Download Physiology – spinal anesthesia MGMC

Dr. S. Parthasarathy
MD., DA., DNB, MD (Acu), Dip. Diab. DCA, Dip.
Software statisticsPhD ( physiology)
Yes we inject local anesthetics into the
subarachnoid space
 Neural
 Cardiovascular
 Respiratory
 Thermal
 GI and hepatic
 Genitourinary
 Coagulation
Changes
Neural
 Local anesthetics block sodium channels to cause
stoppage of conduction
 Spinal rootlets
 SSEM from tibial nerve
blocked
But direct stimulation
the cord – evokes response !!
Neural
 Blockade of the anterior nerve root fibers result in
blockade of efferent motor and autonomic transmission.
 Neural blockade of posterior nerve root fibers results in
the blockade of somatic and visceral impulses.
 sympathetic


Partial parasympathetic-
↓
thoracolumbar
↓
cranio + sacral
Neural - - (differential blockade )
 Small nerves are blocked better
 Sympathetic 2 segments higher than sensory , two segments
higher than motor ( may be 6 also ?)
 Sensory level of T3 – complete sympathetic block
 Local anesthetic concentration – deciding factor
 Thickness , myelination also play roles
 Stimulate the nerve - more channels open – easily blocked
 ( frequency dependent blockade )
Differential block is due to
dilution of local
anesthetics
and
different sensitivity of
nerve fibres
Sedation with spinal
Inhibits ARAS – afferent input from lower limbs blocked and
hence the effect .
(Sedation not related to sedatives )
Think of epidural with GA !!
Decreased dose of sedatives by 30 %
CVS
 Level is below L1 –
 Vasodilation produces sympathetic response to




cause tachycardia !!
Try to maintain output –
T10 sensory is the level where the tilt is towards
hypotension
intrinsic chronotropic stretch receptor of the right
atrium and great veins which in turn decreases the
chronotropic and inotropic drive of heart,
( more blood rt. Atrium – stretch – tachy )
Reverse bainbridge !!
Cardiovascular effects
 Veno and arteriodilatation ( vasodilation )
 Venodilation predominates – 75 %blood

(less smooth muscle )
 Decreased preload and decreased cardiac output
 Arteriodilation – decreased afterload !! But
overall hypotension and decreased cardiac output
 T1 to T4 – cardio accelerator fibres - bradycardia
Combined injection of alpha and beta
blocker
Hypotension incidence is 33 % in non obstetric
 Blockade of splanchnic veins – (T6 to L1) – main
cause
 Sympathetic innervation more in viscera than
limb veins
 Only caudal and lumbar level – venous pooling
less
CVS
 SVR 15 – 18 % reduction - 25 % in old patients
 BP
26 % ----- 32 %
↓
↓
Cerebral
 CBF 12 % ---- 19 % fall. autoregulation works
if the hypotension is
 Clinically insignificant !!
gradual .. 55 – 140 MAP
But LSCS – spinal level
T4
Compress the IVC –
suddenness – auto
regulation ??
BP fall – more ???
 Old age , higher injection site , high level
 the use of head-up posture
 any degree of hypovolaemia – pre-existing or induced
by surgery
 administration of sedatives, opioids.
 induction agents
 positive pressure ventilation.
Some abstracts ??
 Rennin may not increase but Arginine vasopressin
increase after spinal
 Reverse with SNP infusion
 Do these systems complement each other to prevent
hypo ??
 Acute infusion of ACE inhibitors and spinal –
hypotension is more severe
 Chronic intake of ACE inhibitors and spinal – not so –
may continue the drug – says newer studies
Balance is better
 MAP falls – coronary pressure falls -
 Myocardial oxygen supply falls but brady is ok during
earlier tachy ??
 Preload, afterload and heart rate decrease – no
danger
Heart rate (around 13 % incidence ) – non
obstetric
 Increased with low levels
 Decrease with high level
 – cardio accelerator fibers
blocked
 Unopposed vagus
Risks of hypo and
brady are inverse !!
Risks
Young age
ASA I
Beta blocked
Level above T5
Prolonged PR
interval
Basal rate < 60
 Resting sympathetic tone - ↑ - old age
 Resting parasympathetic tone - ↑ -young
age
In a nutshell
Redistributive hypovolumia
and paradoxical bradycardia
Respiratory effects – more with high levels
Parameter
Effect
lung volumes
↓ 5%
VC , FVC , FEV1
( ERV ↓ )
FEV1/FVC
→
TV
→
PEFR
↓
ABG
→
Ventilatory response to hypoxemia and
CO2
→
Bronchial tone
→
sympath/parasympath imbalance
Still no change
→ no change ,
↓ decrease
Respiratory changes
 A rare respiratory arrest associated with spinal
anesthesia is also unrelated to phrenic or
inspiratory
dysfunction
but
rather
to
hypoperfusion of the respiratory centers in the
brainstem -- HOW DO WE KNOW !!
 As soon as we resusucitate, the breathing is
normal to establish – no phrenic palsy !!
In what you think as high spinal ??
 Allow to breathe spontaneous
 The character of spontaneous ventilation is a guide to
medullary blood flow
 Not advisable to control
 IPPV decreases venous return and cardiac output
Respiratory changes
 Except for severely compromised patients with
respiratory failure, inspiratory muscle function during
neuraxial blocks should be adequate to maintain
ventilatory function
Respiratory cripples
 Its not inspiratory – but expiratory we are concerned
for cough out secretions
Thoracic surgeries
 Decreased phrenic nerve activity
 Decreased diaphragmatic activity
 Decreased FRC (functional residual capacity)
 Atelectasis & hypoxia due to V/Q
(ventilation/perfusion) mismatch
 Regional decreases !!
Respiratory system
 Patients with high spinal or epidural blocks may complain
of dyspnea despite normal or elevated minute ventilation.
 This likely results from the patient's inability to feel the
chest wall move while breathing
 Blow to the their own hands to diagnose
 Check BP – reassure
Does spinal do anything ??

Surgery
↓
 Local and systemic endocrine, metabolic
and immune responses
Stress response
Surgery increase the following
 adrenocorticotropic hormone
 cortisol
 epinephrine
Spinal blunts the
increase
 norepinephrine
 vasopressin
 activation of the renin-angiotension-aldosterone
system
 Growth hormone
Insulin and glucagon
spinal ?
What does spinal do ??
parameter
Response
Glucose
↓
Ketones
↓
Lactate
↓
FFA and glycerol
↓
Insulin clearance
↓
Nitrogen balance
?
Oxygen consumption
? Decreased met.
Acute phase reactants
→
Catabolic
↓
anabolic
Gastrointestinal Effects
 Unopposed parasympathetic
 Gastric hyperperistalsis
 Nausea and vomiting
 Atropine !! – think of hypo
 Intestine peristalsis – normal
Contracted gut –
Non gut surgeries
easy !!
Obstructed hernia –
can we do ??
but sphincters relax
 Better pH in stomach
 Hepatic dysfunction not as in GA if MAP is
maintained
Renal Effects
 Neuraxial blockade has little effect on the blood flow
to the renal system.
 Auto regulation maintains adequate blood flow to the
kidneys as long as perfusion pressure is maintained.
 urinary retention, causing delayed patient discharge
from the hospital and frequent catheterization.
Bladder functions
 After the induction of spinal anaesthesia, the urge
to void (normal detrusor function) is abolished
within 60 seconds.
 Recovery does not return until sensory anaesthesia
has regressed to the S3 sacral segment.
 After lignocaine – 235 minutes
 After bupivacaine – 462 minutes
 S3 thin nerve ?? – lot of IV fluids ??
Spinal in already kidney dysfunction
 Maintain MAP
 Less blood loss
 No major fluid shifts
 No ileus
 Then it does not alter
Thermoregulation
 Core hypothermia with spinal anaesthesia develops
primarily from a re-distribution of heat from core
tissues, which are well-perfused tissues such as the
head and trunk, to the peripheral tissues, or arms and
legs.
 Do we monitor temperature in spinals ??
Thermal
 decrease 0.8 degrees centi.
 Tonic vasoconstriction gone
 Threshold set aside
 So muscle contraction is the main compensation
 So shivering – drugs
 Warm air rewarming – faster recovery to normal
because of vasodilation and thermal transfer than GA
Coagulation effects
 Postoperative hypercoagulability is a known problem
 Neuraxial anestheisia modifies as such – virchow triad
 Blood flow better and concentration of clotting factors
are less .
 Platelet count – no effect – but platelet inhibition by
spinal .
 Blood loss decreased by 30 % in major surgeries with
spinal ( THR and prostate )
 The tone is the cause ??
Summary
 Neural – rootlets , sedation (ARAS)
 CVS – BP, SVR, venous return , HR
 RS – PEFR FVC
 Endocrine
 Thermal – hypothermia
 Renal – blood flow ok but bladder dysfunction
 GI – hyperperistalsis, nausea , liver
 Coagulation
Thank you all