anesthesia and cpr

Anesthesia and Cardio-
Pulmonary Resuscitation
Lecture 1
Department Anesthesiology and Intensive
Care
The head of a department: I.Titov, DrPh.

The themes of practical training
1. 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

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

History of anesthesia
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.

Cocaine
South 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 Amide
Cocaine
Procaine (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

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

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

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.

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. Analgesia
3. Loss of reflexes
4. Muscle relaxation
5. 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

The stages of anesthesia
Preparation: physical examanation
(Informed Consent Information)
premedication
Anesthesia: 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

Inhalation Anesthesia.
1. Analgesia
2. Hypnosis (sleep)
and Amnesia
3. Loss of reflexes
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)

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

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

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

 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

Intravenous Anesthesia.
1. Analgesia
2. Hypnosis (sleep)
and Amnesia
3. Loss of reflexes
Narcotic agonists
Ketamine
Thiopental
Propofol Diazepam
Etomidate Midazolam
Muscle Relaxants
Depolarizing – Succinylcholine
Nondepolarizing – 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)

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

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

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%)

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

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

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

 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.

Sudden 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.

Life
 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 arteries
Clinical 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
BLS
Basic life support
Adult, pediatric
A(C)LS
Advanced (Cardiac) Life Support
Adult, pediatric
PRC
Post-resuscitation care
Adult, pediatric

 Adult BLS sequence
Basic 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.

3 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.

 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 cheek
Look, 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

5 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.

 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.

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).

 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.

 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.

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.

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
EARLY
ACCESS
EARLY
ADVANCED
CARE

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