PHYSIOLOGY OF SPINAL ANAESTHESIA.pptx

pugalrockzz1 1,207 views 68 slides Jul 11, 2023
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About This Presentation

Spinal anaesthesia


Slide Content

Physiology of nerve fibers Mechanism of action Systemic effects Types of spinal anesthesia Monitoring of blockade Factors affecting spinal anesthesia Overview

Neurons are basic elements of all rapid signal processing within the body Afferent nerve fiber: transmit impulse from peripheral receptors to CNS Efferent nerve fiber: CNS to periphery Physiology of nerve fibers

On the basis of :fiber DM and velocity of conduction (larger DM larger conduction) Type A ,B ,C Type A further divided into α / β / γ / δ Classification of afferent fibers

Type A- α 1a innervate muscle spindle Type A- α 1b innervate Golgi tendon organ both A- α afferents are important for muscle reflex and muscle tone control ( Proprioception ) Type A- β transmit touch nd pressure signal from cutaneous mechanoreceptors( meisners nd pacinian corpuscles ) Type A- γ for skeletal muscle tone Type A- δ Transmit touch and fast pain and temperature(warm) From free nerve ending

Type B are autonomic preganglionic sympathetic fibers Type C transmit slow pain and temperature(cold) , Postganglionic sympathetic fibers

Type A &B are myelinated and Type C unmyelinated Order of Dm and velocity A>B > C Sensory information from the somatic segments of the body enters the spinal cord through the dorsal roots of the spinal nerves

Spinal Anesthesia in which the injection of small amounts of local anesthetics into the subarachnoid space (CSF) at the level below (L2),where the spinal cord ends, anesthesia of the lower body part below the umbilicus is achieved

Pharmacokinetics :is what the body does to a drug , absorption ,distribution , metabolism,elimination Pharmacodynamics : is what the drug does to the body

Large length of the nerve roots and nerves are bathed in CSF Rootlets, anterior and posterior spinal root nerves and periphery of spinal cord Less drug diffuse into DRG and centre of spinal cord Spinal anesthesia is achieved with a small dose and volume of LA resulting in dense sensory and motor block. Site of action of LA

Lipophilic drugs act at whiter mater ( amides & ester ) Hydrophilic drugs act at grey mater ( quat . Ammonium derivative of lidocaine ) Clonidine induces hyperpolarization at the ventral horn of the spinal cord Receptor for adenosine and potassium channel openers are also demonstrated. Site of action of other drugs

Blockage of the anterior nerve root fibers result in blockage of efferent fibers(somatic and autonomic fibers ) Blockade of posterior nerve root fibers result in blockade of sensory and visceral impulses

Speed of blockade depends on size,surface area&degree of myelination of nerve fiber Smaller nerves more sensitive to LA(high surface area) less myelination more sensitive Concentration of LA highest at point of injection , then LA travels away by diluted with CSF

Small preganglionic sympathetic - B FIBER Type C fibers ( cold,slow pain) type A δ (fast pain) type A β fibers(touch) larger A α fiber last(motor ) regression in reverse order motor first

Relative sensitivity to the effect of LA on nerve fibers observed in block of height is called differential blockade ie sympathetic blockade is 2-6 dermatome segment higher than sensory(order of more cephalad -cold -pinprick-touch ) Sensory is 2 dermatome higher than motor Differential blockade

Anatomic and geometric arrangement of individual fibers in a nerve bundle DM of nerve fibers Difference in firing rate of fibers Variability in longitudinal spread of LA Effects of ion channel Choice of LA Reasons for diffrential blockade

Drug in CSF diffuse through pia mater & penetrate through space of virchow robin (extension of subarachnoid space accompanying blood vessels that invaginate spinal cord from pia mater )to reach DRG Portion of drug diffuse outward through arachnoid and dura mater Some taken up by blood vessels of pia and dura DRUG ABSORPTION

Primary mechanism :diffusion of drug from high concentration to low Elimination Depends on nonneural tissue uptake (vascular) Time for regression inversely correlated with csf volume Greater spread of drug expose to larger vascular absorption so short duration of action Lipid soluble LA bind to epidural fat to form depot , so slow vascular absorption Distribution

sympathetic nervous system (SNS) is described as thoracolumbar since sympathetic fibers exit the spinal cord from T1 to L2. ( cardioaccelator fibers are T1 to T4 ) Main neurotransmiter is norepinephrin and adrenal medulla secrete epinephrine in sympathetic stimulation The parasympathetic nervous system (PNS) has been described as craniosacral since parasympathetic fibers exit in the cranial and sacral regions of the CNS. Autonomic blockade

Sympathetic fibers are small, myelinated, and easily blocked. During neuraxial blockade, sympathetic block occur prior to sensory, followed by motor. End result of neuraxial blockade is a decreased sympathetic and somatic (sensory and motor) with an unopposed parasympathetic tone & compensatory reflexes

Neuraxial blockade can impact the cardiovascular system by causing the following changes: Decrease in blood pressure (33% incidence of hypotension in non-obstetric populations) Decrease in heart rate (13% incidence of bradycardia in non-obstetric populations ) Decrease in stroke volume Decrease in cardiac contractility Cardiovascular effects

Cardiac receptors are liked to CNS through vagus and glossopharyngeal nerve Cardiac receptors are in atria , ventricle ,pericardium , coronary arteries, great vessels and carotid arteries Cardiac reflexes

Baroreceptor reflex (carotid sinus reflex ) Chemoreceptor reflex Bainbridge reflex Bezold-jarisch reflex Cushing reflex Oculocardiac reflex

Its responsible for acute maintenance of blood pressure It’s a negative feedback mechanism Receptors are located in carotid sinus and aortic arch Afferents are glossopharyngeal and vagus nerves Central control by nucleus tractus solitarius located in medulla Cardiovascular center in medulla consists of two areas, areas for increasing BP and decreasing BP When SBP is high , decreased sympathetic activity and thus decrease HR ,contractility and vascular tone and also activation of PNS Baroreceptor reflex

Chemosensitive cells are located in the carotid bodies and aortic bodies They are sensitive to PH , PaO2 , pCO2 paO2 less than 50 mmhg or in acidosis send signal to medulla through 9 th or 10 th CN Chemosensitive area in medulla stimulating respiratory centers and increase ventilatory drive Chemoreceptor reflex

Its elicited by stretch receptors in right atria and cavoatrial junction Increase in right sided filling pressure send vagal afferent signal to cvs centre in medulla Which inhibit parasympathetic activty so HR increase and increase CO Bainbridge reflex

Indirect effects:- Bain bridge reflex predominates during spinal anaesthesia : venous pooling in the periphery reduces stimulation of volume receptors - diminishes the action of cardiac sympathetic nerves- vagal preponderance - bradycardia Oxygen consumption is reduced due to hypotension and muscle relaxation Bain bridge reflex

Its responds to noxious ventricular stimuli It’s a cardioprotective reflex Receptors: Chemoreceptors and mechanoreceptors on the left ventricular wall in severe hypotension receptors are activated send signal through vagus to stimulate parasymapthetic activity and mainatain cardiac blood flow by bradycardia ,coronary artery dilatation and hypotension Bezold-jarisch reflex

Triad of hypertension , bradycardia, irregular breathing Marey's law : baroreceptors in the carotid sinus and the aortic arch normally respond to a fall in blood pressure by producing a compensatory tachycardia Cushing reflex

Sympathectomy results in Venous dilatation and arteriolar dilatation The venous system contains about 75% of the total blood volume while the arterial system contains about 25%.and the arterial system is able to maintain much of its vascular tone. So venodilation is predominate Reduce preload and afterload Reduce stroke volume Result in hypotension Cardiac output is slightly reduced or maintained Stroke volume

Vasodilatory changes depends on patient baseline sympathetic tone High sympathetic tone in elderly so affects more Total peripheral vascular resistance in the normal patient (normal cardiac output and normovolemic ) will decrease 15-18 %. In the elderly the systemic vascular resistance may decrease as much as 25% with a 10% decrease in cardiac output.

Heart rate may decrease in high neuraxial block due to blockade of cardioaccelerator fibers arising from T1-T4 Extensive sympathectomy in T5-L2 and reduction in venous return and right atrial filling causes increase in parasympathetic activity( revers bainbridge reflex) will reduce HR but hypotension causes baroreceptor sympathtic response above the level of blockade So two opposing responses are result in minimal change in HR in T5-L2 blockade Heart rate

If it extends to T1 level ,result in blockade of cardioaccelerator fibers , in addition to marked hypotension ( bezold-jarisch reflex) and unopposed parasympathetic stimulation are all causes severe bradycardia and asystole So spinal anesthesia in presence of hypovolemia may leads to circulatory collapse

Baseline HR <60 High ASA grade Use of beta blockers Sensory level above T6 Age <50yrs Prolonged PR interval Risk factors for bradycardia

Decrease in coronary blood flow from 153 to 74ml/100gm/ mnt Decrease in MAP 119 to 62 mmhg Percent of extraction of myocardial oxygen remain unchanged Coronary blood flow

Hypotension may decreases regional cerebral blood flow (CBF)especially in elderly and hypertensive patients Central nervous system

Neuraxial blockade plays a very minor role in altering pulmonary function Even with high thoracic levels of blockade, tidal volume is unchanged Vital capacity decreases by small amount due to paralysis of abdominal muscle required for forced exhalation Respiratory system

phrenic nerve is innervated by C3-C5 and is responsible for the diaphragm. phrenic nerve is extremely hard to block, even with a high spinal Blockade of abdominal and intercostal muscle is compensated by diapragm and accessory muscle Precaution should taken in respiratory diseased patients , pregnancy and obese Respiratory arrest may happen if hypoperfusion of brainstem

Changes are due to sympathetic blockade and compensatory vagal parasympathetic activation GI hyper peristalsis Contracted gut –it helps excellent surgical condition Hepatic blood flow decreased Gastrointestinal

Neuraxial blockade has little effect on the blood flow to the renal system. Autoregulation maintains adequate blood flow to the kidneys as long as perfusion pressure is maintained. Neuraxial blockade effectively blocks sympathetic and parasympathetic control of the bladder at the lumbar and sacral le v els . Renal effects

Urinary retention can occur due to the loss of autonomic bladder control. Detrusor function of the bladder is blocked by local anesthetics .

Peripheral vasodilatation results in fall in core temperature results in nonbehavioral shivering response Behavioral responses like try to cover body or going to universal flexion are not seen due to somatic blockade Effect on temperature

Continuous spinal anesthesia Unilateral spinal anesthesia Selective spinal anesthesia Special spinal techniques

It allows incremental dosing of local anesthetic and predictable titration of block to an appropriate level It have better hemodynamic stability than single shot spinal Used in severe AS , pregnant women with heart disease or morbid obese, Continuous spinal anesthesia

Needle with laterally facing opening is preferred ( hustead or tuohy needle) Catheter is inserted and threaded 2-3 cm into subarachnoid space

Unilateral spinal anesthesia & Selective spinal anesthesia Both are small dose technique Depends on baricity and patient positioning U/L used in knee arthroscopy , unilateral inguinal hernia In selective spinal anesthetizing only sensory fibers to a specific area

For assesing sympethetic blockade : use HR and blood pressure For sensory : cold sensation(c-fibers) and pinprick sensation (A delta fibers) are used more than mechanical stimuli like touch , pressure(A beta fibers ) Loss of sensation to cold occurs first & verified using ice, ethyl chloride spray ,or alcohol Followed by loss of pinprick &verified using a needle Block monitoring

Dermatomal level, most cephalad is cold then pinprick,then touch For motor block : modified bromage scale is used No motor block 1 inability to raise extended leg ; able to move knees and feet 2 inability to raise extended leg and move knee; able to move feet 3 complete block of motor limb

Dermatomal level of peritoneum is T4 bladder is T10 uterus is T10 Skin incision for these structures are more down as compared to spinal segment

Upper abdominal surgery : T4 Cesarean delivery :T4 TURP: T10 Hip surgry :T10 Foot and ankle surgery :L2 Dermatomal levels

Drug factors Patient factors Procedural factors Factors affecting spinal anesthesia

Dose Volume Concentration Temperature Baricity Drug factors

It is the ratio of density of local anesthetic solution to the density of CSF Density: is mass per unit volume (gm/ml )of solution at specific temperature Density varies inversely with temperature specific gravity : ratio of density of a solution to the density of water No units for baricity and s.gravity Baricity

Density of csf : 1.00059g/L ISOBARIC: LA have same density as csf HYPERBARIC :LA have more denser than csf HYPOBARIC:LA have lower density than csf To make hyperbaric add dextrose to LA To make hypobaric add sterile water to LA

Hyperbaric drug spread to dependent region of spinal canal Hypobaric : nondependent part Isobaric not influenced by gravity and it settle at the site of infiltration Hyperbaric drug in lateral decubitus position settle on dependent side

Patient in sitting position, hyperbaric drug inject into L3-L4/L4-L5 spaces and immediately kept in supine or lateral position drug will rapidly spread to thoracic kyphosis and sacral kyphosis If patient kept in sitting position more sacral fibers are involved so saddle anesthesia for perineal surgeries If patient into lithotomy position lumarlordosis disappear so drug spread cephalad If hypobaric drug injected in sitting position drug will go cephalad Isobaric gives segmental block

More reliable determinent is dose of drug Dose = volume * concentration

CSF volume Advanced age Pregnancy Weight Height(length of lower limb bone more important for height than vertebral column so less important for spread of drug) Spinal anatomy Intra abdominal pressure Menopause Gender Patient factors

CSF volume and spread of LA is inversely related In obese and pregnancy increased abdominal mass and epidural fat ,may decrease csf volume so increase spread Csf density varies with sex ,menopausal status,pregnancy In elderly csf volume decreased and nerve roots more sensitive so more spread

Gender csf is denser in men so reducing baricity of LA so less cephalad spread in lateral position broader shoulders of males relative to hip helps more headup Spinal anatomy : kyphosis more spread scoliosis less changes Pregnancy loss of lumbar lordosis , less volume of csf , progestron mediated neuronal sesitivity increases spread

Patient position Epidural injection post spinal Level of injection Fluid currents Needle orifice direction Needle type Procedural factors

Position should not be affect truly isobaric drug Spreading of drug stop within 20-25 mnts so positioning is important 10 degree headup reduce the spread Trendelenberg position increase spread (loss of lordosis ) Sitting position helps in saddle block

Cephalad orifice of needle tip increase spread More Unilateral block achieved if orifice on one side Injection rate and barbotage (repeated aspiration and reinjection) not affect Slower injection prevent leakage and also increase spread Injection of saline or LA into epidural space after spinal increase the block height
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