ANESTHESIA MACHINE
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Also known as Anesthesia Delivery System Most important in the practice of anesthesia Partner in life of an anesthesiologist functions: 1. supply a mixture of anesthetizing and life sustaining gases 2. permits spontaneous/controlled ventilation 3. provides monitoring devices 4. help anesthesiologist keep patient alive, safe, and adequately anesthetized- MOST IMPT. FXN - after evaluating patient, check first whether or not the equipment is functioning since this is another cause of intraoperative mortality or morbidity - crucial to patient safety - modern anesthesia machine: 1. ventilation 2. monitoring devices Basic elements of an Anesthesia Machine
I. Source of Gases Most commonly used gases: (used inside OR) 1. O2- pure gas 2. NO- liquefied gas Source of compressed gases 1. pipeline system - modern source of gases in higher center; instead of tanks, you see outlets of gas that came from central supply; color coded - back up tanks must however be available in case the system runs out of supply - Oxygen- color green (2/3 liquid; 1/3 gas) - NO- color blue 2. cylinders - full tank of O2 exert 2000-2200 lbs/in 2 w/ a volume of 625- 650 ml - NO exert 750 lbs/in 2 in 1590 L II. Pressure Regulator- reduces gas pressure - Pressure reducing bulb =45-50 lb/in 2 (cylinder pressure) reduced pressure w/c is a workable pressure - Pipeline: 40-45 lb/in 2 III. Flow meter - Control flow of gases - Knob is also color coded IV. CO2 absorber - Prevent accumulation of excess CO2 thru soda lime and bara lime w/c comes in granules that are colored and it changes from white to pink/blue
as it is worked out. INDICATOR: phenolphthalein (pink), ethyl violet (purple) - If the canister has no heat and exhausted, no color change will be noted so that the pt. will manifest tachycardia, inc. HR, inc. BP w/o deepening of anesthetics as the concentration inc. V. Vaporizer - Convert liquid anesthetic to vapor - Calibrated for accuracy and precision VI. Corrugated tubing, rebreathing bags and face masks Rebreathing bags - comes in various sizes depending on the pt - smallest is 500ml for newborns and the largest in adults is 5L - most commonly used: 2 and 3 L masks – also also has varied sizes depending on the pt, transparent face masks – breathing tubing - rubber; reusable, heavy universal connector- fits to any size of the face masks, breathing bag and endotracheal tube corrugated tubing- has the following reasons why it is made as corrugated: 1. to be flexible 2. for moisture trapping 3. resist kinking 4. provide turbulent flow vs laminar flow - kinking of endotracheal tube would cause obstruction escape valve and gas scavenging system - where waste gases accumulate as they are eliminated w/o increasing the risk of the personnel - prevents contamination of the OR with anesthetics Lung exposure to anesthetic gases could cause: 1. spontaneous abortion 2. fetal malformation 3. malignancies personnel of OR Safety measures: 1. color coding 2. Pin Index System 3. O2 fail-safe system – system – stops stops flow of all gases except O 2 4. O2 analyzer- monitors the O 2 content in the patient Additional Notes: Ether- lacks controllability - open drop method - polluting the OR and personnel NO- 1st trimester, can cause abortion
Mechanical Ventilator used to control respiration and allow the anesthesiologist to attend to other matters such as parenteral fluid therapy and other essentials for therapy of the pt. if the body becomes tense, pt. may end up having bronchospasm w/c must be differentiated with laryngospasm since both are managed differently Bronchospasm- bronchodilators are given Laryngospasm- give muscle relaxants Assisted/ controlled respiration
- must be done by manual compression of the bag w/c could result to periodic inflation - anesthesiologist’s focus must always be on the patient Hazards associated with the use of anesthetic machine: 1. inadvertent administration of hypoxic gas mixture - such error usually result from carelessness of anesthesiologist or of the mechanical design of the anesthetic machine - carelessness/failure to open cylinder - loose connection - clogged lines - sticking of flow meters - failure/ faulty installation of the service O 2 supply 2. overdose of anesthetics - observed change of O 2 flow - failure to add diluting O 2 - 1st vaporizer- copper kettle - Ether- is very irritating including OR personnel 3. inadvertent use of several agents caused by leaking valves
Safety devices: *Fail Safe System - eliminates the possibility of administering hypoxic gas mixture - color coded with knobs * Proper use of anesthesia machine rest upon the anesthesiologist and no substitute of VIGILANCE- motto of Anesthesia * Hypoxia must be reversed before 4 minutes Purpose of Anesthesia Machine 1. help anesthesiologist keep the patient alive, safe and adequately anesthetized 2. monitor precise gas mixtures but variable composition delivered to the patient
MONITORING ANESTHETIZED PATIENTS
- Important because anesthesiologist act as guardians of the anesthetized patient in the entire monitoring - Monitor patient as well as the equipment - GOAL: TO KEEP PATIENT ALIVE AND ADEQUATELY ANESTHETIZED Monitoring - from the Latin word “ MONERE” meaning to warn, to keep watch over, to check systematically - process by w/c anesthesiologist recognize and evaluate potential physiologic problems by identifying prognostic trends of patients in a timely manner - vigilance implies monitoring - effective monitoring to the patient and equipment, used in administering anesthesia should: 1. diminish pre ventable mishaps 2. reduce poor outcome that may follow surgical procedures, disease processes or adverse reactions Purpose: 1. To regulate the depth of the anesthesia by knowing how the patient respond to anesthesia Expected: decrease BP, dec. HR, breathing is regular 2. Treatment of physiologic derangements such as arrhythmias, hypotension, organ ischemia, blood loss, hypotension, pulmonary dysfunction Estimated blood volume: Adult male: 60 cc per kilogram Adult female: 55 cc per kilogram Adult allowable blood loss= 20% of EBV Children: 75- 80 cc per kilogram Allowable blood loss in children is only 10% 3. Detect expected catastrophe such as MI and airway obstruction - thru vigilant observation Monitors used: - Physiologic monitoring- continuous assessment of patients conditions with emphasis with change Qualitative- sense Quantitative- measurements
A. Basic Monitors 1. senses- smell, touch, hearing, sight 2. monitoring devices- supplement anesthesiologist perception of more sensitive and continuous assessment of the patient
Limitation: when there is fluctuation, discrepancy of results occur don’t interpret results if it is not a substitute for a good and sound clinical judgment Implication of improved patient safety: - decrease morbidity and mortality for patients - decreased post op. complications - less costly insurance premium and malpractice & diminished legal cost What to observe? 1. surgical field- note for the color of the blood observe oxygenation- bright red = good dark red = poor 2. movement 3. skin color of patient 4. tearing 5. positions B. Essential monitors: 1. PulseOoximeter - O2 sat, HR and peripheral oxygenation - Standard care for monitoring oxygenation in anesthesia to detect adequacy during anesthesia - Normal O2 = 97-100% - Reduces the occurrence of perioperative hypoxemia - Can detect decreases in O2 sat before cyanosis *hypoxemia- when detected early in pulse oximetry may result to a reversible organ injury *93-94% drop, no cyanosis yet *5 minutes with decreased O2 sat results to irreversible brain injury
- Useful in: Titration of O2 therapy Weaning patients from O2 ventilators In neonates, decreases the rate retrolental fibroplasias where 95% O2 sat should be maintained 2. Capnography - Detects adequacy of ventilation - Measure s end tidal CO2 and clinical estimate of partial CO2 - Used to differentiate endotracheal from esophageal intubation
- Normal pCO2=36-44 mmHg - Capnogram- graphic display of airway pCO2 as a function of time - Rapid fall of end tidal CO2 indicates air embolism in sitting craniotomy Factors that influence the shape of the capnogram: Respiratory flow rate Disturbance of pulmonary blood flow Disturbance of ventilation
* Abrupt change in shape signify an acute change in the patient’s physiologic state Capnography can: Detect any breathing circuit problem - Breathing circuit disconnection-decreased in tidal CO2 - Accidental extubation - Airway obstruction - Low cardiac output or hypoperfusion- decreased tidal CO2 - Venous air embolim - Hypothermia - Hypoventilation - Cardiac arrest Can differentiate tracheal and esophageal intubation - In tracheal intubation, there is a consistent concentration of carbon dioxide from the trachea - In esophageal intubation, there is disappearance of CO2 - Clinical way of estimating whether tube is on the right main bronchus -> place tip of tube at the carina and note for : Breath sounds equal on both sides Equal expansion of the chest Endotracheal intubation goes to the right because it is wider and straighter Changes in End tidal CO2 A. sudden decrease Low cardiac output/ hypoperfusion Pulmonary embolism- inc. physiologic dead space Venous air embolism Leak in air breathing circuit Hypothermia Hypometabolism Hyperventilation Extubation
Obstruction to airway Cardiac arrest B. Sudden Increase Hyperthermia- because of inc. CO2 production Sepsis Malignant hyperthermia- Inc. Co2 production - Early manifestation: tachycardia- mottling of the skin, skeletal muscle rigidity, cyanosis, dysrrythmia - Late manifestation: fever Skeletal muscle rigidity Hypoventilation Re- breathing
Slow increase in CO2 concentration: a. partial airway obstruction- kinking of breathing tube b. inspired CO2 is increased- due to malfunction of the breathing circuit c. exhaustion of CO2 absorbent
3. ECG (non-invasive)- monitors cardiac rhythm & conduction - In 1906, invented by Einthoven by using a string Galvanometer - Tells about surface recording of electrical activity of the heart/ myocardium - Usually displays electrical activity of the heart, nothing about the adequacy of myocardial pump function - Detects: rate, rhythm, changes in the ST segment assumed by the degree of oxygenation of the myocardium - TEE: heart anatomy and function; expensive but a useful perioperative monitor - Functions: detection of 1. dysrhythmia 2. conduction abnormality 3. pacemaker malfunction 4. electrolyte disturbance - taken on patients 40 y.o. and above or in younger pt. with the history of palpitations chest pain HPN Previous MI - Most valuable if monitoring begins before induction of anesthesia because any abnormal ECG or marginal ECG findings preoperatively worsens during intraoperative
- Rhythm disturbance Atrial tachycardia- common during anesthesia induction not associated with a hemodynamic instability Ventricular tachycardia- medical emergency associated with hypotension and poor cardiac output 4. BP apparatus - Fundamental to determine the effects of anesthetic agent to the cardiovascular system - Determine adequacy of circulation during anesthesia - Blood pressure- is the pressure exerted by the blood on the walls of the arteries as it flows Changes in systolic BP correlates with myocardial O2 requirement Changes in diastolic BP correlates with changes in coronary perfusion pressure - Pulse pressure= SBP- DBP - Methods: Invasive- intraarterial BP monitoring Non- Invasive- BP cuff apparatus + stethoscope Mean Arterial pressure - (SBP +2DBP)/3 - hydrostatic pressure that provide diffusion 5. Precordial stethoscope and esophageal stethoscope - Stethoscope- note quality of HS & BS - Precordial stethoscope- placed at pts. precordium Bounding- poor vital signs Good volume- good status of pt. Distant HS- inadequate volume Rales and crackles- fluid overload - Esophageal stethoscope- important in thyroidectomy and in pts. with weak pulses (“shock pulses”) - Distant heart sounds: hypovolemia 6. Temperature probe/ monitoring Thermoregulation by hypothalamus is decreased during general anesthesia Hypothalamus- temperature regulating system w/c is affected by general anesthesia but not regional anesthesia
Hypothermia common intraoperatively, a clinical state of subnormal body
temperature where the body is unable to generate body heat and maintain body temperature for bodily function Due to: a. Cold ambient environment in the OR b. Heat loss during surgical operation c. prevents Action of anesthetic Upper limit= 35 degrees Celsius (95 degrees Fahrenheit) Common in extremes of age 1. small children/ infants- inc. ratio of body surface area to body weight 2. elderly- lack compensatory mechanism to generate heat also seen in patients with spinal cord injuries as well as burned patients alters thermoregulation centers shivering peripheral vasodilation drugs that induce hypothermia: 1. opioids- sympatholytic properties 2. barbiturates- peripheral vasodilation 3. muscle relaxants- reduce muscle tone - prevents shivering thermogenesis 4. regional anesthesia- produce sympathetic blockade - sensory blockade for thermal receptors
Adverse effect of hypothermia: 1. decrease O2 availability- ischemia 2. cardiac arrhythmia/ cardiac dysrrhythmia 3. potentiates anesthetic effects and muscle relaxants- inc. sensitivity to anesthetic drugs 4. coagulopathies 5. inc. vascular resistance 6. post operative shivering
7. anticholinergic blockade of sweating Site for monitoring depends on : o o o
Surgical procedure Type of anesthesia Time of monitoring
Route of monitoring or taking temperature: 1. Axilla- 1 degree Celsius below core temperature 2. Skin- 3-4 degrees Celsius below body core temperature 3. Rectal- does not reflect body changes in core temperature - Complication: rectal perforation 4. Mouth- accurately reflects core body temperature 5. nose- reflects brain temperature because of its close proximity to carotid artery (ICA); contraindicated in head trauma and rhinorrhea 6. External auditory meatus- close proximity if tympanic membrane to ICA> core body temp.; can perforate tympanic membrane if placed too deeply 7. Bladder catheter- can approximate body temperature if urine flow is high 8. pulmonary artery catheter- most accurate, expensive and invasive way of taking body temperature 9. Nasopharynx- brain temp. because of its proximity to ICA w/c when probe or placed deeply can cause epistaxis 10. Esophagus- core body temperature, probe must be in lower third or mid esophagus; accurately reflects core body temperature; when deeply placed can cause trauma
Core temperature- reflects the temperature of the vital organs of the body. Accurate temperature in nasopharynx, esophagus, external auditory and pulmonary artery Peri-operative hypothermia - common result of anesthetic induced alteration in thermoregulation - cold temperature of environment in the OR - heat loss during surgical procedure
Hyperthermia Less common; there is increase of 2 degrees Celsius / hour Causes:
1. fever secondary to stress of surgery 2. sepsis 3. inability to warm patients 4. malignant hyperthermia- a late manifestation 5. exposure to endogenous pyrogenes 6. inc. metabolic rate due to thyrotoxixosis and pheochromocytoma
7. Central venous pressure monitoring (CVP) - 80% of circulation is in the atrial circulation - Invasive, central venous catheter is used cannulating central venous circulation - Normal CVP= 5-10 cmH2O or 1.5 – 11 mmHg
Interpreting results of CVP: Low CVP: hypovolemia; no volume loss-> inc. venous capacitance due to vasodilation High CVP; fluid overload
CVP+BP: if decreased and decreased or normal BP, think of hypovolemia - Mgt. inc fluid and monitor if there will be inc in CVP after fluid is increased if inc CVP and normal BP, think of hypervolemia - Mgt: stop giving fluids and give diuretics if inc CVP and decreased BP, think of cardiac failure - Mgt: diuretics and digitalis If heart function fails, there is backflow of blood to venous circulation manifesting as increase in the CVP Central venous pressure (CVP) - pressure exerted by blood returning to the right side of the heart - distinguish between hemorrhage and CHF - decrease CVP: a. vasodilation b. hypovolemia c. secondary to spinal anesthesia - increase CVP: a. Vasoconstriction b. increase intrathoracic pressure c. increase positive pressure ventilation d. Right intraventricular afterload pulmonary embolism pulmonary hypertension condition that impairs diastolic filling time ex.: cardiac tamponade- impaired diastolic filling; incompetence of tricuspid valve Indicators for CVP monitoring: 1. elderly patients: 70 above 2. patients whom large blood or fluid exchange is done- prevents hypervolemia and overtransfusion 3. heart diseases 4. major traumatic injury 5. anticipation of major blood loss
8. Echocardiography: - useful in monitoring continuous heart anatomy and function
- useful in increased myocardial o2 demand (myocardial ischemia) seen as ventricular wall motion on echocardiography where there is abrupt change of ventricular wall motion Transesophageal echocardiography (TEE) - useful in differentiating hypovolemia vs. poor myocardial contractility as a cause for depressed cardiac output syndrome and open heart surgery - assessment of myocardial function and ischemia - valves can be assessed either for valvular replacement or valvular repair - enables surgeon to ensure adequacy of the valve repair before closing the chest - drawback: expensive INHALATIONAL ANESTHETICS
- Sufficient to produce complete anesthesia- amnesia, analgesia, muscle relaxation, unconsciousness - Drawback: in inc. concentration has undesirable effect of cardiorespiratory depression Main purpose of general anesthesia: 1. altered physiologic state; loss of consciousness w/c is reversible 2. amnesia, analgesia, muscle relaxation Property of ideal anesthetic: 1. predictable action and rapid onset of action from induction to emergence from anesthesia 2. provide muscle relaxation 3. cardiostability and bronchodilation 4. not trigger malignant hyperthermia, nausea and vomiting as significant side effect 5. not flammable 6. not undergo biotransformation in the body 7. allow easy instillation of concentration at the site of action
* no anesthetic agent have all the ideal properties * Atropine- used as premedication to prevent salivation *Central anesthesia- depress excitatory transmission in spinal cord at level of dorsal root horn Early inhalational anesthetic: 1. Ether - don’t produce cardiovascular depression - produce very good muscle relaxation
- flammable, cause post-op nausea and vomiting, produce copious salivation; no drop in BP (stimulate sympathetics) 2. Nitrous Oxide - lack potency and can’t be used alone and used as an analgesic today - 2nd gas effect to potentiate effects of other anesthetics 3. Chloroform- hepatotoxic 4. Cyclopropane- highly flammable 5. Trichloroethylene- side effect: produce phosgene 6. Fluoroxene- severe flammability and produce nausea and vomiting; first fluorinated; hepatotoxic 7. Methoxyfluorane- side effect: nephrotoxic due to fluoride ion; slow induction of anesthesia Newer Drugs: Fluorinated volatile anesthetic 1. halothane 2. enflurane- theoretical risk of seizure, not used in epileptic Px 3. isoflurane 4. sevoflurane 5. desflurane *3,4,5-> commonly used today: 3,4,5- substituted halogenated ether *Halothane- substituted halogenated alkane Drugs difficult to use or administer due to: 1. narrow margin of safety of inhalational anesthetic 2. variability among patients- severe side effects because of variations of pts - therefore must be used in titration; requires continuous monitoring To produce its pharmacologic effects: drug administration at an adequate dose sufficient potency deliver to active site of action site of action: Brain site of entry: lung STAGES OF ANESTHESIA:
- introduced by Arthur Guedel STAGE I: - begins in induction and ends in loss of consciousness - use eyelid reflex - eyelid reflex is lost - analgesia and amnesia
STAGE II: - stage excitement and delirium - starts with loss of consciousness and ends at onset of automatic respiration - Px may go into struggling and vomiting may occur - do not stimulate px - don’t start operating - risk of aspiration during laryngospasm and bronchospasm STAGE III: - surgical stage - from automatic respiration to end in onset of respiratory paralysis Phase I- onset of automatic respiration and ends in cessation of eyeball
movement Phase II- cessation of eyeball movement to commencement of intercostals
paralysis Phase III- commencement of intercostal paralysis to complete intercostal
paralysis Phase IV- complete intercostal paralysis to diaphragmatic paralysis
STAGE IV: - breathing and circulation stops - cardiac arrest and death - stage of overdosage *stages of anesthesia is best appreciated using ether *most useful signs: eyelash reflex eyeball movement dilation of pupils changes in respiration - Most sensitive indicator of depth of anesthesia! *Brief Procedures- start incision at stage III, phase I *long procedures (explore lap)- start at stage III, phase II; px may react to insertion of ETA *surgeons should not start operation unless okayed by anesthesiologist 3 GENERAL ANESTHESIA PHASES
I. Induction - induce patient to sleep; critical period since anything can happen to patient - take vital signs as often as possible even at 3-5 mins
- occurs when anesthetizing partial pressure has been achieved by the brain in high concentration - unique in a way since respiratory tract used as entry - immediately during induction, give 3% to achieve anesthetizing partial pressure Factors that increase the speed of induction:
brain anesthetizing partial pressure must be given in high concentration 3. Alveolar Ventilation - faster ventilation, the more rapid is the uptake
II. Maintenance Phase - Goal: To maintain optimal or unchanging anesthetizing partial pressure in the brain as reflected in alveolar partial pressure
II. Circulatory phase - Important factor is cardiac output- where those with apprehension, fear, muscular activity, thyrotoxicosis will be difficult to anesthetize because of inc. blood flow to the peripheral organs causing a decrease blood to the brain - in shock patients, from hemorrhage and dehydration, there is peripheral vasoconstriction less blood flow to the skin brain receives high blood flow anesthesia is easily delivered
III. Emergence/ Recovery Phase - lowers concentration of anesthetic so that partial pressure in the brain also lowers
Barometric pressure- decrease with higher altitude - Higher conc. is needed in inc. altitude vs. in lower altitude because vagometric pressure is lower therefore decrease in pressure
Uptake of Inhalational is divided into; I. Pulmonary phase - should produce significant concentration to build up in the lungs (alveoli) - through diffusion, it goes to the pulmonary circulation
MAC (minimum alveolar concentration - concentration of anesthetic that will prevent movement/ motor response in response to a noxious stimuli (surgical incision) - anesthetics are measured using this - relation between administered dose and quantitative effect produced in an expression of drug potency - concentration of anesthetic that would prevent movement of Pxs - 50% of Pxs in response to (surgical incision)
1. inc alveolar concentration 2. high flow within breathing circuit 3. increase in respiratory flow/ inc minute ventilation
* concentration of anesthetic In tissue - solubility and partial pressure of anesthetic *solubility is constant and partial pressure changes controlled by the concentration of the anesthesia Factors that Affect Pulmonary Uptake: 1. Inhaled concentration/ expired concentration: - maintains concentration in alveoli - the higher the concentration, the higher the uptake - rate of rise of anesthetic to bloodstream
2. Solubility of Anesthetic - affects the rate of diffusion of anesthesia in blood stream - expressed in blood gas partition coefficient where the higher the value, the more soluble - when the anesthetic is more soluble, uptake is slower as well as its induction and recovery this is so because it is taken from the lungs rapidly in large quantities rapid blood solubility goes to the tissues therefore takes time before brain is reached and so can’t attain
BLOOD GAS PARTITION COEFFICIENT NO 0.47 (least potent) Halothane 2.3(most potent & most soluble in blood) Ether 12 Methoxyflurane 12 Enflurane 1.91 Isoflurane 1.4 Desflurane 0.42 (insoluble therefore rapiduptake) Sevoflurane 0.69
MAC 104 (least potent) 0.77
0.16 (most potent) 1.7 1.15 6.0 1.7
*Methoxyflurane- nephrotoxic, not used today * the smaller the MAC value, the more potent is the anesthetic
INHALED ANESTHESIA - easier to measure close but difficult to measure the effect - In 1965, EGER introduced MAC-therapeutic effect of anesthetic Factors that Affect MAC: 1. Age- highest MAC: 6-12 mos.; decrease as age increases and in premature infants 2. health condition 3. hypothermia- 1 degree Celsius – 2.5 % decrease 4. hyponatremia 5. Opioids, Barbiturates and alpha2 blockers, Ca channel blockers 6. Alcohol intoxication 7. Pregnancy Factors that may inc. MAC 1. Young Age- 10% increase in infants and children vs. young adults; infancy @ term- 6 mos. greatest increase 2. chronic alcohol use – inc. amount is required 3. CNS hypo-osmolality 4. Acute ingestion of CNS stimulant (dextroamphetamine, cocaine) 5. inc. CNS neurotransmitters (e.g. MAO inhibitors-antidepressant) 6. Hypothermia
Complete general anesthetic state: can be produced by inhalational anesthetic but must be given in higher dose: 1. loss of consciousness 2. analgesia of the entire body 3. amnesia 4. degree of relaxation Blood- Gas partition coefficient - solubility of inhalational coefficient - inc. Blood- Gas partition coefficient: inc. concentration - inc. solubility: decrease rise of alveolar BGPC
EFFECTS ON ORGAN SYSTEMS CNS — tends to increase cerebral blood flow and it normalizes with time — increases ICP; must be given in titration 1. Nitrous Oxide — increases cerebral blood flow — cerebral vasodilation associated with moderate increase of ICP 2. Halothane — will go back to normal after 2 hours after induction — provides the greatest increase in blood flow due to vasodilation 3. Isoflurane — produces greatest reduction in cerebral blood flow that would result to a flat EEG — has cerebral protecting effect — associated with better maintenance relationship between cerebral metabolic O2 requirement and cerebral blood flow — results in the lowest increase in cerebral blood flow — inhalational anesthetic of choice 4. Enflurane — produces a seizure-like activity exaggerated in the presence of hypocapnia 5. Volatile anesthetics — alter the production and absorption of CSF which tend to normalize with time
Factors that decrease MAC 1. old age- decrease by 6% 2. prematurity 3. hypothermia- for every 1 degree Celsius drop, there is a corresponding decrease of MAC of 2-3% 4. CNS hyperosmolality 5. CNS depressants (opioids, benzodiazepines) 6. decrease CNS neurotransmitters (e.g. anti-HPN drugs) 7. intake of tranquilizers 8. acute alcohol intoxication- no anesthesia required for minor operations 9. alpha2 agonists (e.g. clonidine) 10. pregnancy 11. hyponatremia 12. taking Ca-channel blockers Does NOT affect MAC: 1. Gender 2. Duration of anesthesia 3. Hypo/hypercarbia 4. hyperkalemia 5. thyroid function
Respiratory System — decreases mucociliary clearance — volatile anesthetics produce drug specific and dose related respiratory depression of ventilation through the medullary center (direct) and effects on the intercostals muscles (indirect) — characterized by rapid shallow respiration
— produces a decrease in tidal volume and increase in respiratory rate — inhibits histamine release — decreases airway resistance by relaxation of bronchial smooth muscles and inhibits bronchoconstriction — results in hypocapnia — ventilatory response to hypercapnia is attenuated — loss of intercostals muscle function which results in rocking boat appearance of ventilation where the chest collapses, the abdomen protrudes, and the diaphragm descends during inspiration — relaxation of muscles of the jaw resulting to partial airway obstruction — produces dose dependent decrease of the ventilator response tp CO 2 as well as hypoxemia 1. Halothane — used in patients with asthma — not pungent and so it does not produce irritation and cause laryngospasm — least irritating 2. Sevoflurane — can be given to children before giving isoflurane and desflurane 3. Nitrous Oxide — no airway irritation — 30% more soluble than nitrogen — stimulates the sympathetic system — increases RR; decreases TV — no significant muscle relaxation — increases post-op nausea and vomiting
Cardiovascular System — CV depressant manifested as hypotension; decreased BP — produces drug-specific dose dependent circulatory depression — vasodilation (isoflurane, desflurane) — depressed myocardial contractility (halothane, enflurane) — decreased sympathetic tone 1. Isoflurane — increased heart rate with decreased BP indicates a better maintenance with response to baroreceptor reflex in tha carotid — depresses vagal activity — dilates coronary arteries in the presence of reduced pressure — not as potent as nitroglycerine — do not use in patients with CAD — Coronary Steal Syndrome: dilatation of the LA in normal areas to divert blood flow from stenotic lesion 2. Halothane — minimal to absent chages in HR
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impairment of baroreceptor activity inactivates methionine synthetase by oxidizing cobalt in Vit. B 12 producing a decrease in myelin formation also inhibits thymidelate synthetase produces megaloblastic anemia, pernicious anemia, and neuropathies
3. Nitrous Oxide — rapid discontinuation decreases O 2 tension — diffusion hypoxia can be prevented by allowing the patient to breath O2 for the next 5-10 minutes — increased incidence of spontaneous abortion 4. Halothane — increases sensitivity of myocardium to epinephrine — arrhythmogenic — children are more sensitive — cholinergic; vagally-induced bradycardia effect in children — middle age, obesity, and with familial predisposition to halothane toxicity increase risk — metabolism of more than 20% under hypoxic conditions may cause hepatic necrosis 5. NO plus inhalational anesthetic — decreases BP but minimal due to NO having a mild sympathomimetic effect 6. NO plus high doses of opioids — tremendous drop in blood pressure 7. Isoflurane and Enflurane — less likely than halothane to produce dysrrhythmia in the presence of epinephrine — premature ventricular contraction and tachyarrhythmia — effects commonly seen in adults than in children 8. Halothane and Enflurane — direct myocardial depressant 9. NO and Sevoflurane — produces the least myocardial depression 10. Desflurane — associated with production of CO Myocardial depression from inhalational anesthetics is enhanced by
beta-blockers! Signs and Symptoms of overdose of anesthetics:
a. hypotension b. bradycardia
c. decreased cardiac output d. arrhythmia e. cardiac arrest
Renal System — secondary to decrease in BP decreased GFR
a. b. c. d. e. f. g.
decreased renal blood flow
1. Methoxyflurane — nephrotoxic because it releases fluoride ions when metabolized — 50 mmol/L considered nephrotoxic 2. Sevoflurane — not lipid soluble — produces smooth and rapid induction in pediatric patients — not pungent in odor — soda lime can degrade sevoflurane — vinyl ether/compound A: degradation product of sevoflurane by soda lime is nephrotoxic
GIT — nausea and vomiting 1. Nitrous oxide — not used in cases of pneumothorax, pneumocephalus, and intestinal obstruction — diffuses rapidly into any air space containing cavity — distends air-filled viscera which contributes to nausea and vomiting — decreases splanchnic blood flow — increases uptake of concurrent anesthetics — insoluble in blood — speeds up onset of induction — 2nd gas effect 2. Halothane — affects the liver — increase in liver size; anorexia, nausea, vomiting Halothane Hepatitis
— autoimmune hypersensitivity reaction; occur in repeated exposure to halothane at short intervals — metabolit of halothane has a direct hepatotoxic effect most specifically during the reductive metabolism of halothane that leads to production of free radicals considered hepatotoxic — hepatic necrosis which is immune mediated — decreased hepatic blood flow — predisposing factors:
reduced splanchnic blood flow hypoxemia malnutrition exposure to halothane underlying diseases obesity elevated liver enzyme
Musculoskeletel System — causes relaxation — all inhaled anesthesia w/ exception of NO can trigger malignant hypothermia
Uterus — relaxation; contributes to uterine blood loss; affects the placenta and fetus
BIOTRANSFORMATION — oxidative metabolism occurs in the liver thru the P450 system 1. Nitrous Oxide — methionine synthesis = 20% inc. risk of congenital anomalies; abortion 2. NO + more potent volatile anesthetic — 2nd gas effect, potentiate effects of inhalalational anes.; bld gas partition coefficient of 0.27 — greatest reduction in cerebral metabolic activity (isoflurane) — dose dependent spike wave in EEG (enflurane) INHALATIONAL ANESTHETIC
vs.
INTRAVENOUS ANESTHETIC
rapid induction of anesthetic
to produce general anesthesia:
provides continued adjustment of
- loss of consciousness - amnesia and blunting of some reflexes does not provide complete analgesia and muscle relaxation IV inducing agent allows rapid recovery after its termination
anesthetic depth provides continued monitoring of anesthetic concentration elimination through the lungs provides rapid emergence from anethesia accomplished without an iv access good in pediatric patients choosing of drug is based on the situation cardiovascular depression is greatly affected by halothane
INTRAVENOUS ANESTHETICS
Examples of IV non-opioids anesthetics: 1. Barbiturate (Thiopental) 2. Benzodiazepine 3. Propofol 4. Ketamine 5. Etamidate 6. Opiods – inc. concentration; side effect Characteristics of IV anesthetics: 1. provide rapid nearly instantaneous onset w/o causing pain on injection 2. provide smooth induction w/o any signs of muscular twitching or movement and excitement 3. safe and cause minimal perturbation of cardiovascular and respiratory function 4. short- acting to awaken the patient rapidly to full normal CNS fxn 5. metabolism to inert substance and excretion should be rapid and complete so that no accumulation would occur thereby allowing the drug to be used for a long period of time 6. amnesia for intraoperative events should be complete NOTE: not a single IV conducting agent that possesses all characteristics
Dosing requirement based on: 1. intravascular volume of the patient 2. co-morbidities 3. age 4. chronic medications In the elderly: - inc. volume of distribution, dec. elimination clearance - prolonged effect - adjust dose - more sensitive to IV anesthetics Mechanism of Action: enhance the transmission of GABA interfering the transmission of potential
Effect of barbiturates at the synapses: 1. facilitate the effect of GABA 2. blocks excitatory neurotransmitter – Ach and glutamic acid Barbiturates = urea + malonic acid
Short-acting: 1. Thiobarbiturates – sulfur containing a. Thiopental b. Thiamidal 2. Exybarbiturates a. Methohexetal
Substitution on C 2 and C5 provides CNS effect — loss of consciousness and anticonvulsant — -C5 w/ a phenyl group: Phenobarbital — C5 w/ a methyl group: methohexetal – produce seizure-like movement — -#2 C atom w/ O2: oxybarbiturates — -#2 C atom w/ S: thiobarbiturates
I. Barbiturates A. Thiopental — ultrashort-acting barbiturates used in anesthesia — no analgesic effect ; does not block sensory afferent impulses — should not be used as a sole analgesic — H2O insoluble for weeks — w/ acidic drugs, result in precipitation of barbiturates — pH 10.5-11 (alk solution) — prepared as a 2.5% solution — only given through IV because extravasation can cause tissue necrosis due to high alkalinity given into a vein not into an artery because it will cause chemical endarteritis resulting to vasospasm and damage to inner layer of the artery — give lidocaine and α-adrenergic blocking drug to relieve spasm (phentolamine) — thrombosis: give heparin — 60% of drug exist in an unionized form at pKa = 7.6 — ph of 7.4 – lipid-soluble, rapid diffusion into a vessel- rich group (brain) – conc. inc. rapidly, unconsciousness sets in w/in 15 minutes — 70-85% bound to albumin; 15% free-active subs — onset: 1 hr rate circ. time w/ max. effect w/in 1 min — decreased albumin:decreased CHON binding 1. liver cirrhosis 2. in presence of other drugs (NSAIDS, ASA) – competes w/ Thiopental for the binding site 3. acidosis — dose: 3-5 mg/kg IV — termination of effect : through redistribution to inactive tissues (muscle, fats)
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half life of 6-12 hours contributes to the slow recovery and hang-over sensation sometimes not used to maintain anesthesia because it tends to accumulate IV inducting agents have no analgesic properties except ketamine which cannot be used as a sole anesthetic especially if the procedure is long CNS depression in a dose dependent manner in geriatric patients: 30-40% dose reduction
CNS effects
— induction dose can decrease ICP — does not cause cerebral vasodilation — reduction in cerebral O 2 requirement — maximum decrease in cerebral metabolism requirement as seen in EEG Cardiovascular effects — reduces CO by decreasing venous return — direct myocardial depressant — negative inotropic effect — reduction in sympathetic outflow from CNS — decreases arterial BP which elicits mild compensatory tachycardia — in hypovolemia and in shock: a. don’t give Thiopental since it can be given after resuscitation b. only give 1.5 mg/kg IV c. be ready with a sympathomimetic drug — alternative to Thiopental: a. Etomidate – produces minimal CV depression b. Ketamine – has a tendency to stimulate the CV system c. Propofol and Benzodiazepines – decreases BP Respiratory effects — can produce depression of respiration (apnea) — be ready with resuscitating equipment, ambu bag, laryngeal tube, etc. — never manipulate airway if the patient is anesthetized because it may stimulate laryngospasm and bronchospasm — decreases minute ventilation and tidal volume — right shift in CO 2 response curve — produces a dose dependent medullary and pontine respiratory effects — most likely to have spasms: asthmatics, COPD patients, smokers Contraindications:
A. Absolute 1. porphyria — increased ALA synthetase -> increased porphyrin — involvement of the intercostals and diaphragmatic muscles
2. allergy — histamine release; sulphur molecule B. Relative 1. hypovolemia — may cause profound hypotension — slowly titrated dosage when volume has been normalized 2. hepatic failure — delayed metabolism — prolonged effect B. Methohexital — drawback: presence of muscle twitching limits its usefulness in anesthesia — requirement in anesthetic drug must not produce any excitatory movements II. Ketamine — phencyclidine derivative — N-methyl-D-aspartate receptor antagonist — bioavailability: IM-90%; peak blood concentration is achieved within 15 minutes — awakening is due to redistribution to peripheral compartments — excreted through the kidneys — only one that has analgesic effect; profound analgesia — lamina specific suppression of spinal cord activity that interrupts transmission of pain signals to the brain — dose: 1-2 mg/kg BW IV or 4-8 mg/kg BW IM; produces analgesia for 1020 minutes — a dose of 0.1-0.3 mg/kg only produces analgesia; the patient does not lose consciousness — used for brief surgical procedures — recovery time: 60-90 minutes — may act as a CV depressant in very ill patients — 55% protein bound (α 1- acid glycoprotein) — Norketamine: active metabolite with 1/3 to 1/5 potency of ketamine which prolongs CNS effect of ketamine — associated with increase in airway secretion — must be given with an anti-cholinergic drug (glycopyrrolate) — 0.1 to 0.3 mg/kg for OB patients — can be given in the presence of CV failure, cardiac tamponade
Effects on organ systems CNS — not advisable to give to patients with mental disorders and SOLs — increases cerebral oxygen consumption, cerebral blood flow and ICP — can produce visual/auditory hallucinations which can be reduced by giving benzodiazepines — atropine sulphate increases post-op delirium — induces analgesia, amnesia, and unconsciousness — dose dependent CNS depression Respiratory
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rapid intravenous bolus administration with opioids produces apnea does not produce respiratory depression a potent bronchodilator good induction agent for asthmatic patients increased salivation can be attenuated by premedication with an anticholinergic drug
Diazepam attenuates ketamine’s cardostimulatory effects and prolongs its
halflife Propanolol, Phenoxybenzamine and other sympathetic antagonists unmask
the direct effect myocardial depressant effects of ketamine Halothane + Ketamine produces myocardial depression Lithium prolongs the duration of action of ketamine
III. Propofol — 2,6-diisopropylphenol — derivative of alkyl phenol — insoluble in water — contains soy bean oil, glycerine, and egg lecithin — do not give to persons allergic to eggs — in pregnancy, use with caution for cesarian delivery — can cause anaphylactic reactions — may cause IV pain which can be lessened by prior injection of lidocaine — short-acting — good agent for out-patient anesthesia
Cardiovascular
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increases arterial BP, heart rate, and CO central stimulation of the SNS and inhibition of the reuptake of norepinephrine — increase in pulmonary artery pressure and myocardial work — should be avoided in patients with CAD, hypertension, CHF, and arterial aneurysms — beneficial to patients with acute hypovolemic shock Emergence delirium — 5-30% of patients especially in females — aggravated by tactile and verbal stimulation — minimized by giving benzodiazepines — vivid morbid dreams with morbid contents — floating sensations Dissociative Anesthesia — patient is dissociated from the environment — dissociation of the thalamus from the limbic cortex — the patient appears to be awake and conscious, eyes are open, can produce swallowing movements but cannot respond to sensory input — patient is unaware and has no recollection of events — the presence of nystagmus is a sign that the patient is already asleep Drug Interactions potentiates nondepolarizing muscle relaxants Theophylline + Ketamine predisposes patients to seizures
Effects on Organ Systems Cardiovascular — decrease in arterial BP due to a drop in systemic vascular resistance, cardiac contractility, and preload — hypotension is more pronounced than thiopental — impairs the normalarterial baroreflex response to hypotension — vagally mediated bradycardia — patients with cardiovascular diseases may not tolerate the decrease in MAP Respiratory
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profound respiratory depression causes apnea following an induction dose useful during intubation or laryngeal mask placement causes histamine release which may produce bronchospasm
CNS
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decreases blood flow and ICP can cause a critical reduction cerebral perfusion pressure in patients with elevated ICP antipruritic, antiemetic effect induction is accompanied by muscle twitching, spontaneous movement, opisthotonus, or hiccupping due to subcortical glycine antagonism useful in the termination of status epilepticus decreases intraocular pressure
Drug Interactions older formulations potentiate the effect of nondepolarizing muscle relaxants Fentanyl and Alfentanil concentrations may be increased by concomitant administration of propofol Midazolam + Propofol produces synergistic effect
IV. Benzodiazepines — facilitates GABA receptor binding — Flumazenil reverses most of the CNS effects of benzodiazepines 1. Midazolam — fast acting; water soluble — used as an inducting agent — minimal myocardial depression — maintains MAP and CO — increases heart rate — decreases ABP, CO, and peripheral vascular resistance V. Opioids — effective at producing analgesia — inhibits the presynaptic release and postsynaptic response to excitatory neurotransmitters — transmission of pain impulses can be interrupted at the level of the dorsal horn of the spinal cord — myocardial function is maintained — decreased MAP, secondary bradycardia, casodilation, blockage of sympathetic responses — histamine release with Meperidine and Morphine
VII. Droperidol — a butyrophenone — antagonizes the activation of dopamine receptors — interferes with the transmission mediated by serotonin, norepinephrine, and GABA — tranquilizer and antiemetic properties — α-adrenergic blockade — sedative effects are delayed by extensive protein binding — decreased ABP by peripheral vasodilation; antidysrhythmic effect — do not give to patients with pheochromocytoma — does not depress respiration — may stimulate hypoxic ventilatory drive — addition of an opioid decreases the incidence of dysphoria — Advantage of Benzodiazepines over Barbiturates 1. benzodiazepines produce profound amnesia or anterograde amnesia 2. therapeutic index is high 3. cardiovascular and respiratory depression is less 4. tolerance is rare LOCAL ANESTHETICS
— 40 years after general anesthesia — Niemann observed a numbing effect on the tongue due to cocaine Carl Kohler
— Father of Local Anesthetic — an ophthalmologist — demonstrated the use of topical cocaine for surgical anesthesia of the eye Advantages of Using Local Anesthetics
VI. Etomidate — carboxylated imidazole — depresses the reticular activating system — mimics the inhibitory effects of GABA — disinhibitory effects on parts of the CNS that control extrapyramidal motor activity — 30-60% incidence of myoclonus — dissolved in propylene glycol — pain on injection which can be lessened by lidocaine — used for induction of general anesthesia — rapid onset of action dude to high lipid solubility and large non ionized fraction — adrenocortical response to stress is reduced
1. simplicity 2. most undesirable side effect of general anesthesia is avoided – no loss of consciousness; no danger of aspiration and regurgitation 3. methods are appropriate for ambulatory patients – e.g. excision of cysts Disadvantages
1. lack of patient’s acceptance – may be due to ineffectual approach to patient 2. impracticality to anesthetize certain areas 3. insufficient duration of anesthesia 4. rapid absorption of local anesthetic into the blood stream with fatal and untoward reaction – minimal if precautions are taken 5. uncontrollability of drugs
Local Anesthetic Drugs — blocks neural conduction by their actions on the Na channel — blocks generation of impulses in excitable tissue (spinal cord and peripheral nerves) — produces transient loss of sensory, motor and autonomic function — structural formula determines its physic-chemical properties
Resting Membrane Potential — -90 to -60 mV — spontaneous rapid phase of depolarization which in turn is a result of inward movement of Na from outside into the cell via Na channels Membrane Expansion Theory — local anesthetic acts like general anesthetic that inhibits Na influx by expanding nerve membrane thus decreasing diameter of Na channels preventing Na to go inside
Structure of Local Anesthetic Drugs lipophilic group – benzene ring/aromatic ring hydrophilic group – quaternary amine intermediate group – ester or amide linkage — basis of the classification of local anesthetics Physicochemical Properties of Local Anesthetics depend on: 1. substitution of the benzene ring 2. type of linkage of the intermediate chain 3. alkyl group attached to quaternary ring Physicochemical Properties of Anesthetic Drugs: 1. Potency – correlates with lipid solubility 2. Onset of action – depends on the degree of ionization; pKa; faster onset of effect if unionized 3. Duration of action – associated with plasma protein concentration binding (albumin) 4. Cm – minimum blocking concentration – lowest concentration of local anesthetic that blocks nerve conduction – measure of potency of local anesthetics Factors that affect Potency: 1. nerve fiber size – bigger fibers have lower excitability threshold; motor function; faster conduction velocity – smaller fibers are blocked early by local anesthetics; pain, temperature and autonomic activity
2. nerve fiber type 3. degree of myelination – myelination speeds up nerve conduction from one node of Ranvier to the other – increases speed of neural transmission 4. pH – acidic medium antagonized blockade 5. electrolyte concentration – hypokalemia and hypercalcemia antagonizes blockade Differential Blockade – describes the blockade of the peripheral nerve that occurs at different rates – recovery from anesthetic occurs in the opposite order 1. loss of autonomic function/sympathetic function 2. loss of pinprick or sensory function 3. temperature and touch discrimination 4. motor function
Classification of Local Anesthetics: Ester group 1. cocaine – addictive, systemic toxic effect; potent vasoconstrictor; drying of cornea 2. chloroprocaine 3. procaine – also known as Novocaine 4. tetracaine - pontocaine Amide group 1. lidocaine – also known as Xylocaine; antiarrhythmic – preparations contain preservatives (methylparabene) which may cause allergic reactions 2. bupivacaine – more cardiotoxic than the rest 3. mepivacaine 4. etidocaine 5. prilocaine 6. dubicaine 7. ropivacaine – newest Metabolism Esters – metabolized by pseudocholinesterase in the plasma – hydrolysis is rapid and water-soluble metabolites are excreted through the urine – para-aminobenzoic acid (metabolite) has been associated with allergic reactions – cocaine is partially metabolized in the liver and partially excreted unchanged in the urine
– unstable in solution
– 1 hour before IV insertion especially in children and VIP patients
Amides
– metabolized by microsomal enzymes in the liver – stable in solution – rare allergic reactions Classification of Anesthetics According to Potency: Weak potency a. procaine – 7mg/kg b. chloroprocaine – 8-9 mg/kg Intermediate potency a. lidocaine – 5 mg/kg; w/ epinephrine 7 mg/kg b. mepivacaine – 5 mg/kg High potency a. tetracaine – 1.5 mg/kg b. ropivacaine c. bupivacaine – 2.5 mg/kg Epinephrine
– – – –
prolongs the effect of local anesthetic delay the absorption of local anesthetic due to the vasoconstricting effect reduces its potential toxicity increases effectiveness of local anesthetic promoting more uptake into nerve cells producing profound analgesia – increases neuronal blockade Presenting Symptoms of Overdose of Local Anesthesia: numbness of the tongue tinnitus in an awake patient palpitations blurring of vision; circumoral numbness cardiac dysrhythmias in patients under general anesthesia cardiac collapse Conditions when Epinephrine is contraindicated cardiac arrhythmias hypertension unstable angina pectoris peripheral nerve blocks Eutectic Mixture of Local Anesthetic (EMLA) – eutectic means “easily melted” – composed of 5% lidocaine and 5% prilocaine, 1:1 ratio – dermal anesthesia for beginning an intravenous line
Factors that determine concentration of local anesthetic in the blood: 1. site of absorption 2. redistribution 3. metabolism 4. excretion Intercostal anesthesia – most rapid absorption for regional anesthetics
Toxicity – due to inadvertent intravascular injection causing increased plasma levels of local anesthetic – a result of the systemic effects of local anesthetics CNS
– manifested as convulsions – more sensitive to the effects of local anesthetics – lightheadedness; tinnitus; peri-oral numbness; confusion; muscle twitching; hallucinations; tonic-clonic seizures; respiratory arrest; unconsciousness a. Transient Neurologic Symptoms - moderate to severe pain on lumbar area - disappears within 7 days b. Cauda Equina Syndrome - lumbosacral plexus - non-homogenous distribution of spinally injected anesthetic Cardiovascular
– decreased CO, decreased contractility, hypotension, sinus bradycardia, ventricular dysrhythmias – methemoglobinemia with prilocaine LOCAL ANESTHETIC DRUGS Esters 1. Cocaine – not used due to its systemic toxicity and potential for drug addiction – topical application into nasal mucosa prior to endotracheal intubation – topical anesthetic to the conjunctiva but was withdrawn due to drying effect – only local anesthetic with a vasoconstricting effect 2. Procaine/Novocaine – lacks topical activity
– rapid hydrolysis by plasma cholinesterase; can be used in high dosages – for infiltration and spinal anesthesia 3. Chloroprocaine/Nesacaine – short-acting; does not produce toxicity – cause permanent paraplegia when given inadvertently to the subarachnoid space because of low pH and use of Na bisulfide – EDTA causes severe back pain when given in large epidural doses of the drug 4. Tetracaine/Pontocaine – long-acting and potent – systemic toxicity is greater – for spinal anesthesia providing rapid onset Amides
1. Lidocaine/Xylocaine – introduced by Lofgren in 1948 – first drug of the amide class – topical anesthetic activity, rapid onset – for infiltration, spinal, epidural and peripheral nerve block – IV lidocaine is used as an antiarrhythmic, antiepileptic, analgesic, irritant suppressant, and as a supplement to general anesthesia – lower concentration is used for treatment of cardiac arrhythmia – dose: 5 mg/kg w/o epinephrine; 7 mg/kg with epinephrine – 1.5 mg/kg, 1-3 minutes before intubation to attenuate hypertension 2. Mepivacaine/Carbocaine – dose: 5 mg/kg – metabolism is prolonged in the fetus and newborns – not used in OB anesthesia – longer duration of effect than lidocaine 3. Prilocaine/Citanest – least toxic of the amide anesthetics – useful in regional or IV anesthesia – >600 mg in adults or >10 mg/kg would result to methemoglobinemia in newborns due to metabolites of prilocaine (Toluidine) which converts Hb to methemoglobin – treatment: methylene blue 1-2 mg/kg 4. Bupivacaine/Marcaine – used in OB anesthesia – tends to block cardiac Na channel longer making it cardiotoxic – cardiotoxic effects are enhanced during pregnancy 5. Etidocaine/Duranest – rapid onset, longer duration – motor block exceeds sensory block – useful in operations where muscle relaxation is important
6. Ropivacaine – 0.5% produces less motor effect than bupivacaine – eliminated rapidly thus less myocardial toxicity PHARMACOKINETICS OF LOCAL ANESTHETICS (LA): 1. Absorption - determined by a. site of injection - rapid with IV compared to SQ - intercostally more rapid than brachial plexus because it is more vascular b. dose of local anesthesia- the higher the dose, the higher the absorption c. vascularity - the more vascular, the more rapid is absorption d. addition of vasoconstrictors (e.g. Epinephrine) - delays the absorption e. vasoactive property- all are vasodilators thus rapid absorption except cocaine with its vasoconstrictive prop. 2. Distribution - factors that affect rapidity & extent of diffusion a. pKa- acidosis from local interaction retards diffusion due to ↑ degree of ionization b. concentration- the more the conc. the greater extent of diffusion c. lipid solubility- more extensive diffusion Subarachnoid- rapid onset of action Site of action of LA is the /are the : SC, spinal nerve roots, dorsal root ganglia, & peripheral nerve roots 3. Metabolism - depend on chemical structure of LA - plasma ester → faster rate of metabolism - amide → hepatic enzymes 4. Excretion - physical & pathologic factors that affect excretion/ clearance/elimination: a. ↓ CO- impair removal of LA from plasma b. ↓ hepatic blood flow *e.g. Lidocaine – rate of infusion to treat dysrhythmia should be reduced with CHF to avoid pt. toxic plasma c. liver disease- prolongs elimination half life/time of amine amide group of anesthetics d. age- does not consistently alter initial dose of LA, but the subsequent doses should be modified to avoid cumulative effect - Prolonged half-life in neonates - Adult levels in 6 mo. e. AB imbalance: f etal acidosis → transfer of LA from mother to fetus Drug Interactions Volatile Anesthetic (Cimetidine, Propranolol) alter clearance of LA thus
inhibition of mixed factor from oxidation & ↓ hepatic bids flow (amide LA)
Combination of LA - Mixture of 2 LA to produce l ong duration of action - Disadvantage: toxicity for mixtures is additive
Choice of local Anesthetics depend on: 1. plasma/nerve block 2. Duration of anesthesia desired 3. Speed of onset 4. Potential toxicity Effects of LA on ORGAN System - Most important on: Respiratory system Cardiovascular (CVS) CNS Cardiovascular System - effect of all LA exerts dose dependent, negative isotropic effect in cardiac muscles - ↓ myocardial contractility → ↓ cardiac output → ↓ venous return→ ↓ BP (hypotension) which may be compounded by peripheral vasodilating effect/action of LA
Myocardial contractility- dependent on higher conc. of LA - ↓ contractility when ↓ NA channel blockade block of ANS & affect CVS S/Sx of effect of LA 1. bradycardia 2. hypotension If unrelated→ cardiac arrest Presenting symptoms of local anesthetic overdose during GA: 1. cardiac dysrhythmia 2. circulatory collapse
Cocaine- cardiovascular reaction: vasoconstriction due to inhibition of uptake of norepinephrene by adrenergic nerve terminals HPN Ventricular arrhythmia - Cocaine induced arrhythmia reversed by adrenergic antagonist & Ca channel antagonist Respiratory System - depress hypoxic drive a response to low PaO 2 - apnea can result from phrenic & intercostal nerve paralysis - depression of medullary center - spinal anesthesia – block also intercostal n. but pt. still has adequate response as long as phrenic n. not involved - Local anesthesia tends to relax bronchial muscles LIDOCAINE: block reflex bronchoconstriction w/ intubation Neurological -toxicity for local anesthetics & organ system affected 1. CNS- more vulnerable to toxicity, site of pre-monitoring - signs of overdose in awake patient - first to be affected
Early symptoms: a. circumpolar numbness b. tongue parenthesis c. dizziness Sensory complaint - Tinnitus - blurring of vision If early symptoms cannot be recognized → pt. goes to excitatory stage/phase -restlessness/ agitation -nervousness - Paranoia
* Lidocaine in low conc. can provide treatment of arrhythmia * Bupivacaine – cardiotoxic among the LA because it bounds stronger to NA channels and is compounded in pregnancy by hypoxemia & respiratory acidosis - associated with pronounced depolarization changes -binding to cardiac Na channel at 1 degree of CHON binding, resuscitation more prolonged & difficult to reverse
From CNS excitation → CNS depression Slurring of speech Drowsiness Unconsciousness Muscle twitching heralds onset of tonic clonic seizure → convulsion→ continue → respiratory arrest
Excitatory reaction due to selective blockade of inhibitory pathways if LA is given esp. local infiltration, best precautionary measure is to give pt. benzodiazepine- ↑ threshold of induced seizure Management: 1. oxygenate pt. patent airway maintained 2. give anticonvulsant If convulsion last > 15 min → hypoxia *Diazepam- onset of effect is delayed instead give thiopental (barbiturate) has rapid of effect; if still ineffective may use m. relaxants such as succinylcholine (muscle relaxant of choice) which has a rapid onset of effect Pt. with ↑ ICP - give lidocaine 1.5mg/kg to attenuate ↑ ICP → sympathetic stimulation (pt. not yet adequately anesthetized) Cocaine- stimulate CNS, causes sense of euphoria - restlessness, emesis, tremors, convulsions & respiratory failure during cocaine toxicity Systemic Toxicity of Local Anesthetics Precaution: 1. When you give LA, be ready with “E” drugs Epinephrine – for hypotension, if HR cannot be Atropine- for bradycardia 2. Pt. must be monitored constantly for s/symptoms of toxicity, injection may be stopped, must be given early recognition and prompt treatment 3. large doses of LA best administered in divided doses w/ frequent aspiration - dose of any drug mistakenly given/ N may be limited 4. Add epinephrine solution slows uptake of drugs & provide sensitive marker for side effects like tachycardia 5. Benzodiazepines may serve as anticonvulsant - dose required may be observed by CNS toxicity SPINAL, EPIDURAL AND CAUDAL ANESTHESIA
- major conduction blockade anesthesia Complications: 1. Hypotension - immediate effect of spinal anesthesia - loss of sympathetic mediated peripheral resistance or venous capacitance vessels - vasodilation -> pooling of blood -> decreased IV return -> decreased cardiac output -> decreased BP
- aggravated by: hypovolemia individuals above 40 y.o. block higher than T4 or T5 - management: a. load patient with crystalloids or colloids before procedure 250 mL to 1000 mL 10-20 mL/kg BW b. after spinal anesthesia: give fluids: fast drip 50 cc if no increase in BP: sympathomimetic drugs or vasopressor drugs epinephrine for profound hypotension *sensory level – 2 dermatomes above block * motor level – 2 dermatomes below block * LP above L3 or L4 produces increased level of sympathetic block * Baseline systolic pressure <120/80 mm Hg also increases level of sympathetic block 2. Bradycardia - occurs secondary to unopposed vagal tone from the high sympathetic block - cardiac accelerator fibers at level of T1-T4 - management: anti-cholinergics (atropine sulphate) 3. Increased sensitivity to sedatives - due to the loss of peripheral input to reticular activating system 4. Nausea and vomiting - secondary to hypotension - decreased cerebral blood flow to vomiting center 5. Post-dural puncture headache - delayed complication - results from a leak in the dura mater losing CSF - post-spinal headachce - not produced by epidural anesthesia - severe headache at occipital area - change of position, upright position - use the smallest spinal needle possible - position of needle upon insertion: bevel should face upwards - management: a. analgesics b. hydration c. abdominal binder to increase ICP d. supine position for at least 6 hours e. epidural patch – autologous blood, 20 mL
6. Total spinal - local anesthetic depression of the cervical spinal cord and brainstem - total sympathetic block - SSx: dysphonia, dyspnea, upper extremity numbness, loss of consciousness, papillary dilation, hypotension, bradycardia, cardiac arrest - management: a. ventilation b. support circulation (increase BP, increase HR) with vasopressor drugs or atropine sulfate c. volume infusion A.Spinal Anesthesia - subarachnoid block - deposition of local anesthetic in the SAS - landmark: CSF - lumbar subarachnoid puncture - below L1 in adults; below L3 in children - principal site of effect: spinal nerve roots and spinal cord - Tuffier’s Line: point between the 2 iliac crests corresponding to L2 and L3 - subarachnoid space ends at S2 *Lateral approach - ideal for elderly patients - bypass the ligaments and arthritic structures - structures pierced: 1. skin 2. subcutaneous tissue 3. ligamentum flavum 4. dura mater 5. arachnoid mater * Midline approach - structures pierced: 1. skin 2. subcutanoues tissue 3. supraspinous ligament 4. interspinous ligament 5. ligamentum flavum 6. dura mater 7. arachnoid mater Contraindications: A.Absolute contraindications
1. infection at injection site 2. severe hypovolemia 3. bacteremia 4. infection at the site of procedure 5. intracranial hypertension 6. severe valvular stenotic lesion B. Relative contraindications 1. low back pain 2. sepsis 3. progressive degenerative/demyelinating neurologic diseases Factors that determine effect: 1. resorption of anesthetic agent from CSF into the systemic circulation 2. patient characteristics a. height b. position c. intraabdominal pressure – increased intraabdominal pressure spreads local anesthetic to a higher extent d. anatomic position of spinal cord or configuration of the spinal cord e. pregnancy f. CSF volume 3. direction of the needle - L1-L5 - betweenL1 and L2: higher spread of local anesthetic - direction of bevel upward/downward - total injected dose 4. baricity - ratio of density of CSF to density of the local anesthetic - >1: hyperbaric – gravitates to dependent areas - 1: isobaric - <1: hypobaric – solution will float Complications of Spinal Anesthesia: 1. direct injury to nerve – may produce paresthesias 2. hematoma formation 3. abscess formation – persistent neurologic deficits or severe back pain 4. adhesive arachnoisitis – injection of an irritant to the SAS 5. effect of spinal anesthesia on thermoregulation – vasodilation from spinal anesthesia -> patient cannot shiver in response to hypothermia 6. patients on thrombolytic/fibrinolytic therapy should not receive regional anesthesia except in extreme cirxumstances 7. vagal predominance – suggests risk for cardiovascular collapse during spinal anesthesia
8. cardiac arrest after spinal anesthesia – resuscitation, vasopressor drugs, epinephrine 9. transient neurologic syndrome – from lidocaine – manifestations: pain in the buttocks and dorsal lower extremities – resolves after 1 week in 90% of patients – sharp, lancinating or dull, aching, cramping, or burning pain – symptoms improve during movement and responds to NSAIDS – pain is worse during night time – contributing factor: lithotomy position B. Epidural Anesthesia - epidural block; blind technique - landmark: loss of resistance because of negative pressure in the epidural space - epidural space is widest at L2; contains fat and lymphatic tissue - cervical, thoracic, lumbar, and sacral areas - increased tendency to inject intravascularly - site of action: spinal nerve roots and spinal cord - extends to the foramen magnum and ends at the sacral hiatus - segmental block - requires a larger needle - slower onset of effect than spinal anesthesia *SA: 3 minutes *EA: 10-20 minutes C. Caudal Anesthesia - a form of epidural anesthesia - sacral hiatus (S5) - dense, lower levels of block - ideal for herniorrhaphy in children - limitation: highly variable onset in adults - risk of injection into the venous plexus - difficulty of maintaining stability Advantages: 1. avoidance of airway manipulation – useful in asthmatics, difficult intubation, full stomach 2. decreased stress response – HPN and tachycardia is less 3. decreased thrombogenesis and subsequent thromboembolism in orthopaedic hip surgery 4. improved bowel motility with less distention 5. less post-op nausea and sedation 6. better post-op pain control – abdominal surgery 7. less pulmonary dysfunction
8. faster turnover at the end of anesthesia Complications: gradual and not as profound as spinal anesthesia Advantages of Spinal anesthesia over Caudal anesthesia 1. metabolic stress response to anesthesia and surgery is reduced 2. 20-30% reduction in blood loss 3. decreases the incidence of venous thromboembolic complications by as much as 50% 4. pulmonary compromise appears to be less 5. endotracheal intubation is avoided 6. mental status can be assessed
INTRATHECAL OPIOIDS: - intensive visceral analgesia - prolongs sensory block - opioid receptors at 3rd and 4th lamina of the substantia gelatinosa at dorsal horn of spinal cord - lipophilic opioid receptors: localized effect; rapid onset; >6 hrs duration (fentanyl) - hydrophilic opioid receptors: slower onset, duration 6-24 hours (morphine)