Tugas Anestesi

Rani Purnama Sari Tobing

1. Mnemonic STATICS dalam preparasi anestesi / airway breathing

management
S = Scope (stetoskop, laringoskop)
T = Tubes (endotrakeal tube, LMA)
A = Airway Device (sungkup, orofaring tube)
T = Tape (plester)
I = introducer (stilet)
C = Connector (kabel penghubung ke oksigen)
S = Suction

2. LEMON

www.learnpicu.com/respiratory/intubation-rsi

3. MOANS
- Mask seal
- Obesity/Obstruction
- Aged > 55 Years
- No teeth (replace dentures for Bag Valve Mask Ventilation)
- Stiff lungs requiring increased Ventilatory pressures (Asthma, COPD, ARDS,
term pregnancy)

https://fpnotebook.com/mobile/Lung/Procedure/AdvncdArwy.htm

4. AMPLE or SAMPLE
- Signs and symptoms
- Allergies
- Medication (obat yang diminum saat ini)
- Past illness (penyakit penyerta)/pregnancy
- Last Meal
- Even or environment related to injury

https://fpnotebook.com/mobile/ER/Trauma/TrmHstry.htm
 5. SOAPME

Mnemoni
c–
“SOAP
ME”
• Yankauer suction placed under the mattress on the right
Suction side, head of bed (x2 if GI bleed, vomiting, or lots of
secretions)
• Bag valve mask (with PEEP valve) ready
Oxygen • Non-rebreather mask on patient (O2 wide open)
• Nasal cannula on the patient (with 15L O2) during RSI
• Oral, nasal airways
• 2 ETT (expected size & one size below) w/ balloons
checked, & stylet straight to cuff
Airways
• 1 ETT ready for video laryngoscopy (curved stylet
needed)
• Rescue devices (Laryngeal mask airway, scalpel, etc.)
Positionin 3. Ear-to-sternal notch position
g 4. Ramped if obese
• Continuous monitoring devices
• RSI Meds: Drawn up in carefully considered doses,
Monitors labeled syringes
& Meds ◦ Sedative (Ketamine, etomidate, etc.)
◦ Paralytic (rocuronium, succinylcholine)
• Post intubation sedation meds (Propofol, fentanyl, etc)
• Continuous EtCO2 or at least color-change device to
EtCO2 & confirm successful intubation
other • Bougie placed under the mattress next to yankauer
Equipmen suction
t • 2 laryngoscopes (MAC 3 & 4) with lights checked.
• Video laryngoscope plugged in & turned on

https://em.umaryland.edu/educational_pearls/2577/
6. Kriteria Cormack-Lehane dalam laringoskopi
a. Grade 1 = full view of the glottis
b. Grade 2 = partial view of the glottis or arytenoids
c. Grade 3 = only epiglottis visible
d. Grade 4 = neither glottis nor epiglottis visible

https://openairway.org/tag/cormack-lehane/

7. Macam-macam Laringoskop
a. Indirect menggunakan kaca kecil yang diletakkan pada langit-langit
mulut
b. Direct fiber-optic / flexible menggunakan teleskop pada ujung kabel
dari hidung ke tenggorokan.
c. Direct bentuk paling sering digunakan, dengan mendorong lidah dan
mengangkat epiglottis.

WebMD. What is laryngoscope?. [cited 2019. Available from:

https://www.webmd.com/oral-health/what-is-laryngoscopy#1.

8. Rumus ukuran Endotracheal tube (ETT)

Butterworth, J.F. 2013. Morgan & Mikhail’s Clinical Anesthesiology . New York. Mc Graw
Hill Education. Page : 321

9. Rumus kedalaman ETT dari sudut mulut

For children over 1 year of age:
 For children below 1 year of age:

Adult:
Optimal depth of ET placement can be estimated by the formula “(Height in
cm/7)-2.5.”

Sumber: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3237149/
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1460-9592.2006.01982.x

10. Ventilasi tekanan positif (VTP)

Positive-pressure ventilation means that airway pressure is applied at the
patient's airway through an endotracheal or tracheostomy tube. The positive
nature of the pressure causes the gas to flow into the lungs until the ventilator
breath is terminated. As the airway pressure drops to zero, elastic recoil of the
chest accomplishes passive exhalation by pushing the tidal volume out.

Sumber: https://emedicine.medscape.com/article/304068-overview#a1

11. Teknik EC clamp

Pasien diposisikan terlentang (supine), penolong menggunakan 3 jari
pada 1 tangan untuk mengangkat rahang kearah masker, membuka
jalan napas. Penempatan 3 jari ini menyerupai huruf E. Kemudian Ibujari
dan jari telunjuk memegang masker, membentuk huruf C. Ini membantu
penutupan erat antara masker dan wajah korban, sehingga ventilasi
bag-mask menjadi efektif.

https://eccguidelines.heart.org/index.php/figures/the-ec-clamp-technique-of-
bag-mask-ventilations-2/
12. Airway, Breathing, Circulation, Disability, Exposure (ABCDE)

Assessment Treatment
A– Voice Head tilt and chin
Airways Breath sounds lift
Oxygen (15 l
min−1) Suction
B– Respiratory rate Seat comfortably
Breathing (12–20 min−1) Rescue breaths
Chest wall Inhaled
movements medications
Chest percussion Bag-mask
Lung auscultation ventilation
Pulse oximetry Decompress
(97%–100%) tension
pneumothorax
C– Skin color, sweating Stop bleeding
Circulation Capillary refill time Elevate legs
(<2 s) Intravenous access
Palpate pulse rate Infuse saline
(60–100 min−1)
Heart auscultation
Blood pressure
(systolic 100–140
mmHg)
Electrocardiography
monitoring
D– Level of Treat Airway,
Disability consciousness – Breathing, and
AVPU Circulation
 list- problems
behavior=unordered Recovery position
prefix-word= mark- Glucose for
type=disc max-label- hypoglycemia
size=0
• Alert
• Voice
responsive
• Pain
responsive
• Unresponsive
Limb movements
Pupillary light
reflexes
Blood glucose
E– Expose skin Treat suspected
Exposure Temperature cause

Troels Thim. 2012. Initial assessment and treatment with the Airway, Breathing, Circulation,
Disability, Exposure (ABCDE) approach. International Journal of General Medicine

13. Pedriatric assesment triangle

Appearance Work of breathing Circulation

Tone Abnormal breath sound Pallor

Interactivity Abnormal positioning Mottling
Consolability Retractions Cyanosis
Look/gaze Flaring Bleeding
Speech/cry

Namigar. Correlation between the Ramsay sedation scale, Richmond sedation-agitation scale,
and Riker sedation-agitation scale during sedation with midazolam-remifentanil. Rev. Bras.
Anestesiol. 2017; 67(4).
14. Ramsay score sedation scale

15. Status fisik ASA

ASA
Definition
Classification

ASA I A normal healthy patient

ASA II A patient with mild systemic disease

ASA III A patient with severe systemic

disease

ASA IV A patient with severe systemic

disease that is a constant threat to life

ASA V A moribund patient who is not

expected to survive without the
operation

ASA VI A declared brain-dead patient whose

organs are being removed for donor
purposes

American Society of Anesthesiologists. ASA Physical Status Classification

System. https://www.asahq.org/standards-and-guidelines/asa-physical-status-
classification-system
16. Mnemonic FAST HUGS BID

Sumber: Nair, AS, Naik, VM, & Rayani, BK. 2017. FAST HUGS BID: Modified
Mnemonic for Surgical Patient. Indian Journal of Critical Care Medicine, 21(10),
pp.713-714.

17. Skor Candida

Patient Population: Medical/ surgical ICUs for ≥ 7 days

Risk Factor: Severe sepsis (2 points), major surgery (1 point), total parenteral
nutrition (1 point), multi-focal candida colonization (1 point). Cut off: score ≥ 3

Sumber: https://www.accp.com/docs/bookstore/ccsap/c16b1_sample.pdf

18. Skor Tetanus

Dakar Score:
 Variables are scored either 0 (absent) or 1 (present), giving a maximum score
of six for disease with the worst prognosis. Outcome was classified as ‘survived
(to discharge from hospital)’ or ‘died’.

Phillips Score:

A final score’s maximum value is 3, with higher scores associated with worse
outcome.

Sumber: http://www.antimicrobe.org/b100tab.htm
https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-3156.2006.01562.x

19. CPIS (clinical pulmonary infection score)

 Sumber: Basyigit, S. 2017. Clinical Pulmonary Infection Score (CPIS) as a
Screening Tool in Ventilatory Associated Penumonia (VAP). The Medical
Bulletin of Sisli Etfal Hospital. 51(2)

20. Derajat perdarahan menurut ATLS

21. Fluid challenge test

Fluid challenge adalah pemberian cepat bolus cairan pada pasien kritis, yang
secara umum tidak stabil secara hemodinamik. Dianggap sebagai intervensi
diagnostic untuk mengetahui apakah pasien tersebut membaik dengan
pemberian cairan tambahan.

Prosedur:
Tipe cairan: tidak ada cairan intravena yang paling tepat, pilihan terbaik melihat
dari penyakit yang mendasari, jenis kehilangan cairan, keparahan kegagalan
sirkulatori, dan kadar albumin serum.
Saat ini cairan yang direkomendasikan adalah cairan kristaloid untuk bolus
cairan, contohnya NaCl 0,9% (Normal Saline). Contoh lain adalah cairan
Hartmann’s (compound sodium lactate), dapat digunakan sebagai cairan bolus
namun mengandung potassium dan lactate yang mungkin menjadi
kontraindikasi di beberapa kondisi. Cairan Hartmann’s mirip cairan Ringer
Lactate, namun kandungan ion-nya berbeda.

Laju pemberian cairan:

Tergantung pasien dan penyakit yang mendasari. Penting untuk menentukan
jumlah cairan yang diberikan dalam interval waktu yang telah ditentukan pula
(contoh: 250-1000ml cairan kristaloid dalam 30 menit. Selain itu, pikirkan
 diagnosis dan treatment lainnya jika pemberian cairan bolus awal ini
memberikan respon yang buruk.

Hal-hal yang harus diperhatikan sebelum fluid challenge:

- Hipotensi akibat hipovolemia.
Secara klinis ditunjukkan dengan MAP <65-70 mmHg
- Takikardia
- Urine output rendah akibat hipovolemia, yaitu kurang dari 0,5cc/kg/jam

Kenaikan 10% atau lebih dari cardiac output (CO) setelah fluid challenge
mengindikasikan hipovolemia. Jika tidak ada monitor CO, dapat menggunakan
central venous pressure (CVP). Jika CVP tidak berubah setelah fluid challenge,
ini mengindikasikan adanya hipovolemia dan fluid challenge dapat dilanjutkan.
Jika CVP meningkat 3cm H20 atau lebih, menunjukkan tidak adanya
hipovolemia dan fluid challenge dihentikan.

Sumber:
https://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0007/306475/liverpoolFluid
_Challenge.pdf
https://scottishintensivecare.org.uk/training-education/sics-induction-
modules/assessment-fluid-challenge/

22. Perbedaan laringoskop Miller dan Macintosh

Laryngoscope blades are typically used as the primary tool for the examination
of the interior of the airway and for placement of an endotracheal tube.
Choosing the correct size laryngoscope blade is critical to successful
endotracheal intubation.

Mac

In 1943, Macintosh introduced the curved laryngoscope blade. At this time, the
blade was utilized for the intubation of older children whose anatomy resembles
that of an adult. In 1947, modifications were implemented to the original blade
to better suit the pediatric population. The Macintosh laryngoscope blade is
popular even for small children. This blade is the predominate model of all the
curve blades. The Mac blade is designed to lift the epiglottis indirectly and
provide a view of the larynx by placing the tip of the blade in the vallecula. In
infants and young children who have a floppy epiglottis, the Mac blade may not
provide adequate exposure of the larynx.

 Less traumatic
 Less of a view
 Less stimulating (less tachycardia and/or arrythmias)
 Favored in patients with BIG TONGUES
 Lifts the epiglottis INDIRECTLY

Miller

In 1946, Miller described a modification of the original adult laryngoscope,

introducing a pediatric laryngoscope blade. The blade could be inserted either
anterior or posteriorly to the epiglottis. Today, the Miller blade is one of the most
popular laryngoscopes for pediatrics and difficult-to-intubate patients. Many
practitioners prefer a straight blade laryngoscope on pediatric patient due to the
unique upper airway anatomy of an infant or a small child. A straight blade is
favorable in elevating the tongue so it is then removed from the field to facilitate
optimal visualization of the infant larynx; however, there is a greater potential to
damage the epiglottis with a straight blade, with the direct elevation of the
epiglottis itself rather and applying the indirect method.
  More traumatic
 More of a view
 More stimulating
- The direct contact by the Miller blade on the epiglottis may trigger
tachycardia and / or arrythmias.
- The Superior Laryngeal Nerve (SLN), a branch of the vagus, divides
into an external-motor nerve and an internal-sensory nerve that provide
sensory innervation to the larynx between the epiglottis and the vocal
cords.
 Preffered in neonates/infants, pediatrics, and patients with LONG,
FLOPPY, and/or ANTERIOR Epiglottis
 Lifts the Epiglottis DIRECTLY

Sumber: http://difficultairwayusf.wixsite.com/srna-senior-project/visit

23. Aldrete score

NO KRITERIA SCORE SCORE

1. Warna kulit
 Kemerahan/ normal 2
 Pucat 1
 Cianosis 0
2. Aktifitas Motorik
 Gerak 4 anggota tubuh 2
 Gerak 2 anggota tubuh 1
 Tidak ada gerakan 0
3. Pernafasan
 Nafas dalam, batuk & tangis kuat 2
 Nafas dangkal dan adekuat 1
 Apnea atau nafas tidak adekuat 0
4. Tekanan darah
 ± 20 mmhg dari pre operasi 2
 20 – 50 mmhg dari pre operasi 1
 + 50 mmhg dari pre operasi 0
5. Kesadaran
 Sadar penuh mudah di panggil 2
 Bangun jika di panggil 1
 Tidak ada respon 0
Ket :
 Pasien dapat di pindah ke bangsal, jika score minimal 8
pasien.
 Pasien di pindah ke ICU, jika score < 8 setelah di rawat
selama 2 jam.
24. Bromage score
NO KRITERIA SCORE SCORE
1. Dapat mengangkat tungkai 0
bawah.
2. Tidak dapat menekuk lutut tetapi 1
dapat mengangkat kaki.
 3. Tidak dapat mengangkat tungkai 2
bawah tetapi masih dapat
menekuk lutut.
4. Tidak dapat mengangkat kaki 3
sama sekali.
Ket :
 Pasien dapat di pindah ke bangsal, jika score kurang
dari 2

Sumber: https://www.scribd.com/doc/97464041/Aldrete-Bromage-Steward-Score

25. Triple airway maneuver

 Sumber:
https://www.ambulance.qld.gov.au/docs/clinical/cpp/CPP_Triple%20airway%20mano
euvre.pdf

26. Farmakologi obat anestesi:

a. Ketamine: Ketamine neuropharmacology is complex. Ketamine
essentially acts on glutamate binding sites, NMDA (N‐Methyl‐D‐
Aspartate), and non‐NMDA receptors 70. The antagonism of NMDA
receptor is responsible for the specific ketamine properties (amnesic and
psychosensory effects, analgesia, and neuroprotection). There are also
other glutamate‐independent mechanisms.

Sumber: https://onlinelibrary.wiley.com/doi/full/10.1111/cns.12099#cns12099-
sec-0017-title

b. Fentanyl
Fentanyl is similar to other opioid drugs. Fentanyl molecules target a
subclass of opioid receptor systems in the body, many of which are
localized in the brain within specialized neuroanatomical structures
particularly regarded to the control of emotions, pain, and speaking to
the point of its infamous addictive properties, reward. Biochemically, it is
referred to as a Mu-selective opioid agonist. However, it has the
capabilities to activate other opioid system receptors such as the delta,
and potentially the kappa-receptors. Consequently, the activation of
these receptors, particularly the Mu-receptors, produce analgesia. Also,
the neurotransmitter dopamine (Da) is increased in the reward areas of
the brain, which elicits the stereotypical exhilaration and relaxation
effects, and is typically associated with the addiction to the drug.

Sumber: https://www.ncbi.nlm.nih.gov/books/NBK459275/#_article-
21694_s2_
c. Pethidine
Meperidine is primarily a kappa-opiate receptor agonist and also has
local anesthetic effects. Meperidine has more affinity for the kappa-
receptor than morphine. Opiate receptors are coupled with G-protein
receptors and function as both positive and negative regulators of
synaptic transmission via G-proteins that activate effector proteins.
Binding of the opiate stimulates the exchange of GTP for GDP on the G-
protein complex. As the effector system is adenylate cyclase and cAMP
located at the inner surface of the plasma membrane, opioids decrease
intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the
release of nociceptive neurotransmitters such as substance P, GABA,
dopamine, acetylcholine and noradrenaline is inhibited. Opioids also
inhibit the release of vasopressin, somatostatin, insulin and glucagon.
Opioids close N-type voltage-operated calcium channels (OP2-receptor
agonist) and open calcium-dependent inwardly rectifying potassium
channels (OP3 and OP1 receptor agonist). This results in
hyperpolarization and reduced neuronal excitability.

Sumber: https://www.drugbank.ca/drugs/DB00454

d. Midazolam
The actions of benzodiazepines such as midazolam are mediated
through the inhibitory neurotransmitter gamma-aminobutyric acid
(GABA), which is one of the major inhibitory neurotransmitters in the
central nervous system. Benzodiazepines increase the activity of GABA,
thereby producing a sedating effect, relaxing skeletal muscles, and
inducing sleep, anesthesia, and amnesia. Benzodiazepines bind to the
benzodiazepine site on GABA-A receptors, which potentiates the effects
of GABA by increasing the frequency of chloride channel opening. These
receptors have been identified in different body tissues including the
heart and skeletal muscle, although mainly appear to be present in the
central nervous system.

Sumber: https://www.drugbank.ca/drugs/DB00683

e. Diazepam
Diazepam is a benzodiazepine tranquilliser with anticonvulsant,
sedative, muscle relaxant and amnesic properties. Benzodiazepines,
such as diazepam, bind to receptors in various regions of the brain and
spinal cord. This binding increases the inhibitory effects of gamma-
aminobutyric acid (GABA). GABAs functions include CNS involvement in
sleep induction. Also involved in the control of hypnosis, memory,
anxiety, epilepsy and neuronal excitability.

Sumber: https://www.drugbank.ca/drugs/DB00829

f. Propofol
The action of propofol involves a positive modulation of the inhibitory
function of the neurotransmitter gama-aminobutyric acid (GABA)
through GABA-A receptors
 Sumber: https://www.drugbank.ca/drugs/DB00818

g. Phenobarbital: potentiates GABAergic inhibition AMPA receptor

blockade

Sumber: Morgan’s Clinical Anesthesiology

h. Phenytoin : Blocks voltage sensitive Na+ channels

Sumber: Morgan’s Clinical Anesthesiology

27. Farmakologi obat simpatomimetik:

a. Adrenaline: sympathetic agonist (mydriasis, decrease IOP)

b. Dobutamine
Dobutamine directly stimulates beta-1 receptors of the heart to increase
myocardial contractility and stroke volume, resulting in increased cardiac
output.

c. Dopamine
Dopamine is a precursor to norepinephrine in noradrenergic nerves and
is also a neurotransmitter in certain areas of the central nervous system.
Dopamine produces positive chronotropic and inotropic effects on the
myocardium, resulting in increased heart rate and cardiac contractility.
This is accomplished directly by exerting an agonist action on beta-
adrenoceptors and indirectly by causing release of norepinephrine from
storage sites in sympathetic nerve endings. In the brain, dopamine actas
as an agonist to the five dopamine receptor subtypes (D!, D2, D3, D4,
D5).

d. Norepinephrine
Norepinephrine functions as a peripheral vasoconstrictor by acting on
alpha-adrenergic receptors. It is also an inotropic stimulator of the heart
and dilator of coronary arteries as a result of it's activity at the beta-
adrenergic receptors

Sumber: Drugbank

28. Syok
a. Hypovolemic shock
Hypovolemic shock develops because of a lack of fluid in the
bloodstream. The vessels might still be intact and the pump still works,
but the fluid is low. Hypovolemic shock can be from bleeding directly
(hemorrhagic shock) or from other losses of fluid. Dehydration is a
common cause of hypovolemia, as is sepsis (which also causes
distributive shock).

b. Distributive shock
Distributive shock comes from the container (blood vessels) expanding
too large for the amount of fluid in the system. The amount of blood in
the system can be low or normal, but the blood vessels expand too large
 to maintain adequate pressure. Distributive shock usually occurs from
the vessels dilating as a result of a communication failure with the brain
(neurogenic shock from a spinal cord injury, for example) or the release
of histamines (anaphylactic shock).

c. Cardiogenic shock
Cardiogenic shock is all about the pump. When the heart fails, such as
in heart attacks, cardiogenic shock is the result. Congestive heart failure
is an example of cardiogenic shock. Congestive heart failure is a back
up of blood into the body or into the lungs as a result of one side of the
heart being damaged from a heart attack. The good side of the heart
pumps at full speed while the damaged side can't keep up and blood
pressure suffers as a result.

d. Obstructive shock
Obstructive shock is a special example. This occurs when the flow of
blood is blocked by an outside force. One of the most common examples
of obstructive shock is from a tension pneumothorax (also called
a collapsed lung). Air accumulates in the chest outside of the lungs and
puts pressure on the heart and other vessels. As the pressure grows,
the heart is not able to adequately pump and blood flow is restricted
through the vessels that are squeezed. The other common example of
obstructive shock is from pericardial tamponade. The sac around the
heart (pericardium) traps blood between it and the heart inside it. The
trapped blood begins to exert pressure on the heart and squeezes it hard
enough to slow blood flow.

Sumber: https://www.verywellhealth.com/types-of-shock-4018329

29. SOFA score, quick SOFA (sequential organ failure assessment)

mengidentifikasi pasien suspek infeksi memiliki risiko buruk jika diluar ICU
 qSOFA score of ≥2 points indicates organ dysfunction

Sumber: Marik, PE, & Taeb, AM. 2017. SIRS, qSOFA, and new sepsis definition.
Journal of Thoracic Disease. 9(4). p.943-945.

30. Defibrillator monofasik dan bifasik

Monofasik
Gelombang shock dari satu vector /
satu arah, dari satu elektroda
Energi 360 Joule
Bifasik
Gelombang shock dari arah sejalur
dan berlawanan (dua arah), dengan
mengubah polaritas elektroda ketika
shock dihantarkan
Energi 200 Joule

Sumber: https://www.emsworld.com/article/10324825/biphasic-defibrillation-shape-
resuscitation-today

31. Terapi oksigen

Oxygen therapy is a treatment that delivers oxygen gas for you to
breathe. You can receive oxygen therapy from tubes resting in your nose, a
face mask, or a tube placed in your trachea, or windpipe. This treatment
increases the amount of oxygen your lungs receive and deliver to your blood.
Oxygen therapy may be prescribed for you when you have a condition that
causes your blood oxygen levels to be too low. Low blood oxygen may make
you feel short of breath, tired, or confused, and can damage your body.
Oxygen therapy can be given for a short or long period of time in the
hospital, another medical setting, or at home. Oxygen is stored as a gas or
liquid in special tanks. These tanks can be delivered to your home and contain
a certain amount of oxygen that will require refills. Another device for use at
home is an oxygen concentrator, which pulls oxygen out of the air for immediate
use. Because oxygen concentrators do not require refills, they won’t run out of
oxygen. Portable tanks and oxygen concentrators may make it easier for you
to move around while using your therapy.
Oxygen poses a fire risk, so you should never smoke or use flammable
materials when using oxygen. You may experience side effects from this
treatment, such as a dry or bloody nose, tiredness, and morning headaches.
Oxygen therapy is generally safe.

Sumber: https://www.nhlbi.nih.gov/health-topics/oxygen-therapy
32. IV Catheter

Sumber: https://www.maxhealthcare.in/sites/default/files/Sizes-of-IV-Cannulas-and-
Flow-Rate-Calculations.pdf
33. Early warning score system
Early Warning Scores have been developed to facilitate early detection of
deterioration by categorising a patient’s severity of illness and prompting
nursing staff to request a medical review at specific trigger points (Mitchell et
al., 2010) utilising a structured communication tool while following a definitive
escalation plan. Adopting a National Early Warning Score (NEWS) is beneficial
for standardising the assessment of acute illness severity, enabling a more
timely response using a common language across acute hospitals nationally.

Sumber: https://www.ncbi.nlm.nih.gov/pubmed/25806463

34. Bezold Jarisch Reflex

The Bezold-Jarisch reflex originates in cardiac sensory receptors with

nonmyelinated vagal afferent pathways. The left ventricle, particularly the
inferoposterior wall, is a principal location for these sensory receptors.
Stimulation of these inhibitory cardiac receptors by stretch, chemical
substances or drugs increases parasympathetic activity and inhibits
sympathetic activity. These effects promote reflex bradycardia, vasodilation
 and hypotension (Bezold-Jarisch reflex) and also modulate renin release and
vasopressin secretion. Conversely, decreases in the activity of these inhibitory
sensory receptors reflexly increase sympathetic activity, vascular resistance,
plasma renin activity and vasopressin. Long regarded as pharmacologic
curiosities, it is now clear that reflexes originating in these inhibitory cardiac
sensory receptors are important to the pathophysiology of many cardiovascular
disorders.

Sumber: https://www.ncbi.nlm.nih.gov/pubmed/6826948

35. Trias Cushing pada peningkatan tekanan intracranial

Cushing triad is a clinical syndrome consisting of hypertension, bradycardia and
irregular respiration and is a sign of impending brain herniation. This occurs
when the ICP is too high the elevation of blood pressure is a reflex mechanism
to maintain CPP. High blood pressure causes reflex bradycardia and brain stem
compromise affecting respiration. Ultimately the contents of the cranium are
displaced downwards due to the high ICP, causing a phenomenon known as
herniation which can be potentially fatal.

Sumber: https://www.ncbi.nlm.nih.gov/books/NBK482119/

36. Nyeri
Nyeri adalah pengalaman sensorik dan emosional yang tidak
menyenangkan akibat kerusakan jaringan, baik aktual maupun potensial atau
yang digambarkan dalam bentuk kerusakan tersebut. Nyeri adalah suatu
pengalaman sensorik yang multidimensional. Fenomena ini dapat berbeda
dalam intensitas (ringan,sedang, berat), kualitas (tumpul, seperti terbakar,
tajam), durasi (transien, intermiten,persisten), dan penyebaran (superfisial atau
dalam, terlokalisir atau difus). Meskipun nyeri adalah suatu sensasi, nyeri
memiliki komponen kognitif dan emosional, yang digambarkan dalam suatu
bentuk penderitaan. Nyeri juga berkaitan dengan reflex menghindar dan
perubahan output otonom.
Fisiologi Nyeri
Mekanisme timbulnya nyeri didasari oleh proses multipel yaitu
nosisepsi, sensitisasi perifer, perubahan fenotip, sensitisasi sentral,
eksitabilitas ektopik, reorganisasi struktural, dan penurunan inhibisi. Antara
stimulus cedera jaringan dan pengalaman subjektif nyeri terdapat empat
proses tersendiri : tranduksi, transmisi, modulasi, dan persepsi. Transduksi
adalah suatu proses dimana akhiran saraf aferen menerjemahkan stimulus
(misalnya tusukan jarum) ke dalam impuls nosiseptif. Ada tiga tipe serabut
saraf yang terlibat dalam proses ini, yaitu serabut A-beta, A-delta, dan C.
Serabut yang berespon secara maksimal terhadap stimulasi non noksius
dikelompokkan sebagai serabut penghantar nyeri, atau nosiseptor. Serabut ini
adalah A-delta dan C. Silent nociceptor, juga terlibat dalam proses transduksi,
merupakan serabut saraf aferen yang tidak bersepon terhadap stimulasi
eksternal tanpa adanya mediator inflamasi. Transmisi adalah suatu proses
dimana impuls disalurkan menuju kornu dorsalis medula spinalis, kemudian
sepanjang traktus sensorik menuju otak. Neuron aferen primer merupakan
pengirim dan penerima aktif dari sinyal elektrik dan kimiawi. Aksonnya berakhir
di kornu dorsalis medula spinalis dan selanjutnya berhubungan dengan banyak
neuron spinal. Modulasi adalah proses amplifikasi sinyal neural terkait nyeri
(pain related neural signals). Proses ini terutama terjadi di kornu dorsalis
medula spinalis, dan mungkin juga terjadi di level lainnya. Serangkaian
reseptor opioid seperti mu, kappa, dan delta dapat ditemukan di kornu dorsalis.
Sistem nosiseptif juga mempunyai jalur desending berasal dari korteks
frontalis, hipotalamus, dan area otak lainnya ke otak tengah (midbrain) dan
medula oblongata, selanjutnya menuju medula spinalis. Hasil dari proses
inhibisi desendens ini adalah penguatan, atau bahkan penghambatan (blok)
sinyal nosiseptif di kornu dorsalis. Persepsi nyeri adalah kesadaran akan
pengalaman nyeri. Persepsi merupakan hasil dari interaksi proses transduksi,
transmisi, modulasi, aspek psikologis, dan karakteristik individu lainnya.
Reseptor nyeri adalah organ tubuh yang berfungsi untuk menerima rangsang
nyeri. Organ tubuh yang berperan sebagai reseptor nyeri adalah ujung syaraf
bebas dalam kulit yang berespon hanya terhadap stimulus kuat yang secaara
potensial merusak. Reseptor nyeri disebut juga Nociseptor. Secara anatomis,
reseptor nyeri (nociseptor) ada yang bermiyelin dan ada juga yang tidak
bermiyelin dari syaraf aferen. (Anas Tamsuri, 2006)
Jalur Nyeri di Sistem Syaraf Pusat
Jalur Asenden Serabut saraf C dan A delta halus, yang masing-masing
membawa nyeri akut tajam dan kronik lambat, bersinap disubstansia gelatinosa
kornu dorsalis, memotong medula spinalis dan naik ke otak di cabang
neospinotalamikus atau cabang paleospinotalamikus traktus spino talamikus
anterolateralis. Traktus neospinotalamikus yang terutama diaktifkan oleh
aferen perifer A delta, bersinap di nukleus ventropostero lateralis (VPN)
talamus dan melanjutkan diri secara langsung ke kortek somato sensorik girus
pasca sentralis, tempat nyeri dipersepsikan sebagai sensasi yang tajam dan
berbatas tegas. Cabang paleospinotalamikus, yang terutama diaktifkan oleh
aferen perifer serabt saraf C adalah suatu jalur difus yang mengirim kolateral-
kolateral ke formatio retikularis batang otak dan struktur lain. Serat-serat ini
mempengaruhi hipotalamus dan sistem limbik serta kortek serebri (Price A.
Sylvia,2006).
Jalur Desenden Salah satu jalur desenden yang telah di identifikasi
adalah mencakup 3 komponen yaitu : a. Bagian pertama adalah substansia
grisea periaquaductus (PAG) dan substansia grisea periventrikel
mesenssefalon dan pons bagian atas yang mengelilingi aquaductus Sylvius. b.
Neuron-neuron di daerah satu mengirim impuls ke nukleus ravemaknus (NRM)
yang terletak di pons bagian bawah dan medula oblongata bagian atas dan
nukleus retikularis paragigantoselularis (PGL) di medula lateralis. c. Impuls
ditransmisikan ke bawah menuju kolumna dorsalis medula spinalis ke suatu
komplek inhibitorik nyeri yang terletak di kornu dorsalis medula spinalis (Price
A. Sylvia,2006). Untuk lebih jelasnya dapat dilihat pada gambar dibawah ini.
 Sumber: http://ejournal.umm.ac.id/index.php/sainmed/article/viewFile/5449/5246
https://www.surgeryjournal.co.uk/article/S0263-9319(15)00236-7/pdf

37. Seorang pasien BB 50 kg, berikut titrasi dengan syringe pump

a. Adrenaline (4mg/50ml): Pengenceran = 4mg/50cc = 80mcg/cc
Jika dosis 0,1mcg, maka = (0,1mcg x 50kg x 60) / 80mcg/cc =
3,75cc/jam
b. Norepinephrine (8mg/50ml): Pengenceran = 8mg/50cc = 160mcg/cc
Jika dosis 0,05mcg, maka = (0,05mcg x 50kg x 60) / 160mcg/cc =
0,94cc/jam
c. Dobutamine (250mg/50ml): Pengenceran = 250mg/50ml = 5000
mcg/cc
Jika dosis 2mcg, maka = (2mcg x 50kg x 60) / 5000mcg/cc = 1,2cc/jam
d. Dopamine (200mg/50ml): Pengenceran = 200mg/50ml = 4000 mcg/cc
Jika dosis 5mcg, maka = (5mcg x 50kg x 60) / 4000mcg/cc =
3,75cc/jam
e. Nicardipine (10mg/50ml): Pengenceran = 10mg/50cc = 200 mcg/cc
Jika dosis 1mcg, maka = (1mcg x 50kg x 60) / 200mcg/cc = 15cc/jam
f. Fentanyl (500mcg/50ml): Pengenceran = 500mcg/50ml = 10mcg/ml
Jika dosis 2mcg/kgBB, maka = (2mcg x 50kg x 60) / 10mcg/cc =
600cc/jam

Sumber: Medscape, Morgan Clinical Anesthesiology

38. Perbedaan CPR AHA 2005,2010, 2015

2005 2010 2015
Use of the “A-B-C” A change in the basic
basic life support life support (BLS)
sequence sequence of steps for
trained rescuers from
“A-B-C” (Airway,
Breathing, Chest
compressions) to “C-A-
 B” (Chest
compressions, Airway,
Breathing) for adults
and pediatric patients
(children and infants,
excluding newborns).
“Look, Listen and Feel” “Look, Listen and Feel”
Included in BLS has been removed
algorithm from the BLS algorithm
A compression rate of A compression rate of In adult victims of
“approximately” at least 100/min cardiac arrest, it is
100/min reasonable for rescuers
to perform chest
compressions at a rate
of 100 to 120/min
Depress adult The new During manual CPR,
breastbone recommendation for rescuers should
approximately 1 1/2 to chest compression perform chest
2 inches (approximately depth: push down on compressions to a
4 to 5 cm) the adult breastbone at depth of at least 2
least 2 inches (5 cm). inches (5 cm) for an
average adult, while
avoiding excessive
chest compression
depths (greater than 2.4
inches [6 cm])
The 2005 AHA If a bystander is not Untrained lay rescuers
Guidelines for CPR and trained in CPR, the should provide
ECC did not provide bystander should compression-only
different provide Hands-Only™ (Hands-Only™) CPR,
recommendations for (compression-only) with or without
trained versus CPR for the adult dispatcher guidance, for
untrained rescuers but victim who suddenly adult victims of cardiac
did recommend that collapses, with an arrest. The rescuer
dispatchers provide emphasis to “push hard should continue
compression-only CPR and fast” on the center compression-only CPR
instructions to untrained of the chest, or follow until the arrival of an
bystanders. The 2005 the directions of the AED or rescuers with
AHA Guidelines for EMS dispatcher. All additional training. All
CPR and ECC did note trained lay rescuers lay rescuers should, at
that if the rescuer was should, at a minimum, a minimum, provide
unwilling or unable to provide chest chest compressions for
provide ventilations, the compressions for victims of cardiac
rescuer should provide victims of cardiac arrest. In addition, if the
chest compressions arrest. In addition, if the trained lay rescuer is
only trained lay rescuer is able to perform rescue
able to perform rescue breaths, he or she
breaths, compressions should add rescue
and breaths should be breaths in a ratio of 30
provided in a ratio of 30 compressions to 2
compressions to 2 breaths. The rescuer
breaths should continue CPR
until an AED arrives
and is ready for use,
EMS providers take
over care of the victim,
or the victim starts to
move
To help bystanders To help bystanders
recognize cardiac recognize cardiac
arrest, dispatchers arrest, dispatchers
should ask about an should inquire about a
adult victim’s victim’s absence of
responsiveness, if the responsiveness and
victim is breathing, and quality of breathing
if the breathing is (normal versus not
normal, in an attempt normal). If the victim is
to distinguish victims unresponsive with
with agonal gasps (i.e., absent or abnormal
in those who need breathing, the rescuer
CPR) from victims who and the dispatcher
are breathing normally should assume that the
and do not need CPR victim is in cardiac
arrest. Dispatchers
should be educated to
identify
unresponsiveness with
abnormal and agonal
gasps across a range of
clinical presentations
and descriptions.
For patients with known
or suspected opioid
addiction who are
unresponsive with no
normal breathing but a
pulse, it is reasonable
for appropriately trained
lay rescuers and BLS
providers, in addition to
providing standard BLS
care, to administer
intramuscular (IM) or
intranasal (IN)
naloxone. Opioid
overdose response
education with or
without naloxone
distribution to persons
at risk for opioid
 overdose in any setting
may be considered.
Sumber:
https://www.emt-national-training.com/aha2005-2010.pdf
https://www.sca-
aware.org/sites/default/files/comparison_chart_2015_aha_guidelines_for_cpr_and_e
cc.pdf

39. Apa yang dimaksud dengan dextrose 40%, dextrose 5%, mannitol 20%,
albumin 20%
Dextrose 40% : dalam 1000 ml terdapat 400 gr glukosa
Dextrose 5% : dalam 1000 ml terdapat 50 gr glukosa
Mannitol 20% : dalam 1000 ml terdapat 200 gr mannitol
Albumin 20% : dalam 1000 ml terdapat 200 gr human albumin

40. Farmakologi Obat :

a. Ranitidine: These agents competitively inhibit histamine binding to H 2
receptors, thereby reducing gastric acid output and raising gastric pH.
b. Omeprazole: These agents, including omeprazole (Prilosec),
lansoprazole (Prevacid), rabeprazole (Aciphex), esomeprazole
(Nexium), and pantoprazole (Protonix), bind to the proton pump of
parietal cells in the gastric mucosa and inhibit secretion of hydrogen
ions.
c. Ketorolac: Ketorolac is a parenteral nonsteroidal antiinflammatory drug
(NSAID) that provides analgesia by inhibiting prostaglandin synthesis.
d. Paracetamo (acetaminophen): is generally considered to be a weak
inhibitor of the synthesis of prostaglandins (PGs).
However, the in vivo effects of paracetamol are similar to those of the
selective cyclooxygenase-2 (COX-2) inhibitors. Paracetamol also
decreases PG concentrations in vivo, but, unlike the selective COX-2
inhibitors, paracetamol does not suppress the inflammation of
rheumatoid arthritis. It does, however, decrease swelling after oral
surgery in humans and suppresses inflammation in rats and mice.
Paracetamol is a weak inhibitor of PG synthesis of COX-1 and COX-2 in
broken cell systems, but, by contrast, therapeutic concentrations of
paracetamol inhibit PG synthesis in intact cells in vitro when the levels
of the substrate arachidonic acid are low (less than about 5 mumol/L).
When the levels of arachidonic acid are low, PGs are synthesized largely
by COX-2 in cells that contain both COX-1 and COX-2. Thus, the
apparent selectivity of paracetamol may be due to inhibition of COX-2-
dependent pathways that are proceeding at low rates. This hypothesis
is consistent with the similar pharmacological effects of paracetamol and
the selective COX-2 inhibitors. COX-3, a splice variant of COX-1, has
been suggested to be the site of action of paracetamol, but genomic and
kinetic analysis indicates that this selective interaction is unlikely to be
clinically relevant. There is considerable evidence that the analgesic
effect of paracetamol is central and is due to activation of descending
serotonergic pathways, but its primary site of action may still be inhibition
of PG synthesis. The action of paracetamol at a molecular level is
unclear but could be related to the production of reactive metabolites by
 the peroxidase function of COX-2, which could deplete glutathione, a
cofactor of enzymes such as PGE synthase.
e. Dexamethasone:
Dexamethasone is a glucocorticoid agonist. Unbound dexamethasone
crosses cell membranes and binds with high affinity to specific
cytoplasmic glucocorticoid receptors. This complex binds to DNA
elements (glucocorticoid response elements) which results in a
modification of transcription and, hence, protein synthesis in order to
achieve inhibition of leukocyte infiltration at the site of inflammation,
interference in the function of mediators of inflammatory response,
suppression of humoral immune responses, and reduction in edema or
scar tissue. The antiinflammatory actions of dexamethasone are thought
to involve phospholipase A2 inhibitory proteins, lipocortins, which control
the biosynthesis of potent mediators of inflammation such as
prostaglandins and leukotrienes.

Sumber: Morgan’s Clinical Anesthesiology + Drugbank