Anesthesia

31Juli 2015
Anestesi merupakan suatu peristiwa hilangnya sensasi,
perasaan nyeri bahkan hilangnya kesadaran sehingga
memungkinkan dilakukan pembedahan.

Tujuan anestesi yaitu :

Hipnotik
Analgesi
Relaksasi otot

Klasifikasi anestesi, yaitu :

Anestesi Umum
Anestesi Lokal
Anestesi Regional
Mendelson's syndrome is chemical pneumonitis caused by
aspiration during anaesthesia, especially during pregnancy.

First described in obstetrical cases by Mendelson1 in 1946.

Aspiration contents may include gastric juice, blood, bile,

water or an association of them.

Historically it is said that a patient is at risk if they have:

- Residual gastric volume of greater than 25ml

- pH of less than 2.5
Two to five hours after aspiration there is a dramatic onset of:
- cyanosis
- dyspnea
- tachycardia
- shock.
- Examination of the patient shows no localized signs of lung
disease but generalized adventitious sounds and
bronchospasm. The condition simulates pulmonary edema
with rales, wheezes, and rhonchi throughout both lungs. There
is a bloody, frothy sputum and marked pulmonary congestion.
- A very high pulse and respiratory rate are common, and
gross pulmonary edema may supervene, with a rapidly
deteriorating course resulting in death from cardiac failure.
- X-ray of the chest shows soft patchy mottling scattered
through the lung fields but no evidence of lung collapse.
examination of the lungs will show gross swelling of
Muscle relaxant fall into two groups:

1. Non-depolarizing blocking agents:

- These agents constitute the majority of the clinically relevant
neuromuscular blockers.
- act by competitively blocking the binding of ACh to its
receptors, and in some cases, they also directly block the
inotropic activity of the ACh receptors.

2. Depolarizing blocking agents:

depolarizing the sarcolemma of the skeletal muscle fiber -->
persistent depolarization makes the muscle fiber resistant to
further stimulation by ACh.
 Global view of a
neuromuscular junction:
1. Axon
2. Motor end-plate
3. Muscle fiber
4. Myofibril

Neuromuscular junction:
1. Presynaptic terminal
2. Sarcolemma
3. Synaptic vesicle
4. Nicotinic acetylcholine
receptor
5. Mitochondrion

botulinum toxin and tetanus toxin act presynaptically

Most neuromuscular blockers function by blocking
transmission at the end plate of the neuromuscular junction.
Normally, a nerve impulse arrives at the motor nerve terminal,
initiating an influx of calcium ions, which causes the exocytosis
of synaptic vesicles containing acetylcholine.
Acetylcholine then diffuses across the synaptic cleft. It may be
hydrolysed by acetylcholine esterase (AchE) or bind to the
nicotinic receptors located on the motor end plate. The binding
of two acetylcholine molecules results in a conformational
change in the receptor that opens the sodium-potassium
channel of the nicotinic receptor. This allows Na+ and Ca2+
ions to enter the cell and K+ ions to leave the cell, causing a
depolarization of the end plate, resulting in muscle contraction.
Following depolarization, the acetylcholine molecules are then
removed from the end plate region and enzymatically
hydrolysed by acetylcholinesterase.
- Normal end plate function can be blocked by two
mechanisms.
- Nondepolarizing agents, such as tubocurarine, block the
agonist, acetylcholine, from binding to nicotinic receptors
and activating them, thereby preventing depolarization.
- Alternatively, depolarizing agents, such as succinylcholine,
are nicotinic receptor agonists which mimic Ach, block
muscle contraction by depolarizing to such an extent that it
desensitizes the receptor and it can no longer initiate an
action potential and cause muscle contraction.
- Both of these classes of neuromuscular blocking drugs are
structurally similar to acetylcholine, the endogenous ligand,
in many cases containing two acetylcholine molecules
linked end-to-end by a rigid carbon ring system, as in
pancuronium (a nondepolarizing agent).
- Suxamethonium acts as a depolarizing neuromuscular
blocker.
- Act on nicotinic receptors resulting in persistent
depolarization of the motor end plate.
- It is degraded by butyrylcholinesterase into succinic acid and
choline. This hydrolysis by butyrylcholinesterase is much
slower than that of acetylcholine by acetylcholinesterase.
It is perennially popular in emergency medicine because it has
the fastest onset and shortest duration of action of all muscle
relaxants

Suxamethonium is also commonly used as the sole muscle

relaxant during electroconvulsive therapy, favoured for its
short duration of action.
 succinylcholine (suxamethonium)

more resistant to degradation by acetylcholinesterase -->the

enzyme responsible for degrading acetylcholine, and can thus
more persistently depolarize the muscle fibers.

There are two phases to the depolarizing block.

- phase I (depolarizing phase), they cause muscular
fasciculations (muscle twitches) while they are depolarizing
the muscle fibers.
- phase II (desensitizing phase) sets in and the muscle is no
longer responsive to acetylcholine released by the
motoneurons. At this point, full neuromuscular block has
been achieved.
rapid onset (30 seconds) but very short duration of action (5–
10 minutes) because of hydrolysis by various cholinesterases
(such as butyrylcholinesterase in the blood).

Succinylcholine was originally known as diacetylcholine

because structurally it is composed of two acetylcholine
molecules joined with a methyl group.

suxamethonium may trigger a transient release of large

amounts of potassium from muscle fibers. This puts the patient
at risk for life-threatening complications, such as hyperkalemia
and cardiac arrhythmias.
 - Succinylcholine is comprised of two acetylcholine molecules
joined together and acts as a depolarizing neuromuscular
blocker by binding acetylcholine receptors at the post-
synaptic neuromuscular junction end plate.
- The resultant end plate depolarization initially stimulates
muscle contraction; however, because succinylcholine is
not degraded by acetylcholinesterase, it remains in the
neuromuscular junction to cause continuous end plate
depolarization and subsequent muscle relaxation. This is
termed a phase I block.

are membrane depolarization and transient fasciculations, followe

Phase 2 block
- This phase is not abnormal and is a part of its mechanism
of action.
- It is caused by the blood concentration of suxamethonium
exceeding the therapeutic window. Desensitization occurs
at the nerve terminal, and the myocyte becomes less
sensitive to acetylcholine; the membrane repolarizes and
cannot be depolarized again.
- With increasing doses of succinylcholine (i.e., a large single
dose, repeated doses, or a continuous infusion), a phase II
block may occur.
- Continuous activation of acetylcholine receptors leads to
ongoing shifts of sodium into the cell and potassium out of
the cell. Despite this, the post-junctional membrane
potential eventually moves in the direction of normal even in
the continued presence of succinylcholine. This is due to
increased activity of the sodium-potassium ATPase pump,
which brings potassium into the cell in exchange for
sodium. The receptor does not respond appropriately to
acetylcholine, and neuromuscular blockade is prolonged.
- Phase II block may be seen clinically with doses of
succinylcholine >4mg/kg, but some characteristics of this
blockade have been reported at 0.3mg/kg.
- Side effects include malignant hyperthermia, muscle pains,
acute rhabdomyolysis with high blood levels of potassium,
transient ocular hypertension, constipation and changes in
cardiac rhythm, including slow heart rate, and cardiac arrest.
In
- people with neuromuscular disease or burns, an injection of
suxamethonium can lead to a large release of potassium
from skeletal muscles, potentially resulting in cardiac arrest.
- Conditions having susceptibility to suxamethonium-induced
high blood potassium are burns, closed head injury,
acidosis, Guillain–Barré syndrome, cerebral stroke,
drowning, severe intra-abdominal sepsis, massive trauma,
myopathy, and tetanus.
- The side effect of high blood potassium may occur because
the acetylcholine receptor is propped open, allowing
continued flow of potassium ions into the extracellular fluid.
- A typical increase of potassium ion serum concentration on
administration of suxamethonium is 0.5 mmol per liter.
- High blood potassium does not generally result in adverse
effects below a concentration of 6.5 to 7 mEq per liter.
Therefore, the increase in serum potassium level is usually
not catastrophic in otherwise healthy patients.
- Severely high blood levels of potassium will cause changes
in cardiac electrophysiology, which, if severe, can result in
asystole.
- Malignant hyperthermia from suxamethonium administration
can result in a drastic and uncontrolled increase in skeletal
muscle oxidative metabolism.
- This overwhelms the body's capacity to supply oxygen,
remove carbon dioxide, and regulate body temperature,
eventually leading to circulatory collapse and death if not
treated quickly.

inherited as an autosomal dominant disorder

- The normal short duration of Suxamethonium is due to the
rapid metabolism of the drug by non-specific plasma
cholinesterases. However plasma cholinesterase activity is
reduced in some people due to either genetic variation or
acquired conditions, this results in a prolonged duration of
neuromuscular block.
- Genetically ninety six percent of the population have a
normal (Eu:Eu) genotype and block duration, however some
people have abnormal genes (Ea, Es, Ef). All will result in a
longer duration of block from 20 minutes up to several hours.
- Acquired factors that affect plasma cholinesterase activity
include pregnancy, liver disease, kidney failure, heart failure,
thyrotoxicosis, cancer and a number of other drugs.

https://en.m.wikipedia.org/wiki/Suxamethonium_chloride#
https://en.m.wikipedia.org/wiki/Suxamethonium_chloride#
Non-depolarizing blockers are reversed by
acetylcholinesterase inhibitor drugs since they are competitive
antagonists at the ACh receptor so can be reversed by
increases in ACh.

Certain drugs such as aminoglycoside antibiotics and

polymyxin and some fluoroquinolones also have neuromuscular
blocking action as their side-effect.
- Methods for estimating the degree of neuromuscular block
include valuation of muscular response to stimuli from
surface electrodes, such as in the train-of-four test, wherein
four such stimuli are given in rapid succession.
- With no neuromuscular blockade, the resultant muscle
contractions are of equal strength, but gradually decrease in
case of neuromuscular blockade.
- It is recommended during use of continuous-infusion
neuromuscular blocking agents in intensive care.
Sugammadex is a newer drug for reversing neuromuscular
block by rocuronium in general anaesthesia. It is the first
selective relaxant binding agent (SRBA)
Guedel's classification is a means of assessing of depth of
general anesthesia introduced by Arthur Ernest Guedel (1883-
1956) in 1937.
 Stages of Anesthesi

Stage I (stage of analgesia or disorientation): from beginning of i

Stage II (stage of excitement or delirium): from loss of

consciousness to onset of automatic breathing.
- Eyelash reflex disappear but other reflexes remain intact and
coughing, vomiting and struggling may occur
- respiration can be irregular with breath-holding.
Stage III (stage of surgical anesthesia): from onset of automatic respiration
to respiratory paralysis.

It is divided into four planes:

Plane I - from onset of automatic respiration to cessation of eyeball

movements.
- Eyelid reflex is lost, swallowing reflex disappears, marked eyeball
movement may occur but conjunctival reflex is lost at the bottom of the
plane

Plane II - from cessation of eyeball movements to beginning of paralysis of

intercostal muscles.
- Laryngeal reflex is lost although inflammation of the upper respiratory tract
increases reflex irritability, corneal reflex disappears, secretion of tears
increases (a useful sign of light anesthesia)
- respiration is automatic and regular, movement and deep breathing as a
response to skin stimulation disappears.
Plane III - from beginning to completion of intercostal muscle paralysis.
- Diaphragmatic respiration persists but there is progressive intercostal
paralysis, pupils dilated and light reflex is abolished.
- The laryngeal reflex lost in plane II can still be initiated by painful stimuli
arising from the dilatation of anus or cervix.
- This was the desired plane for surgery when muscle relaxants were not
used.

Plane IV - from complete intercostal paralysis to diaphragmatic paralysis

(apnea).
Stage IV: from stoppage of respiration till death.
- Anesthetic overdose cause medullary paralysis with
respiratory arrest and vasomotor collapse.
- Pupils are widely dilated and muscles are relaxed.

This classification was designed for use of a sole inhalational

anesthetic agent, diethyl ether (commonly referred to as
simply "ether"), in patients who were usually premedicated
with morphine and atropine.
- At that time, intravenous anesthetic agents were not yet in
common use, and neuromuscular-blocking drugs were not
used at all during general anesthesia.
RUMUS PERHITUNGAN DARAH UNTUK TRANSFUSI

1. Rumus : Hb normal – Hb pasien = hasil

2. hasil x BB x jenis darah

Keterangan :
Hb normal : Hb yang diharapkan atau Hb normal
Hb pasien : Hb pasien saat ini
Hasil : hasil pengurangan Hb normal dan Hb pasien
Jenis darah : darah yang dibutuhkan
= PRC dikalikan 3
= WB dikalikan 6
Hipotermi juga dapat diklasifikasikan berdasarkan temperature tubuh, yaitu :

Ringan = 34-36°C
Kebanyakan orang bila berada pada suhu ini akan menggigil secara hebat, teru

Sedang = 30–34°C
Terjadi penurunan konsumsi oksigen oleh sistem saraf secara besar yang meng

Berat = <30°C
Pasien rentan mengalami fibrilasi ventrikular, dan penurunan kontraksi miokardi
Terima Kasih
 Estimated energy requirements for various activities.

Authors/Task Force Members et al. Eur Heart J 2014;35:2383-2431

©The European Society of Cardiology 2014. All rights reserved. For permissions please email:
journals.permissions@oup.com.