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ANESTHESIA MACHINE as it is worked out.

INDICATOR: phenolphthalein (pink), ethyl violet

- Also known as Anesthesia Delivery System (purple)
- Most important in the practice of anesthesia - If the canister has no heat and exhausted, no color change will be noted so
- Partner in life of an anesthesiologist that the pt. will manifest tachycardia, inc. HR, inc. BP w/o deepening of
- functions: anesthetics as the concentration inc.
1. supply a mixture of anesthetizing and life sustaining gases V. Vaporizer
2. permits spontaneous/controlled ventilation - Convert liquid anesthetic to vapor
3. provides monitoring devices - Calibrated for accuracy and precision
4. help anesthesiologist keep patient alive, safe, and adequately VI. Corrugated tubing, rebreathing bags and face masks
anesthetized- MOST IMPT. FXN Rebreathing bags
- after evaluating patient, check first whether or not the equipment is - comes in various sizes depending on the pt
functioning since this is another cause of intraoperative mortality or morbidity - smallest is 500ml for newborns and the largest in adults is 5L
- crucial to patient safety - most commonly used: 2 and 3 L
- modern anesthesia machine: face masks also has varied sizes depending on the pt, transparent
1. ventilation breathing tubing - rubber; reusable, heavy
2. monitoring devices universal connector- fits to any size of the face masks, breathing bag and
endotracheal tube
Basic elements of an Anesthesia Machine corrugated tubing- has the following reasons why it is made as corrugated:
I. Source of Gases 1. to be flexible
Most commonly used gases: (used inside OR) 2. for moisture trapping
1. O2- pure gas 3. resist kinking
2. NO- liquefied gas 4. provide turbulent flow vs laminar flow
Source of compressed gases - kinking of endotracheal tube would cause obstruction
1. pipeline system escape valve and gas scavenging system
- modern source of gases in higher center; instead of tanks, you see - where waste gases accumulate as they are eliminated w/o increasing the
outlets of gas that came from central supply; color coded risk of the personnel
- back up tanks must however be available in case the system runs out - prevents contamination of the OR with anesthetics
of supply
- Oxygen- color green (2/3 liquid; 1/3 gas) Lung exposure to anesthetic gases could cause:
- NO- color blue 1. spontaneous abortion
2. cylinders 2. fetal malformation
- full tank of O2 exert 2000-2200 lbs/in2 w/ a volume of 625- 650 ml 3. malignancies personnel of OR
- NO exert 750 lbs/in2 in 1590 L
II. Pressure Regulator- reduces gas pressure Safety measures:
- Pressure reducing bulb =45-50 lb/in2 (cylinder pressure) reduced pressure 1. color coding
w/c is a workable pressure 2. Pin Index System
- Pipeline: 40-45 lb/in2 3. O2 fail-safe system stops flow of all gases except O2
III. Flow meter 4. O2 analyzer- monitors the O2 content in the patient
- Control flow of gases
- Knob is also color coded Additional Notes:
IV. CO2 absorber Ether- lacks controllability
- Prevent accumulation of excess CO2 thru soda lime and bara lime w/c - open drop method
comes in granules that are colored and it changes from white to pink/blue - polluting the OR and personnel
NO- 1st trimester, can cause abortion
used to control respiration and allow the anesthesiologist to attend to other - Important because anesthesiologist act as guardians of the anesthetized
matters such as parenteral fluid therapy and other essentials for therapy of patient in the entire monitoring
the pt. - Monitor patient as well as the equipment
if the body becomes tense, pt. may end up having bronchospasm w/c must - GOAL: TO KEEP PATIENT ALIVE AND ADEQUATELY ANESTHETIZED
be differentiated with laryngospasm since both are managed differently
Bronchospasm- bronchodilators are given Monitoring
Laryngospasm- give muscle relaxants - from the Latin word MONERE meaning to warn, to keep watch over, to
check systematically
Assisted/ controlled respiration - process by w/c anesthesiologist recognize and evaluate potential physiologic
- must be done by manual compression of the bag w/c could result to problems by identifying prognostic trends of patients in a timely manner
periodic inflation - vigilance implies monitoring
- anesthesiologists focus must always be on the patient - effective monitoring to the patient and equipment, used in administering
anesthesia should:
Hazards associated with the use of anesthetic machine: 1. diminish preventable mishaps
1. inadvertent administration of hypoxic gas mixture 2. reduce poor outcome that may follow surgical procedures, disease
- such error usually result from carelessness of anesthesiologist or of the processes or adverse reactions
mechanical design of the anesthetic machine Purpose:
- carelessness/failure to open cylinder 1. To regulate the depth of the anesthesia by knowing how the patient respond
- loose connection to anesthesia
- clogged lines Expected: decrease BP, dec. HR, breathing is regular
- sticking of flow meters 2. Treatment of physiologic derangements such as arrhythmias, hypotension,
- failure/ faulty installation of the service O2 supply organ ischemia, blood loss, hypotension, pulmonary dysfunction
2. overdose of anesthetics Estimated blood volume:
- observed change of O2 flow Adult male: 60 cc per kilogram
- failure to add diluting O2 Adult female: 55 cc per kilogram
- 1st vaporizer- copper kettle Adult allowable blood loss= 20% of EBV
- Ether- is very irritating including OR personnel Children: 75- 80 cc per kilogram
3. inadvertent use of several agents caused by leaking valves Allowable blood loss in children is only 10%
3. Detect expected catastrophe such as MI and airway obstruction
Safety devices: - thru vigilant observation
*Fail Safe System
- eliminates the possibility of administering hypoxic gas mixture Monitors used:
- color coded with knobs - Physiologic monitoring- continuous assessment of patients conditions with
* Proper use of anesthesia machine rest upon the anesthesiologist and no emphasis with change
substitute of VIGILANCE- motto of Anesthesia Qualitative- sense
* Hypoxia must be reversed before 4 minutes Quantitative- measurements

Purpose of Anesthesia Machine A. Basic Monitors

1. help anesthesiologist keep the patient alive, safe and adequately anesthetized 1. senses- smell, touch, hearing, sight
2. monitor precise gas mixtures but variable composition delivered to the patient 2. monitoring devices- supplement anesthesiologist perception of more
sensitive and continuous assessment of the patient
Limitation: - Normal pCO2=36-44 mmHg
when there is fluctuation, discrepancy of results occur - Capnogram- graphic display of airway pCO2 as a function of time
dont interpret results if it is not a substitute for a good and sound - Rapid fall of end tidal CO2 indicates air embolism in sitting craniotomy
clinical judgment
Factors that influence the shape of the capnogram:
Implication of improved patient safety: Respiratory flow rate
- decrease morbidity and mortality for patients Disturbance of pulmonary blood flow
- decreased post op. complications Disturbance of ventilation
- less costly insurance premium and malpractice & diminished legal
cost * Abrupt change in shape signify an acute change in the patients physiologic
What to observe?
1. surgical field- note for the color of the blood Capnography can:
observe oxygenation- bright red = good Detect any breathing circuit problem
dark red = poor - Breathing circuit disconnection-decreased in tidal CO2
2. movement - Accidental extubation
3. skin color of patient - Airway obstruction
4. tearing - Low cardiac output or hypoperfusion- decreased tidal CO2
5. positions - Venous air embolim
- Hypothermia
B. Essential monitors: - Hypoventilation
1. PulseOoximeter - Cardiac arrest
- O2 sat, HR and peripheral oxygenation Can differentiate tracheal and esophageal intubation
- Standard care for monitoring oxygenation in anesthesia to detect - In tracheal intubation, there is a consistent concentration of carbon
adequacy during anesthesia dioxide from the trachea
- Normal O2 = 97-100% - In esophageal intubation, there is disappearance of CO2
- Reduces the occurrence of perioperative hypoxemia - Clinical way of estimating whether tube is on the right main bronchus ->
- Can detect decreases in O2 sat before cyanosis place tip of tube at the carina and note for :
Breath sounds equal on both sides
*hypoxemia- when detected early in pulse oximetry may result to a Equal expansion of the chest
reversible organ injury Endotracheal intubation goes to the right because it is wider and
*93-94% drop, no cyanosis yet straighter
*5 minutes with decreased O2 sat results to irreversible brain injury
Changes in End tidal CO2
- Useful in: A. sudden decrease
Titration of O2 therapy Low cardiac output/ hypoperfusion
Weaning patients from O2 ventilators Pulmonary embolism- inc. physiologic dead space
In neonates, decreases the rate retrolental fibroplasias where 95% O2 Venous air embolism
sat should be maintained Leak in air breathing circuit
2. Capnography Hypometabolism
- Detects adequacy of ventilation Hyperventilation
- Measure s end tidal CO2 and clinical estimate of partial CO2 Extubation
- Used to differentiate endotracheal from esophageal intubation
Obstruction to airway - Rhythm disturbance
Cardiac arrest Atrial tachycardia- common during anesthesia induction not
B. Sudden Increase associated with a hemodynamic instability
Hyperthermia- because of inc. CO2 production Ventricular tachycardia- medical emergency associated with
Sepsis hypotension and poor cardiac output
Malignant hyperthermia- Inc. Co2 production
- Early manifestation: tachycardia- mottling of the skin, skeletal muscle 4. BP apparatus
rigidity, cyanosis, dysrrythmia - Fundamental to determine the effects of anesthetic agent to the
- Late manifestation: fever cardiovascular system
Skeletal muscle rigidity - Determine adequacy of circulation during anesthesia
Hypoventilation - Blood pressure- is the pressure exerted by the blood on the walls of the
Re- breathing arteries as it flows
Changes in systolic BP correlates with myocardial O2 requirement
Slow increase in CO2 concentration: Changes in diastolic BP correlates with changes in coronary perfusion
a. partial airway obstruction- kinking of breathing tube pressure
b. inspired CO2 is increased- due to malfunction of the breathing circuit - Pulse pressure= SBP- DBP
c. exhaustion of CO2 absorbent - Methods:
Invasive- intraarterial BP monitoring
3. ECG (non-invasive)- monitors cardiac rhythm & conduction Non- Invasive- BP cuff apparatus + stethoscope
- In 1906, invented by Einthoven by using a string Galvanometer
- Tells about surface recording of electrical activity of the heart/ Mean Arterial pressure
myocardium - (SBP +2DBP)/3
- Usually displays electrical activity of the heart, nothing about the - hydrostatic pressure that provide diffusion
adequacy of myocardial pump function
- Detects: rate, rhythm, changes in the ST segment assumed by the degree 5. Precordial stethoscope and esophageal stethoscope
of oxygenation of the myocardium - Stethoscope- note quality of HS & BS
- TEE: heart anatomy and function; expensive but a useful perioperative - Precordial stethoscope- placed at pts. precordium
monitor Bounding- poor vital signs
- Functions: detection of Good volume- good status of pt.
1. dysrhythmia Distant HS- inadequate volume
2. conduction abnormality Rales and crackles- fluid overload
3. pacemaker malfunction - Esophageal stethoscope- important in thyroidectomy and in pts. with
4. electrolyte disturbance weak pulses (shock pulses)
- taken on patients 40 y.o. and above or in younger pt. with the history of - Distant heart sounds: hypovolemia
chest pain 6. Temperature probe/ monitoring
HPN Thermoregulation by hypothalamus is decreased during general
Previous MI anesthesia
- Most valuable if monitoring begins before induction of anesthesia Hypothalamus- temperature regulating system w/c is affected by
because any abnormal ECG or marginal ECG findings preoperatively general anesthesia but not regional anesthesia
worsens during intraoperative
Hypothermia 7. anticholinergic blockade of sweating
common intraoperatively, a clinical state of subnormal body Site for monitoring depends on :
temperature where the body is unable to generate body heat and o Surgical procedure
maintain body temperature for bodily function o Type of anesthesia
Due to: o Time of monitoring
a. Cold ambient environment in the OR
b. Heat loss during surgical operation Route of monitoring or taking temperature:
c. prevents Action of anesthetic 1. Axilla- 1 degree Celsius below core temperature
Upper limit= 35 degrees Celsius (95 degrees Fahrenheit) 2. Skin- 3-4 degrees Celsius below body core temperature
Common in extremes of age 3. Rectal- does not reflect body changes in core temperature
1. small children/ infants- inc. ratio of body surface area to body - Complication: rectal perforation
weight 4. Mouth- accurately reflects core body temperature
2. elderly- lack compensatory mechanism to generate heat 5. nose- reflects brain temperature because of its close proximity to carotid
also seen in patients with spinal cord injuries as well as burned artery (ICA); contraindicated in head trauma and rhinorrhea
patients 6. External auditory meatus- close proximity if tympanic membrane to ICA-
alters thermoregulation centers > core body temp.; can perforate tympanic membrane if placed too
shivering deeply
peripheral vasodilation 7. Bladder catheter- can approximate body temperature if urine flow is
drugs that induce hypothermia: high
1. opioids- sympatholytic properties 8. pulmonary artery catheter- most accurate, expensive and invasive way
2. barbiturates- peripheral vasodilation of taking body temperature
3. muscle relaxants- reduce muscle tone 9. Nasopharynx- brain temp. because of its proximity to ICA w/c when
- prevents shivering thermogenesis probe or placed deeply can cause epistaxis
4. regional anesthesia- produce sympathetic blockade 10. Esophagus- core body temperature, probe must be in lower third or
- sensory blockade for thermal receptors mid esophagus; accurately reflects core body temperature; when
deeply placed can cause trauma
Adverse effect of hypothermia:
1. decrease O2 availability- ischemia Core temperature- reflects the temperature of the vital organs of the
2. cardiac arrhythmia/ cardiac dysrrhythmia body. Accurate temperature in nasopharynx, esophagus, external
3. potentiates anesthetic effects and muscle relaxants- inc. sensitivity auditory and pulmonary artery
to anesthetic drugs
4. coagulopathies Peri-operative hypothermia
5. inc. vascular resistance - common result of anesthetic induced alteration in thermoregulation
6. post operative shivering - cold temperature of environment in the OR
- heat loss during surgical procedure
Less common; there is increase of 2 degrees Celsius / hour 7. Central venous pressure monitoring (CVP)
Causes: - 80% of circulation is in the atrial circulation
1. fever secondary to stress of surgery - Invasive, central venous catheter is used cannulating central venous
2. sepsis circulation
3. inability to warm patients - Normal CVP= 5-10 cmH2O or 1.5 11 mmHg
4. malignant hyperthermia- a late manifestation
5. exposure to endogenous pyrogenes
6. inc. metabolic rate due to thyrotoxixosis and pheochromocytoma
Interpreting results of CVP: - useful in increased myocardial o2 demand (myocardial ischemia) seen as
Low CVP: hypovolemia; no volume loss-> inc. venous capacitance due ventricular wall motion on echocardiography where there is abrupt
to vasodilation change of ventricular wall motion
High CVP; fluid overload Transesophageal echocardiography (TEE)
- useful in differentiating hypovolemia vs. poor myocardial
CVP+BP: contractility as a cause for depressed cardiac output syndrome and
if decreased and decreased or normal BP, think of hypovolemia open heart surgery
- Mgt. inc fluid and monitor if there will be inc in CVP after fluid is - assessment of myocardial function and ischemia
increased - valves can be assessed either for valvular replacement or valvular
if inc CVP and normal BP, think of hypervolemia repair
- Mgt: stop giving fluids and give diuretics - enables surgeon to ensure adequacy of the valve repair before
if inc CVP and decreased BP, think of cardiac failure closing the chest
- Mgt: diuretics and digitalis - drawback: expensive
If heart function fails, there is backflow of blood to venous circulation
manifesting as increase in the CVP INHALATIONAL ANESTHETICS
- Sufficient to produce complete anesthesia- amnesia, analgesia, muscle
Central venous pressure (CVP) relaxation, unconsciousness
- pressure exerted by blood returning to the right side of the heart - Drawback: in inc. concentration has undesirable effect of cardiorespiratory
- distinguish between hemorrhage and CHF depression
- decrease CVP:
a. vasodilation Main purpose of general anesthesia:
b. hypovolemia 1. altered physiologic state; loss of consciousness w/c is reversible
c. secondary to spinal anesthesia 2. amnesia, analgesia, muscle relaxation
- increase CVP:
a. Vasoconstriction Property of ideal anesthetic:
b. increase intrathoracic pressure 1. predictable action and rapid onset of action from induction to emergence
c. increase positive pressure ventilation from anesthesia
d. Right intraventricular afterload 2. provide muscle relaxation
pulmonary embolism 3. cardiostability and bronchodilation
pulmonary hypertension 4. not trigger malignant hyperthermia, nausea and vomiting as significant side
condition that impairs diastolic filling time effect
ex.: cardiac tamponade- impaired diastolic filling; 5. not flammable
incompetence of tricuspid valve 6. not undergo biotransformation in the body
7. allow easy instillation of concentration at the site of action
Indicators for CVP monitoring:
1. elderly patients: 70 above * no anesthetic agent have all the ideal properties
2. patients whom large blood or fluid exchange is done- prevents * Atropine- used as premedication to prevent salivation
hypervolemia and overtransfusion *Central anesthesia- depress excitatory transmission in spinal cord at level of
3. heart diseases dorsal root horn
4. major traumatic injury
5. anticipation of major blood loss Early inhalational anesthetic:
1. Ether
8. Echocardiography: - dont produce cardiovascular depression
- useful in monitoring continuous heart anatomy and function - produce very good muscle relaxation
- flammable, cause post-op nausea and vomiting, produce copious STAGE II:
salivation; no drop in BP (stimulate sympathetics) - stage excitement and delirium
2. Nitrous Oxide - starts with loss of consciousness and ends at onset of automatic
- lack potency and cant be used alone and used as an analgesic today respiration
- 2nd gas effect to potentiate effects of other anesthetics - Px may go into struggling and vomiting may occur
3. Chloroform- hepatotoxic - do not stimulate px
4. Cyclopropane- highly flammable - dont start operating
5. Trichloroethylene- side effect: produce phosgene - risk of aspiration during laryngospasm and bronchospasm
6. Fluoroxene- severe flammability and produce nausea and vomiting; first
fluorinated; hepatotoxic STAGE III:
7. Methoxyfluorane- side effect: nephrotoxic due to fluoride ion; slow induction - surgical stage
of anesthesia - from automatic respiration to end in onset of respiratory paralysis

Newer Drugs: Phase I- onset of automatic respiration and ends in cessation of eyeball
Fluorinated volatile anesthetic movement
1. halothane Phase II- cessation of eyeball movement to commencement of intercostals
2. enflurane- theoretical risk of seizure, not used in epileptic Px paralysis
3. isoflurane Phase III- commencement of intercostal paralysis to complete intercostal
4. sevoflurane paralysis
5. desflurane Phase IV- complete intercostal paralysis to diaphragmatic paralysis
*3,4,5-> commonly used today: 3,4,5- substituted halogenated ether
*Halothane- substituted halogenated alkane STAGE IV:
- breathing and circulation stops
Drugs difficult to use or administer due to: - cardiac arrest and death
1. narrow margin of safety of inhalational anesthetic - stage of overdosage
2. variability among patients- severe side effects because of variations of pts
- therefore must be used in titration; requires continuous monitoring *stages of anesthesia is best appreciated using ether
*most useful signs:
To produce its pharmacologic effects: eyelash reflex
drug administration at an adequate dose eyeball movement
sufficient potency dilation of pupils
deliver to active site of action changes in respiration - Most sensitive indicator of depth of
site of action: Brain anesthesia!
site of entry: lung
*Brief Procedures- start incision at stage III, phase I
STAGES OF ANESTHESIA: *long procedures (explore lap)- start at stage III, phase II; px may react to
- introduced by Arthur Guedel insertion of ETA
*surgeons should not start operation unless okayed by anesthesiologist
- begins in induction and ends in loss of consciousness 3 GENERAL ANESTHESIA PHASES
- use eyelid reflex I. Induction
- eyelid reflex is lost - induce patient to sleep; critical period since anything can happen to
- analgesia and amnesia patient
- take vital signs as often as possible even at 3-5 mins
- occurs when anesthetizing partial pressure has been achieved by the brain anesthetizing partial pressure must be given in high
brain in high concentration concentration
- unique in a way since respiratory tract used as entry
- immediately during induction, give 3% to achieve anesthetizing partial 3. Alveolar Ventilation
pressure - faster ventilation, the more rapid is the uptake

Factors that increase the speed of induction: II. Circulatory phase

1. inc alveolar concentration - Important factor is cardiac output- where those with apprehension,
2. high flow within breathing circuit fear, muscular activity, thyrotoxicosis will be difficult to anesthetize
3. increase in respiratory flow/ inc minute ventilation because of inc. blood flow to the peripheral organs causing a decrease
blood to the brain
II. Maintenance Phase - in shock patients, from hemorrhage and dehydration, there is
- Goal: To maintain optimal or unchanging anesthetizing partial pressure in peripheral vasoconstriction less blood flow to the skin brain
the brain as reflected in alveolar partial pressure receives high blood flow anesthesia is easily delivered

III. Emergence/ Recovery Phase Barometric pressure- decrease with higher altitude
- lowers concentration of anesthetic so that partial pressure in the brain also - Higher conc. is needed in inc. altitude vs. in lower altitude because
lowers vagometric pressure is lower therefore decrease in pressure

Uptake of Inhalational is divided into; MAC (minimum alveolar concentration

I. Pulmonary phase - concentration of anesthetic that will prevent movement/ motor
- should produce significant concentration to build up in the lungs (alveoli) response in response to a noxious stimuli (surgical incision)
- through diffusion, it goes to the pulmonary circulation - anesthetics are measured using this
- relation between administered dose and quantitative effect produced in
* concentration of anesthetic In tissue - solubility and partial pressure of an expression of drug potency
anesthetic - concentration of anesthetic that would prevent movement of Pxs
*solubility is constant and partial pressure changes controlled by the - 50% of Pxs in response to (surgical incision)
concentration of the anesthesia
Factors that Affect Pulmonary Uptake: NO 0.47 (least potent) 104 (least potent)
1. Inhaled concentration/ expired concentration: Halothane 2.3(most potent & most 0.77
- maintains concentration in alveoli soluble in blood)
- the higher the concentration, the higher the uptake Ether 12
- rate of rise of anesthetic to bloodstream Methoxyflurane 12 0.16 (most potent)
Enflurane 1.91 1.7
2. Solubility of Anesthetic Isoflurane 1.4 1.15
- affects the rate of diffusion of anesthesia in blood stream Desflurane 0.42 (insoluble therefore 6.0
- expressed in blood gas partition coefficient where the higher the rapiduptake)
value, the more soluble Sevoflurane 0.69 1.7
- 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 *Methoxyflurane- nephrotoxic, not used today
rapidly in large quantities rapid blood solubility goes to the * the smaller the MAC value, the more potent is the anesthetic
tissues therefore takes time before brain is reached and so cant attain
INHALED ANESTHESIA Complete general anesthetic state: can be produced by inhalational anesthetic
- easier to measure close but difficult to measure the effect but must be given in higher dose:
- In 1965, EGER introduced MAC-therapeutic effect of anesthetic 1. loss of consciousness
2. analgesia of the entire body
Factors that Affect MAC: 3. amnesia
1. Age- highest MAC: 6-12 mos.; decrease as age increases and in premature 4. degree of relaxation
2. health condition Blood- Gas partition coefficient
3. hypothermia- 1 degree Celsius 2.5 % decrease - solubility of inhalational coefficient
4. hyponatremia - inc. Blood- Gas partition coefficient: inc. concentration
5. Opioids, Barbiturates and alpha2 blockers, Ca channel blockers - inc. solubility: decrease rise of alveolar BGPC
6. Alcohol intoxication
Factors that may inc. MAC tends to increase cerebral blood flow and it normalizes with time
1. Young Age- 10% increase in infants and children vs. young adults; infancy increases ICP; must be given in titration
@ term- 6 mos. greatest increase
2. chronic alcohol use inc. amount is required 1. Nitrous Oxide
3. CNS hypo-osmolality increases cerebral blood flow
4. Acute ingestion of CNS stimulant (dextroamphetamine, cocaine) cerebral vasodilation associated with moderate increase of ICP
5. inc. CNS neurotransmitters (e.g. MAO inhibitors-antidepressant) 2. Halothane
6. Hypothermia will go back to normal after 2 hours after induction
provides the greatest increase in blood flow due to vasodilation
Factors that decrease MAC 3. Isoflurane
1. old age- decrease by 6% produces greatest reduction in cerebral blood flow that would result
2. prematurity to a flat EEG
3. hypothermia- for every 1 degree Celsius drop, there is a corresponding has cerebral protecting effect
decrease of MAC of 2-3% associated with better maintenance relationship between cerebral
4. CNS hyperosmolality metabolic O2 requirement and cerebral blood flow
5. CNS depressants (opioids, benzodiazepines) results in the lowest increase in cerebral blood flow
6. decrease CNS neurotransmitters (e.g. anti-HPN drugs) inhalational anesthetic of choice
7. intake of tranquilizers 4. Enflurane
8. acute alcohol intoxication- no anesthesia required for minor operations produces a seizure-like activity exaggerated in the presence of
9. alpha2 agonists (e.g. clonidine) hypocapnia
10. pregnancy 5. Volatile anesthetics
11. hyponatremia alter the production and absorption of CSF which tend to normalize
12. taking Ca-channel blockers with time

Does NOT affect MAC: Respiratory System

1. Gender decreases mucociliary clearance
2. Duration of anesthesia volatile anesthetics produce drug specific and dose related respiratory
3. Hypo/hypercarbia depression of ventilation through the medullary center (direct) and
4. hyperkalemia effects on the intercostals muscles (indirect)
5. thyroid function characterized by rapid shallow respiration
produces a decrease in tidal volume and increase in respiratory rate impairment of baroreceptor activity
inhibits histamine release inactivates methionine synthetase by oxidizing cobalt in Vit. B12
decreases airway resistance by relaxation of bronchial smooth muscles producing a decrease in myelin formation
and inhibits bronchoconstriction also inhibits thymidelate synthetase
results in hypocapnia produces megaloblastic anemia, pernicious anemia, and
ventilatory response to hypercapnia is attenuated neuropathies
loss of intercostals muscle function which results in rocking boat
appearance of ventilation where the chest collapses, the abdomen 3. Nitrous Oxide
protrudes, and the diaphragm descends during inspiration rapid discontinuation decreases O 2 tension
relaxation of muscles of the jaw resulting to partial airway obstruction diffusion hypoxia can be prevented by allowing the patient to breath
produces dose dependent decrease of the ventilator response tp CO 2 O2 for the next 5-10 minutes
as well as hypoxemia increased incidence of spontaneous abortion
1. Halothane 4. Halothane
used in patients with asthma increases sensitivity of myocardium to epinephrine
not pungent and so it does not produce irritation and cause arrhythmogenic
laryngospasm children are more sensitive
least irritating cholinergic; vagally-induced bradycardia effect in children
2. Sevoflurane middle age, obesity, and with familial predisposition to halothane
can be given to children before giving isoflurane and desflurane toxicity increase risk
3. Nitrous Oxide metabolism of more than 20% under hypoxic conditions may cause
no airway irritation hepatic necrosis
30% more soluble than nitrogen 5. NO plus inhalational anesthetic
stimulates the sympathetic system decreases BP but minimal due to NO having a mild sympathomimetic
increases RR; decreases TV effect
no significant muscle relaxation 6. NO plus high doses of opioids
increases post-op nausea and vomiting tremendous drop in blood pressure
7. Isoflurane and Enflurane
Cardiovascular System less likely than halothane to produce dysrrhythmia in the presence of
CV depressant manifested as hypotension; decreased BP epinephrine
produces drug-specific dose dependent circulatory depression premature ventricular contraction and tachyarrhythmia
vasodilation (isoflurane, desflurane) effects commonly seen in adults than in children
depressed myocardial contractility (halothane, enflurane) 8. Halothane and Enflurane
decreased sympathetic tone direct myocardial depressant
1. Isoflurane 9. NO and Sevoflurane
increased heart rate with decreased BP indicates a better produces the least myocardial depression
maintenance with response to baroreceptor reflex in tha carotid 10. Desflurane
depresses vagal activity associated with production of CO
dilates coronary arteries in the presence of reduced pressure
not as potent as nitroglycerine Myocardial depression from inhalational anesthetics is enhanced by
do not use in patients with CAD beta-blockers!
Coronary Steal Syndrome: dilatation of the LA in normal areas to
divert blood flow from stenotic lesion Signs and Symptoms of overdose of anesthetics:
2. Halothane a. hypotension
minimal to absent chages in HR b. bradycardia
c. decreased cardiac output a. reduced splanchnic blood flow
d. arrhythmia b. hypoxemia
e. cardiac arrest c. malnutrition
d. exposure to halothane
Renal System e. underlying diseases
secondary to decrease in BP decreased renal blood flow f. obesity
decreased GFR g. elevated liver enzyme

1. Methoxyflurane Musculoskeletel System

nephrotoxic because it releases fluoride ions when metabolized causes relaxation
50 mmol/L considered nephrotoxic all inhaled anesthesia w/ exception of NO can trigger malignant
2. Sevoflurane hypothermia
not lipid soluble
produces smooth and rapid induction in pediatric patients Uterus
not pungent in odor relaxation; contributes to uterine blood loss; affects the placenta and
soda lime can degrade sevoflurane fetus
vinyl ether/compound A: degradation product of sevoflurane by
soda lime is nephrotoxic BIOTRANSFORMATION
oxidative metabolism occurs in the liver thru the P450 system
nausea and vomiting 1. Nitrous Oxide
1. Nitrous oxide methionine synthesis = 20% inc. risk of congenital anomalies;
not used in cases of pneumothorax, pneumocephalus, and intestinal abortion
obstruction 2. NO + more potent volatile anesthetic
diffuses rapidly into any air space containing cavity 2nd gas effect, potentiate effects of inhalalational anes.; bld gas
distends air-filled viscera which contributes to nausea and vomiting partition coefficient of 0.27
decreases splanchnic blood flow greatest reduction in cerebral metabolic activity (isoflurane)
increases uptake of concurrent anesthetics dose dependent spike wave in EEG (enflurane)
insoluble in blood
2nd gas effect rapid induction of anesthetic to produce general anesthesia:
2. Halothane provides continued adjustment of - loss of consciousness
affects the liver anesthetic depth - amnesia and blunting of some
increase in liver size; anorexia, nausea, vomiting provides continued monitoring of reflexes
anesthetic concentration does not provide complete analgesia
Halothane Hepatitis elimination through the lungs and muscle relaxation
autoimmune hypersensitivity reaction; occur in repeated provides rapid emergence from IV inducing agent allows rapid
exposure to halothane at short intervals anethesia recovery after its termination
metabolit of halothane has a direct hepatotoxic effect most accomplished without an iv access
specifically during the reductive metabolism of halothane that good in pediatric patients
leads to production of free radicals considered hepatotoxic choosing of drug is based on the
hepatic necrosis which is immune mediated situation
decreased hepatic blood flow cardiovascular depression is greatly
predisposing factors: affected by halothane
INTRAVENOUS ANESTHETICS 1. Thiobarbiturates sulfur containing
Examples of IV non-opioids anesthetics: a. Thiopental
1. Barbiturate (Thiopental) b. Thiamidal
2. Benzodiazepine 2. Exybarbiturates
3. Propofol a. Methohexetal
4. Ketamine
5. Etamidate Substitution on C2 and C5 provides CNS effect
6. Opiods inc. concentration; side effect loss of consciousness and anticonvulsant
Characteristics of IV anesthetics: -C5 w/ a phenyl group: Phenobarbital
1. provide rapid nearly instantaneous onset w/o causing pain on injection C5 w/ a methyl group: methohexetal produce seizure-like movement
2. provide smooth induction w/o any signs of muscular twitching or movement -#2 C atom w/ O2: oxybarbiturates
and excitement -#2 C atom w/ S: thiobarbiturates
3. safe and cause minimal perturbation of cardiovascular and respiratory
function I. Barbiturates
4. short- acting to awaken the patient rapidly to full normal CNS fxn A. Thiopental
5. metabolism to inert substance and excretion should be rapid and complete ultrashort-acting barbiturates used in anesthesia
so that no accumulation would occur thereby allowing the drug to be used no analgesic effect ; does not block sensory afferent impulses
for a long period of time should not be used as a sole analgesic
6. amnesia for intraoperative events should be complete H2O insoluble for weeks
w/ acidic drugs, result in precipitation of barbiturates
NOTE: not a single IV conducting agent that possesses all characteristics pH 10.5-11 (alk solution)
prepared as a 2.5% solution
Dosing requirement based on: only given through IV because extravasation can cause tissue necrosis
1. intravascular volume of the patient due to high alkalinity given into a vein not into an artery because it will
2. co-morbidities cause chemical endarteritis resulting to vasospasm and damage to inner
3. age layer of the artery
4. chronic medications give lidocaine and -adrenergic blocking drug to relieve spasm
In the elderly: thrombosis: give heparin
- inc. volume of distribution, dec. elimination clearance 60% of drug exist in an unionized form at pKa = 7.6
- prolonged effect ph of 7.4 lipid-soluble, rapid diffusion into a vessel- rich group (brain)
- adjust dose conc. inc. rapidly, unconsciousness sets in w/in 15 minutes
- more sensitive to IV anesthetics 70-85% bound to albumin; 15% free-active subs
onset: 1 hr rate circ. time w/ max. effect w/in 1 min
Mechanism of Action: enhance the transmission of GABA interfering the decreased albumin:decreased CHON binding
transmission of potential 1. liver cirrhosis
2. in presence of other drugs (NSAIDS, ASA) competes w/ Thiopental
Effect of barbiturates at the synapses: for the binding site
1. facilitate the effect of GABA 3. acidosis
2. blocks excitatory neurotransmitter Ach and glutamic acid dose: 3-5 mg/kg IV
termination of effect : through redistribution to inactive tissues (muscle,
Barbiturates = urea + malonic acid fats)
half life of 6-12 hours contributes to the slow recovery and hang-over 2. allergy
sensation histamine release; sulphur molecule
sometimes not used to maintain anesthesia because it tends to
accumulate B. Relative
IV inducting agents have no analgesic properties except ketamine which 1. hypovolemia
cannot be used as a sole anesthetic especially if the procedure is long may cause profound hypotension
CNS depression in a dose dependent manner slowly titrated dosage when volume has been normalized
in geriatric patients: 30-40% dose reduction 2. hepatic failure
delayed metabolism
CNS effects prolonged effect
induction dose can decrease ICP
does not cause cerebral vasodilation B. Methohexital
reduction in cerebral O2 requirement drawback: presence of muscle twitching limits its usefulness in
maximum decrease in cerebral metabolism requirement as seen in EEG anesthesia
Cardiovascular effects requirement in anesthetic drug must not produce any excitatory
reduces CO by decreasing venous return movements
direct myocardial depressant
negative inotropic effect II. Ketamine
reduction in sympathetic outflow from CNS phencyclidine derivative
decreases arterial BP which elicits mild compensatory tachycardia N-methyl-D-aspartate receptor antagonist
in hypovolemia and in shock: bioavailability: IM-90%; peak blood concentration is achieved within 15
a. dont give Thiopental since it can be given after resuscitation minutes
b. only give 1.5 mg/kg IV awakening is due to redistribution to peripheral compartments
c. be ready with a sympathomimetic drug excreted through the kidneys
alternative to Thiopental: only one that has analgesic effect; profound analgesia
a. Etomidate produces minimal CV depression lamina specific suppression of spinal cord activity that interrupts
b. Ketamine has a tendency to stimulate the CV system transmission of pain signals to the brain
c. Propofol and Benzodiazepines decreases BP dose: 1-2 mg/kg BW IV or 4-8 mg/kg BW IM; produces analgesia for 10-
Respiratory effects 20 minutes
can produce depression of respiration (apnea) a dose of 0.1-0.3 mg/kg only produces analgesia; the patient does not
be ready with resuscitating equipment, ambu bag, laryngeal tube, etc. lose consciousness
never manipulate airway if the patient is anesthetized because it may used for brief surgical procedures
stimulate laryngospasm and bronchospasm recovery time: 60-90 minutes
decreases minute ventilation and tidal volume may act as a CV depressant in very ill patients
right shift in CO2 response curve 55% protein bound (1- acid glycoprotein)
produces a dose dependent medullary and pontine respiratory effects Norketamine: active metabolite with 1/3 to 1/5 potency of ketamine
most likely to have spasms: asthmatics, COPD patients, smokers which prolongs CNS effect of ketamine
associated with increase in airway secretion
Contraindications: must be given with an anti-cholinergic drug (glycopyrrolate)
A. Absolute 0.1 to 0.3 mg/kg for OB patients
1. porphyria can be given in the presence of CV failure, cardiac tamponade
increased ALA synthetase -> increased porphyrin
involvement of the intercostals and diaphragmatic muscles
Effects on organ systems Diazepam attenuates ketamines cardostimulatory effects and prolongs its
CNS halflife
not advisable to give to patients with mental disorders and SOLs Propanolol, Phenoxybenzamine and other sympathetic antagonists unmask
increases cerebral oxygen consumption, cerebral blood flow and ICP the direct effect myocardial depressant effects of ketamine
can produce visual/auditory hallucinations which can be reduced by Halothane + Ketamine produces myocardial depression
giving benzodiazepines Lithium prolongs the duration of action of ketamine
atropine sulphate increases post-op delirium
induces analgesia, amnesia, and unconsciousness III. Propofol
dose dependent CNS depression 2,6-diisopropylphenol
derivative of alkyl phenol
Respiratory insoluble in water
rapid intravenous bolus administration with opioids produces apnea contains soy bean oil, glycerine, and egg lecithin
does not produce respiratory depression do not give to persons allergic to eggs
a potent bronchodilator in pregnancy, use with caution for cesarian delivery
good induction agent for asthmatic patients can cause anaphylactic reactions
increased salivation can be attenuated by premedication with an may cause IV pain which can be lessened by prior injection of lidocaine
anticholinergic drug short-acting
good agent for out-patient anesthesia
increases arterial BP, heart rate, and CO Effects on Organ Systems
central stimulation of the SNS and inhibition of the reuptake of Cardiovascular
norepinephrine decrease in arterial BP due to a drop in systemic vascular resistance,
increase in pulmonary artery pressure and myocardial work cardiac contractility, and preload
should be avoided in patients with CAD, hypertension, CHF, and arterial hypotension is more pronounced than thiopental
aneurysms impairs the normalarterial baroreflex response to hypotension
beneficial to patients with acute hypovolemic shock vagally mediated bradycardia
Emergence delirium patients with cardiovascular diseases may not tolerate the decrease in
5-30% of patients especially in females MAP
aggravated by tactile and verbal stimulation
minimized by giving benzodiazepines Respiratory
vivid morbid dreams with morbid contents profound respiratory depression
floating sensations causes apnea following an induction dose
Dissociative Anesthesia useful during intubation or laryngeal mask placement
patient is dissociated from the environment causes histamine release which may produce bronchospasm
dissociation of the thalamus from the limbic cortex
the patient appears to be awake and conscious, eyes are open, can CNS
produce swallowing movements but cannot respond to sensory input decreases blood flow and ICP
patient is unaware and has no recollection of events can cause a critical reduction cerebral perfusion pressure in patients
the presence of nystagmus is a sign that the patient is already asleep with elevated ICP
antipruritic, antiemetic effect
Drug Interactions induction is accompanied by muscle twitching, spontaneous movement,
potentiates nondepolarizing muscle relaxants opisthotonus, or hiccupping due to subcortical glycine antagonism
Theophylline + Ketamine predisposes patients to seizures useful in the termination of status epilepticus
decreases intraocular pressure
Drug Interactions VII. Droperidol
older formulations potentiate the effect of nondepolarizing muscle a butyrophenone
relaxants antagonizes the activation of dopamine receptors
Fentanyl and Alfentanil concentrations may be increased by concomitant interferes with the transmission mediated by serotonin, norepinephrine,
administration of propofol and GABA
Midazolam + Propofol produces synergistic effect tranquilizer and antiemetic properties
-adrenergic blockade
IV. Benzodiazepines sedative effects are delayed by extensive protein binding
facilitates GABA receptor binding decreased ABP by peripheral vasodilation; antidysrhythmic effect
Flumazenil reverses most of the CNS effects of benzodiazepines do not give to patients with pheochromocytoma
does not depress respiration
1. Midazolam may stimulate hypoxic ventilatory drive
fast acting; water soluble addition of an opioid decreases the incidence of dysphoria
used as an inducting agent
minimal myocardial depression Advantage of Benzodiazepines over Barbiturates
maintains MAP and CO 1. benzodiazepines produce profound amnesia or anterograde amnesia
increases heart rate 2. therapeutic index is high
decreases ABP, CO, and peripheral vascular resistance 3. cardiovascular and respiratory depression is less
4. tolerance is rare
V. Opioids
effective at producing analgesia LOCAL ANESTHETICS
inhibits the presynaptic release and postsynaptic response to excitatory 40 years after general anesthesia
neurotransmitters Niemann observed a numbing effect on the tongue due to cocaine
transmission of pain impulses can be interrupted at the level of the
dorsal horn of the spinal cord Carl Kohler
myocardial function is maintained Father of Local Anesthetic
decreased MAP, secondary bradycardia, casodilation, blockage of an ophthalmologist
sympathetic responses demonstrated the use of topical cocaine for surgical anesthesia of the eye
histamine release with Meperidine and Morphine
Advantages of Using Local Anesthetics
VI. Etomidate 1. simplicity
carboxylated imidazole 2. most undesirable side effect of general anesthesia is avoided no loss of
depresses the reticular activating system consciousness; no danger of aspiration and regurgitation
mimics the inhibitory effects of GABA 3. methods are appropriate for ambulatory patients e.g. excision of cysts
disinhibitory effects on parts of the CNS that control extrapyramidal motor
activity Disadvantages
30-60% incidence of myoclonus 1. lack of patients acceptance may be due to ineffectual approach to patient
dissolved in propylene glycol 2. impracticality to anesthetize certain areas
pain on injection which can be lessened by lidocaine 3. insufficient duration of anesthesia
used for induction of general anesthesia 4. rapid absorption of local anesthetic into the blood stream with fatal and
rapid onset of action dude to high lipid solubility and large non ionized untoward reaction minimal if precautions are taken
fraction 5. uncontrollability of drugs
adrenocortical response to stress is reduced
Local Anesthetic Drugs 2. nerve fiber type
blocks neural conduction by their actions on the Na channel 3. degree of myelination
blocks generation of impulses in excitable tissue (spinal cord and myelination speeds up nerve conduction from one node of Ranvier to the
peripheral nerves) other
produces transient loss of sensory, motor and autonomic function increases speed of neural transmission
structural formula determines its physic-chemical properties 4. pH acidic medium antagonized blockade
5. electrolyte concentration hypokalemia and hypercalcemia antagonizes
Resting Membrane Potential blockade
-90 to -60 mV
spontaneous rapid phase of depolarization which in turn is a result of Differential Blockade
inward movement of Na from outside into the cell via Na channels describes the blockade of the peripheral nerve that occurs at different rates
recovery from anesthetic occurs in the opposite order
Membrane Expansion Theory 1. loss of autonomic function/sympathetic function
local anesthetic acts like general anesthetic that inhibits Na influx by 2. loss of pinprick or sensory function
expanding nerve membrane thus decreasing diameter of Na channels 3. temperature and touch discrimination
preventing Na to go inside 4. motor function

Structure of Local Anesthetic Drugs Classification of Local Anesthetics:

lipophilic group benzene ring/aromatic ring Ester group
hydrophilic group quaternary amine 1. cocaine addictive, systemic toxic effect; potent vasoconstrictor; drying of
intermediate group ester or amide linkage cornea
basis of the classification of local anesthetics 2. chloroprocaine
3. procaine also known as Novocaine
Physicochemical Properties of Local Anesthetics depend on: 4. tetracaine - pontocaine
1. substitution of the benzene ring Amide group
2. type of linkage of the intermediate chain 1. lidocaine also known as Xylocaine; antiarrhythmic
3. alkyl group attached to quaternary ring preparations contain preservatives (methylparabene) which may cause
allergic reactions
Physicochemical Properties of Anesthetic Drugs: 2. bupivacaine more cardiotoxic than the rest
1. Potency correlates with lipid solubility 3. mepivacaine
2. Onset of action depends on the degree of ionization; pKa; faster onset of 4. etidocaine
effect if unionized 5. prilocaine
3. Duration of action associated with plasma protein concentration binding 6. dubicaine
(albumin) 7. ropivacaine newest
4. Cm minimum blocking concentration
lowest concentration of local anesthetic that blocks nerve conduction Metabolism
measure of potency of local anesthetics Esters
metabolized by pseudocholinesterase in the plasma
Factors that affect Potency: hydrolysis is rapid and water-soluble metabolites are excreted through
1. nerve fiber size the urine
bigger fibers have lower excitability threshold; motor function; faster para-aminobenzoic acid (metabolite) has been associated with allergic
conduction velocity reactions
smaller fibers are blocked early by local anesthetics; pain, temperature and cocaine is partially metabolized in the liver and partially excreted
autonomic activity unchanged in the urine
unstable in solution 1 hour before IV insertion especially in children and VIP patients
metabolized by microsomal enzymes in the liver Factors that determine concentration of local anesthetic in the blood:
stable in solution 1. site of absorption
rare allergic reactions 2. redistribution
3. metabolism
Classification of Anesthetics According to Potency: 4. excretion
Weak potency
a. procaine 7mg/kg Intercostal anesthesia most rapid absorption for regional anesthetics
b. chloroprocaine 8-9 mg/kg
Intermediate potency Toxicity
a. lidocaine 5 mg/kg; w/ epinephrine 7 mg/kg due to inadvertent intravascular injection causing increased plasma levels of
b. mepivacaine 5 mg/kg local anesthetic
High potency a result of the systemic effects of local anesthetics
a. tetracaine 1.5 mg/kg
b. ropivacaine CNS
c. bupivacaine 2.5 mg/kg manifested as convulsions
more sensitive to the effects of local anesthetics
Epinephrine lightheadedness; tinnitus; peri-oral numbness; confusion; muscle
prolongs the effect of local anesthetic twitching; hallucinations; tonic-clonic seizures; respiratory arrest;
delay the absorption of local anesthetic due to the vasoconstricting effect unconsciousness
reduces its potential toxicity a. Transient Neurologic Symptoms
increases effectiveness of local anesthetic promoting more uptake into nerve - moderate to severe pain on lumbar area
cells producing profound analgesia - disappears within 7 days
increases neuronal blockade
b. Cauda Equina Syndrome
Presenting Symptoms of Overdose of Local Anesthesia: - lumbosacral plexus
numbness of the tongue - non-homogenous distribution of spinally injected anesthetic
in an awake patient
palpitations Cardiovascular
blurring of vision; circumoral numbness decreased CO, decreased contractility, hypotension, sinus bradycardia,
cardiac dysrhythmias ventricular dysrhythmias
cardiac collapse in patients under general anesthesia methemoglobinemia with prilocaine

Conditions when Epinephrine is contraindicated LOCAL ANESTHETIC DRUGS

cardiac arrhythmias Esters
hypertension 1. Cocaine
unstable angina pectoris not used due to its systemic toxicity and potential for drug addiction
peripheral nerve blocks topical application into nasal mucosa prior to endotracheal intubation
topical anesthetic to the conjunctiva but was withdrawn due to drying
Eutectic Mixture of Local Anesthetic (EMLA) effect
eutectic means easily melted only local anesthetic with a vasoconstricting effect
composed of 5% lidocaine and 5% prilocaine, 1:1 ratio 2. Procaine/Novocaine
dermal anesthesia for beginning an intravenous line lacks topical activity
rapid hydrolysis by plasma cholinesterase; can be used in high dosages 6. Ropivacaine
for infiltration and spinal anesthesia 0.5% produces less motor effect than bupivacaine
3. Chloroprocaine/Nesacaine eliminated rapidly thus less myocardial toxicity
short-acting; does not produce toxicity
cause permanent paraplegia when given inadvertently to the PHARMACOKINETICS OF LOCAL ANESTHETICS (LA):
subarachnoid space because of low pH and use of Na bisulfide 1. Absorption - determined by
EDTA causes severe back pain when given in large epidural doses of the a. site of injection - rapid with IV compared to SQ
drug - intercostally more rapid than brachial plexus because it is more vascular
4. Tetracaine/Pontocaine b. dose of local anesthesia- the higher the dose, the higher the absorption
long-acting and potent c. vascularity - the more vascular, the more rapid is absorption
systemic toxicity is greater d. addition of vasoconstrictors (e.g. Epinephrine)
for spinal anesthesia providing rapid onset - delays the absorption
e. vasoactive property- all are vasodilators thus rapid absorption except
Amides cocaine with its vasoconstrictive prop.
1. Lidocaine/Xylocaine 2. Distribution
introduced by Lofgren in 1948 - factors that affect rapidity & extent of diffusion
first drug of the amide class a. pKa- acidosis from local interaction retards diffusion due to degree of
topical anesthetic activity, rapid onset ionization
for infiltration, spinal, epidural and peripheral nerve block b. concentration- the more the conc. the greater extent of diffusion
IV lidocaine is used as an antiarrhythmic, antiepileptic, analgesic, irritant c. lipid solubility- more extensive diffusion
suppressant, and as a supplement to general anesthesia Subarachnoid- rapid onset of action
lower concentration is used for treatment of cardiac arrhythmia Site of action of LA is the /are the : SC, spinal nerve roots, dorsal root
dose: 5 mg/kg w/o epinephrine; 7 mg/kg with epinephrine ganglia, & peripheral nerve roots
1.5 mg/kg, 1-3 minutes before intubation to attenuate hypertension 3. Metabolism
2. Mepivacaine/Carbocaine - depend on chemical structure of LA
dose: 5 mg/kg - plasma ester faster rate of metabolism
metabolism is prolonged in the fetus and newborns - amide hepatic enzymes
not used in OB anesthesia 4. Excretion
longer duration of effect than lidocaine - physical & pathologic factors that affect excretion/ clearance/elimination:
3. Prilocaine/Citanest a. CO- impair removal of LA from plasma
least toxic of the amide anesthetics b. hepatic blood flow
useful in regional or IV anesthesia *e.g. Lidocaine rate of infusion to treat dysrhythmia should be reduced
>600 mg in adults or >10 mg/kg would result to methemoglobinemia in with CHF to avoid pt. toxic plasma
newborns due to metabolites of prilocaine (Toluidine) which converts Hb c. liver disease- prolongs elimination half life/time of amine amide group of
to methemoglobin anesthetics
treatment: methylene blue 1-2 mg/kg d. age- does not consistently alter initial dose of LA, but the subsequent doses
4. Bupivacaine/Marcaine should be modified to avoid cumulative effect
used in OB anesthesia - Prolonged half-life in neonates
tends to block cardiac Na channel longer making it cardiotoxic - Adult levels in 6 mo.
cardiotoxic effects are enhanced during pregnancy e. AB imbalance: fetal acidosis transfer of LA from mother to fetus
5. Etidocaine/Duranest
rapid onset, longer duration Drug Interactions
motor block exceeds sensory block Volatile Anesthetic (Cimetidine, Propranolol) alter clearance of LA thus
useful in operations where muscle relaxation is important inhibition of mixed factor from oxidation & hepatic bids flow (amide LA)
Combination of LA Cocaine- cardiovascular reaction: vasoconstriction due to inhibition of uptake of
- Mixture of 2 LA to produce long duration of action norepinephrene by adrenergic nerve terminals
- Disadvantage: toxicity for mixtures is additive HPN
Ventricular arrhythmia
Choice of local Anesthetics depend on: - Cocaine induced arrhythmia reversed by adrenergic antagonist & Ca channel
1. plasma/nerve block antagonist
2. Duration of anesthesia desired
3. Speed of onset Respiratory System
4. Potential toxicity - depress hypoxic drive a response to low PaO2
- apnea can result from phrenic & intercostal nerve paralysis
Effects of LA on ORGAN System - depression of medullary center
- Most important on: - spinal anesthesia block also intercostal n. but pt. still has adequate response
Respiratory system as long as phrenic n. not involved
Cardiovascular (CVS) - Local anesthesia tends to relax bronchial muscles
CNS LIDOCAINE: block reflex bronchoconstriction w/ intubation

Cardiovascular System Neurological

- effect of all LA exerts dose dependent, negative isotropic effect in cardiac -toxicity for local anesthetics & organ system affected
muscles 1. CNS- more vulnerable to toxicity, site of pre-monitoring
- myocardial contractility cardiac output venous return BP - signs of overdose in awake patient
(hypotension) which may be compounded by peripheral vasodilating - first to be affected
effect/action of LA
Early symptoms:
Myocardial contractility- dependent on higher conc. of LA a. circumpolar numbness
- contractility when NA channel blockade block of ANS & affect CVS b. tongue parenthesis
c. dizziness
S/Sx of effect of LA
1. bradycardia Sensory complaint
2. hypotension - Tinnitus
If unrelated cardiac arrest - blurring of vision

Presenting symptoms of local anesthetic overdose during GA: If early symptoms cannot be recognized pt. goes to excitatory stage/phase
1. cardiac dysrhythmia -restlessness/ agitation
2. circulatory collapse -nervousness
- Paranoia
* Lidocaine in low conc. can provide treatment of arrhythmia
From CNS excitation CNS depression
* Bupivacaine cardiotoxic among the LA because it bounds stronger to NA Slurring of speech
channels and is compounded in pregnancy by hypoxemia & respiratory acidosis Drowsiness
- associated with pronounced depolarization changes Unconsciousness
-binding to cardiac Na channel at 1 degree of CHON binding, resuscitation more
prolonged & difficult to reverse 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 - aggravated by:
esp. local infiltration, best precautionary measure is to give pt. benzodiazepine- hypovolemia
threshold of induced seizure individuals above 40 y.o.
block higher than T4 or T5
Management: - management:
1. oxygenate pt. patent airway maintained a. load patient with crystalloids or colloids before procedure
2. give anticonvulsant 250 mL to 1000 mL
If convulsion last > 15 min hypoxia 10-20 mL/kg BW
*Diazepam- onset of effect is delayed instead give thiopental (barbiturate) has b. after spinal anesthesia:
rapid of effect; if still ineffective may use m. relaxants such as succinylcholine give fluids: fast drip 50 cc
(muscle relaxant of choice) which has a rapid onset of effect if no increase in BP: sympathomimetic drugs or vasopressor drugs
epinephrine for profound hypotension
Pt. with ICP
- give lidocaine 1.5mg/kg to attenuate ICP sympathetic stimulation (pt. not *sensory level 2 dermatomes above block
yet adequately anesthetized) * motor level 2 dermatomes below block
* LP above L3 or L4 produces increased level of sympathetic block
Cocaine- stimulate CNS, causes sense of euphoria * Baseline systolic pressure <120/80 mm Hg also increases level of
- restlessness, emesis, tremors, convulsions & respiratory failure during cocaine sympathetic block
toxicity 2. Bradycardia
- occurs secondary to unopposed vagal tone from the high sympathetic
Systemic Toxicity of Local Anesthetics block
Precaution: - cardiac accelerator fibers at level of T1-T4
1. When you give LA, be ready with E drugs - management: anti-cholinergics (atropine sulphate)
Epinephrine for hypotension, if HR cannot be 3. Increased sensitivity to sedatives
Atropine- for bradycardia - due to the loss of peripheral input to reticular activating system
2. Pt. must be monitored constantly for s/symptoms of toxicity, injection may be 4. Nausea and vomiting
stopped, must be given early recognition and prompt treatment - secondary to hypotension
3. large doses of LA best administered in divided doses w/ frequent aspiration - decreased cerebral blood flow to vomiting center
- dose of any drug mistakenly given/ N may be limited 5. Post-dural puncture headache
4. Add epinephrine solution slows uptake of drugs & provide sensitive marker for - delayed complication
side effects like tachycardia - results from a leak in the dura mater losing CSF
5. Benzodiazepines may serve as anticonvulsant - post-spinal headachce
- dose required may be observed by CNS toxicity - not produced by epidural anesthesia
- severe headache at occipital area
SPINAL, EPIDURAL AND CAUDAL ANESTHESIA - change of position, upright position
- major conduction blockade anesthesia - use the smallest spinal needle possible
- position of needle upon insertion: bevel should face upwards
Complications: - management:
1. Hypotension a. analgesics
- immediate effect of spinal anesthesia b. hydration
- loss of sympathetic mediated peripheral resistance or venous c. abdominal binder to increase ICP
capacitance vessels d. supine position for at least 6 hours
- vasodilation -> pooling of blood -> decreased IV return -> decreased e. epidural patch autologous blood, 20 mL
cardiac output -> decreased BP
6. Total spinal 1. infection at injection site
- local anesthetic depression of the cervical spinal cord and brainstem 2. severe hypovolemia
- total sympathetic block 3. bacteremia
- SSx: dysphonia, dyspnea, upper extremity numbness, loss of 4. infection at the site of procedure
consciousness, papillary dilation, hypotension, bradycardia, cardiac 5. intracranial hypertension
arrest 6. severe valvular stenotic lesion
- management: B. Relative contraindications
a. ventilation 1. low back pain
b. support circulation (increase BP, increase HR) with vasopressor 2. sepsis
drugs or atropine sulfate 3. progressive degenerative/demyelinating neurologic diseases
c. volume infusion
Factors that determine effect:
A. Spinal Anesthesia 1. resorption of anesthetic agent from CSF into the systemic circulation
- subarachnoid block 2. patient characteristics
- deposition of local anesthetic in the SAS a. height
- landmark: CSF b. position
- lumbar subarachnoid puncture c. intraabdominal pressure increased intraabdominal pressure spreads
- below L1 in adults; below L3 in children local anesthetic to a higher extent
- principal site of effect: spinal nerve roots and spinal cord d. anatomic position of spinal cord or configuration of the spinal cord
- Tuffiers Line: point between the 2 iliac crests corresponding to L2 and L3 e. pregnancy
- subarachnoid space ends at S2 f. CSF volume
3. direction of the needle
*Lateral approach - L1-L5
- ideal for elderly patients - betweenL1 and L2: higher spread of local anesthetic
- bypass the ligaments and arthritic structures - direction of bevel upward/downward
- structures pierced: - total injected dose
1. skin 4. baricity
2. subcutaneous tissue - ratio of density of CSF to density of the local anesthetic
3. ligamentum flavum - >1: hyperbaric gravitates to dependent areas
4. dura mater - 1: isobaric
5. arachnoid mater - <1: hypobaric solution will float

* Midline approach Complications of Spinal Anesthesia:

- structures pierced: 1. direct injury to nerve may produce paresthesias
1. skin 2. hematoma formation
2. subcutanoues tissue 3. abscess formation persistent neurologic deficits or severe back pain
3. supraspinous ligament 4. adhesive arachnoisitis injection of an irritant to the SAS
4. interspinous ligament 5. effect of spinal anesthesia on thermoregulation vasodilation from spinal
5. ligamentum flavum anesthesia -> patient cannot shiver in response to hypothermia
6. dura mater 6. patients on thrombolytic/fibrinolytic therapy should not receive regional
7. arachnoid mater anesthesia except in extreme cirxumstances
7. vagal predominance suggests risk for cardiovascular collapse during
Contraindications: spinal anesthesia
A. Absolute contraindications
8. cardiac arrest after spinal anesthesia resuscitation, vasopressor drugs, 8. faster turnover at the end of anesthesia
9. transient neurologic syndrome from lidocaine Complications: gradual and not as profound as spinal anesthesia
manifestations: pain in the buttocks and dorsal lower extremities
resolves after 1 week in 90% of patients Advantages of Spinal anesthesia over Caudal anesthesia
sharp, lancinating or dull, aching, cramping, or burning pain 1. metabolic stress response to anesthesia and surgery is reduced
symptoms improve during movement and responds to NSAIDS 2. 20-30% reduction in blood loss
pain is worse during night time 3. decreases the incidence of venous thromboembolic complications by as
contributing factor: lithotomy position much as 50%
4. pulmonary compromise appears to be less
B. Epidural Anesthesia 5. endotracheal intubation is avoided
- epidural block; blind technique 6. mental status can be assessed
- landmark: loss of resistance because of negative pressure in the epidural
- epidural space is widest at L2; contains fat and lymphatic tissue - intensive visceral analgesia
- cervical, thoracic, lumbar, and sacral areas - prolongs sensory block
- increased tendency to inject intravascularly - opioid receptors at 3rd and 4th lamina of the substantia gelatinosa at dorsal
- site of action: spinal nerve roots and spinal cord horn of spinal cord
- extends to the foramen magnum and ends at the sacral hiatus - lipophilic opioid receptors: localized effect; rapid onset; >6 hrs duration
- segmental block (fentanyl)
- requires a larger needle - hydrophilic opioid receptors: slower onset, duration 6-24 hours (morphine)
- 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

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