materi kuliah 

REVERSAL PELUMPUH OTOT 

EKSTUBASI  
PERAWATAN PASCA ANESTESI 
REVERSAL   
 PELUMPUH OTOT 
Cholinesterase Inhibitors  

• ​Drugs that prevent the degradation of 

acetylcholine (ACh) by acetylcholinesterase ​•
Viewed as indirect-acting cholinergic agonists ​•
Lack selectivity (muscarinic, ganglionic, and 
neuromuscular)  
• ​Limited therapeutic applications 
 Transmisi rangsangan saraf ​ ​otot  
melalui Neuromuscular junction  

Acetyl cholin ​ ​Perangsang saraf ( Neurotransmitter) yang dibuat di ujung 

s​erabut saraf melalui Acetylasi cholin dgn ko-enzym A ​ ​bantuan enzym 
Asetyl transferase  

​Asetil kolin disimpan dalam vesikel  

​Dalam keadaan istirahat ( Resting Membran Potential), Membran lebih mudah 

ditembus (permeabel) ion K​+ ​Ekstra sel dibanding ion Na​+. ( - 90 mV)  

​Saat pelepasan Ach ​ ​membran lebih permeabel thd Na​+ ​ ​Terjadi 

depolarisasi dan aksi potensial. 
 ​Bila depolarisasi cukup kuat ​ ​diikuti kontraksi otot ​ ​Repolarisasi (+) : 
o.k. kerja Acetyl Cholin berakhir ( Hidrolisa oleh enzym Acetyl 
Cholinesterase ) 
  

NEUROMUSCULAR TRANSMISSION 
Cholinergic Pharmacology: The Basics

The two receptors types are nicotinic and muscarinic.

• ​Nicotinic receptors ​stimulate autonomic ganglia and skeletal muscle. ​•

​ uscarinic
These receptors are also activated by the nicotine alkaloid. ​• M
receptors ​stimulate end-organ receptors. These receptors are also
activated by the alkaloid muscarine.
Cholinergic Pharmacology: Clinical Aspects  

• ​Normal muscle action: ​Neuromuscular transmission depends on the 

re​lease of ACh from presynaptic neurons and activation of postsynap​tic 
 nicotinic cholinergic receptors on the motor end plate.   

• ​Nondepolarizing  muscle  relaxants:  ​Neuromuscular  transmission  is 

blocked by nondepolarizing muscle relaxants that bind to postsynaptic 
nicotinic cholinergic receptors 
Reversal of Nondepolarizing Muscle Relaxants  
• ​Spontaneous reversal: ​Occurs with gradual diffusion, redistribution,   
metabolism, and excretion of nondepolarizing muscle relaxants.  

• ​Pharmacologic reversal: ​Occurs with the administration of specific reversal   

agents​. Reversal with acetylcholinesterase inhibitors should be monitored   
with a peripheral nerve stimulator. At least one twitch with train-of-four   
(TOF) stimulation should be present before reversal. Suggested endpoints for   
 recovery are sustained tetanus for 5 s in response to a 100-Hz stimulus in   
anesthetized patients, an adequate TOF ratio greater than 0.9 as   
assessed by acceleromyography, or sustained head or leg lift in awake patients.  

• ​Organophosphates ​are used in ophthalmology and pesticides. They irreversibly bind to cholinesterase inhibitors​. 
Cholinergic Pharmacology: Clinical Aspects  

Side effects of acetylcholinesterase inhibitors:   

In addition to increasing the availability of acetylcholine at the neuromuscular junction, inhibition of 
acetylcholinesterase can increase cholinergic receptor activity elsewhere, leading to side effects.  

• ​Cardiovascular system: ​The predominant muscarinic effect on the heart is a vagal-like bradycardia that can 
progress to sinus arrest.  
• ​Pulmonary receptors: ​Muscarinic stimulation can result in bronchospasm and increased ​respiratory 
secretions.  
• ​Cerebral receptors: ​Physostigmine is a cholinesterase inhibitor that can cross the blood– brain barrier 
(BBB). It can cause diffuse activation of the electroencephalogram by stimulating muscarinic and nicotinic 
receptors within the central nervous system (CNS). ​• ​Gastrointestinal receptors: ​Muscarinic stimulation 
increases peristaltic activity ​(esophageal, gastric, and intestinal) and glandular secretions (e.g., salivary, parietal). 
Perioperative bowel anastomotic leakage, nausea and vomiting, and fecal incontinence have been attributed to 
the use of cholinesterase inhibitors. 
  
Fig. 15-1. ​Structural formulas of reversible cholinesterase inhibitors.
Antagonis Pelumpuh otot Non 
 Depolarisasi ( Reversal )  
Neostigmin Methyl Sulfat ( Prostigmin® )   

​Sediaan : Ampul 0,5 mg/cc   

​Merupakan Anticholinesterase ​ ​mencegah hidrolisis & menyebabkan 
akumulasi Ach  
​Memp. Efek : - Muskarinik  
- Nikotinik  
- Stimulasi otot   
​Efek samping ​ ​sering karena efek muskarinik ;  
1. Bradikardia  
2. Hyperperistaltik, Spasme sal. Cerna  
3. Hipersekresi kel. Ludah & sal. Nafas  
4. Bronkospasme  
5. Kontraksi Vesika urinaria  
6. Miosis 
Neostigmine…  
 ​Efek samping tersebut Dapat dihambat dgn pemb.  
R/ ​Sulfas atropin  

​Dosis Prostigmin : 0,02 – 0,08 mg/kgbb/iv  

​Biasa diberikan bersama R/Sulfas Atropin dengan 

dosis : 0,01 – 0,04 mg/kgbb/iv 
Cholinergic Pharmacology: Drugs  
Neostigmine  
• ​Mechanism of action: ​Acetylcholinesterase inhibitor.  
• ​Dosage: ​Up to 0.08 mg/kg in children; 5 mg in adults.  
• ​Onset: ​Effects apparent in 5 to 10 minutes; peak at 10 minutes and last more than 1 
hour.  
• ​Clinical note: ​Typically administered with glycopyrrolate to prevent bradycardia. 
• ​Structure: ​Carbamate moiety (binds to acetylcholinesterase) and quaternary 
ammonium group (prevents passage across the BBB 
Cholinergic Pharmacology: Drugs  
Pyridostigmine  
• ​Mechanism of action: ​Acetylcholinesterase inhibitor.  
• ​Dosage: ​Up to 0.4 mg/kg in children; 20 mg in adults.  
• ​Onset: ​Effects apparent in 10 to 15 minutes and lasts more than 2 hours. ​•
Clinical note: ​Typically administered with glycopyrrolate to prevent bradycardia. ​•
Structure: ​Carbamate moiety (binds to acetylcholinesterase) and quaternary 
ammonium incorporated into phenol ring (prevents passage across the BBB). 
Cholinergic Pharmacology: Drugs  
Edrophonium  
• ​Mechanism of action: ​Acetylcholinesterase inhibitor.  
• ​Dosage: ​0.5 to 1 mg/kg.  
• ​Onset: ​Most rapid onset and shortest duration for class. Effects apparent in 1 to 2 
minutes. Higher dosages last up to 1 hour.  
• ​Clinical note: ​Typically administered with atropine to prevent bradycardia. If used 
with glycopyrrolate, should be given several minutes after glycopyrrolate so that 
onset time matches.  
• ​Structure: ​Noncovalent binding to acetylcholinesterase. Quaternary ammonium 
group (prevents passage across the BBB). 
Cholinergic Pharmacology: Drugs  
Physostigmine  
• ​Mechanism of action: ​Acetylcholinesterase inhibitor.  
• ​Dosage: ​0.01 to 0.03 mg/kg.  
• ​C​linical note: ​Can be used to treat central anticholinergic toxicity from scopolam​ine 
or atropine overdose.  
• ​Also reverses some of the CNS depression from benzodiazepines and volatile 
anesthetics.  
• ​Structure: ​Carbamate moiety. Lack of quaternary ammonium allows passage across 
the BBB 
Cholinergic Pharmacology: Drugs  
Sugammadex  
• ​Mechanism of action: ​Hydrophobic structural interactions trap aminosteroid 
neuromuscular blocking agents  
• ​(r​ocuronium, vecuronium) within cyclodextrin cavity, terminating neuromuscular  
block.  
• ​Dosage: ​4 to 8 mg/kg.  
• ​Onset: ​Can reverse shallow and deep neuromuscular blockade within 2 minutes. ​•
Clinical note: ​Because of concerns about hypersensitivity and allergic reactions, not 
yet approved by the U.S.  
• ​Food and Drug Administration. Currently is available and used in Europe. 
• ​Structure: ​Modified cyclodextrin 
Peripheral Nerve Stimulation ​ ​Monitor untuk melihat efek , 
pengaruh Muscle relaxant pada otot masih ada/tidak. 
  
Test utk melihat 
fungsi otot rangka 
sudah baik/belum 
​bila nerve stimulator (-) post relaksan :  

1. Hand grip test  

2. Angkat kepala  
3. Buka mata lebar  
4. Keluarkan lidah   

5. Ventilasi paru / TV

sudah baik 
 TERIMA KASIH 
EKSTUBASI 
• ​Intubasi dan ekstubasi trakea adalah rutinitas dan tidak dapat dipisahkan teknik 
dalam anestesi dan perawatan intensif.   

• ​Meski begitu umum diterapkan, kepentingannya tidak boleh diremehkan.  

• ​Dalam beberapa kasus, intubasi dan / atau ekstubasi trakea dapat dilakukan 
menantang dan masih merupakan penyebab penting morbiditas dan kematian dalam 
anestesiologi. 
KRITERIA EKSTUBASI 
 
 LANGKAH LANGKAH EKSTUBASI  
• ​1. RENCANA EKSTUBASI  
• ​2. PERSIAPAN EKSTUBASI  
• ​3. MELAKUKAN TINDAKAN EKSTUBASI  
• ​4. PERAWATAN PASCA EKSTUBASI 
LANGKAH LANGKAH EKSTUBASI 
RENCANA EKSTUBASI 
 EKSTUBASI   
DALAM ATAU AWAKE ? 
TERIMA KASIH 
PERAWATAN PASCA ​PROSEDUR OPERASI

MENINGKAT ​ ​KOMPLIKASI
ANESTESI ​LATAR
ANESTESI / BEDAH ​
BELAKANG :
KEMATIAN 24 JAM PASCA

BEDAH

PR / PACU / RPS ( 1950 )

TUJUAN : PENGAWASAN / PERAWATAN

 SECARA KETAT SETELAH ANESTESI

UMUM / REGIONAL.

Phases of Recovery  

Phase 1 ​is the immediate intensive care level recovery that cares for patients during 
emergence and awakening from anesthesia and continues until standard PACU criteria 
are met.  

Phase 2 ​is a lower level care that ensures the patient is ready to go home. 
Emergence from General Anesthesia  

Problems such as airway obstruction, shivering, agitation, delirium, pain, nausea and 
vom​iting, hypothermia, and autonomic labiality are frequently encountered. 
Delayed emergence  
• ​The  most  frequent  cause  of  delayed  emergence  (when  the  patient  fails  to  regain 
consciousness  30–60  min  after  general anesthesia) is residual anesthetic, sedative, 
and analgesic drug effect.  
• ​A​dministration of naloxone (80-mcg increments) and flumazenil (0.2-mg  
increments) readily reverses the effects of an opioid and benzodiazepine, 
respectively.  
• ​Nerve stimulator used to exclude significant neuromuscular blockade in patients on 
a mechanical ventilator who have inadequate spontaneous tidal volumes. ​• L​ ess 
common causes of delayed emergence include hypothermia, marked metabolic 
disturbances, and perioperative stroke.  
• ​Core temperature less than 33°C has an anesthetic effect and greatly potentiates the 
actions of central nervous system (CNS) depressants.  
• ​Forced-air warming devices are most effective in raising body temperature 
KOMPLIKASI SAAT PERJALANAN
DARI OK RR :

❖ ​MONITORING YANG KURANG

❖ ​OVERDOSIS OBAT
❖ ​ALAT RESUSITASI ( - )

PERSYARATAN PASIEN TAK STABIL

DARI OK RR :

❖ ​TERPASANG ET
 ❖ ​MONITOR PORTABLE
❖ ​OBAT – OBAT EMERGENCY ( + )
PENYULIT PASCA ANESTESI :

A. UMUM :

• ​MUAL – MUNTAH.

• ​PERUBAHAN MENTAL.

• ​SALURAN NAFAS ATAS.

• ​HIPOTENSI.
 • ​DISRITMIA.

• ​HIPERTENSI.
B. SPESIFIK :
I. MASALAH JALAN NAFAS ​:

1. OBSTRUKSI / SALURAN NAFAS ATAS :

WOUND HEMATOM. -
- SPASME LARING.
PARALISIS PITA SUARA.
- EDEMA JLN NAFAS Th / -
- ELEVASI
KEPALA. ​-​O​2
 HUMIDIFIKASI. KORTIKOSTEROID. ​-
- ​NEBULIZER RESTRIKSI CAIRAN. ​-
EPINEPRIN. ​- REINTUBASI.
2. HIPOVENTILASI :

​LAJU NAFAS

​REVERSE PELEMAS OTOT TIDAK ADEKUAT.

​OBSTRUKSI SALURAN NAFAS ATAS.

​NYERI HEBAT.

​PENYAKIT PARU DASAR.

 ​BRONKHOSPASME.

​PNEUMOTHORAKS.
3. HIPOKSEMIA :
- ​ATELEKTASIS.
- OBSTRUKSI SALURAN NAFAS ATAS. -
HIPOVENTILASI.
- GANGGUAN DIFUSI.
- BRONKHOSPASME.
- ASPIKSIA.
- EDEMA PARU
- PNEUMOTHORAX
- EMBOLI PARU.
4. MASIH TERINTUBASI , O.K. :

- KEADAAN EMERGENCY.

- REVERSE TIDAK ADEKUAT.

- OBSTRUKSI JALAN NAFAS.

- LAMBUNG PENUH.

- HEMODINAMIK TAK STABIL.

- PERTUKARAN GAS TAK ADEKUAT.

 - HIPOTERMI / MENGGIGIL.

II. MASALAH HEMODINAMIK

1. HIPOTENSI :
HIPOVOLEMI.
PNEUMOTHORAKS.
a. VASKULER TAMPONADE JANTUNG​.
TIDAK ADEKUAT
VENTILASI >>.
TENSION - SPINAL / EPIDURAL.
b. PE AN TONUS VASKULER c. DISFUNGSI MIOKARD

- ​ANAFILAKSIS.
- ​SEPSIS / ADRENAL INSUF. ​- ​OBAT – OBATAN.

• ​ISKHEMIK / INFARK.
• ​GAGAL JANTUNG KONGESTIF. ​• ​SEPSIS.
• ​HIPERTIROID.
• ​ARITMIA.
• ​INOTROPIK NEGATIF.
2. HIPERTENSI , OK : ​
• ​NYERI. ​•
AGITASI.
 • ​HIPOKSEMIA.
• ​HIPERKARBIA.
• ​T I K NAIK.

3. DISRITMIA :
VENTRIKULER :
a. SUPRA

• ​SINUS TAKIKARDI. ​•
VENTRIKULER : b. SINUS BRADIKARDI.
• ​IRAMA CEPAT.
 • ​TERAPI : LIDOKAIN : 1,5 mg /
kgBB. ​• ​dilanjutkan Drips : 1 – 4 mg /
menit.
III. MASALAH OLIGURI : ( < 0,5 ml / kg BB / jam )
• ​PRE RENAL.
• ​RENAL.
• ​POST RENAL.

IV. MASALAH NEUROLOGI :

a​. TERLAMBAT BANGUN, OLEH KARENA :
• ​KERUSAKAN NEUROLOGI.
• ​GANGGUAN METABOLISME.
 • ​DELIRIUM YANG GAWAT.
b. DEFISIT NEUROLOGIK FOKAL, OLEH KARENA : ​•
STROKE INTRA OPERATIF
• ​KERUSAKAN SYARAF PERIFER AKIBAT
OPERASI/ DAN POSISI OPERASI.

V. HIPOTERMIA :
• ​Vasokontriksi ok. Hipoperfusi / asidosis
metabolisme ​• ​Gangguan platelet
• ​Gangguan gelombang T pada EKG.

THERAPI : ​O​2 ;​ 25 mg MEPERIDIN; SELIMUT TEBAL;

KOMPRES HANGAT; LAMPU PENGHANGAT; ISI
VOLUME ​VASKULER + VASODILATOR.
VI. HIPERTERMIA :
• ​INFEKSI.
• ​HIPERTERMIA MALIGNA. ​•

KOMPLIKASI PARU.

• ​KRISIS HIPERTIROID.

• ​SINDROMA NEUROLEPTIK THERAPI :

• ​EKSTERNAL COOLING. ​•
MALIGNA ANTI PIRETIK.

KRITERIA KEMBALI KE BANGSAL :

• ​HEMODINAMIK STABIL.
 ALDRETE SCORE
• ​VENTILASI SPONTAN • ​SUHU NORMAL.

ADEKUAT. ​• ​NYERI • ​MUAL / MUNTAH

MINIMAL.
TERKONTROL. BROMAGE SCALE

KRITERIA PINDAH DARI PACU 

III.
 0.

Jika skore bernilai <2, maka pasien dapat dipindahkan dari ruangan pemulihan ke
ruangan/bangsal perawatan.
BROMAGE SCALE :​Untuk menilai blokade
motoris ekstremitas inferior
oleh spinal
anestesia
0 : Gerakan penuh dari tungkai.
1 : Tidak mampu meng-ekstensi tungkai.
2 : Tidak mampu mem – fleksi lutut.
3 : Tidak mampu mem – fleksi
pergelangan kaki.