CVT / Veterinary Technician Feature Article

Principles of Anesthesia

By:  Valerie Johnson, DVM, ACVECC resident
Animal Emergency & Critical Care Center
The following is a lecture outline discussing the basic principles of small animal anesthesia.  As veterinary technicians, it is critical for you to understand basic anesthetic concepts- especially when you are given the responsibility of administering anesthesia and monitoring your veterinary patients during surgical procedures.  The goal of....     If you have any questions, please feel free to Email our hospital at ce@neamc.com.

Stages of Anesthesia

Stage I - Stage of voluntary movement

Encompasses period of time from initial administration of anesthesia to loss of consciousness Increased HR, pupil dilation, ataxia, recumbency, salivation, increased jaw tone, increased blood pressure Eyeball position normal, palpebral reflex present

Stage II - Stage of delirium and involuntary movement

From loss of consciousness to onset of regular pattern of breathing Increased HR, struggling, breath holding or tachypnea, increased blood pressure, increased jaw tone, laryngospasm in cats Dilated pupils, variable eye position

Stage III - Stage of surgical anesthesia

Unconsciousness with progressive depression of reflexes, divided into 3 planes

Light Plane - considered light until eye movement ceases Medium Plane - stable respiration and pulse, sluggish palpebral reflex, strong corneal reflex Deep Plane - decreased tidal volume, increased respiratory rate, central pupil, palpebral and corneal reflex absent, PLRs not present, progressive bradycardia and hypotension, as progresses closer to Stage IV patient loses diaphragmatic function and can become cyanotic

Stage IV - Dangerous for patient- high risk of anesthetic death.

CNS extremely depressed, respiration ceases, severely decreased blood pressure, anal and bladder sphincters relaxed Pupils dilated, palpebral and corneal reflexes absent

Preanesthetic Medications

Anticholinergics

Atropine

decreased secretions- oral, pharyngeal and respiratory secretions dilate bronchi - causes increased respiratory dead space decreased motor and secretory activity in GI tract suppresses vagal influence on heart minimal effect on blood pressure at normal preanesthetic doses dilates pupils (relaxes sphincter muscle of iris) suppresses muscarinic action of anticholinesterase (used to reverse nondepolarizing muscle relaxants) if given IV may initially increase vagal tone increases incidence of cardiac arrhythmias and sinus tachycardia (most common arrhythmia prior to induction of anesthesia if 2nd degree AV block, most common arrhythmia after induction of anesthesia is VPCs and ventricular bigeminy) contraindicated if preexisting tachycardia cleared from blood quickly in dogs and excreted unchanged in urine, cats clear via atropine esterase in liver

Glycopyrrolate

physiologic effects similar to atropine but longer duration of action vagal inhibition lasts 2-3 hours, antisialagogue effects can last up to 7 hours

Tranquilizers

Acepromazine (Promace®)

phenothiazine derivative - blocks post synaptic dopamine receptors in CNS, may inhibit release of and increased turnover rate of dopamine, thought to depress portions of the RAS in brain (responsible for control of temperature, basal metabolic rate, emesis, vasomotor tone, hormonal balance, and alertness) decreases arterial blood pressure hypothermia decreased seizure threshold? antiemetic prevents or decreases the severity of malignant hyperthermia

Diazepam  (Valium®)

Benzodiazepine - acts on benzodiazepine receptor in CNS - causes increase in inhibitory neurotransmitter glycine in spine (muscle relaxation effects), sedation and anticonvulsant effects mediated by GABA minimal respiratory and cardiac depression low toxicity overdose treated with flumazenil ( 1 part flumazenil to 13 parts diazepam)

Midazolam

also benzodiazepine- physiological effects similar to diazepam shorter duration of action, water soluble (nonirritating)

Opioids- Receptors - mu, kappa, sigma, delta

Mu - supraspinal analgesia, respiratory depression, euphoria, physical dependence Kappa - spinal analgesia, miosis, sedation, dysphoria Sigma - psychomimetic activity, hallucinations, respiratory and vasomotor stimulation Delta - modifies mu activity

Mu  Kappa Morphine agonist agonist Naloxone  antagonist   antagonist Butorphanol   partial agonist  partial agonist Buprenorphine partial agonist antagonist?

Morphine

increased seritonin synthesis - causes analgesia decreases medullary respiratory, cough and vasomotor center activity stimulates medullary vomiting center decreases basal metabolic rate - decreases body temp 1° to 3° F respiratory depression - decreases respiratory minute volume, increases alveolar CO2  no significant myocardial depression can cause histamine release, peripheral vasodilation, bradycardia, incresease in ADH release (can decrease urine production up to 90%) stimulates sphincters of GI tract - can cause constipation but increased peristalsis combats this effect can cause excitation in cats miosis metabolized by liver

Oxymorphone- mu opiate agonist

10x more potent than morphine induces more sedation and less hypnosis little respiratory and cough suppression

Fentanyl- mu opiate agonist

250 x more potent than morphine analgesia, sedation, respiratory depression and exaggerated response to loud noises short duration of action but respiratory depression can last for several hours can have respiratory depression, apnea of panting usually does not cause vomiting causes vagal mediated bradycardia but has little effect on cardiac output or blood pressure unless given with barbiturates (can cause hypotension if given with barbiturates) transdermal patches - significant variability in time to achieve therapeutic levels and levels themselves, cats achieve therapeutic levels faster (usually in about 6 hours),  duration of action persists for 72-104 hours (3-5 days), duration of action generally longer in cats than dogs

Butorphanol  (Torbugesic®)

mixed agonist/antagonist less respiratory depressant effects no change in bile flow (morphine decreases bile flow) no change in histamine excreted in urine (small amt excreted in bile)

Buprenorphine  (Buprenex®)

partial agonist/antagonist 30x more potent than morphine respiratory depression lasts 6-8 hours

Alpha-Adrenergic Agonists

Anxiolysis Sedation Sympatholytic Easily reversed by antagonists No profound respiratory depression Some analgesic effect Contraindicated if cardiac or pulmonary disease due to myocardial depression and pulmonary hypertension Duration of analgesia is about half the duration of sedation

Xylazine  (Rompum®)

cardiac depressant effects arrhythmogenic (AV block) when given IV causes bradycardia followed by 5-10 minutes of hypertension followed by longer periods of decreased cardiac output and hypotension decreases heart rate by increasing vagal tone decreases respiratory rate but increases tidal volume duration of sedation approx 30-40 minutes, duration of analgesia 15-20 min frequently causes vomiting, decreases GI motility and prolongs gastric emptying time may inhibit platelet aggregation

Medetomidine  (Domitor®)

more selective for alpha-2 receptors duration 2-3 times xylazine - sedation 60-90 min with analgesia for 30-45 min dose 10ug-30ug produces sedation and analgesia, cats often need larger dose for comparable sedation effects similar to xylazine, however hypertension often persists and may not be followed by hypotensive period

Injectable Anesthetics

Barbiturates

classified according to duration of action mechanism of action- barbiturates act on CNS neurons in a manner similar to GABA - cause depression of the CNS by interference with passage of impulses to the cerebral cortex metabolized by kidney and biotransformation in the liver, the short acting barbiturates (pentobarbital, amobarbital and secobarbital) are primarilty metabolized by the liver all highly protein bound - change in blood pH can affect anesthetic depth - acidosis causes increased depth, alkalosis causes dissociation and therefore decreases anesthetic depth (only undissociated form can penetrate cell membranes)

Pentobarbital

Subanesthetic doses can cause hyperexcitability Cardiovascular effects - decreases BP, CVP, PaO2, pH, body temp and stroke volume Respiratory effects - respiratory depression Deep anesthesia depresses renal blood flow and urine flow by circulatory depression and reflex vasoconstriction, stimulates release of ADH Leukocyte counts decrease by 20% with pentobarbital anesthesia Red blood cell numbers and Hct decrease - may be due to splenic dilation (oral administration does not affect blood values of RBCs or WBCs) Pentobarb freely crosses the placental barrier (high mortality of neonates if used for C-section) Complete recovery from anesthetic effects takes 6-18 hours and may be prolonged in cats (24-72 hours)

Methohexital

Ultrashort acting barbiturate - short action due to redistribution Overdose causes temporary apnea - lethal dose is 2.5 times median anesthetic dose

Thiopental Sodium (Pentothal®)

Main excretion via urine and liver, high fat levels in blood bind drug and cause decreased duration of action Causes marked depression of respiratory centers Five minutes after administration heart rate, aortic pressure, PVR and left ventricular systolic and end diastolic pressures increase - arrhythmias are common - bigeminy, extrasystole, V tach, V fib Prolonged anesthesia with  thiopentothal causes pronounced hyperglycemia, lactic acid and amino acids in blood and decreased liver glycogen

Nonbarbiturates

Etomidate

Imidazole derivative single injection produces brief anesthesia No depression of cardiovascular or respiratory systems, causes minimal respiratory depression in neonates in utero  Decreases cerebral metabolic rate of oxygen consumption and has anticonvulsant properties (may be brain-protective) Causes depression in adrenal function for up to 3 hours following single injection can cause addisonian crisis with prolonged infusion Stored in propylene glycol - can cause acute hemolysis Can cause nausea, vomiting with multiple doses

Propofol

Nonbarbiturate sedative/hypnotic Limited solubility in aqueous solution, formulated in emulsion Preparations support bacterial growth – should be discarded 6 hours after opening vial No excitement phase with induction and so can be used for sedation, induction or maintenance as a CRI Metabolized by redistribution, cytochrome P450 enzymes in liver and elsewhere and glucoronidation in liver, drugs affecting cyt P450 will prolong propofol anesthesia Minimal change in HR, causes vasodilation and can induce hypotension which does not trigger a reflex increase in HR, arrhythmias uncommon Respiratory depression and apnea most common adverse effect, caused by reduction in TV and RR with depression of hypoxic drive, rapid administration of drug more likely to cause apnea In people most common adverse event is pain on injection, not as commonly noted in veterinary patients Safe to use with increased intracranial pressure, liver disease, kidney disease

Contraindications to propofol use

moderate to severe cardiac disease hypovolemia hypotension cats that are anemic epilepsy or hx of seizures

Adverse effects associated with propofol use

Excitatory effects – occasionally see myoclonus, twitching, opisthotonous, unsure if this activity is a form of a seizure Pancreatitis – increase in FFA and TG levels after propofol administration, anecdotal reports of pancreatitis following propofol administration Heinz body anemia in cats, cats show prolonged recovery after propofol anesthesia if used daily for procedures lasting longer than 30 minutes (this effect was not seen with daily doses of propofol given only as an induction injection)

Dissociatives

Dissociative anesthetic agents induce and anesthetic state by interruption of ascending transmission from the unconscious to conscious parts of the brain rather than by generalized depression of all brain centers varying degrees of hypertonus and purposeful or reflexive movement of skeletal muscle occur unrelated to surgical stimulation eyes remain open with nystagmic gaze analgesia is intense but of short duration – greater analgesia for somatic pain than for visceral pain

Ketamine

CNS effects – significant increase in cerebral blood flow, intracranial pressure and cerebrospinal fluid as a  result of cerebral vasodilation and elevated systemic blood pressure Hallucinations may occur during emergence from ketamine anesthesia Premedication with acepromazine, xylazine or benzodiazepine may decrease incidence of adverse reaction CV effects – sympathomimetic effects – increased HR and arterial BP, Mean arterial pressure, HR, cardiac outpout increase while peripheral vascular resistance remains unchanged – causes increased cardiac work and myocardial oxygen demand – effects blunted by premedication and concurrent gas anesthesia Resp effects – Unlike most anesthetics ketamine does not depress the ventilatory responses to hypoxia, with higher doses transient apnea and shallow breathing can be seen, - can cause increased salivatin and respiratory mucous production -  can be prevented with anticholinergic Ketamine metabolized by the liver in dog and human, in cat mostly metabolized by kidney Mild increase in intraocular pressure

Telazol

Tiletamine with zolazepam – tiletamine has a longer duration of action and greater analgesic effect than ketamine effective in producing general anesthesia in cats and primates, inconsistent response in dogs and other species  causes seizure activity at higher doses causes tachycardia and hypertension, minimal respiratory signs expect at high doses (apnea, shallow breathing)

Inhalational Anesthetics

Isoflurane- most popular anesthetic gas used Sevoflurane- newest agent, most expensive, rapid induction & recovery Halothane- older agent, used primarily in large animal practice

MAC = minimal alveolar concentration of an anesthetic gas required to keep a dog from gross movement in response to painful stimuli

Increased catecholamines increase MAC, decreased catecholamines decrease MAC Hypothermia decreases MAC, hyperthermia increases MAC Premedication decreases MAC

Inhalational anesthetic induction and elimination

Anesthesia is taken into the alveoli and then equilibrates with the blood in a manner similar to O2 and CO2, anesthetic agent is then taken up by the tissues until equilibrium is reached between the blood and tissues, when venous blood returning to the lungs has the same amount of anesthetic as the alveoli the blood will not take up more anesthetic (at equilibrium) Induction of anesthesia depends on alveolar ventilation, cardiac output and solubility of the gas Elimination occurs via the same route,  to recover from anesthesia, concentrations in the brain have to decrease, with no anesthesia entering the alveoli, anesthetic goes from the higher concentration in the blood to the lower concentration in the alveoli Duration of anesthesia affects recovery – longer duration prolongs recovery

Effects of anesthetic gas on organ systems

Cardiovascular

inhalant anesthetics all decrease cardiac output due to a decrease in stroke volume from depression of myocardial contractility Isoflurane is least depressant to cardiac output Heart rate is variable but generally normal to increased Blood pressure is decreased in a dose dependent fashion Myocardium is sensitized to arrhythmogenic effects of catecholamines – halothane most arrhythmogenic, isoflurane and sevoflurane least arrhythmogenic

Kidneys

decrease renal blood flow and glomerular filtration in a dose dependent fashion reduction in renal function highly dependent on animal’s state of hydration and hemodynamics during surgery

Liver

depression of hepatic function and hepatocellular damage may be caused by any of the inhalant anesthetics decreased clearance of drugs from the liver occurs during anesthesia due to decreased blood flow through the liver as well as decreased intrinsic clearance  isoflurane least likely to cause liver damage due to less compromise of cardiac output and therefore better tissue oxygenation

Skeletal Muscle

Malignant Hyperthermia can occur in susceptible patients

Anesthetic Machines

Vaporizers- Convert liquid anesthetic to gas, picked up by carrier gas (oxygen) and delivered to patient,  increased flow of carrier gas (oxygen) increases anesthetic delivery to patient Each agent has its own type of vaporizer- ie isoflurane can not be used in a vaporizer designed for halothane or sevoflurane.

Breathing Systems

Rebreathing systems – exhaled gas flows back to patient after removal of CO2 – conserves oxygen, anesthetic gas, heat and moisture Tubing – pediatric if <15#,  Adult if >15# Exhaled gas flows through one way valve- goes through reservoir bag and CO2 absorbent canister then through inspiratory valve and tube, Pop off valve vents gas to scavenger system – prevents buildup of excess pressure Semiclosed systems– fresh gas inflow exceeds uptake of oxygen and anesthetic by patient    **gas flow is set at  2-4 times patient’s tidal volume** Nonrebreathing systems – animals <8#, incorrect terminology – some rebreathing of exhaled gases occurs especially  at low flow rates,  fresh gas goes to patient and is exhaled through the reservoir bag and not recycled

Signs of Inhalational Anesthesia

Respiratory

increased RR +/- breath holding in stage I irregular respiration and breath holding in stage II  regular breathing that depends on threshold of stimulation in stage III as anesthesia progresses through stage III intercostals muscles weaken and thoracic movement decreases, breathing becomes abdominal - abdomen bulges while thorax collapses during inspiration, reverse occurs during expiration, after abdominal breathing respiration will cease with further increase in anesthetic depth

Circulation

stage I and stage II – pulses are strong and accelerated as anesthesia increases blood pressure decreases and pulses weaken

Ocular

ocular signs can be variable – circulatory and respiratory signs more reliable during light and medium anesthesia eyeballs turn downwards and 3rd eyelids come up pupils become dilated during stage II then become constricted (this varies with premedication such as atropine or opiates) with deep anesthesia or overdose pupils become dilated and unresponsive palpebral reflex is  lost on transition from light to medium anesthesia, corneal reflex is lost shortly thereafter

Pharyngeal Reflex

increased muscle tone during Stage II then progressively declines lose resistance to opening mouth fully during medium anesthesia

Factors affecting Anesthesia

Age

Very young animals have limited muscles and fat to which anesthesia can be redistributed Very old animals can have decreased cardiac, hepatic and renal function

Breed

Brachycephalic dogs – enlarged soft palate, restricted respiratory passages-avoid prolonged anesthetic recovery (use quick acting anesthetics), leave ET tube in as long as possible Sighthounds – greyhound, borzoi, afghan etc. – complications include: hypothermia from low body fat malignant hyperthermia impaired biotransformation of drugs in liver causes prolonged recovery especially from thiobarbiturates recommended drugs include propofol, ket/val, methohexital

Changes in clearance of anesthetic

Liver and kidney - has the most effect if liver or kidney extracts a high fraction of drug from the blood eg. lidocaine and morphine have high hepatic clearance Lungs – major pathway of elimination of inhalation anesthetics – drugs that decrease ventilation eg. opiods may delay pulmonary excretion of gas Changes in distribution – with IV induction agents concentration of drug leaving blood and going to tissues determines anesthetic plane – since concentration of drug in arterial blood is a function of cardiac output anything that decreases cardiac output will cause more drug to go to brain and myocardium where most of the output is being distributed – this can further compromise cardiac function

Monitoring of Anesthesia

Cardiovascular

EKG – bradycardia, tachycardia or arrhythmias – does not measure mechanical performance and so can be normal with poor myocardial function and poor tissue perfusion Blood Pressure – product of cardiac output, vascular capacity and blood volume – vasodilation causes increased perfusion but can cause hypotension, agents to increase blood pressure cause vasoconstriction which can decrease peripheral perfusion,  blood pressure needs to be maintained to perfuse the brain and heart Indirect BP – if cuff is too tight BP erroneously low, if too loose – falsely high Doppler – more accurate in smaller animals,  all techniques are least accurate when BP is low and vessels constricted Normal BP 100/80 to 160/120, MAP 60-100 At systolic pressure <80 or MAP <60 blood flow is inadequate to perfuse brain and heart Causes of hypotension  hypovolemia  peripheral vasodilation  decreased myocardial contractility

Respiratory

Rate is of limited value, change in breathing rate is a more sensitive indicator Tidal volume 10-20 ml/kg End tidal CO2 (ETCO2) is a measurement of CO2 in expired gas at the end of exhalation, since alveolar and capillary PCO2 are equilibrated it is an estimate of PaCO2

PaCO2 as a parameter

PaCO2     35-45 mmHg- normal, <35 = Hypoventilation, >35 = Hyperventilation PaCO2 >60    indicates severe respiratory acidosis requiring mechanical ventilation PaCO2<20   indicates severe respiratory alkalosis and decreased cerebral blood flow causing impaired cerebral oxygenation  Causes of increased PaCO2: Hypoventilation – airway obstruction, thoracic or abdominal restrictive disease, pleural space disorder, pulmonary parenchymal disease, inappropriate ventilator settings Dead space rebreathing  Hyperthermia or increased CO2 production Recent bicarbonate therapy Decreased PaCO2 caused by hyperventilation Venous PCO2 is 3-6mmHg higher than arterial

PO2 as a parameter

PO2 is the tension of oxygen dissolved in plasma, value is irrespective of hemoglobin concentration SaO2 is a measurement of hemoglobin saturation of oxygen O2 content = (Hb x 1.34 x % saturation) + (.003 x PO2) Pulse oximeter (SpO2) measures pulse rate and hemoglobin saturation of oxygen – measures absorption of infrared light through a blood sample- oxyhemoglobin, reduced hemoglobin, methemoglobin and carboxyhemoglobin all absorb red to infrared light differently Pulse ox is designed to measure oxyhemoglobin and reduced hemoglobin – if methemoglobin or carboxyhemoglobin are present they will affect measurement Oxyhemoglobin absorbs at 660 Reduced hemoglobin absorbs at 940 Methemoglobin absorbs at both frequencies so SpO2 reads at 85% Carboxyhemoglobin absorbs at 660 so falsely increases reading Pulse ox accuracy is greatest at range of 80-95% hemoglobin saturation  Poor performance of pulse ox – can be caused by peripheral vasoconstriction – can’t pick up pulse, thickness of tissue can interfere with light transmission, electrical or optical interference

Blood oxygenation level PaO2 SaO2 Normal >80   >95  Serious hypoxemia <60 <90 Very serious hypoxemia <40 <75