general surgery anaesthesia

Anesthesia and Cardio-Pulmonary Resuscitation

Lecture 1Department General Surgery

The themes of practical training1. Cardiopulmonary resuscitation. Symptoms of

clinical death. Safar’s triple manoeuvre. Breathing.2. Cardiopulmonary resuscitation. Chest compression.

Complications of the CPR.3. Anesthesia. Local anesthesia.4. Anesthesia. General anesthesia.

Part I: Anesthesia

• The word is derived from the Greek words an, which means “without” and aithesia which means “feeling”

• The use of medical anesthesia was first reported in 1846

• The development of anesthesia has made today’s modern surgical techniques possible

History of Anesthesia

1771-Karl Scheel & Joseph Priestly

- discovery of O2

1772-Joseph Priestly -

discovery of N2O

History of Anesthesia

1846-Dr. William T.G. Morton First anesthesia specialist Oct. 16, 1846 - Ether Day

at Harvard Medical School

Oliver Wendell Holmes suggested the name

"Anesthesia"

History of anesthesia

• Ether synthesized in 1540 by Cordus• Ether used as anesthetic in 1842 by Dr.

Crawford W. Long• Ether publicized as anesthetic in 1846 by Dr.

William Morton• Chloroform used as anesthetic in 1853 by Dr.

John Snow

• Endotracheal tube discovered in 1878• Local anesthesia with cocaine in 1885• Thiopental first used in 1934• Curare first used in 1942 - opened the “Age of

Anesthesia”

Part I: Anesthesia

All methods of anesthesia divides into two large groups:

local Elimination of painful sensation from a specific part of the body without

loss of consciousness

general Drug-induced depression of CNS to prevent all perception of sensation

during a procedure or surgery

Part I: Anesthesia. Local anesthesia.

Local anesthesia: topical block local infiltration nerve block – intercostal anesthesia, brachial plexus

blocks, peripheral nerve block of the arm, etc. spinal anesthesia epidural anesthesia caudal anesthesia

• A local anesthetic is an agent that interrupts pain impulses in a specific region of the body without a loss of patient consciousness.

• Normally, the process is completely reversible -- the agent does not produce any residual effect on the nerve fiber.

CocaineSouth American Indians used to induce

euphoria, reduce hunger, and increase work tolerance in sixth century

• The first local anesthetic was Cocaine which was isolated from coca leaves by Albert Niemann in Germany in the 1860s.

• The very first clinical use of Cocaine was in 1884 by Sigmund Freud who used it to wean a patient from morphine addiction. It was Freud and his colleague Karl Kollar who first noticed its anesthetic effect.

• Kollar first introduced it to clinical ophthalmology as a topical ocular anesthetic. Also in 1884, Dr. William Stewart Halsted was the first to describe the injection of cocaine into a sensory nerve trunk to create surgical anesthesia.

• Cocaine remains popular in medicine today, but only as a topical anesthetic, because of its unique vasoconstrictive properties.

All local anesthetics are weak bases, classified as tertiary amines.

Typical structure of local Anesthetic Molecule

Ester AmideCocaineProcaine (Novocaine) (1905)

Benzocaine (1900)

Tetracaine (1930)

Chloroprocaine (1952)

Lidocaine (Xylocaine) (1944)

Mepivacaine (1957)

Prilocaine (1960)

Bupivacaine (1963)

Ropivacaine (1995)

Esters are hydrolyzed in plasma by pseudo-cholinesterase. One of the by-products of metabolism is paraaminobenzoic acid, the common cause of allergic reactions seen with these agents.

Amides are metabolized in the liver to inactive agents. True allergic reactions are rare.

• Local anesthetics work to block nerve conduction by reducing the influx of sodium ions into the nerve cytoplasm.

• Sodium ions cannot flow into the neuron, thus the potassium ions cannot flow out, thereby inhibiting the depolarization of the nerve.

• If this process can be inhibited for just a few Nodes of Ranvier along the way, then nerve impulses generated downstream from the blocked nodes cannot propagate to the ganglion.

Topical anesthesia.

Cream “EMLA”

10% lidocaine solution

• Injection of local anesthetic around a peripheral nerve

• Can be used for anesthesia during surgery or for post-op pain relief

• Examples: ankle block for foot surgery, supraclavicular block for post-operative pain control after shoulder surgery

Spinal anesthesia.

• A local anesthetic agent (lidocaine or bupivacaine) is injected into the subarachnoid space- Spinal anesthesia is also known as a subarachnoid block

• Blocks sensory and motor nerves, producing loss of sensation and temporary paralysis

Possible Complications of Spinal Anesthesia• Hypotension• Post-dural puncture headache (“Spinal headache”)

caused by leakage of spinal fluid through the puncture hole in the dura - can be treated by blood patch

• “High Spinal”- can cause temporary paralysis of respiratory muscles. Patient will need ventilatory support until block wears off

Part I: Anesthesia. Local anesthesia. Epidural anesthesia.

• Local anesthetic agent is injected through an intervertebral space into the epidural space.

• May be administered as a one-time dose, or as a continuous epidural, with a catheter inserted into the epidural space to administer anesthetic drug

Part I: Anesthesia. Local anesthesia. Systemic toxicity.

Adverse effects of local anesthetics• Allergic reactions

– Mild or severe• Systemic toxicity

– Most often due to accidental intravascular injection

– Lightheadedness, visual changes, muscular twitching, seizures, coma,

– Arrhythmias, cardiac depression

Part I: Anesthesia. Local anesthesia. Systemic toxicity.

Essentially all systemic toxic reactions associated with local anesthetics are the result of over-dosage leading to high blood levels of the agent given. Therefore, to avoid a systemic toxic reaction to a local anesthetic, the smallest amount of the most dilute solution that effectively blocks pain should be administered.

• Injection of Local Anesthetic.wmv

Part I: Anesthesia. General anesthesia

General anesthesia (narcosis)

Inhalation A. Noninhalation

Intravenous (IV)

Intramuscular (IM)

Rectal Oral

• Effects of general anesthesia:1. Hypnosis (sleep) and Amnesia 2. Analgesia3. Loss of reflexes4. Muscle relaxation5. Neurovegetative protection• Effects produced by depression of the CNS &

blocking pain stimuli at the level of the cerebral cortex

• Perioperative — begins with decision to have surgery, lasts until patient is transferred to operating room

• Intraoperative — extends from admission to surgical department to transfer to recovery room

• Postoperative — lasts from admission to recovery room to complete recovery from surgery

Three Phases of Perioperative Period

Part I: Anesthesia. General anesthesiaThe stages of anesthesia

Preparation: physical examanation (Informed Consent Information)

premedicationAnesthesia: Stages of anesthesia • Induction — from administration of anesthesia to

ready for incision• Maintenance — from incision to near completion of

procedure• Emergence — starts when patient emerges from

anesthesia and is ready to leave operating room

Informed Consent Information• Description of procedure and alternative therapies• Underlying disease process and its natural course• Name and qualifications of person performing

procedure• Explanation of risks and how often they occur• Explanation that patient has the right to refuse

treatment or withdraw consent

Anesthesia Monitoring Devices:• Electrocardiograph (EKG or ECG)• Pulse oximeter (SpO2 and HR)• Blood pressure monitor • Temperature probe

Part I: Anesthesia. General anesthesiaInhalation Anesthesia.

• Effects of general anesthesia:

1. Analgesia

2. Hypnosis (sleep)

and Amnesia

3. Loss of reflexes

4. Muscle relaxation

5. Neurovegetative protection

Nitrous Oxide

Halothane

Isoflurane

Desflurane

Sevoflurane

Enflurane

Part I: Anesthesia. Inhalation Anesthesia.Nitrous Oxide• Prepared by Priestly in 1776• Anesthetic properties described by Davy in 1799• Characterized by inert nature with minimal metabolism• Colorless, odorless, tasteless, and does not burn• Simple linear compound• Not metabolized• Only anesthetic agent that is inorganic• Major difference is low potency• MAC value is 105%• Weak anesthetic, powerful analgesic• Needs other agents for surgical anesthesia• Low blood solubility (quick recovery)

Part I: Anesthesia. Inhalation Anesthesia.Nitrous Oxide• Minimal effects on heart rate and blood pressure• May cause myocardial depression in sick patients• Little effect on respiration• Safe, efficacious agent• Manufacturing impurities toxic• Hypoxic mixtures can be used• Large volumes of gases can be used• Beginning of case: second gas effect• End of case: diffusion hypoxia

Part I: Anesthesia. Inhalation Anesthesia.Halothane• Synthesized in 1956 by Suckling• Halogen substituted ethane• Volatile liquid easily vaporized, stable, and nonflammable• Most potent inhalational anesthetic• MAC of 0.75%• Efficacious in depressing consciousness• Very soluble in blood and adipose• Prolonged emergence• Inhibits sympathetic response to painful stimuli• Inhibits sympathetic driven baroreflex response (hypovolemia)• Sensitizes myocardium to effects of exogenous catecholamines-- ventricular

arrhythmias• Decreases respiratory drive-- central response to CO2 and peripheral to O2

– Respirations shallow-- atelectasis– Depresses protective airway reflexes

• Depresses myocardium-- lowers BP and slows conduction• Mild peripheral vasodilation

Part I: Anesthesia. Inhalation Anesthesia.Halothane Side Effects• “Halothane Hepatitis” -- 1/10,000 cases

– fever, jaundice, hepatic necrosis, death– metabolic breakdown products are hapten-protein conjugates– immunologically mediated assault– exposure dependent

• Malignant Hyperthermia-- 1/60,000 with succinylcholine to 1/260,000 without– halothane in 60%, succinylcholine in 77%

• Classic-- rapid rise in body temperature, muscle rigidity, tachycardia, rhabdomyolysis, acidosis, hyperkalemia, DIC– most common masseter rigidity– family history

Part I: Anesthesia. Inhalation Anesthesia.• Malignant Hyperthermia (continued)

– high association with muscle disorders– autosomal dominant inheritance– diagnosis--previous symptoms, increase CO2, rise in CPK

levels, myoglobinuria, muscle biopsy– physiology--hypermetabolic state by inhibition of calcium

reuptake in sarcoplasmic reticulum– treatment--early detection, d/c agents, hyperventilate,

bicarb, IV dantrolene (2.5 mg/kg), ice packs/cooling blankets, lasix/mannitol/fluids. ICU monitoring

– Susceptible patients-- preop with IV dantrolene, keep away inhalational agents and succinylcholine

• Learn to Intubate During General Anaesthesia....wmv

Part I: Anesthesia. General anesthesiaIntravenous Anesthesia.

• Effects of general anesthesia:

1. Analgesia

2. Hypnosis (sleep)

and Amnesia

3. Loss of reflexes

4. Muscle relaxation

5. Neurovegetative protection

Narcotic agonists

Ketamine

ThiopentalPropofol Diazepam

Etomidate Midazolam

Muscle RelaxantsDepolarizing – SuccinylcholineNondepolarizing – Vecuronium

Droperidol

Part I: Anesthesia. Intravenous Anesthesia.• First attempt at intravenous anesthesia by Wren in

1656-- opium into his dog• Use in anesthesia in 1934 with thiopental• Many ways to meet requirements-- muscle relaxants,

opoids, nonopoids• Appealing, pleasant experience

Thiopental• Barbiturate• Water soluble• Alkaline• Dose-dependent suppression of CNS activity--

decreased cerebral metabolic rate (EEG flat)

Part I: Anesthesia. Intravenous Anesthesia.Thiopental• Varied effects on cardiovascular system in people--

mild direct cardiac depression-- lowers blood pressure-- compensatory tachycardia (baroreflex)

• Dose-dependent depression of respiration through medullary and pontine respiratory centers

• Noncompatibility• Tissue necrosis--gangrene• Tissue stores• Post-anesthetic course

Part I: Anesthesia. Intravenous Anesthesia.Etomidate• Structure similar to ketoconozole• Direct CNS depressant (thiopental) and GABA agonist• Redistribution• Little change in cardiac function in healthy and cardiac

patients• Mild dose-related respiratory depression• Decreased cerebral metabolism• Pain on injection (propylene glycol)• Myoclonic activity• Nausea and vomiting (50%)• Cortisol suppression

Part I: Anesthesia. Intravenous Anesthesia.Ketamine• Structurally similar to PCP (phencyclidine)• Interrupts cerebral association pathways --

“dissociative anesthesia”• Stimulates central sympathetic pathways• Characteristic of sympathetic nervous system

stimulation-- increase HR, BP, CO• Maintains laryngeal reflexes and skeletal muscle tone• Emergence can produce hallucinations and

unpleasant dreams (15%)

Part I: Anesthesia. Intravenous Anesthesia.Propofol• Rapid onset and short duration of action• Myocardial depression and peripheral

vasodilation may occur-- baroreflex not suppressed

• Not water soluble-- painful (50%)• Minimal nausea and vomiting

Part I: Anesthesia. Intravenous Anesthesia.

Narcotic agonists (opiods)• Used for years for analgesic action-- civil war for wounded soldiers• Predominant effects are analgesia, depression of sensorium and respirations• Mechanism of action is receptor mediated

• Minimal cardiac effects-- no myocardial depression• Bradycardia in large doses• Some peripheral vasodilation and histamine release -- hypotension• Side effects nausea, chest wall rigidity, seizures, constipation, urinary retention

Narcotic agonists (opoids)• Meperidine (demerol), morphine, alfentanil,

fentanyl, sufentanil. But morphine and fentanyl are commonly used.

• Naloxone is pure antagonist that reverses analgesia and respiratory depression nonselectively-- acts 30 minutes, effects may recur when metabolized

Muscle Relaxants• Current use of inhalational and previous intravenous agents do not fully provide control of

muscle tone• First used in 1942-- many new agents developed to reduce side effects and lengthen duration

of action• Mechanism of action occurs at the neuromuscular junction

Neuromuscular Junction

Part I: Anesthesia. Intravenous Anesthesia.Nondepolarizing Muscle Relaxants• Competitively inhibit end plate nicotinic cholinergic receptor• Intermediate acting (15-60 minutes): atracurium, vecuronium,

mivacurium• Long acting (over 60 minutes): pancuronium, tubocurarine,

metocurine• Difference-- renal function• Tubocurare-- suppress sympathetics, mast cell degranulation• Pancuronium-- blocks muscarinics• Reversal by anticholinesterase-- inhibit acetylcholinesterase

– neostigmine, pyridostigmine, edrophonium– side effects muscarinic stimulation

Depolarizing Muscle Relaxants• Depolarize the end-plate nicotinic receptor• Succinylcholine used clinically

– short duration due to plasma cholinesterase– side effects-- fasiculations, myocyte rupture,

potassium extravasation, myalgias– sinus bradycardia-- muscarinic receptor– malignant hyperthermia

Part I: Anesthesia. General anesthesia• Aspiration

– Inhalation of GI contents & acids• Results in mild respiratory status changes to sudden death

• Pulmonary dysfunction– Hypoventilation

• Treated with increased oxygenation, reversal of drugs, positive pressure ventilation

Postoperative anesthesia complications• Respiratory: atalectasis, aspiration, pneumonia• GI: Nausea, vomiting, decreased peristalsis, paralytic

ileus• U: Urinary retention, kidney dysfunction

Part II. Cardiopulmonary resuscitation

2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations was approved on November 2005.

A lot of regulations was changed.

Part II. Cardiopulmonary resuscitationSudden death Unexpected death of the patient, who is in

good general health condition. Appearance of the death within few hours from the onset of first symptoms of illness.

Cardiac sudden death.

Every tenth (third) of patients could be saved by proper life support.

Part II. Cardiopulmonary resuscitationLife For normal functioning all cells of the body

require oxygen. If oxygen is not provided, death of organism appears within 4..5 minutes.

Brain is the tissue most susceptible to anoxia (absence of oxygen).

Process of the death

Is not a momentary but stepwise process, which can take certain time.

Five steps of the death:– Preagony– Terminal pause– Agony– Clinical death (reversible injury) Biological death (irreversible injury)

Agony is a stadium which preceeds to the death. Function of vital organs is severly disturbed, and conditions required for survival of organism cannot be met.

Unconsciousness Blood pressure is undetectable No pulse on arteriesClinical death: circulation stops completely and

that leads to the cessation of breathing and nervous system activity.

Symptoms of clinical death

No pulse on arteries (carotid or femoral)

Change of skin colour Unconsciousness Gasping, cessation of breathing Dilatation of eye pupils

Duration of clinical death is 3(5) minutes

Biological death is irreversible condition. Metabolism of and functioning of vital organs has completely ceased. Organ damage is as extensive that resuscitation of the body is impossible.

Evident symptoms of the death: Rigor mortis Death spots on the body Drop of body temperature to the level of the

surrounding

Cardiopulmonary Resuscitation – CPR

BLSBasic life supportAdult, pediatric

A(C)LSAdvanced (Cardiac) Life SupportAdult, pediatric

PRCPost-resuscitation care Adult, pediatric

Adult BLS sequenceBasic life support consists of the following sequance

of actions:1. Make sure the victim, any bystanders, and you

are safe.2. Check the victim for a response (gently shake his

shoulders and ask loudly, “Sir. Or Ms., are you all right?”)

3 A. If he responds: Leave him in the position in which you find him

provided there is no further danger. Try to find out what is wrong with him and get

help if needed. Reassess him regularly.

Adult BLS sequence3 B. If he does not respond: Shout for help, call 911 (USA and Canada)

or 03 (Ukraine and Russian Fed) Turn the victim onto his back and then

open the airway using head tilt and chin lift:

- place your hand on his forehead and gently tilt head back.- with your fingertips under the point of the victim’s chin, lift the chin to open the airway.

Adult BLS sequence 4. Keep the airway open, look, listen, and

feel for normal breathing. Look for chest movement Listen at the victim’s mouth for breath

sounds. Feel for air on your cheekLook, listen and feel for no more than 10

sec to determine if the victim breathing normally. If you have any doubt whether breathing is normal, act as if it is not normal.

Safar’s triple manoeuvre Head tilt Jaw thrust Open mouth

Triple Airway Manoeuvre.wmv

Adult BLS sequence5 A. If he is breathing normally:• Turn him into the recovery position• Send or go for help, or call for an ambulance.• Check for continuated breathing.5 B. If he is not breathing normally:Ask someone to call for an ambulance. Kneel by the side of the victim. Pinch the soft part of the victim’s nose closed, using the

index finger and thumb of your hand on his forehead. Allows his mouth to open, but maintain chin tilt. Take a normal breath and place your lips around his mouth,

making sure that you have a good seal.

Recovery position

Adult BLS sequence (cont)5B. Cont. Blow steadily into his mouth whilst watching for

his chest to rise; take about one second to make his chest rise as in normal breathing; this is an effective rescue breath.

Maintaining head tilt and chin lift, take your mouth away from the victim and watch for his chest to fall as air comes out.

Take another normal breath and blow into the victim’s mouth once more to give a total of two effective rescue breaths.

Give each rescue breath over 1 sec rather than 2 sec.

Adult BLS sequence (cont)6. Check the victim’s pulse.6 A. If pulse on the carotid artery is not palpable –

begin chest compression. Place the heel of one hand in the centre of the

victim’s chest. Place the heel of your other hand on the top of

the first hand. Interlock the fingers of your hands and ensure

that pressure is not applied over the victim’s ribs. Do not apply any pressure over the upper abdomen or the bottom end of the bony sternum (breastbone).

Adult BLS sequence (cont) Position yourself vertically above the victim’s

chest and, with your arms straight, press down on the sternum 4-5 cm.

After each compression, release all the pressure on the chest without losing contact between your hands and the sternum. Repeat at a rate of about 100 times a minute (a little less than 2 compressions a second).

Compression and release should take an equal amount of time.

Perform 30 compressions and after that open the airway again using head tilt and chin lift.

Adult BLS sequence (cont) Perform 2 inflations. Then return your hands without delay to correct

position on the sternum and give a further 30 chest compressions.

Continue with the chest compressions and rescue breaths in the ratio of 30:2.

Stop to recheck the victim only if he starts breathing normally; otherwise do not interrupt resuscitation.

Adult BLS sequence (cont)If your rescue breaths do not make the chest

rise as in normal breathing, then before your next attempt:

Сheck the victim’s mouth and remove any visible obstruction.

Recheck that there is adequate head tilt and chin lift.

Do not attempt more than two breaths each time before returning to chest compressions.

Adult BLS sequence (cont)If there is more than one rescuer present,

another should take over CPR about every 2 min to prevent fatigue. Ensure the minimum of delay during the changeover of rescuers.

Chain of survival

EARLY CPR

EARLY DEFIBRILLATION

EARLYACCESS

EARLY ADVANCED

Key - Life

CPR.wmv

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