. Severe hypotension
b. Blunt chest trauma
c. Unexplained hypoxia
d. Uncertain volume status
8. To assess complications following MI i.e. valves
defects, ventricular septal defect, free wall rupture
with tamponade.

C. The contraindications for TOE both relative and

absolute

Relative:
1. Altered mental status
2. Oesophageal stricture or malignancy
3. Cervical spine arthritis with reduced movement
4. Severe thrombocytopaenia
Fig. 29. Transoesophageal echo 5. Surgical interposion of oesophagus

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 Cardiac anaesthesia

6. Tenuous CVS status

7. Hx of odynophgia and dysphagia
A. The causes of low cardiac output post cardiac
Absolute: surgery
1. Patient who is not fasted for 6 hours
2. Patient refusal 1. Reduced preload:
3. absence of oesophagus a. Absolute hypovolaemia (bleeding)
b. Relative hypovolaemia (sedatives,
rewarming, vasodilators)
D. The complications of TOE c. Cardiac tamponade
d. Right ventricular dysfunction
Incidence:
Complications: 1­3% in clinical setting and up to 13% in 2. Reduced contractility:
emergency setting a. Myocardial stunning
Complications: b. Preexisting poor left ventricular function
1. Sore throat c. Acid­base abnormalities
2. Airway device displacement d. Inadequate revascularisation
3. Airway obstruction
4. Oropharyngeal/ dental trauma 3. Increased afterload:
5. Gastric/ oesophageal trauma a. Vasoconstriction
6. Reflex stimulation (sympathetic): Arrhythmia, MI, b. Fluid overload and left ventricular
ST segment changes distension
7. Aneurysmal rupture c. Left ventricular outflow tract obstruction
8. Infection (post MVR)
4. Arrhythmias
E. Haemodynamic variables can be measured or 5. Diastolic dysfunction
derived from TOE 6. Co­existing pathologies
7. Sepsis, SIRS
Measured: 8. Anaphylaxis
1. CO 9. Adrenal insufficiency
2. LV filling pressure
3. Pulmonary artery pressures
4. atrial interaction B. The mechanism of action and physiological effects of
5. chamber preload the intra­aortic balloon pump (IABP)

Derived:
1. Using flow signals of pulmonary artery, aortic and 1. Circulatory assist device, consists of double lumen
mitral and tricuspid valves and body surface area 8­9.5 French catheter with 25­50 ml balloon
(BSA): attached at distal end and console with a pump to
a. Can calculate stroke volume (SV). drive balloon.
b. Can calculate stroke volume index (SVI). 2. Outer lumen used for gas delivery to balloon and
inner lumen for monitoring systemic arterial
pressure.
3. Helium often used because of low density and
18. Postoperative cardiac output failure easy absorption in case of balloon rupture.
4. Inserted via femoral artery using Seldinger
and the intra­aortic balloon pump technique into descending aorta.
5. Tip 2­3 cm distal to origin left subclavian artery.
A. What are the causes of low cardiac output post 6. Console detects trigger for balloon deflation.
cardiac surgery? Commonly ECG waveform and systemic arterial
B. What is the mechanism of action pressure waveform.
C. What are the physiological effects of the 7. Counter pulsation ­ Inflates with helium during
intra­aortic balloon pump (IABP)? diastole (middle of T wave/dicrotic notch) and
D. What are the indications and contraindications for
deflates during systole (peak of R wave/just
the use of an IABP?
before upstroke on arterial pressure waveform)
E. What complications may be suffered as the result
8. Diastolic augmentation (see below)
of use of the IABP?

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 Cardiac anaesthesia

9. Balloon inflation causes volume displacement Contra­indications for IABP:

within the aorta, both proximally and distally. Absolute:
10. Assistance every beat (1:1) or less often (1:2, 1:4, Aortic regurgitation
1:8) depending on haemodynamic status. Aortic dissection
Chronic end stage heart disease with no anticipation of
recovery
Aortic stents
C. The physiological effects of the intra­aortic balloon
pump (IABP) Relative:
Uncontrolled sepsis
Haemodynamic effects: Abdominal aortic aneurysm
1. Aorta: reduced systolic and increased diastolic Tachyarrhythmias
pressure. Severe peripheral vascular disease
2. Left ventricle: decreased systolic Major arterial reconstruction surger
pressure/end­diastolic pressure/volume/wall
tension. E. Complications may be suffered as the result of use of
3. Heart: decreased afterload, decreased preload and the IABP
increased cardiac output.
4. Blood flow: increase or no effect on coronary 1. Transient loss of peripheral pulse
blood flow. 2. Limb ischaemia
5. Overall decrease in myocardial oxygen demand 3. Thromboembolism
and increased oxygen supply. 4. Compartment syndrome
5. Aortic dissection
Renal effects: 6. Local vascular injury—false aneurysm,
1. Blood flow can increase by 25% secondary to haematoma, bleeding from the wound
increased cardiac output 7. Infection
2. If positioned juxta­renal may decrease blood flow 8. Balloon rupture (gas embolus)
and urine output 9. Balloon entrapment
10. Haematological changes eg thrombocytopenia,
Haematological effects: haemolysis
1. Haemolysis of red blood cells causes reduction in 11. Malpositioning causing cerebral or renal
haemoglobin and haematocrit by 5% compromise
2. Thrombocytopenia through mechanical damage, 12. Cardiac tamponade
heparin or both

D. Indications and contraindications for the use of an

IABP

Indications for IABP:

1. Unstable angina refractory to medical treatment
2. Cardiogenic shock post myocardial infarction
3. Decompensated left ventricular failure
4. Mechanical complications of acute MI: mitral
regurgitation and ventricular septal defect
5. Ischaemia related ventricular arrhythmias
6. Perioperative low cardiac output
7. Acute ischaemia associated with coronary
angioplasty
8. Weaning from cardiopulmonary bypass
9. Bridge to cardiac surgery/transplantation
10. Paediatric complex cardiac anomalies Fig. 30. Intra­aortic ballon effects

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 Cardiac anaesthesia

19. Adult congenital heart disease 13. Ventricular septal defect with associated anomaly, e.g.
aortic regurgitation, absent valve, subaortic
(ACHD) stenosis, mitral valve disease, right ventricular
outflow tract obstruction, straddling
A. How may grown­up congenital heart disease atrioventricular valve
(CHD) be classified?
B. What are the specific considerations in Severe complexity ACHD
anaesthetising adult patients with CHD?
C. What are the factors increasing and decreasing 1. Conduits valved or non­valved
pulmonary vascular resistance? 2. All types of cyanotic heart disease
D. What factors make patients with CHD more prone 3. Double­outlet ventricle
to haemorrhage? 4. Eisenmenger syndrome
E. Which groups of patients should receive antibiotic 5. Fontan procedure or TCPC
prophylaxis against infective endocarditis? 6. Mitral, tricuspid, or pulmonary atresia
7. Pulmonary hypertension
A. Classification of the grown­up congenital heart 8. Any single­ventricle circulation
disease (CHD) 9. Transposition of the great vessels
10. Truncus arteriosus
Simple ACHD 11. Very rare complex anomalies, e.g. crisscross
heart, isomerism, ventricular inversion, heterotaxy
1. Unrepaired lesion syndromes
a. Isolated aortic valve disease (13/1000
live births)
b. Isolated mitral valve disease (excluding B. The specific considerations in anaesthetising adult
mitral cleft or parachute valve) patients with CHD
c. Isolated patent foramen ovale, small
atrioseptal defect, or ventricular septal Factors to consider before undertaking anaesthesia in a
defect patient with ACHD:
d. Mild pulmonary stenosis
1. A clear understanding of the anatomical
2. Repaired lesion configuration of the heart and great vessels and its
a. Previously ligated or occluded ductus associated pathophysiology is essential
arteriosus 2. A clear understanding of any associated
b. Repaired sinus venosus or secundum non­cardiac disease and the often fragile
atrioseptal defect without residual defect emotional state of these patients when they
c. Repaired ventricular septal defect discover they need to undergo anaesthesia and
without residual defect surgery
3. The risk of associated cardiac arrhythmias,
Moderate complexity ACHD including the management of pacemakers and
implanted defibrillators
1. Aorta to left ventricular fistula 4. The possible negative inotropic, vasodilatory
2. Partial or total anomalous pulmonary venous effects of anaesthesia, or both, particularly in the
drainage presence of heart failure
3. Atrioventricular canal defects partial or complete 5. The impact of the chosen ventilatory strategy on
4. Coarctation of the aorta the distribution of blood flow
5. Ebstein’s anomaly 6. Awareness of possible residual defects in patients
6. Significant infundibular right ventricular outflow who have undergone previous repair (paradoxical
tract obstruction embolism, air embolism, pulmonary hypertension,
7. Ostium primum or sinus venosus atrioseptal defect Eisenmenger’s syndrome)
8. Unrepaired ductus arteriosus 7. The need for antibiotic and thromboprophylaxis
9. Moderate­to­severe pulmonary stenosis or 8. The risk of bleeding
regurgitation 9. In older patients, additional co­morbid disease
10. Sinus of valsalva fistula or aneurysm should be considered, e.g. coronary artery disease,
11. Subvalvular or supravalvular aortic stenosis heart failure, diabetes mellitus, renal impairment
12. Tetralogy of Fallot

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 Cardiac anaesthesia

C. Factors increasing and decreasing pulmonary 8. Hypoxic vasoconstriction – a powerful

vascular resistance physiological reflex which diverts perfusion away
from hypoxic areas of the lung. (See below)
The pulmonary vascular system is a low­pressure,
low­resistance system in series with the right ventricle.
Pressures in the pulmonary circulation are about 20% of Hypoxic pulmonary vasoconstriction (HPV)
those in the systemic circulation. 1. Hypoxic pulmonary vasoconstriction (HPV) is an
important mechanism that improves the match
Pulmonary vascular resistance (PVR) is influenced by the between perfusion and ventilation by diverting
following factors: blood from poorly ventilated areas to better
ventilated areas.
1. Autonomic innervation – vasomotor tone is 2. HPV maintains this balance of ventilation to
minimal in the normal resting state and pulmonary perfusion on a breath­to­breath basis. The
vessels are maximally dilated. The autonomic predominant site of HPV lies in the small
system exerts a relatively weak influence on PVR, pulmonary arteries (30–50 μm), with the
increases in sympathetic tone giving rise to remaining resistance arising from the capillary bed
vasoconstriction. and venous system.
3. HPV may also affect the pulmonary vessels in
2. Nitric oxide (NO) – an important mediator of general rather than on a regional basis.
pulmonary vascular tone causing vasodilatation (it 4. Low PaO2 levels are responsible for generalised
is also active in systemic vessels). Nitric oxide has HPV in the fetus, reducing blood flow through the
been identified as endothelium­derived relaxing pulmonary vascular bed to about 10­15% of the
factor (EDRF), which also mediates other fetal cardiac output.
processes by the relaxation of smooth muscle. It is 5. This generalised response also causes a significant
derived from L­arginine and increases increase in PVR at high altitude.
intracellular concentrations of cyclic guanosine 6. The exact mechanism of HPV is unknown. It is
monophosphate (cGMP). Its actions as a potent potentiated by acidosis and modified by various
vasodilator have led to its use in severe acute lung drugs.
disease, where inhaled concentrations of5–80 ppm a. Drugs that attenuate HPV
can improve oxygenation. i. Volatile anaesthetic agents
ii. Nitrates
3. Prostacyclin (prostaglandin I2) – an iii. Nitroprusside
arachidonate, which is a potent vasodilator also of iv. Calcium channel blockers
endothelial origin. v. Bronchodilators

4. Endothelins – potent vasoconstrictor peptides b. Drugs that potentiate HPV

released by the pulmonary endothelial cells. i. Cyclo­oxygenase inhibitors
ii. Propranolol
5. Vascular transmural pressure – important in the iii. Almitrine
pulmonary circulation because the thinner vessel
walls make them more prone to collapse when
alveolar pressure exceeds intravascular pressure. D. Factors make patients with CHD more prone to
During controlled ventilation, high positive haemorrhage
alveolar pressures can cause increased PVR and
decrease perfusion in some areas of the lung. 1. Patients with ACHD may exhibit a mild bleeding
tendency manifested by:
6. Lung volume – which also determines the calibre a. Easy bruising
ofthe vessels embedded in the lung parenchyma. b. Epistaxis
PVR is least at FRC. As the lung increases in c. Haemoptysis
volume, the vessels become narrowed and 2. This may become life threatening in the context of
elongated; as it decreases in volume, the vessels major surgery or trauma.
become tortuous. 3. Platelet counts tend to be in the low normal range
and their function is often abnormal.
7. Lung disease – both acute and chronic lung 4. In addition, patients may be taking anticoagulants
disease can result in significant increases in PVR. or antiplatelet agents to maintain shunt patency
Long­term increases in PVR due to chronic and there may also be associated abnormalities of
disease can lead to right­sided heart failure. the intrinsic and extrinsic clotting systems.
5. Conversely, patients with cyanosis may develop a

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 Cardiac anaesthesia

compensated erythrocytosis and although 2. Moderate/intermediate risk group

symptoms related to hyperviscosity are usually a. Patients with a previous history of
absent or mild, if the haematocrit is < 65­70%, the rheumatic fever
risk of venous thromboembolism is generally b. Patients with any other form of native
increased. valve disease (including: bicuspid aortic
6. The use of low molecular weight heparin valve, MVP and calcific aortic stenosis)
thromboprophylaxis, elastic stockings, and early c. Patients with unrepaired congenital
mobilization after surgery is essential. anomalies of the heart valves
3. High risk procedures group
a. All dental procedures that involve
E. The groups of patients that should receive antibiotic manipulation of the gingival tissue or the
prophylaxis against infective endocarditis periapical region of teeth or perforation
of the oral mucosa.
Groups of patients at risk of developing infective b. Procedures on respiratory tract or
endocarditis according to AHA guidelines are: infected skin, skin structures or
musculoskeletal tissue.
1. Highest risk group
a. Prosthetic cardiac valve or prosthetic
material used for valve repair Recommended Antibiotic regimen
b. Previous IE
c. Unrepaired cyanotic CHD, including 1. For those not allergic to penicillin:
palliative shunts and conduits Amoxicillin 2g oraly 30­60 mins before the
d. Completely repaired congenital heart procedure
defect with prosthetic material or device,
whether placed by surgery or catheter 2. For those allergic to penicillin:
intervention during the first 6 months Clindamycin 600mg orally 30­60 mins before the
after the procedure procedure
e. Repaired CHD with residual defects at
the site or adjacent to the site of a
prosthetic patch
f. Cardiac transplantation recipients who
develop valvulopathy

59 Revision Notes in Anaesthesia and ICU

Chapter 3

Comorbidities and anaesthesia

 Comorbidities and anaesthesia

__________________________________________________________________________________________________

A widely prevalent co­morbidities such as hypertension, diabetes, obesity, myocardial ischemia, thyroid, kidney and
liver disease are having special relevance to an anaesthetic plan. Sound knowledge of physiology is necessary for
understanding the pathophysiology of a diseases process, this together with knowledge of the effects of drugs and their
mechanisms of action will form an efficient guide to a safer management and events prediction specially in the intra, and
postoperative courses. It's also important to determine when to consult a speciality and what to request from the laboratory
or X­ray department.
In a study conducted by Eyelade O, et al. in Apr­Jun 2016, 165 adult patients aged between 18 and 84 years were studied.
Hypertension was the most common comorbidity in this cohort of patients. The number of patients submitted to major
surgery affected by one or more comorbidities is progressively increasing. Outcome is the final output measured as
postoperative morbidity, mortality and quality of life.
Strategies to improve outcome can be divided in some fundamental steps including preoperative evaluation and
optimization, no discontinuation of preoperative drug treatments specially in cardiac patient; choice of adequate
monitoring techniques, checking of patient metabolic state and oxidative balance; choice of the best anesthesia;
postoperative care, particularly due to identify the best management of the critical patient between the different levels of
assistance. In conclusion, a patient with comorbidities scheduled for major surgery needs a full anesthetist­intensivist
involvement, which broadens the role of the anaesthetist in the perioperative medicine. Outcome is the result of many
interventions during patient course, including economic costs and the importance of an appropriate treatment.

__________________________________________________________________________________________________

62 Revision Notes in Anaesthesia and ICU

To be issued Insha Allh in August 08-2018