1.

Early Goal Directed Therapy

Early Goal Directed Therapy (EGDT) definition

 Within 6 hours of presentation to the Emergency Department intensive monitoring of specific
circulatory parameters with the aggressive management of 5 key parameters to specified targets to
optimise oxygen delivery to tissues.

Parameters :
1. CVP 8-12 mmHg
2. MAP 65 – 90 mmHg
3. Urine output >0.5 ml/kg/hr
4. Mixed venous oxygen saturation >65% / ScvO2 >70%
5. Haematocrit >30%

Interventions :
1. Reduce work of breathing by early use of mechanical ventilation
2. Fluid resuscitation
3. Use of vasoactive agents: noradrenaline, dobutamine
4. Transfusion

Goal-directed therapy has been used for severe sepsis and septic shock in the intensive care unit. This
approach involves adjustments of cardiac preload, afterload, and contractility to balance oxygen
delivery with oxygen demand. The purpose of this study was to evaluate the efficacy of early goal-
directed therapy before admission to the intensive care unit.
The systemic inflammatory response syndrome can be self-limited or can progress to severe sepsis
and septic shock. Along this continuum, circulatory abnormalities (intravascular volume depletion,
peripheral vasodilatation, myocardial depression, and increased metabolism) lead to an imbalance
between systemic oxygen delivery and oxygen demand, resulting in global tissue hypoxia or
shock.2 An indicator of serious illness, global tissue hypoxia is a key development preceding
multiorgan failure and death.2 The transition to serious illness occurs during the critical “golden
hours,” when definitive recognition and treatment provide maximal benefit in terms of outcome.
These golden hours may elapse in the emergency department, hospital ward, or the intensive care
unit.
Early hemodynamic assessment on the basis of physical findings, vital signs, central venous pressure,
and urinary output7 fails to detect persistent global tissue hypoxia. A more definitive resuscitation
strategy involves goal-oriented manipulation of cardiac preload, afterload, and contractility to achieve
a balance between systemic oxygen delivery and oxygen demand. End points used to confirm the
achievement of such a balance (hereafter called resuscitation end points) include normalized values
for mixed venous oxygen saturation, arterial lactate concentration, base deficit, and pH. Mixed
venous oxygen saturation has been shown to be a surrogate for the cardiac index as a target for
hemodynamic therapy.9In cases in which the insertion of a pulmonary-artery catheter is impractical,
venous oxygen saturation can be measured in the central circulation.
Whereas the incidence of septic shock has steadily increased during the past several decades, the
associated mortality rates have remained constant or have decreased only slightly. Studies of
interventions such as immunotherapy, hemodynamic optimization, or pulmonary-artery
catheterization14 enrolled patients up to 72 hours after admission to the intensive care unit. The
negative results of studies of the use of hemodynamic variables as end points (“hemodynamic
optimization”), in particular, prompted suggestions that future studies involve patients with similar
causes of disease13 or with global tissue hypoxia (as reflected by elevated lactate
concentrations)15 and that they examine interventions begun at an earlier stage of disease.
We examined whether early goal-directed therapy before admission to the intensive care unit
effectively reduces the incidence of multiorgan dysfunction, mortality, and the use of health care
resources among patients with severe sepsis or septic shock.
The patients assigned to early goal-directed therapy received a central venous catheter capable of
measuring central venous oxygen saturation (Edwards Lifesciences, Irvine, Calif.); it was connected
to a computerized spectrophotometer for continuous monitoring. Patients were treated in the
emergency department according to a protocol for early goal-directed therapy for at least six hours
and were transferred to the first available inpatient beds. Monitoring of central venous oxygen
saturation was then discontinued. Critical-care clinicians (intensivists, fellows, and residents
providing 24-hour in-house coverage) assumed the care of all the patients; these physicians were
unaware of the patients' study-group assignments. The study investigators did not influence patient
care in the intensive care unit.
The protocol was as follows. A 500-ml bolus of crystalloid was given every 30 minutes to achieve a
central venous pressure of 8 to 12 mm Hg. If the mean arterial pressure was less than 65 mm Hg,
vasopressors were given to maintain a mean arterial pressure of at least 65 mm Hg. If the mean
arterial pressure was greater than 90 mm Hg, vasodilators were given until it was 90 mm Hg or
below. If the central venous oxygen saturation was less than 70 percent, red cells were transfused to
achieve a hematocrit of at least 30 percent. After the central venous pressure, mean arterial pressure,
and hematocrit were thus optimized, if the central venous oxygen saturation was less than 70 percent,
 dobutamine administration was started at a dose of 2.5 μg per kilogram of body weight per minute, a
dose that was increased by 2.5 μg per kilogram per minute every 30 minutes until the central venous
oxygen saturation was 70 percent or higher or until a maximal dose of 20 μg per kilogram per minute
was given. Dobutamine was decreased in dose or discontinued if the mean arterial pressure was less
than 65 mm Hg or if the heart rate was above 120 beats per minute. To decrease oxygen
consumption, patients in whom hemodynamic optimization could not be achieved received
mechanical ventilation and sedatives
Sumber :
1. https://litfl.com/early-goal-directed-therapy-in-septic-shock/
2. https://www.nejm.org/doi/full/10.1056/NEJMoa010307

2. Setting Ventilator
Setting Ventilator
1. Tentukan “Minute Volume” (M.V.) yaitu :
· M.V = Tidal Volume (T.V) x Respiratory Rate (R.R)
· Normal T.V = 10 – 15 cc/kg BB
· Normal R.R =
- Dewasa = 10 – 12 x/menit
- Pada pasien dengan COPD, T.V lebih kecil, yaitu 6 – 8 cc/kg BB.
- Pada Servo Ventilator 900 C :
o M.V < 4 liter, pakai standar “infant”
o M.V. > 4 liter, pakai standar “adult”
2. Modus
· Tergantung dari keadaan klinis pasien.
· Bila mempergunakan “IMV”, harus dikombinasikan dengan “PEEP”.
3. PEEP
· Ditentukan tergantung dari keadaan klinis pasien.
· Pada pasien dengan edema paru, PEEP dimulai dengan 5 mmHg.
· Pada pasien tidak dengan edema paru, PEEP dimulai dari nol, tetapi FiO2 dinaikan sampai 50%. Bila FiO2 tidak
naik, baru diberikan PEEP mulai dari 5 mmHg.
· Catatan :
- Selama pemakaian Ventilator, FiO2 diusahakan kurang dari 50 %
- PEEP dapat dinaikkan secara bertahap 2,5 mmHg, sampai batas maximal 15 mmHg.
4. Pengaturan Alarm
· Oksigen = batas terendah : 10 % dibawah yang diset
· batas tertinggi : 10 % diatas yang diset
· “Expired M.V = kira-kira 20 % dari M.V yang diset
· “Air Way Pressure” = batas tertinggi 10 cm diatas yang diset

Prosedur Pemberian Ventilator

Sebelum memasang ventilator pada pasien. Lakukan tes paru pada ventilator untuk memastikan pengesetan
sesuai pedoman standar. Sedangkan pengesetan awal adalah sebagai berikut:
· Fraksi oksigen inspirasi (FiO2) 100%
· Volume Tidal: 4-5 ml/kg BB
· Frekwensi pernafasan: 10-15 kali/menit
· Aliran inspirasi: 40-60 liter/detik
· PEEP (Possitive End Expiratory Pressure) atau tekanan positif akhir ekspirasi: 0-5 Cm, ini diberikan pada pasien
yang mengalami oedema paru dan untuk mencegah atelektasis. Pengesetan untuk pasien ditentukan oleh tujuan
 terapi dan perubahan pengesetan ditentukan oleh respon pasien yang ditujunkan oleh hasil analisa gas darah
(Blood Gas)

Pemantauan
1. Observasi keadaan kardiovaskuler pasien : denyut jantung, tekanan darah, sianosis, temperatur.
2. Auskultasi paru untuk mengetahui :
- Letak tube
- Perkembangan paru-paru yang simetris
- Panjang tube
3. Periksa AGD tiap 6 jam, kecuali ada perubahan seting, analisa gas darah diperiksa 20 menit setelah ada
perubahan seting.
· Nilai standar : PCO2 = 35 – 45 mmHg
· Saturasi O2 = 96 – 97 %
· PaO2 = 80 – 100 mmHg
- PaO2 > 100 mmHg → FiO2 diturunkan bertahap 10 %.
- PCO2 > 45 mmHg → M.V dinaikkan.
- PCO2 < 35 mmHg → M.V diturunkan.
4. Periksa keseimbangan cairan setiap hari
5. Periksa elektrolit setiap hari
6. “Air Way Pressure” tidak boleh lebih dari 40 mmHg
7. “Expired Minute Volume” diperiksa tiap 2 jam
8. Usahakan selang nasogastrik tetap berfungsi.
9. Foto Thorax setiap hari → untuk melihat perkembangan klinis, letak ETT dan komplikasi yang terjadi akibat
pemasangan Ventilator.
10. Perhatikan ada tidaknya “tension pneumothorax” dengan melihat tanda-tanda sebagai berikut :
- Gelisah, kesadaran menurun
- Sianosis
- Distensi vena leher
- Trachea terdorong menjauh lokasi “tension pneumothorax”
- Salah satu dinding torak jadi mengembang
- Pada perkusi terdapat timpani.

Perawatan :
1. Terangkan tujuan pemakaian ventilator pada pasien dan atau pada keluarganya bagi pasien yang tidak sadar.
2. Mencuci tangan sebelum dan sesudah melakukan tindakan, untuk mencegah infeksi.
3. “Breathing circuit” sebaiknya tidak lebih tinggi dari ETT, agar pengembunan air yang terjadi tidak masuk ke
paru pasien.
4. Perhatikan permukaan air di “humidifier”, jaga jangan sampai habis, air diganti tiap 24 jam.
5. Fiksasi ETT dengan plester dan harus diganti tiap hari, perhatikan jangan sampai letak dan panjang tube berubah.
1. Tulis ukuran dan panjang tube pada “flow sheet”
6. Cegah terjadinya kerusakan trachea dengan cara :
2. Tempatkan tubing yang dihubungkan ke ETT sedemikian rupa sehingga posisinya berada diatas pasien. Tubing
harus cukup panjang untuk memungkinkan pasien dapat menggerakkan kepala.
7. Memberikan posisi yang menyenangkan bagi pasien, dengan merubah posisi tiap 2 jam. Selain itu perubahan
posisi berguna untuk mencegah terjadinya dekubitus.
8. Memberi rasa aman dengan tidak meninggalkan pasien sendirian.
9. Teknik mengembangkan “cuff” :
- Kembangkan “cuff” dengan udara sampai tidak terdengar suara bocor.
- “cuff” dibuka tiap 2 jam selama 15 menit.

Mode Jenis Ventilasi Mekanik

Klasifikasi Ventilasi mekanik berdasarkan cara alat tersebut mendukung ventilasi, dua kategori umum adalah
ventilator tekanan negatif dan tekanan positif. Berdasarkan mekanisme kerjanya ventilator mekanik tekanan
positif dapat dibagi menjadi empat jenis yaitu :

1. Volume Cycled Ventilator.

 Volume cycled merupakan jenis ventilator yang paling sering digunakan di ruangan unit perawatan kritis.
Perinsip dasar ventilator ini adalah cyclusnya berdasarkan volume. Mesin berhenti bekerja dan terjadi ekspirasi
bila telah mencapai volume yang ditentukan. Keuntungan volume cycled ventilator adalah perubahan pada
komplain paru pasien tetap memberikan volume tidal yang konsisten.

Jenis ventilator ini banyak digunakan bagi pasien dewasa dengan gangguan paru secara umum. Akan tetapi jenis
ini tidak dianjurkan bagi pasien dengan gangguan pernapasan yang diakibatkan penyempitan lapang paru
(atelektasis, edema paru). Hal ini dikarenakan pada volume cycled pemberian tekanan pada paru-paru tidak
terkontrol, sehingga dikhawatirkan jika tekanannya berlebih maka akan terjadi volutrauma. Sedangkan
penggunaan pada bayi tidak dianjurkan, karena alveoli bayi masih sangat rentan terhadap tekanan, sehingga
memiliki resiko tinggi untuk terjadinya volutrauma.

2. Pressure Cycled Ventilator

Prinsip dasar ventilator type ini adalah cyclusnya menggunakan tekanan. Mesin berhenti bekerja dan terjadi
ekspirasi bila telah mencapai tekanan yang telah ditentukan. Pada titik tekanan ini, katup inspirasi tertutup dan
ekspirasi terjadi dengan pasif. Kerugian pada type ini bila ada perubahan komplain paru, maka volume udara
yang diberikan juga berubah. Sehingga pada pasien yang setatus parunya tidak stabil, penggunaan ventilator tipe
ini tidak dianjurkan, sedangkan pada pasien anak-anak atau dewasa mengalami gangguan pada luas lapang paru
(atelektasis, edema paru) jenis ini sangat dianjurkan.
3. Time Cycled Ventilator
Prinsip kerja dari ventilator type ini adalah cyclusnya berdasarkan waktu ekspirasi atau waktu inspirasi yang
telah ditentukan. Waktu inspirasi ditentukan oleh waktu dan kecepatan inspirasi (jumlah napas permenit).
Normal ratio I : E (inspirasi : ekspirasi) 1 : 2.

4. Berbasis aliran (Flow Cycle)

Memberikan napas/ menghantarkan oksigen berdasarkan kecepatan aliran yang sudah disetting terlebih dahulu.

Mode Ventilator Mekanik

1. Mode control (pressure control, volume control, continuous mode).
Pasien mendapat bantuan pernafasan sepenuhnya, pada mode ini pasien dibuat tidak sadar (tersedasi) sehingga
pernafasan di kontrol sepenuhnya oleh ventilator. Tidal volume yang didapat pasien juga sesuai yang di set pada
ventilator. Pada mode control klasik, pasien sepenuhnya tidak mampu bernafas dengan tekanan atau tidal volume
lebih dari yang telah di set pada ventilator. Namun pada mode control terbaru, ventilator juga bekerja dalam
mode assist-control yang memungkinkan pasien bernafas dengan tekanan atau volum tidal lebih dari yang telah
di set pada ventilator.
2. Mode Intermitten Mandatory Ventilation (IMV).
Pada mode ini pasien menerima volume dan frekuensi pernafasan sesuai dengan yang di set pada ventilator.
Diantara pernafasan pemberian ventilator tersebut pasien bebas bernafas. Misalkan respiratory rate (RR) di set
10, maka setiap 6 detik ventilator akan memberikan bantuan nafas, diantara 6 detik tersebut pasien bebas
bernafas tetapi tanpa bantuan ventilator. Kadang ventilator memberikan bantuan saat pasien sedang bernafas
mandiri, sehingga terjadi benturan antara kerja ventilator dan pernafasan mandiri pasien. Hal ini tidak akan
terjadi pada
3. Mode Synchronous Intermitten Mandatory Ventilation (SIMV) yang sama dengan mode IMV hanya saja
ventilator tidak memberikan bantuan ketika pasien sedang bernafas mandiri. Sehingga benturan terhindarkan.
4. Mode Pressure Support atau mode spontan.
Ventilator tidak memberikan bantuan inisiasi nafas lagi. Inisiasi nafas sepenuhya oleh pasien, ventilator hanya
membantu pasien mencapai tekanan atau volume yang di set di mesin dengan memberikan tekanan udara positif.
Mode of ventilation

The mode of ventilation should be tailored to the needs of the patient. In the emergent situation, the practitioner may need
to order initial settings quickly. SIMV and A/C are versatile modes that can be used for initial settings. In patients with a
good respiratory drive and mild-to-moderate respiratory failure, PSV is a good initial choice.

Tidal volume

Observations of the adverse effects of barotrauma and volutrauma have led to recommendations of lower tidal volumes
than in years past, when tidal volumes of 10-15 mL/kg were routinely used.

An initial TV of 5-8 mL/kg of ideal body weight is generally indicated, with the lowest values recommended in the
presence of obstructive airway disease and ARDS. The goal is to adjust the TV so that plateau pressures are less than 35
cm water.

Respiratory rate

A respiratory rate (RR) of 8-12 breaths per minute is recommended for patients not requiring hyperventilation for the
treatment of toxic or metabolic acidosis, or intracranial injury. High rates allow less time for exhalation, increase mean
airway pressure, and cause air trapping in patients with obstructive airway disease. The initial rate may be as low as 5-6
breaths per minute in asthmatic patients when using a permissive hypercapnic technique.

Supplemental oxygen therapy

The lowest FiO2 that produces an arterial oxygen saturation (SaO2) greater than 90% and a PaO2 greater than 60 mm Hg
is recommended. No data indicate that prolonged use of an FiO2 less than 0.4 damages parenchymal cells.

Inspiration/expiration ratio

The normal inspiration/expiration (I/E) ratio to start is 1:2. This is reduced to 1:4 or 1:5 in the presence of obstructive
airway disease in order to avoid air-trapping (breath stacking) and auto-PEEP or intrinsic PEEP (iPEEP). Use of inverse
I/E may be appropriate in certain patients with complex compliance problems in the setting of ARDS.

Inspiratory flow rates

Inspiratory flow rates are a function of the TV, I/E ratio, and RR and may be controlled internally by the ventilator via
these other settings. If flow rates are set explicitly, 60 L/min is typically used. This may be increased to 100 L/min to
deliver TVs quickly and allow for prolonged expiration in the presence of obstructive airway disease.

Positive end-expiratory pressure

Positive end-expiratory pressure (PEEP) has several beneficial effects and, when used at optimal levels in combination
with low tidal volumes, may reduce the incidence of ventilator-induced lung injury. In particular, there is a significant
amount of ongoing research evaluating the use of high levels of PEEP in acute lung injury (ALI) and ARDS. PEEP has
been found to reduce the risk of atelectasis trauma by increasing the number of "open" alveoli participating in ventilation,
thereby minimizing trauma due to the cyclical collapse and reopening of alveoli. However, note that in disease states such
as ARDS, the degree to which alveoli function has been compromised varies tremendously within the lungs and there is
no single ideal PEEP appropriate for all alveoli; rather, a compromise PEEP must be selected.

In addition to alveolar recruitment, an additional beneficial effect of PEEP is to shift lung water from the alveoli to the
perivascular interstitial space. It does not decrease the total amount of extravascular lung water. This is of clear benefit in
cases of cardiogenic as well as noncardiogenic pulmonary edema. An additional benefit of PEEP in cases of CHF is to
decrease venous return to the right side of the heart by increasing intrathoracic pressure.

Applying physiologic PEEP of 3-5 cm water is common to prevent decreases in functional residual capacity in those with
normal lungs. The reasoning for increasing levels of PEEP in critically ill patients is to provide acceptable oxygenation
and to reduce the FiO2 to nontoxic levels (FiO2< 0.5). The level of PEEP must be balanced such that excessive
intrathoracic pressure (with a resultant decrease in venous return and risk of barotrauma) does not occur.

Sensitivity

With assisted ventilation, the sensitivity typically is set at -1 to -2 cm water. The development of iPEEP increases the
difficulty in generating a negative inspiratory force sufficient to overcome iPEEP and the set sensitivity. Newer
ventilators offer the ability to sense by inspiratory flow instead of negative force. Flow sensing, if available, may lower
the work of breathing associated with ventilator triggering.

Monitoring During Ventilatory Support

Cardiac monitor, blood pressure, and pulse oximetry (SaO2) are recommended. The authors’ practice with stable patients
is to titrate down FiO2 to the minimum value necessary to maintain maximal SaO2. An arterial blood gas (ABG)
measurement is frequently obtained 10-15 minutes after the institution of mechanical ventilation. The measured arterial
PaO2 should verify the transcutaneous pulse oximetry readings and direct the reduction of FiO2 to a value less than 0.5.
The measured PaCO2 can suggest adjustments of minute ventilation but should be interpreted in light of the patient's
overall acid-base status. For example, full correction of PaCO2 in a chronically hypercarbic COPD patient will lead to
unopposed metabolic alkalosis.

Reasonable alternatives to arterial blood gas measurement in more stable patients include measuring the venous blood
gas, which will give values close to arterial pH and PaCO2 or monitoring an end-tidal carbon dioxide. An additional
advantage of end-tidal carbon dioxide monitoring is that it can detect acute ventilator dysfunction such as endotracheal
tube obstruction or dislodgement.[10]

Peak inspiratory and plateau pressures should be assessed frequently, although it should be recognized that both pressures
will be increased by extrapulmonary pressure, for example from stiff chest walls or a distended abdomen, and do not
reflect the true risk of barotrauma. In general, however, parameters may be altered to limit pressures to less than 35 cm
water. Expiratory volume is checked initially and periodically (continuously if ventilator is capable) to ensure that the set
tidal volume is delivered. Any indication of an air leak must prompt a search for underinflated tube cuffs, open tubing
ports, or worsening pneumothorax. In patients with airway obstruction, monitor auto-PEEP.

Initial Ventilator Settings in Various Disease States

In the ED setting, patients frequently require full respiratory support. For most ED patients who are paralyzed as a
component of rapid-sequence induction, CMV and A/C are good choices as an initial ventilatory mode. SIMV may be
better tolerated in nonparalyzed patients with obstructive airway disease and an intact respiratory effort. PSV can be used
when respiratory effort is intact and respiratory failure is not severe.[11]

Noninvasive ventilation (CPAP, BiPAP) can be used effectively in many cases of severe COPD and CHF to avoid
tracheal intubation. Initial ventilator settings are guided by the patient's pulmonary pathophysiology and clinical status.
Adjustments can then be made to limit barotrauma, volutrauma, and oxygen toxicity. CPAP and BiPAP require alert,
cooperative patients capable of independently maintaining their airways and are contraindicated in the presence of facial
trauma.
Asthma and COPD

Hypoxia can generally be corrected through a high FiO2, but patients with airway obstruction are at risk of high airway
pressures, breath stacking leading to intrinsic PEEP, barotrauma, and volutrauma. To minimize intrinsic PEEP, it is
recommended that expiratory flow time be increased as much as possible and that tidal volumes and respiratory rates are
set at low values.[12] Permissive hypercapnia enables a low respiratory rate of 6-8 breaths per minute to be used, as well
as an increased I:E ratio of 1:1.5 or 1:2.

PEEP may benefit some asthmatic patients by reducing the work of breathing and maintaining open airways during
expiration, but its effects are difficult to predict and must be carefully monitored. Patients with asthma and COPD are at
particular risk of barotraumatic progression to tension pneumothorax, a complication that can initially appear similar to
runaway intrinsic PEEP. These conditions may be distinguished by temporary detachment of the patient from positive-
pressure ventilation; if exhalation results in a recovery of pulse or normal blood pressure, the diagnosis is intrinsic PEEP.

CPAP and BiPAP will benefit some asthmatics and many patients with COPD. These patients will require careful
monitoring as they can easily deteriorate from hypercarbia, intrinsic PEEP, or respiratory exhaustion. Nevertheless, a
CochraneDatabase Systematic Review analysis of trials including patients with severe COPD exacerbations demonstrated
that the use of noninvasive positive-pressure ventilation absolutely reduced the rate of endotracheal intubation by 59%
(95% confidence interval [CI] of relative risk [RR]: 0.33-0.53), the length of hospital stay by 3.24 days (95% CI: 2.06-
4.44 days), and the risk of mortality by 48% (95% CI of RR: 0.35-0.76).[2]

Acute respiratory distress syndrome

ARDS lungs are typically irregularly inflamed and highly vulnerable to atelectasis as well as barotrauma and volutrauma.
Their compliance is typically reduced, and their dead space increased. The standard of care for the ventilatory
management of patients with ARDS changed dramatically in 2000 with the publication of a large multicenter, randomized
trial comparing patients with ARDS initially ventilated with either the traditional tidal volume of 12 mL/kg or a lower TV
of 6 mL/kg. This trial was stopped early because the lower tidal volume was found to reduce mortality by an absolute
8.8% (P=.007). Intriguingly, plasma interleukin 6 concentrations decreased in the low TV group relative to the high TV
group (P< .001), suggesting a decrease in lung inflammation.[13, 14, 15, 16]

The authors recommend initiating ventilation of patients with ARDS with A/C ventilation at a tidal volume of 6 mL/kg,
with a PEEP of 5 and initial ventilatory rate of 12, titrated up to maintain a pH greater than 7.25. There is not yet adequate
evidence to routinely recommend PEEP greater than 5 cm water, but, in appropriately monitored circumstances, it may be
attempted.[17] Intrinsic PEEP may occur in patients with ARDS at high ventilatory rates and should be watched for and
treated by reducing the rate of ventilation under direct observation until plateau pressures decrease. The authors
recommend a target plateau pressure of less than 30 cm water. Once a patient has been stabilized with adequate tidal
volumes at a plateau pressure of less than 30 cm water, considering a trial of pressure- cycled ventilation is reasonable.

Several recruitment maneuvers have been devised to increase the proportion of alveoli ventilated in ARDS. These
techniques typically attempt short-term increased PEEP or volume to open occluded or collapsed alveoli. Gattinoni et al,
for example, found that among ARDS patients undergoing whole-lung CT, applying 45 cm water PEEP recruited a mean
of 13% new lung tissue.[18]

A recent meta-analysis that compared high versus low levels of PEEP in patients with ALI and ARDS found no
difference in mortality before hospital discharge amongst studies that used the same tidal volume in both control and
intervention arms.[17] In a subsequent subgroup analysis that assessed lung-protective ventilation (low tidal volume, high
PEEP) versus conventional mechanical ventilation, the authors found a decrease in mortality with the use of a lung-
protective ventilation strategy. The same review also found that high levels of PEEP do improve oxygenation in patients
with ALI and ARDS.

In a recent prospective, randomized, controlled trial, Guerin et al examined whether early prone positioning during
mechanical ventilation can improve outcomes in patients with severe ARDS. The authors found that both the 28-day and
unadjusted 90-day mortalities in the prone group were significantly lower (16% and 23.6%, respectively) than in the
supine group (32.8% and 41%, respectively).[19] Although they found no difference between the groups with regard to
duration of invasive mechanical ventilation or length of stay in the ICU, they found a higher incidence of cardiac arrest in
the supine group (31% vs 16% in the prone group).

Permissive hypercapnia is a ventilatory strategy that has won particular favor in the management of patients with ARDS
and COPD/asthma who would otherwise require dangerously high tidal volumes and airway pressures. In patients without
contraindications such as head injury, cerebrovascular accident (CVA), elevated intracranial pressure, or cardiovascular
instability, permissive hypercapnia has permitted much decreased tidal volumes, airway pressures, and respiratory rates,
though evidence for a decrease in mortality rates is incomplete.[20] The typically recommended target pH is 7.25.

Noninvasive ventilatory strategies have met with little success in the treatment of patients with ARDS. The authors
recommend great caution and close monitoring if noninvasive positive pressure ventilation (NIPPV) is attempted among
patients with ARDS.

In trials of NIPPV among patients with undifferentiated hypoxemia, the presence of pneumonia or ARDS was associated
with significantly increased risk of failure. Some subgroups of patients with ARDS may benefit from NIPPV; however,
Antonelli et al demonstrated greater success in applying noninvasive positive pressure ventilation to patients with lower
simplified acute physiology scores and higher PaO2/FiO2 ratios.[21]

Congestive heart failure

CHF responds very well to positive-pressure ventilation, which serves the dual role of opening alveoli and reducing
preload. Many patients with CHF benefit from a trial of noninvasive CPAP or BiPAP. Some of these patients will
clinically improve so rapidly that admitting services may request discontinuation of noninvasive ventilatory support, but
great caution must be maintained if this is attempted, as fluid may unpredictably reaccumulate, resulting in hypoxia and
respiratory failure.

Intubated patients usually manage to adequately oxygenate. PEEP can be increased as tolerated to improve oxygenation
and reduce preload. However, in some patients, cardiac output can be particularly dependent on preload and such patients
may easily develop postintubation hypotension. Management of this common complication includes a combination of
fluid therapy, discontinuation of nitroglycerin or other medical therapies, and, if necessary, medical or mechanical
hemodynamic support interventions.[22]

Traumatic brain injury

Hyperventilation was traditionally recommended in the management of severe traumatic brain injury, but recent studies
have demonstrated poor outcomes thought to be secondary to excessive cerebral vasoconstriction and reduced cerebral
perfusion. However, retrospective data have demonstrated decreased mortality among traumatic brain injury ventilated to
PCO2 between 30 and 39 mm Hg, though this has not been prospectively validated.

Sumber : https://emedicine.medscape.com/article/810126-overview

3. Breathing Circuit
Anaesthesia Breathing System (formerly known as anaesthesia Breathing Apparatus or Anaesthesia
Breathing Circuit) is an interface between the anaesthetic machine and the patient. They evolved over 160
years from the open systems used by Morton to the present day closed systems using carbon dioxide
absorbents. The main purpose of these systems is to deliver the required oxygen and anaesthetic gases, and
maintain carbon dioxide homeostasis. In addition they help us to assess, assist, or control ventilation, and
condition temperature and humidity. Present day systems are constructed to facilitate scavenging of exhaled
gases as well.
Components
1. Connectors and Adaptors (Figure 1): These connectors ensure quick connection between the breathing
systems, and masks or endotracheal tubes. Their sizes are universal and either male or female 15/22
mm connections. Some of them also incorporate gas sampling ports.
 1. HME filter with sampling port
2. T-Piece
3. Straight connector with a side gas sampling
port.
4. Right angle connection
5. Right angle swivel connector for insertion
of a flexible fiberscope. It can
accommodate different sized fiberscopes
by changing the diaphragm. The large cap
Figure 1. Connectors
is used if no diaphragm is present.
6. Right angle connector with gas sampling
port.
7. Flexible corrugated extension

2. Reservoir Bag
a. Acts as a reservoir for gases to be stored during exhalation
b. Acts as a reservoir and ensures adequate supply of required flows during inhalation
c. Helps anaesthesiologist to assess, assist or control ventilation manually
d. Protects the patient from excessive pressure
3. Corrugated tubes: Flexible, low-resistance, light weight connection from one part to other
4. Valves:
a. Adjustable Pressure Limiting (APL) Valves: The APL valve is a user-adjustable valve that
releases gases to a scavenging system. It is used to control the pressure in the breathing system.
b. Unidirectional Valves: These valves ensure a required direction of flow in breathing systems.
c. Non-rebreathing Valves: These valves are used more commonly in manual resuscitators

5. Filters:
a. Bacterial filters: These are meant to prevent transmission of infection to the patient or
contamination of the equipment. The recommendations for their use vary for different countries.
Generally a new filter should be used for every patient or in the absence of a filter a disposable
system should be used for every patient. Filters are generally not preferred for paediatric patients.
b. Heat and Moisture Exchange (HME) filters: Administration of dry gases at room temperature
could lead to heat loss and increased pulmonary complication. The function of the nose is to
warm and humidify inhaled gases. When the nose is bypassed it is advisable to use HME filters to
achieve this objective. These devices also help to dehumidify the gases that are being sampled for
analysis by side stream devices.
Apparatus Dead Space: Some components that connect the breathing system to the patient act as an
extension of patient’s anatomical dead space. Since this dead space is imposed by a piece of apparatus it is
termed as apparatus dead space. Apparatus dead space can be defined as that part of the breathing system
from which exhaled alveolar gases are rebreathed without any significant change in their carbon dioxide
concentration. The volume of the apparatus dead space should be kept to as small as possible or else
rebreathing of carbon dioxide could result in hypercapnia.

Classification of Breathing Systems

Historical (Table 1):

Table 1. Classification of Breathing Systems

Type Inhalation Exhalation To Reservoir Rebreathing Example
Open Air + Agent Atmosphere nil Nil Open drop
T-Piece
Semi Open Air + Agent Atmosphere small minimal T-Piece with small
from Machine reservoir
Semi Closed From Machine Atmosphere + large possible Magill attachment
Machine Mapleson systems
Closed From Machine Machine large Yes + CO2 Circle system
absorbent

Recommended (Table 2): Many classifications used in the literature are a source of confusion and
inconsistency. Since it is important for an anesthesiologist to understand carbon dioxide homeostasis while
using different systems, it is advisable to classify the systems based on CO2 elimination. One should also
understand whether a system is efficient during spontaneous breathing, controlled ventilation or both, and
whether it can be used for paediatric patients, adults or both.

Table 2. Classification based on CO2 Rebreathing (normal working condition)

No CO2 Rebreathing CO2 Rebreathing is possible, but the CO2 level in

patient is determined by the interaction of:
1. Minute ventilation
2. Fresh Gas Flow and
3. Arrangement of Components
1. Non-Rebreathing Valves: These separate
exhaled gases from inhaled gases.
 Non-Rebreathing circuits,
 Self inflating resuscitation equipment
2. CO2 Absorbent systems:
 To-and-Fro system
 Circle system
2. T-Piece Systems:
1. Mapleson Systems
a. Efficient for spontaneous respiration
Mapleson A, Lack’s
b. Efficient for controlled ventilation
Mapleson D, Bain’s
c. Efficient for both spontaneous and
controlled
 A-D switches
 Enclosed Afferent Reservoir System
 Ayre’s T –piece, Jackson-Rees, Bain’s
Systems using Non-rebreathing Valves
These systems have largely disappeared from anaesthetic practice. However, manual resuscitators (Figure
2) are used commonly in the medical practice. Self inflating bags with non-rebreathing valves (Ambu bag
is one of the common names) are principally used for transport of patients and for resuscitation of patients
by paramedics, emergency room staff, critical care staff, and the operating room personnel.

The non-rebreathing valve allows the gases from the bag to be delivered to the patient and prevents any
exhaled gases to enter the self inflating bag and thus prevent CO2 rebreathing. The bag is filled with oxygen
enriched air through another set of unidirectional valves. The inspired oxygen concentration depends on the
oxygen flow and size of the reservoir. A PEEP valve can be added to the system at the patient exhalation
port to optimize gaseous exchange. A pressure monitoring and limiting valve is also added to prevent any
barotrauma.

Figure 2. Schematic diagram of self inflating resuscitator. (© Cambridge University Press. Reproduced
with permission: Kumar AY, Wang J. Anesthesia breathing systems. In: Vacanti C. et al Eds. Essential
Clinical Anesthesia. 1st Edition. Boston: Cambridge university press 2010: In Print)
These units are available in different sizes to suit different patient populations. Patients breathing
spontaneously will either breathe ambient air or oxygen enriched ambient. The equipment is portable, and
simple to use. However failure to familiarize oneself with the available equipment can lead to adverse
outcomes.
Systems using CO2 Absorbents
These systems were developed to conserve gases, to save costs, minimize pollution, and to some degree
retain heat and moisture. All the exhaled gases are rebreathed except the carbon dioxide which is removed
by different formulations of carbon dioxide absorbents (Soda lime, Baralyme, Amsorb®, Drägersorb®
etc.). Fresh gases are added to the system based on the leaks in the system, uptake of oxygen and
inhalational anesthetic agents by the body, arrangements of various components of the system, and clinical
state and duration of anesthesia.
The CO2 from exhaled gases combines with water to become a weak acid, carbonic acid, which reacts with
a strong alkali (calcium hydroxide) producing a carbonate and water. This reaction of neutralization is
exothermic and steps are as follows:
 1. CO2 + H2O ⇔ H2CO3
2. H2CO3 + Ca(OH)2 ⇔ CaCO3 + 2H2O + Heat

The reaction with calcium hydroxide is slow, hence catalysts are used to improve the performance.
Traditionally soda lime has sodium and potassium hydroxides as catalysts. The modern day soda lime has
only sodium hydroxide as a catalyst. Baralyme has barium hydroxide octahydrate as a catalyst. Some
formulations of Amsorb® and Drägersorb®Free contain calcium chloride, a humectant (hygroscopic
substance with the affinity to form hydrogen bonds with molecules of water).

The absorbent is presented as porous granules or pellets with a size between 4-8 mesh. Traditionally silica
is added to give hardness to the granules, but the modern technology makes this unnecessary. The
absorbents can either be packed into canisters or available as pre-packed canisters.

Theoretically 100 grams of wet soda lime contains approximately 74 grams of calcium hydroxide (one gram
molecular weight). This can absorb one gram molecular weight of CO2 (44 g CO2 is equivalent to 24 liters
at room temperature and pressure according to Avogadro’s principle). Assuming that a resting adult
produces CO2 at the rate of 12 liters/hour (200 ml/min), 100 g of soda lime at 100% efficiency is expected
to last for about two hours. However in practice one can never achieve this level of efficiency particularly
in single chamber canisters and 100 g soda lime roughly lasts for about 60 minutes. Dual chamber canisters
demonstrate better efficiency if canisters are changed one at a time and reversed. However in order to
minimize the effects of desiccation of the absorbent, the consensus statement from Anesthesia Patient Safety
Foundation recommends that the absorbent from both canisters be changed at the same time. Amsorb® is
reported to be 50% less efficient when compared to soda lime.

Inhaled Anaesthetic agents and CO2 absorbents

The absorbents will, to some extent, interact with inhaled anesthetics and result in the production of
degradation products.
Compound A: Sevoflurane decomposes to form several degradation products. However, only ‘Compound
A’ has a dose dependent nephrotoxicity in rats. Human studies have produced contradicting results.
The circumstances that produce higher levels of ‘compound A’ include
1. low total gas flow rate (below 1 L/min),
2. higher concentration of sevoflurane,
3. the use of Baralyme rather than Soda lime,
4. higher absorbent temperatures, and
5. desiccated carbon dioxide absorbent (hence the addition of calcium chloride reduces the
production of compound A).
Absorbents free of strong alkali, having smaller concentration of sodium hydroxide, or containing
calcium chloride produce little or no ‘compound A’ (Amsorb®, Drägersorb® Free).
Carbon Monoxide: Carbon monoxide (CO) is produced when desflurane, enflurane, or isoflurane is passed
through dry absorbent containing a strong alkali. The factors that increase the carbon monoxide production
include (1) higher anaesthetic concentration, (2) higher temperature, and (3) dry absorbent. The magnitude
of CO production from greatest to least is desflurane > enflurane > isoflurane > halothane
= sevoflurane. The use of Baralyme produces more CO rather than Soda lime. Amsorb® and Drägersorb®
free do not produce significant levels of CO. In view of the above and also because of the production of
high temperature with sevoflurane, leading to reports of fires, the manufacturers of Baralyme have stopped
the distribution of Baralyme since late 2004.

Indication of Absorbent exhaustion:

1. Capnography: Appearance of CO2 in the inspired gas is the best way to detect absorbent exhaustion
2. Indicators: An indicator is an acid or base whose color depends on the pH and the color change is
indicative of absorbent exhaustion. Several indicators like Phenolphthalein (White to pink), Ethyl violet
(white to purple), Clayton yellow (red to yellow), Ethyl orange (orange to yellow), and Mimosa Z (red
to white) are used by different manufacturers. Color change could be misleading in certain
circumstances particularly due to regeneration (peaking) after a period of rest. Amsorb® turns purple
when desiccated; an additional advantage to prevent use of desiccated soda lime.
3. Temperature in canister: Since the CO2 neutralization is an exothermic reaction, changes in the
absorbent temperature occur earlier than color change. Studies have suggested that when temperature
of the downstream canister is higher than that of the upstream canister the absorbent should be changed
in both canisters.
4. Clinical signs: Clinical signs of hypercapnia like tachycardia, hypertension, cardiac arrhythmias, and
sweating are usually late signs and are non-specific.

To and Fro System (Figure 3)

Ralph Waters (anesthetist in Kansas City) in 1921 described the clinical use of a canister filled with soda
lim. Patients exhaled through the canister (placed close to the patient's airway) into a reservoir bag and
inhaled the next breath, free of CO2, from the reservoir bag, passing again through the canister (i.e., a to-
and-fro canister). This revolutionary innovation meant that inhalation anaesthesia could be given without
dilution by room air. High concentrations of oxygen could be given, heat was conserved, and pollution of
the operating room air was avoided (pollution was considered to be a problem even in 1926). The principle
of CO2 absorption using the to-and-fro canister was eventually supplanted by soda lime canisters in circle
systems. The to-and-fro canister, however, set the stage for the subsequent introduction of cyclopropane
and, even later, halogenated inhalational anaesthetics that could not be given using open techniques. The
stage was also set for initiation of assisted and, finally, controlled respiration, the need for which did not
become apparent for another 25 years.
Figure 3. Waters ‘To and Fro’ system. (© Cambridge University Press. Reproduced with permission)
Circle System (Figure 4)
In 1926, Brian Sword developed a unidirectional rebreathing system, referred to as a circle system. The
gases flow in a circle through the soda lime canister to the patient and back. The unidirectional flow is
maintained by two separate unidirectional valves one for inspiration (IUDV) and another for expiration
(EUDV) mounted on the canister. The placement of the other components like Fresh Gas Flow (FGF),
Adjustable Pressure Limiting Valve (APL), and Reservoir bag determine the efficiency of the system.

FGF: The fresh gas flow usually enters the system between the canister and the IUDV. The system is
classified into three functional types based on the FGF:
1. High flow: FGF > patient’s Alveolar Ventilation. In an ideal arrangement this results in selective
elimination of all the exhaled gases from the patient and hence there is no rebreathing of alveolar gases.
The inspired concentration of oxygen and anaesthetic agents will be the same as that are set on the
machine. This technique is recommended usually at induction, intermittently during a long anaesthetic,
whenever patient’s depth of anaesthesia needs to be changed rapidly, and during recovery.
2. Low flow: FGF < patient’s Alveolar Ventilation (but not basal). These flows result in conservation of
part of the exhaled gases. This technique allows for a bit of flexibility, requires less sophisticated
technology, and lessens the effects due to accumulation of compound A and carbon monoxide.
3. Closed system or Basal flow: The use of very low FGF makes these systems economical and exciting.
FGF supplies only the consumed oxygen and anaesthetic agents by the patients. The currently available
sophisticated machines (Zeus, Aisys) make this technique practically easy to master and use.
Monitoring of oxygen and inhaled agents between the system and patient is mandatory.
Figure 4. Schematic representation of circle system. (© Cambridge University Press. Reproduced with
permission)

Reservoir Bag (RB): The reservoir bag should ideally be located between EUDV and the canister. It will
be less efficient to have it between IUDV and the canister. It should never be located between either of the
unidirectional valves and the patient. During mechanical ventilation the reservoir bag is switched to the
ventilator bellows using a switch (Man/Auto).
APL: The location of the APL valve in conjunction with the reservoir bag determines the efficiency of
expelling exhaled gases out of the system. The ideal location is between the EUDV and the canister along
with the RB. This location allows for efficient elimination of exhaled alveolar gases preferentially out of
the system. Modifications to the APL valve facilitate scavenging.
Breathing tubes: Two corrugated tubes connect the Y-piece at the patient end to either of the unidirectional
valves. Corrugated tubes are used to allow flexibility and prevent kinking. These tubes expand and contract
during positive pressure ventilation resulting in loss of tidal volume (internal compliance of the tubes). This
could be as high as 200 ml at pressures of 20 cm H2O. Hence appropriate changes should be made
particularly for paediatric patients.
Advantages and disadvantages
The main advantages of circle system include economy, reduced pollution, and conservation of heat and
humidity. The disadvantages include the need for more vigilance, need for extensive monitoring of inspired
gases, and accumulation of by-products of anaesthetic agent degradation.
Mapleson Systems (Figure 5)

Figure 4. Mapleson Classification. (© Cambridge University Press. Reproduced with permission)

The Magill attachment has been in use since 1928. In 1954 on the advice of William Mushin, Mapleson
assembled various components used in the Magill circuit in different ways and reported on the functional
analysis to eliminate rebreathing. Mapleson systems A-E were thus born and system F (Jackson Rees
modification of T-piece) was added to the analysis in 1975. The amount of carbon dioxide rebreathing
associated with each system is multifactorial, and variables that dictate the ultimate carbon dioxide
concentration are as shown in Table 3. The following summarizes the relative efficiency of different
Mapleson systems with respect to prevention of rebreathing:
 During spontaneous ventilation: A > DFE > CB.
 During controlled ventilation, DFE > BC > A.
The Mapleson A, B, and C systems are rarely used today, but the D, E, and F systems are commonly
used.
 Table 3. Factors affecting CO2 rebreathing
1. the fresh gas inflow rate, 8. the peak inspiratory flow rate,
2. the minute ventilation, 9. the volume of the reservoir tube,
3. the mode of ventilation (spontaneous or 10. the volume of the breathing bag,
controlled), 11. ventilation by mask,
4. the tidal volume, 12. ventilation through an endotracheal tube, and
5. the respiratory rate, 13. the carbon dioxide sampling site.
6. the inspiratory to expiratory ratio,
7. the duration of the expiratory pause,

Mapleson A (Magill attachment – 1928; Lack system – 1972): This is the most efficient system during
spontaneous respiration. FGF equalling minute ventilation eliminates rebreathing, while PaCO2 is
determined by the patient’s minute ventilation. The following figures depict plug type movement of gases
from various compartments, however, mixing of gases at various interfaces occurs all the time. The
apparatus dead space in this system extends from the APL valve to the patient.
During spontaneous ventilation the APL valve is kept in the fully open position, however it remains closed
till its opening pressure is exceeded. As the patient exhales, the dead space gases followed by alveolar gases
enter the corrugated tube and travel towards the reservoir bag. Simultaneously the fresh gas also flows into
the bag. Once the bag is full the pressure in the system rises and the APL valve opens. From this point the
alveolar gases from the patient are vented through APL valve. The fresh gas entering the corrugated tube
forces the alveolar gases in the corrugated tube out through the open APL valve. If the FGF is equal to or
higher than patient’s minute volume, all the alveolar gases and the dead space gases will be vented through
APL valve (Figure 6). At the beginning of next inspiration patient inhales alveolar gases from apparatus
dead space followed by fresh gases from the corrugated tube. If the FGF is equal to the alveolar ventilation
then the gas from the dead space that entered the corrugated tube will be conserved (Figure 7). Since these
gases do not contain any CO2, rebreathing of these dead space gases will not result in CO2 accumulation in
patient. However if the FGF were to be less than the alveolar ventilation, then significant rebreathing of
CO2 cotaining alveolar gases could result in hypercapnea (Figure 8).
During controlled ventilation the Mapleson A is the least efficient system (Figure 9). The APL valve has
to be partially closed to inflate the lungs. Hence the opening pressure of the APL valve is high and the gases
are not vented out of the system during exhalation. At the end of exhalation the patient end of the corrugated
tube is filled with alveolar gases. The reservoir bag and the machine end of the corrugated tube contain
fresh gases. During the early part of the next inspiration a portion of the alveolar gases enters the patient
and some is vented out through the APL valve. During the later part of inspiration fresh gases enter the
patient’s lungs and some are vented out. This results in wastage of fresh gases and significant rebreathing
of alveolar gases making this system unsuitable for controlled ventilation.
However enclosing the reservoir bag and APL valve as done in Enclosed Afferent Reservoir System
(EARS) makes the system efficient both for spontaneous and controlled ventilation.

Figure 6. Disposition of gases at the end of spontaneous exhalation when FGF equals or slightly more than
minute ventilation. During next inspiration patient breathes gases from apparatus dead space and fresh gas.
(© Cambridge University Press. Reproduced with permission)

Figure 7. Disposition of gases at the end of spontaneous exhalation when FGF equals alveolar ventilation.
During next inspiration patient breathes gases from apparatus dead space, dead space gas and fresh gas. (©
Cambridge University Press. Reproduced with permission)
Figure 8. Disposition of gases at the end of spontaneous exhalation when FGF is less than alveolar
ventilation. During next inspiration patient breathes alveolar gas, dead space gas, and fresh gas. (©
Cambridge University Press. Reproduced with permission)

Figure 9. Disposition of gases at the end of exhalation (controlled ventilation). During next inspiration
patient is ventilated with alveolar gas, dead space gas, and fresh gas. There will be significant wastage of
fresh gas. (© Cambridge University Press. Reproduced with permission
Lack System: This system is a co-axial version of Mapleson A. The expiratory tube runs coaxially within
the inspiratory limb and the APL valve is situated at the machine end of the system, facilitating easy access
and scavenging. In view of the expiratory limb running inside the inspiratory limb, the system is bulky and
imposes a higher resistance.

Figure 10. Lack System. (© Cambridge University Press. Reproduced with permission)

Mapleson D: The Mapleson D, E, and F systems function as T-piece systems. The apparatus dead space
in these systems extend from the patient to the point of entry of FGF.
All through the exhalation the dead space gases and alveolar gases mix thoroughly with fresh gases and
collect in the reservoir bag and corrugated tubing. During the expiratory pause the fresh gases collect at the
patient end of the corrugated tube (Figure 11). During the next inspiration the fresh gas flowing from the
machine and fresh gas in the corrugated tube enters the patient first. The contribution of this to the tidal
volume will depend upon the FGF and the expiratory pause. During later part of inspiration the mixture of
fresh gas, dead space gas and alveolar gas enters the patient. Some of these gases remain in the anatomical
dead space of the patient, hence minimizing the effect of rebreathing. The functional analysis is similar in
both spontaneous and controlled ventilation. Hence this system can be used safely during both spontaneous
and controlled ventilation. Fresh gas flow of 1.5 to 2 times the minute ventilation of the patient was reported
to produce adequate PaCO2, which depends primarily on the minute ventilation.
The system is slightly more efficient during controlled ventilation because of the control over the expiratory
pause. When high FGF (> 2 times the minute volume) is used, there is no rebreathing and the minute
ventilation determines the arterial CO2 levels. This principle is commonly employed in paediatric
population. Whereas, in adults, the patient is hyperventilated (minute Volume > 150 ml/Kg/min with normal
to low respiratory rate) and CO2 levels are controlled by adjusting FGF and hence the rebreathing. Studies
using Bain circuit have demonstrated that a FGF of 70 ml/Kg/min maintains normocapnia, whereas a FGF
of 100 ml/Kg/min maintains mild hypocapnia.
Figure 11. Disposition of gases at the end of exhalation. The patient end of the corrugated tube is filled
with fresh gases and the remaining part of corrugated tube and reservoir bag is filled with a mixture of
fresh gas, dead space gas, and alveolar gas. (© Cambridge University Press. Reproduced with
permission)
Bain Circuit (Figure 12): The Bain circuit is a modification of the Mapleson D system and was
introduced in 1972. It is a coaxial circuit in which the fresh gas flows through a narrow inner tube within
the outer corrugated tubing. Traditionally the length of the system is 1.8 meters. The length can be
increased by adding additional corrugated tube at the machine end without altering its functionality.
This may be of particular benefit for remote anaesthesia in magnetic resonance imaging units.

Advantages: It is lightweight, convenient, easily sterilized, and reusable. Scavenging of the gases from
the expiratory valve is facilitated because the valve is located away from the patient. Exhaled gases in
the outer reservoir tubing add warmth to inspired fresh gases.
Hazards: Kinking, leakage or disconnections in inner tube can cause severe hypercapnia. The outer
tube should be transparent to allow inspection of the inner tube. The integrity of the inner tube should
be checked by the following tests:
1. Set a low flow on the oxygen flowmeter and occlude the inner tube (with a finger or the barrel of a
small syringe) at the patient end while observing the flowmeter indicator. If the inner tube is intact
and correctly connected, the indicator will fall slightly.
2. Activate the oxygen flush and observe the bag (Pethick test). A Venturi effect caused by the high
flow at the patient end will create a negative pressure in the outer exhalation tubing, and this will
cause the bag to deflate. If the inner tube is not intact, this manoeuvre will cause the bag to inflate
slightly.

Figure 12. Bain Circuit. (© Cambridge University Press. Reproduced with permission)
T -Piece Systems
Ayre’s T-piece was introduced in 1937. It is light weight, simple and has no valves. The resistance was
considered to be lower than systems containing valves. Numerous modifications of the T-piece system
were made. The Jackson-Rees modification is widely used in paediatric anaesthesia (Figure 13). In this
system the APL valve is replaced by open ended reservoir bag.
Functionally the Jackson-Rees attachment performs like Mapleson D. Rebreathing is prevented by
using FGF about two times the minute ventilation. This system is used in children for both
spontaneous and controlled ventilation. The T-piece systems are widely used for paediatric
anaesthesia, oxygen therapy, paediatric and neonatal resuscitation, and in paediatric ventilators.

Figure 13. T-Piece system - Jackson-Rees modification. (© Cambridge University Press. Reproduced
with permission)
Monitoring
Inspired Oxygen Concentration
The current recommendations require that all modern machines must have inspired oxygen
concentration monitoring along with low O2 and high O2 alarms. Most units incorporate oxygen
concentration monitor either at the CGO or in the inspiratory limb of the circle system to ensure that
hypoxic mixtures are not delivered. In addition inspired oxygen concentration is also monitored at the
patient end using paramagnetic analysers. Causes of inadequate O2 concentration in the breathing system
include:
1. a hypoxic gas being delivered via the pipeline or tanks,
2. disconnected fresh gas hose during use of a hanging bellows ventilator,
3. O2 flow control valve turned off,
4. failure of oxygen fail-safe system ,
5. proportioning system failure,
6. O2 leak in the low pressure system of the machine, and
7. a closed system with inadequate O2 inflow rate.
Airway Pressure
Airway pressure monitoring warns the user about high pressures, low pressures, and disconnections.
Many traditional anaesthesia breathing systems incorporate an analogue pressure gauge, as well as an
electronic pressure monitoring and alarm system. Most currently used anaesthesia machines incorporate
low pressure, high pressure, sustained pressure, or disconnection alarms. Airway pressure monitoring
can give us an approximate idea of changes in airway resistance, and lung and thoracic compliance. The
modern anaesthesia machine can give us real time pressure tracing plotted against time. During volume
 controlled ventilation, when inspiratory pause is used, changes in plateau pressure indicate changes in
lung and thoracic compliance, whereas changes in the peak to plateau pressure gradient indicate changes
in airway resistance provided there are no alterations in tidal volume.
Spirometry
Spirometry is used to monitor the tidal volume, compliance, resistance, and breathing system integrity.
These values provide valuable information regarding changing pulmonary mechanics during
anaesthesia. The ventilator bellows are marked to give us an approximate idea of tidal volume. In
traditional anesthesia machines monitoring of expired tidal and minute volumes is achieved using a
spirometer placed in the vicinity of the expiratory unidirectional valve. The modern machines use flow
sensors (D- lite flow sensor, heated wire anemometer, ultrasonic flow sensor etc.) between the patient
and breathing system, and give an accurate idea of minute volume, compliance and resistance. These
modules enable us to monitor flow-volume and pressure-volume loops as well.
Capnography
It is interesting and essential to have a good understanding of functional analysis of breathing systems.
However for all practical purposes one depends on capnography to maintain CO2 homeostasis.
Monitoring end tidal carbon dioxide levels (PETCO2) gives us an estimate of PaCO2, and hence the FGF
and minute ventilation can be manipulated to maintain desired CO2 levels. Evaluation of the inspiratory
phase of the capnogram gives us an idea of rebreathing of exhaled CO2 (Figure 14). The ideal site to
sample gases is between the patient and the elbow adaptor after the breathing system.

Figure 14. Capnography and rebreathing

A: Normal capnogram. PETCO2 is normal

B: Exhaustion of soda lime. Base line is elevated
above zero indicating rebreathing (shaded area
during inspiration). PETCO2 is
increased
C: Camel hump during inspiration indicating
rebreathing of mixed gas (alveolar and fresh)
during later part of inspiration. This is typical of
Mapleson D in controlled ventilation. The
PETCO2 may remain normal despite rebreathing.

D: Rebreathing during controlled ventilation

with Mapleson A or malfunctioning inspiratory
unidirectional valve in circle system.
expiration appears prolonged due to any
rebreathing of alveolar gases without
change in CO2 content. PETCO2 is increased.

Sumber :
http://www.capnography.com/Circuits/Breathingsys/ravi.htm last accessed June 30, 2012
http://www.asevet.com/resources/circuits/index.htm last accessed June 30, 2012
4. Ventilasi, difusi, perfusi
Pada sistem respirasi ada tiga langkah dalam proses oksigenasi yaitu ventilasi, perfusi paru dan difusi. 1) Ventilasi
adalah proses keluar masuknya udara dari dan ke paru-paru, jumlahnya sekitar 500 ml. Udara yang masuk dan
keluar terjadi karena adanya perbedaan tekanan antara intrapleura dengan tekanan atmosfer, dimana pada saat
inspirasi tekanan intrapleural lebih negatif (752 mmHg) daripada tekanan atmosfer (760 mmHg) sehingga udara
akan masuk ke alveoli. Faktor-faktor yang mempengaruhi kepatenan ventilasi yaitu kebersihan jalan nafas
(adanya sumbatan atau obstruksi jalan nafas akan menghalangi masuk dan keluarnya udara dari dan ke paru-paru),
adekuatnya sistem saraf pusat dan pusat pernafasan, adekuatnya pengembangan dan pengempisan paru,
kemampuan otot-otot pernafasan seperti diafragma, eksternal interkosta, internal interkosta, otot abdominal
(Wartonah, 2006). Universitas Sumatera Utara

2) Perfusi Paru Perfusi paru adalah pergerakan aliran darah melalui sirkulasi paru untuk dioksigenasi dimana
pada sirkulasi paru darah yang dioksigenasi mengalir dalam arteri pulmonalis dari ventrikel kanan jantung. Darah ini
ikut serta dalam proses pertukaran oksigen dan karbon dioksida di kapiler dan alveolus. Fungsi utama sirkulasi
pulmonal adalah mengalirkan darah yang dioksigenasi dari dan ke paruparu agar dapat terjadi pertukaran gas.
Sirkulasi paru merupakan 8-9% dari curah jantung. Dengan demikian, adekuatnya pertukaran gas dalam
paru dipengaruhi oleh keadaan ventilasi dan perfusi. Pada orang dewasa sehat pada saat istirahat ventilasi alveolar
(volume tidal = V) sekitar 4 lt/menit, sedangkan aliran darah kapiler pulmonal (Q) sekitar 5 lt/menit (Wartonah,
2006). 3) Difusi Dalam difusi pernafasan, komponen yang berperan penting adalah alveoli dan darah. Untuk
memenuhi kebutuhan O2 dari jaringan, proses difusi gas pada system respirasi haruslah optimal. Difusi gas adalah
bergeraknya O2 dan CO2 atau partikel lain dari area bertekanan tinggi ke arah yang bertekanan rendah. Di dalam
alveoli, O2 melintasi membran alveoli-kapiler dari alveoli berdifusi kedalam darah karena adanya perbedaan
tekanan PO2 yang tinggi dialveolus (100 mmHg) dan tekanan pada kapiler lebih rendah (PO2 40 mmHg),
sedangkan CO2 berdifusi keluar alveoli akibat adanya perbedaan tekanan PCO2 darah 45 mmHg dan di alveoli 40
mmHg. Proses difusi dipengaruhi oleh faktor ketebalan membran, luas permukaan membran, komposisi membran,
koefisien difusi O2 dan CO2, serta perbedaan tekanan gas O2 dan CO2 (Muttaqin, 2010)
 CO

Dinding dada
Proses fonasi
Sistem saraf
Saluran napas atas & bawah
Paru

Tiga komponen :

16 X
percabangan

23 X
percabangan
 Zona Zona
konduksi respirasi

 Tidak mengandung alveoli

 Tidak ambil bagian pada
proses pertukaran gas
 Ruang rugi anatomi
 Mengandung alveoli
 Terlibat pada proses
pertukaran gas


tubuh untuk memenuhi O2 untuk proses metabolisme
dan mengeluarkan CO2 SEBAGAI hasil metabolisme
 Proses masuk dan keluarnya udara melalui saluran
napas ke dalam paru meliputi inspirasi dan ekspirasi

Ekspirasi adalah proses pasif dimana tidak didapatkan

kontaksi otot untuk menurunkan volume intratorakal

Tekanan
Fase inspirasi
pada saluran Akhir Tekanan
awal
napas inspirasi saluran napas
menjadi > tekanan
tekanan
negatif Recoil paru atmosfer
intrapleura
menurun
aliran udara rongga dada
sekitar ekspirasi
masuk ke ke posisi
– 6 mmHg
dalam paru semula

VE = VT X F VT = volume tidal
F = frekuensi napas
Ventilasi Alveolar dan Ruang Rugi (dead space)

 Pertukaran gas terjadi di dalam alveoli ketika udara inspirasi masuk dan terjadi difusi
dengan pembuluh darah kapiler

 Tidak semua udara inspirasi mencapai alveoli dan berpartisipasi dalam pertukaran gas

 Volume udara pada akhir inspirasi yang tetap ada di dalam saluran napas konduksi
disebut ruang rugi anatomis\ Ruang rugi fisiologis = ruang rugi anatomi + ruang rugi
alveolar

 Ruang rugi alveolar sangat sedikit sehingga ruang rugi fisiologik sama dengan ruang
rugi anatomic

 Volume gas di dalam alveolus yang tidak mendapat perfusi disebut shunt dan kelebihan
volume gas dalam alveolus disebut dead space
 Volume ruang rugi anatomis (Vdan) pada laki-laki
dewasa normal 150 – 180 ml

Volume ruang rugi fisiologis (VD ) orang muda normal

sedikit lebih besar / sekitar 25- 35% VT (rasio VD/VT)

Volume udara yang berperan dalam pertukaran gas

disebut ventilasi alveolar (VA) dengan persamaan
VA = VE – VD

Gangguan proses ventilasi

Kelainan saraf pusat, neuromuskuler, trauma cervical,

kelumpuhan saraf frenicus

Keracunanobat‐obatanyangmenyebabkandepresinapas

Toksin botulisme, tetanus, polio

Deformitas dindingdada

Ketidakseimbangan elektrolit

Distensi abdomenmassif

Obstruksi jalannapas
 Difusi

Perpindahan molekul gas secara pasif dari area

dengan tekanan parsial tinggi ke area dengan
tekanan parsial rendah sampai kedua area
memiliki tekanan parsial sama

Perpindahan O2 dari alveoli ke dalam darah dan

CO2 dari darah ke alveoli

Proses pertukaran gas terjadi karena perbedaan

tekanan parsial O2 dan CO2 antara alveoli dan
kapiler paru
 alveolokapiler

intraalveolar
sel epitel alveolar
membran basal sel epitel alveolar
jaringan ikat longgar (ruang interstisial)
membran basal endotelium kapiler
endotelium kapiler
plasma darah kapiler

hemoglobin (Hb)

Proses difusi melalui membran semipermeabel

Cardiopulmonary
Delmar;

Gangguan difusi

Rendahnya tekanan parsial oksigen inspirasi (pada ketinggian diatas 10.000 kaki)

Ketidakseimbangan antara ventilasi dengan perfusi baik shunt maupun dead space

Kelainan pirau kanan ke kiri pada kelainan jantung

Peningkatan kebutuhan oksigen jaringan yang meningkat (sepsis, luka bakar hebat,
pancreatitis, keracunan sianida, overdosis salisilat atau obat-obatan lainnya)
 Distribusi yang

Aliran darah dalam paru

sistemik

oleh gravitasi bumi

Rasio ventilasi-perfusi (V/Q)

Ventilasi alveolar normalnya 4L/menit
kecepatan aliran darah kapiler paru adalah 5L/menit
€ rata-rata V/Q = 4/5 atau 0,8.

Rasio ventilasi-perfusi pada setiap bagian paru bervariasi

Apeks paru menerima ventilasi lebih banyak dibanding basal

paru, tetapi menerima aliran darah (perfusi) lebih sedikit
dibanding basal paru

V/Q bagian apeks lebih besar dari basal paru

 Spirometri
Inert gas dilution
Body plethysmography
Nitrogen washout

Analisa Gas Darah

Volume paru
 5. Jenis shock dan terapi

Introduction
Shock is a life-threatening manifestation of circulatory failure. Circulatory shock leads to cellular
and tissue hypoxia resulting in cellular death and dysfunction of vital organs. Effects of shock are
reversible in the early stages and a delay in diagnosis and/or timely initiation of treatment can lead to
irreversible changes including multiorgan failure (MOF) and death.

Etiology
Shock is characterized by decreased oxygen delivery and/or increased oxygen consumption or
inadequate oxygen utilization leading to cellular and tissue hypoxia. It is a life-threatening condition
of circulatory failure and most commonly manifested as hypotension (systolic blood pressure less
than 90 mm Hg or MAP less than 65 mmHg). Shock is the final manifestation of a complex list of
etiologies and could be fatal without timely management. There are mainly four broad categories of
shock: distributive, hypovolemic, cardiogenic and obstructive. The wide range of etiologies can
contribute to each of these categories and are manifested by the final outcome of shock.
Undifferentiated shock means that the diagnosis of shock has been made; however, the underlying
etiology has not been uncovered.
1. Distributive Shock
Characterized by peripheral vasodilatation.
Types of distributive shock include:
Septic shock
Sepsis is defined as a life-threatening organ dysfunction resulting from dysregulated host response to
infection. Septic shock is a subset of sepsis with severe circulatory, cellular, and metabolic
abnormalities resulting in tissue hypoperfusion, manifested as hypotension which requires
vasopressor therapy and elevated lactate levels (more than 2 mmol/L)
Most common pathogens associated with sepsis and septic shock in the United States are gram-
positive bacteria, including streptococcal pneumonia and Enterococcus.
Systemic inflammatory response syndrome
Systemic inflammatory response syndrome (SIRS) is a clinical syndrome of vigorous inflammatory
response caused by either infectious or noninfectious causes. Infectious causes include pathogens
such as gram-positive (most common) and gram-negative bacteria, fungi, viral infections (e.g.,
respiratory viruses), parasitic (e.g., malaria), rickettsial infections. Noninfectious causes of SIRS
include but are not limited to pancreatitis, burns, fat embolism, air embolism, and amniotic fluid
embolism
Anaphylactic shock
Anaphylactic shock is a clinical syndrome of severe hypersensitivity reaction mediated by
immunoglobulin E (Ig-E), resulting in cardiovascular collapse and respiratory distress due to
bronchospasm. The immediate hypersensitivity reactions can occur within seconds to minutes after
presentation of the inciting antigen. Common allergens include drugs (e.g., antibiotics, NSAIDs),
food, insect stings, and latex.
Neurogenic shock
Neurogenic shock can occur in the setting of trauma to the spinal cord or to the brain. The underlying
mechanism is the disruption of autonomic pathway resulting in decreased vascular resistance and
changes in vagal tone.
Endocrine shock
Due to underlying endocrine etiologies such as adrenal failure (Addisonian crisis) and myxedema.
2. Hypovolemic Shock
Hypovolemic shock is characterized by decreased intravascular volume and increased systemic
venous assistance (compensatory the mechanism to maintain perfusion in the early stages of shock).
In the later stages of shock due to progressive volume depletion, cardiac output also decreases and
manifest as hypotension. Hypovolemic shock can be divided into two broad subtypes: hemorrhagic
and nonhemorrhagic.
Common causes of hemorrhagic hypovolemic shock include
 Gastrointestinal bleed (both upper and lower gastrointestinal bleed (e.g., variceal bleed, portal
hypertensive gastropathy bleed, peptic ulcer, diverticulosis) trauma.
 Vascular etiologies (e.g., aortoenteric fistula, ruptured abdominal aortic aneurysm, tumor
eroding into a major blood vessel).
 Spontaneous bleeding in the setting of anticoagulant use (in the setting of supratherapeutic
INR from drug interactions).
Common causes of nonhemorrhagic hypovolemic shock include:
 GI losses - the setting of vomiting, diarrhea, NG suction or drains.
 Renal losses - medication induced diuresis, endocrine disorders such as hypoaldosteronism.
 Skin losses/insensible losses - burns, Steven Johnson syndrome, Toxic epidermal necrolysis,
heat stroke, pyrexia.
 Third-space loss - in the setting of pancreatitis, cirrhosis, intestinal obstruction, trauma.
3. Cardiogenic Shock
Due to intracardiac causes leading to decreased cardiac output and systemic hypoperfusion. Different
subtypes of etiologies contributing to cardiogenic shock include:
 Cardiomyopathies - include acute myocardial infarction affecting more than 40% of the left
ventricle, acute myocardial infarction in the setting of multi-vessel coronary artery disease,
right ventricular myocardial infarction, fulminant dilated cardiomyopathy, cardiac arrest (due
to myocardial stunning), myocarditis.
 Arrhythmias - both tachy- and bradyarrhythmias.
 Mechanical - severe aortic insufficiency, severe mitral insufficiency, rupture of papillary
muscles, or chordae tendinae trauma rupture of ventricular free wall aneurysm.
4. Obstructive Shock
Mostly due to extracardiac causes leading to decrease in the left ventricular cardiac output
  Pulmonary vascular - due to impaired blood flow from the right heart to the left heart.
Examples include hemodynamically significant pulmonary embolism, severe pulmonary
hypertension.
 Mechanical - impaired filling of right heart or due to decreased venous return to the right heart
due to extrinsic compression. Examples include tension pneumothorax, pericardial
tamponade, restrictive cardiomyopathy, constrictive pericarditis.

Pathophysiology
Hypoxia at the cellular level causes a series of physiologic and biochemical changes, resulting in
acidosis and a decrease in regional blood flow which further worsens the tissue hypoxia.[4] In
hypovolemic, obstructive, and cardiogenic shock there is a decrease in cardiac output and decreased
oxygen transport. In distributive shock, there is decreased peripheral vascular resistance and
abnormal oxygen extraction. Excitement is a spectrum of physiologic changes, ranging from early
stages which are reversible to final stages which are irreversible with multiorgan failure and death.
Generally, shock has the following three stages:
1. Pre-shock or compensated shock - As the name suggests, this stage is characterized by
compensatory mechanisms to counter the decrease in tissue perfusion, including tachycardia,
peripheral vasoconstriction, and changes in systemic blood pressure
2. Shock - During this stage, most of the classic signs and symptoms of shock appear due to
early organ dysfunction, resulting from progression of the pre-shock stage as the
compensatory mechanisms become insufficient.
3. End-organ dysfunction - This is the final stage, leading to irreversible organ dysfunction,
multiorgan failure, and death

Evaluation
Resuscitation should not be delayed while investigating the etiology of undifferentiated shock.
Physicians should have a high clinical suspicion for the presence of shock and an attempt to stratify
the severity of the shock should also be done to assess the need for emergent or early interventions.
Evaluation of undifferentiated shock should begin with a thorough history and physical examination.
Besides telemetry monitoring, a 12-lead electrocardiogram should be obtained. ECGs might show
evidence of acute coronary syndrome, arrhythmias or provide diagnostic clues suggestive of
pericardial effusion or pulmonary embolism.
Laboratory tests in a patient with undifferentiated shock should include a CBC and differential, renal
and liver function tests, serum lactate level, cardiac biomarkers, D-dimer level, coagulation profile,
type and screen for a possible blood transfusion if appropriate (if concern for hemorrhagic shock),
blood and urine cultures, and blood gas analysis. Initial imaging studies recommended in patients
with undifferentiated shock and hypotension include chest x-rays to look for the source of infection
such as pneumonia, complications of shock such as ARDS, clinical findings supporting the diagnosis
of pulmonary edema in cardiogenic shock, widened mediastinum in aortic dissection. CT scans can
also assist in unmasking the etiology of shock in appropriate clinical scenarios. Point of care
ultrasonography or focused cardiac ultrasound is also a useful bedside diagnostic tool.[7]

Treatment / Management
The initial approach to management is stabilization of airway and breathing with oxygen and oral
mechanical ventilation when needed. Peripheral IV or intraosseous infusion (IO) access should
be obtained. Central venous access may be needed in the setting of shock if there is difficulty
securing peripheral venous access or the patient needs prolonged vasopressor therapy or large volume
resuscitation. Immediate treatment with intravenous (IV) fluid should be initiated followed by
vasopressor therapy, if needed, to maintain tissue perfusion. Depending on the underlying etiology of
shock, specific therapies might also be needed.
Septic shock - initial aggressive fluid resuscitation with IV isotonic crystalloids 30 mL/kg within 3
hrs with additional fluid based on frequent reassessment, empiric antibiotic therapy within one
hr. [8] For patients with septic shock requiring vasopressors, target a mean arterial pressure (MAP) of
65 mmHg. The first choice of vasopressor is a norepinephrine with the addition of vasopressin if
refractory.[9]
Anaphylactic shock - aggressive IV fluid resuscitation with 4 to 6 L of IV crystalloids. Stop the
offending agent, intramuscular epinephrine, antihistamines, corticosteroids, nebulized albuterol.
In adrenal crisis - judicious fluid resuscitation, IV dexamethasone.
Hypovolemic shock - obtain two large-bore IVs or central line. Place the patient in the Trendelenburg
position. Aggressive IV fluid resuscitation with 2-4 L of isotonic crystalloids. PRBC transfusion if
ongoing bleed. Appropriate medical or interventional strategies to treat the underlying etiology.
Continue with isotonic crystalloids and use vasopressors if needed
Obstructive shock - the judicious use of IV crystalloids. If shock persists, early initiation of
vasopressors-norepinephrine is the first choice and add vasopressin if refractory. Continue IV fluids
but monitor very closely.
If acute massive pulmonary embolism -thrombolysis. Judicious use of IV fluids has paradoxical
worsening of hypotension; it may develop due to severe right ventricular dilatation and septal bowing
compromising left ventricle filling.
If tension pneumothorax - needle thoracotomy followed by tube thoracotomy. If cardiac tamponade-
pericardiocentesis, significant clinical improvement is possible, even with minimal fluid removal).
Cardiogenic shock - if unstable tachyarrhythmia or bradyarrhythmias, initiate ACLS protocol and
cardioversion. Judicious use of IV fluids in the absence of pulmonary edema. Consider inotropes
(dobutamine is the most commonly used agent) or intra-aortic balloon pump (IABP), if refractory
shock, and vasopressor (norepinephrine) with inotropes.
If STEMI - consider a thrombolysis or coronary revascularization procedures and or IABP.
Sumber : https://www.ncbi.nlm.nih.gov/books/NBK531492/?report=printable

6. Kebutuhan cairan selama operasi

1. Kebutuhan cairan selama operasi

Usia Kebutuhan Cairan Rutin

Dewasa  2 cc/kgBB/jam

 10 kg I: 4 cc/kgBB/jam
Anak-anak  10 kg II: 2 cc/kgBB/jam
 10 kg III: 1 cc/kgBB/jam
Contoh: Anak usia 12 tahun dengan berat badan 30 kg membutuhkan cairan rutin perhari:

 10 kg I: 4 cc/kgBB/jam x 10 kg = 40
 10 kg II: 2 cc/kgBB/jam x 10 kg = 20
 10 kg III: 1 cc/kgBB/jam x 10 kg = 10
–––––––––––––––––––––––––––––––––––––––––––– +

 30 kg: 70 cc/jam x 24 jam/hari = 1680 cc/hari -> 1700 cc/hari (dibulatkan)

Kebutuhan Cairan Selama Operasi (Stres Operasi)

Jenis Operasi Kebutuhan Cairan Selama Operasi

Ringan 4 cc/kgBB/jam

Sedang 6 cc/kgBB/jam

Berat 8 cc/kgBB/jam

Penggantian Cairan Selama Puasa

 50 % selama jam I operasi

 25 % selama jam II operasi
 25 % selama jam III operasi

Terapi Cairan untuk Koreksi Suhu

Untuk setiap kenaikan 1°C membutuhkan terapi cairan tambahan:

 10 % x kebutuhan cairan rutin

Contoh: Anak usia 12 tahun dengan berat badan 30 kg dan suhu 38°C untuk koreksi suhu membutuhkan
terapi cairan tambahan:

 10 % x 1700 cc/hari = 170 cc/hari

Contoh :

Aa XX
BB 60kg
Maintenance =
4 x 10 kg pertama = 40ml
2 x 10 kg kedua = 20 ml
1 x 40 kg sisanya = 40 ml +
Maintenance = 100ml x lama puasa (misal 8 jam) = 100 x 8 = 800 ml (puasa)

Operasi kecil = 4
Operasi sedang = 6
Operasi berat = 8
 Bb x jenis operasi
Co : laparotomy

60 x 8 = 480 ml

Jam = maintenance + operasi + ½ puasa

Jam ke 1 = 100 + 480 + 400 = 980 ml
Jam ke 2 = 100 + 480 + 200 = 780 ml
Jam ke 3 = 100 + 480 + 200 = 780 ml

7. Anestesi pada laparoskopi

Laparoscopic surgery is a principle technique for minimally invasive surgery of the abdomen, and it has been
employed in procedures ranging across multiple surgical disciplines. Gynecologic surgeries were among its
first applications. The advantages of laparoscopy in comparison to open abdominal surgery include reduced
surgical trauma, less pain, fewer post-operative pulmonary complications, and shorter recovery times. The
disadvantages include longer surgical times and higher equipment costs.1
Laparascopic surgery is most routinely performed with general anesthesia. It is furthermore facilitated by
proper decompression of the gastrointestinal tract (GI), and by establishment of adequate muscle relaxation,
pneumoperitoneum, and Trendelenburg position. These conditions collectively improve exposure of the
abdominal organs and decrease the risk of operative mechanical injury to the patient. However, they also
induce specific and potentially deleterious pathophysiologic changes to the patient. While the goal of the
surgeon is to operate safely and efficaciously, the goal of the anesthesiologist is to help improve surgical
conditions when possible, while also preventing (or mitigating) the side effects of these conditions and
mantaining vital organ function. These goals must be achieved concurrently. Thus, it is critical for both the
surgeon and the anesthesiologist to understand the physiologic consequences of laparascopy and to work in
cooperation to achieve a good surgical outcome.
ESTABLISHMENT OF SURGICAL CONDITIONS
To provide optimal surgical conditions for laparascopy, the abdominal organs must be adequately exposed and
the laparascopic ports and instruments must be inserted safely and in proper position. This is achieved with a
multi-part approach that includes decompression of the GI tract followed by establishment of general
anesthesia, muscle relaxation, pneumoperitoneum, and Trendelenburg position.
GI tract decompression starts preoperatively with a bowel preparation and continues intraoperatively with the
placement of an oro- or naso-gastric tube immediately after induction of anesthesia. Both maneuvers decrease
intraabdominal volume. The latter maneuver, in particular, decompresses the stomach of air that may have
been insufflated from mask ventilation during induction of anesthesia and is important for reducing the risk of
gastric injury from insertion of the Veress needle. With induction of anesthesia, neuromuscular blockade is
established to relax the abdominal wall muscles, thereby facilitating placement of laparascopic ports and
induction of the pneumoperitoneum. Neuromuscular blockade also prevents sudden patient movement that can
lead to accidental injuries of intra-abdominal structures by laparascopic instruments. The pneumoperitoneum is
then achieved by insufflating the abdomen, most commonly with carbon dioxide (CO2). Finally, the patient is
positioned in Trendelenburg, so that the abdominal contents fall away from the lower abdomen to reveal the
pelvic organs. These maneuvers induce a number of clinically relevant pathophysiologic effects during
surgery. We will review these effects by organ system.
PHYSIOLOGIC EFFECTS OF LAPAROSCOPIC SURGERY
I. Cardiovascular System
A. Hemodynamic Effects of Pneumoperitoneum
Hemodynamic disturbances during laparascopy are primarily due to pneumoperitoneum. The
pneumoperitoneum is established by insufflating the abdomen with pressures of 15 to 20 mm Hg. Normal
intra-abdominal pressure (IAP) is 0 to 5 mm Hg. Increases in IAP above 10 mm Hg are clinically significant,
and above 15mm Hg can result in an abdominal compartment syndrome, which affects multiple organ systems.
The cardiovascular manifestations can be understood via the following simple relationship, which expresses
the determinants of blood pressure:
Mean Arterial Pressure (MAP) = Cardiac Output (CO) x Systemic Vascular Resistance (SVR)
Pneumoperitoneum causes an increase in SVR while causing a decrease in CO. However, MAP
is increased overall because increases in SVR exceed decreases in CO.2 These effects are proportional to the
increase in IAP. The mechanism for increased SVR is compression of the abdominal organs and vessels.
Resistance to flow through arterial beds is increased due to both mechanical and neurohumoral factors (e.g.,
release of catecholamines and vasopressin, and activation of the renin-angiotensin system). The decreases in
CO are due to decreased venous return (i.e., decreased cardiac preload) from compression of the inferior vena
cava, from increased resistance in the venous circulation, and from hypovolemia due to preoperative bowel
preparation. CO typically decreases from 10 to 30%. However, despite a decrease in intracardiac blood
volume, intracardiac filling pressures may be elevated due to pressure transmitted across the diaphragm to the
heart. There are analagous effects in the pulmonary circulation that manifest as an increase in pulmonary
vascular resistance (PVR) and decrease in CO to the lungs.
Healthy patients appear to tolerate these hemodynamic effects well. Several studies demonstrate that end organ
perfusion is maintained in these patients despite a decrease in CO.3 However, patients with cardiac disease
may be at increased risk for further cardiac compromise. Patients with intravascular volume depletion appear
to tolerate these effects the least well.4 To minimize these effects, the lowest insufflation pressure required to
achieve adequate surgical exposure should be used. Ideally, insufflation pressure should be less than 15 mm
Hg. Increases in SVR may be treated with vasodilating agents, centrally acting alpha-2 agonists, or opioids.
Decreases in venous return and CO may be attenuated by appropriate intravenous fluid loading prior to the
induction of pneumoperitoneum.
B. Hemodynamic Effects of Positioning
Relative to the supine position and in the absence of a pneumoperitoneum, the Trendelenburg position
generally increases venous return and CO. However, in the presence of a pneumoperitoneum, venous return
and CO are decreased overall. If the patient is placed in extreme Trendelenburg, a decrease in venous return
from the head may result, thus leading to increased intracranial and intraocular pressures. If this position is
maintained for an extended duration, cerebral edema and retinal detachment may occur.5 Because of venous
stagnation, cyanosis and edema in the face and neck may be expected. The head up (reverse Trendelendburg)
position reduces venous return, which may lead to a fall in cardiac output and arterial pressure. The lithotomy
position will induce auto-transfusion by redistributing blood from vessels of the lower extremities into the
central body compartment, which thus will increase the preload of the heart.
C. Cardiovascular Complications
Bradyarrhythmias, dysrhythmias, and even asystole can occur during insertion of laparoscopic ports or during
insufflation of the abdomen. Sudden stretching of the peritoneum can precipitate a sudden, reflexive, and
sometimes profound increase in vagal tone. Slow insufflation of CO2 can decrease the risk of
arrhythmias. Administration of anticholinergic medications may be appropriate in bradyarrhythmias. If the
arrhythmia persists or results in hemodynamic compromise, prompt interruption of the surgery and release of
the pneumoperitoneum is indicated.
II. Pulmonary and Respiratory System:
A. Pulmonary and Respiratory Effects of Pneumoperitneum
Pneumoperitoneum transmits pressure to the thorax. The upward pressure elevates the diaphragm, compresses
the lungs, and impedes expansion of the lungs and chest cavity (i.e., decreases thoracopulmonary
compliance). The pulmonary implications of this mechanical effect are two-fold. First, compression of the
lungs leads to decreased functional residual capacity (FRC), i.e., the volume of gas remaining in the lungs
after a normal exhalation. This circumstance exacerbates the decrease in FRC that normally occurs under
general anesthesia. The decreased end-expiratory lung volume is insufficient to maintain patent alveoli, and
thus atelectasis results. Atelectasis alters the normal relationship between ventilation and perfusion of the
lungs. The atelectatic areas of lung are underventilated relative to their perfusion and therefore cause
hypoxemia. Older patients are particularly at risk for atelectasis, because the minimum end-expiratory lung
volume that is required to prevent atelectasis – known as the closing capacity – increases with age. Institution
of positive end-expiratory pressure (PEEP) can mitigate the decreases in FRC by stenting alveoli open at end
expiration. The second mechanical effect of pneumoperitoneum is that controlled mechanical ventilation is
more difficult due to the decrease in thoracopulmonary compliance. Greater airway pressure is required to
generate a given tidal volume. Conversely, a mechnically delivered tidal volume will result in higher airway
pressures. As with hemodynamic effects, these effects are proportional to the increase in IAP. In addition, they
may be further exacerbated by Trendelenburg position and by conditions resulting in restrictive lung disease
(e.g., obesity). Thoracopulmonary compliance may be decreased by up to 50% during pneumoperitoneum.6,7
Pneumoperitoneum furthermore causes hypercapnea from systemic absorption of CO2.2 CO2 is the most
commonly chosen gas for peritoneal insufflation. CO2is a convenient choice because it is easily absorbed into
the blood, is buffered by the principle physiologic buffer (bicarbonate), and is easily eliminated via the
respiratory system. In uncomplicated laparoscopy, the partial pressure of arterial CO2 (PaCO2) rises on
induction of pneumoperitoneum and plateaus from 15 to 30 minutes later, thus signifying
CO2 equilibrium. PaCO2 can be reliably monitored via analysis of end-tidal gasses. The degree of
hypercapnea depends on CO2 insufflation pressure, but in routine cases under general anesthesia and
controlled mechanical ventilation, hypercapnea is easily managed by increasing alveolar ventilation by 10% to
25%.8 In cases where the degree of hypercapnea becomes unmanageable with hyperventilation alone, the
pneumoperitoneum can be temporarily released to allow for CO2 elimination.
B. Pulmonary Effects of Positioning
The head-down position generally decreases FRC, overall lung volumes, and lung compliance. Morbidly obese
patients will have greater peak airway pressures and often cannot sustain prolonged Trendelenburg position.
Although laparoscopic surgery can be performed on the morbidly obese, each operation should be evaluated
carefully for the feasibility of success and potential risk.
C. Pulmonary and Respiratory Complications
i. CO2 Subcutaneous Emphysema.
Subcutaneous emphysema is the most common respiratory complication during laparoscopy. It is suggested by
an increase in end-tidal CO2 (etCO2) greater than 25% or an increase that occurs > 30 minutes after abdominal
CO2 insufflation. Subcutaneous emphysema can often be palpated. The cause is extraperitoneal insufflation of
CO2. Although in some cases this is unintentional, in other cases it is required to operate on extraperitoneal
structures.9 The hypercapnea is managed by increasing mechanical ventilation. CO2 subcutaneous emphysema
itself is not a contraindication to extubation at the end of surgery provided that other extubation criteria are
satisfied.10
ii. Pneumothorax
Movement of gas from the peritoneum into the thorax can occur under pressure through weak areas and
defects in the diaphragm. The resulting pneumothorax may be asymptomatic, or it may manifest as increased
peak airway pressure, decreased O2 saturation, and hypotension. In severe cases, there can be profound
hypotension and cardiac arrest.9
Early diagnosis and treatment can be life saving. Surgery should be stopped and the pneumoperitoneum
released. Supportive measures should be continued while confirming the diagnosis, either clinically or with
chest radiography. Depending on the degree of cardiopulmonary compromise, the pneumothorax may be
observed or treated with an intercostal cannula or a thoracostomy tube. After stabilization of the patient,
conversion to an open procedure may be indicated.10
iii. Endobronchial intubation
Elevation of the diaphragm by the pneumoperitoneum can alter the position of the endotracheal (ET) tube
within the trachea. In some cases, the lungs are pushed cephalad such that the ET tube is advanced past beyond
the carina and into a mainstem bronchus. When this occurs, only one lung is ventilated. The non-ventilated
lung still remains perfused, and as such becomes a large source of intrapulmonary shunt. Endobronchial
intubation is suspected when there is a decrease in O2 saturation and pulmonary compliance. The decrease in
compliance occurs because a given volume is being delivered into one lung rather than two. The diagnosis is
often confirmed by the finding of unequal breath sounds when the lungs are auscultated. The ET tube should
then be slightly withdrawn as needed to reestablish two-lung ventilation.
iv. Gas (CO2) Embolism
Gas embolism, although rare, has a mortality rate of nearly 30%. Profound hypotension, arrhythmias, or
asystole can occur as a result of a “gas lock” in the vena cava or right ventricle (RV) that interrupts circulation.
An increase in etCO2 is observed. This may be followed by an acute decrease in etCO2 if there is severe
hypotension. The major cause is intravascular insufflation of gas from misplacement of the Veress needle or
trocar either directly into a vessel or into a parenchymal organ. Risk factors include hysteroscopy,
hypovolemia, and a history of prior abdominal surgeries. Gas embolism most frequently occurs on induction of
pneumoperitoneum but can occur at any point during surgery.9
Initial steps include immediate deflation of the pneumoperitoneum, institution of 100% FiO2, placement of the
patient in the left lateral head-down position to remove air from the RV outflow track, and hyperventilation to
eliminate the increased PaCO2 caused by the sudden increase in pulmonary dead space. A central line may be
required to aspirate gas from the RV. CPR may be required. Hyperbaric O2 treatment should be considered if
there is suspicion of cerebral gas embolism.10
ANESTHETIC MANAGEMENT
I. Patient Monitoring
Standard patient monitors for laparoscopy include electrocardiogram, noninvasive blood pressure monitor,
pulse oximetry, capnography, and temperature monitor. Monitors of the neuromuscular junction can be used to
ensure adequate muscle relaxation. An airway pressure monitor is routinely used during mechnical ventilation,
and can aid detection of high IAP, endobronchial intubation, or even inadequate anesthesia. Invasive arterial
blood pressure monitoring and arterial blood gas analysis should be considered in patients with advanced age
or cardiopulmonary comorbidities.4
II. Anesthetic Technique
A wide variety of anesthetic techniques have been used for laparoscopic procedures. Although general
anesthesia with endotracheal intubation is most routinely used and is considered to be the safest anethetic
technique, local and regional anesthesia have also been used safely for laparascopic surgeries.
As more laparascopic procedures are performed on an outpatient basis, the choice of maintenance agents is
likely to be reduced to short acting drugs such as sevoflurane, desflurane, and infusions of propofol. There is
apparently no clinical advantage to omitting nitrous oxide, and any benefit from its elimination must be
balanced against a greater risk of awareness. An Ultrashort-acting opioids analgesic such as remifentanil has
allowed bypassing Phase I recovery in ambulatory setting. Because laparoscopic surgery has generally been
performed with tracheal intubation and controlled ventilation short or intermediate-acting neuromuscular
blockers should be administered based on surgical length. General anesthesia can be performed without
intubation safely and effectively with ProSeal laryngeal mask airway in non-obese patients. Careful attention
should be paid to patients with high airway pressures (>30 cmH2O) or where extreme head-down tilt will be
applied. Reversal drugs such as neostigmine and glycopyrrolate have not been implicated in PONV. More
important, it has been demonstrated that even minor degrees of residual neuromuscular block can produce
distressing symptoms. Regional anesthesia (spinal, epidural) can be used in laparoscopic procedures
(diagnostic, infertility, and tubal sterilization).
III. Post-operative Recovery
A. Post-Operative Monitoring
Routine postoperative care should consist of adequate monitoring of vital organ functions. This includes
continuous monitoring of peripheral oxygen saturation, respiratory rate, ECG, blood pressure measurement
and heart rate and rhythm. Advanced postoperative monitoring may be required in cardiovascularly debilitated
ASA III and IV patients.
B. Post-Operative Nausea and Vomitting
Postoperative nausea and vomiting (PONV) is common after laparoscopic surgery, although its etiology is not
quite clear. Ondansetron given at the end of surgery results in a significantly greater anti-emetic effect
compared with preinduction dosing. Other 5-HT3 antagonists are effective as well. In addition, prophylactic
dexamethasone decreases the incidence for nausea and vomiting after laparoscopic cholecystectomy relative to
placebo and may decrease the severity of pain with no adverse effects noted from this single steroid dose.
C. Post-operative Pain
Postoperative pain in laparoscopic surgery is less severe compared to an open procedure, but is still
considerable. The most effective pain relief can be obtained by combining opioids, local anesthetics, and
NSAIDS into balanced analgesia. This approach at least allows the opioids dose to be reduced by the use of
other modalities, thereby limiting side effects, reducing postoperative pain and analgesics, and facilitating an
earlier return to normal activities. Rectus sheath block, local infiltration of the laparoscopy portals and
intraperitoneal local anesthesia can be used as regional techniques for pain relieve.

CHOICE OF ANAESTHETIC TECHNIQUE FOR LAPAROSCOPY–THE BEST

ONE
With the recent trend towards the use of laparoscopy in day-care surgeries, anaesthetic techniques
have changed, with more emphasis on shorter and more favourable techniques. The ideal anaesthetic
technique for laparoscopic surgery should maintain stable cardiovascular and respiratory functions,
provide rapid post-operative recovery, lead to minimal post-operative nausea and vomiting (PONV)
and provide good post-operative pain relief for early mobility.
THE TRADITIONAL ANAESTHETIC TECHNIQUE — GA
The use of GA with controlled ventilation has been considered the most acceptable technique for
laparoscopic procedures owing to the various effects of pneumoperitoneum. The use of rapidly-acting
and shorter-duration intravenous agents such as propofol and etomidate as well as inhalational agents
such as sevoflurane and desflurane has made GA a favourable technique for day-care laparoscopic
procedures. Use of the ultra-short-acting opioid analgesic remifentanil also favours GA in fast-track
laparoscopic procedures. The use of nitrous oxide in laparoscopic procedures has been controversial,
but the recent literature does not convey any clinical advantage of avoiding it against a greater risk of
intraoperative awarenessThe only advantage of avoiding nitrous oxide may be a lower incidence of
PONV. The use of short-acting, non-depolarizing muscle relaxants has replaced depolarizing muscle
relaxants such as succinylcholine from the balanced GA technique for laparoscopic surgeries,
allowing for less post-operative muscle pain. Moreover, the increasing usage of newer drugs like
alpha-2 agonists apart from traditionally used opioids is quite effective in the attenuation of stressor
response during intubation.
The use of Proseal laryngeal mask airway (LMA) with controlled ventilation can avoid endotracheal
intubation in selected non-obese patients undergoing laparoscopic procedures, thus reducing the
incidence of post-operative sore throat, but it should be limited to procedures with the use of low
intra-abdominal pressures and mild tilt.
The safest technique of anaesthesia remains GA with endotracheal intubation in those with no
contraindications, with maintenance of intra-operative end-tidal carbon dioxide (EtCO2) around 35
mmHg with adjustments in tidal volume or respiratory rate. The agents which directly depress the
heart should be avoided, with the provision of anticholinergic drugs in case of sudden surge in vagal
tone during laparoscopy.
EMERGENCE OF RA IN LAPAROSCOPIC SURGERY
The use of RA for laparoscopy had not gained popularity until recently due to the risk of aspiration
and respiratory embarrassment caused by pneumoperitoneum, making it less favourable for a
conscious patient. However, RA does provide numerous advantages over GA in terms of quicker
recovery, effective post-operative pain relief, no airway manipulation, shorter post-operative stay,
cost-effectiveness and reduced PONV. Most of the uses of RA in the past have been limited to the
patient population with significant co-morbidities, where it proved to be beneficialThere is evidence
that the use of RA in laparoscopy performed on awake patients may produce fewer changes in
respiratory mechanics and arterial blood gases. The various regional techniques that can be safely
used in laparoscopic procedures are as follows.
Epidural anaesthesia
It has emerged as a very safe technique for lower abdominal surgeries as well as for post-operative
analgesia, with only occasional complications reported. It has been used safely in laparoscopic
procedures involving the upper abdomen, and has been shown to have no deleterious effects on
respiratory mechanics. The effectiveness of the epidural technique is enhanced and a prolonged post-
operative analgesic period is achieved with the use of adjuvant with local anaesthetics. Epidural
anaesthesia can be used in patients deemed unfit for GA with the provision of effective post-operative
analgesia.
Spinal anaesthesia
The spinal anaesthesia may be more feasible and can provide better laparoscopic surgical conditions
due to profound muscle relaxation and shorter recovery. There has been several reports in the
literature for the safe use of spinal anaesthesia for laparoscopic upper abdominal and lower
abdominal procedures. The main advantages of spinal anaesthesia are: An awake, spontaneously
breathing patient; prevention of airway manipulation; less incidence of PONV; and the provision of
effective post-operative analgesia with a shorter recovery time
There are a few concerns related to the use of spinal anaesthesia for laparoscopic procedures. The
incidence of hypotension has been noted to be up to 20.5% and can be augmented by the
Trendelenburg position and increased intra-abdominal pressures. However, various studies show that
it can be easily prevented by liberally preloading the patient, reducing the head tilt, reducing the intra-
abdominal pressure and the liberal use of vasopressors
The incidence of referred shoulder-tip pain varies 25-43%; it may be distressing to the patient in the
post-operative period. The etiology is thought to be subdiaphragmatic irritation of the peritoneum by
the carbon dioxide pneumoperitoneum. This can be reduced by lowering of the intra-abdominal
pressures to 8-10 mmHg, the instillation of local anaesthetics into the peritoneal cavity or the use of\8
parenteral opioids
The changes in respiratory mechanics due to pneumoperitoneum may cause increase in PaCO2 due to
absorption from peritoneum, resulting in ventilatory changes. However, various reports in the
literature support non-significant changes in either PaO2 or PaCO2 during laparoscopic surgery under
spinal anaesthesia
Combined spinal-epidural anaesthesia
The use of combined spinal-epidural anaesthesia offers many advantages over either of the
techniques by ensuring rapid onset of anaesthesia compared to epidural alone and reduced intrathecal
doses of local anaesthetics required compared to spinal anaesthesia. It also entails the provision of
effective post-operative analgesia and early ambulation of patients. The incidence of side effects is
low with slight alterations in the positioning of the patient and by restriction of intra-abdominal
pressures.
GA VS RA — CURRENT EVIDENCE
Evidence is lacking from developing nations regarding various advancements, mainly owing to the
practice of scarce reporting of advancements and innovations. However, recently data reporting has
witnessed a slight uptrend in the developing nations imbibing empiricism and scientific
evidence.[43,44] RA provides various advantages over GA, such as reduction of surgical stress
response, prevention of airway instrumentation, provision of effective post-operative analgesia, and
early ambulation with lower incidence of deep vein thrombosis. There are numerous studies in the
literature comparing GA and RA for laparoscopic surgery, which suggests that RA may be a good
alternative. The main concerns associated with the use of RA are accelerated hypotension due to
sympathetic blockade, ventilatory changes due to the higher sensory levels required, occurrence of
shoulder-tip pain due to diaphragmatic irritation, and increased surgical time due to limitation of the
intra-abdominal pressure.
Turkstani et al. compared GA with spinal anaesthesia in 50 patients undergoing laparoscopic
cholecystectomy (LC) and found significantly lower pain scores with lower analgesic consumption in
the post-operative period in those with spinal anaesthesia. The total length of hospital stay was not
significantly different but the total cost of anaesthesia was significantly less in the spinal anaesthesia
group. Shoulder-tip pain was recorded in 48% of patients and the hypotension was also seen in 8
patients, but both of these complications were easily controlled.
Imbelloni et al. in their comparison of 68 patients undergoing LC under general or spinal anaesthesia
also found spinal anaesthesia to be a safe and cost-effective technique, with 47% incidence of
shoulder-tip pain and 41% incidence of significant hypotension, both of which responded to
pharmacological treatment with opioids and vasopressors, respectively.
Ellakany, in his study of 40 patients receiving either general or segmental thoracic spinal anaesthesia,
found comparable surgical conditions with superior post-operative analgesia and significantly better
satisfaction scores among patients in the spinal anaesthesia group. He also found a 40% incidence of
significant hypotension and about 25% incidence of abdominal discomfort, which were easily
managed. He found no patients with nausea and vomiting in the spinal anaesthesia group. However,
the use of newer, long-acting anti-emetics like palonosetron reduces the incidence of PONV to a
significant extent.
Mehta et al., in their study of 60 patients, also found better post-operative analgesia with spinal
anaesthesia in comparison to GA for LC. They found no significant difference between the groups
regarding intraoperative complications, recovery, length of hospital stay and degree of satisfaction.
There was no incidence of nausea and vomiting in the patients who received spinal anaesthesia.
All the studies in the literature suggest that RA may be considered comparable to GA in laparoscopic
procedures regarding surgical conditions, intra- and post-operative complications, and hospital length
of stay, but may be superior to GA with respect to the PONV, post-operative analgesia and early
recovery.

1. https://laparoscopy.blogs.com/prevention_management_3/2010/10/anesthesia-for-laparoscopic-surgery.html
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4746973/