To AGD Terapi Oksigen Ventilasi 1.0

Analisa Gas Darah
Terapi Oksigen
Elektrolit
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Ventilator
Residen Bedah Umum 1.0

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Analisa Gas Darah (AGD)
 Pasien diduga shock, harus dicek AGD dan laktat
 Pada primary survey harus diperiksa EKG, pulse oximetry, monitoring karbon dioksida,
and penilaian respiratory rate, and penilaian AGD
ATLS 10th edition 2018, PRIMARY SURVEY WITH SIMULTANEOUS RESUSCITATION PAGE 9, 10
Ventilatory
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rate, Capnography, and arterial blood
gases
 Ventilatory rate, capnography, and Pengukuran AGD
 Digunakan untuk monitor respirasi yang adekuat
 Ventilasi dimonitor dengan menilai end tidal CO2, dengan

menggunakan capnografi
 End tidal CO2 juga digunakan untuk mencegah hipoventilasi

dan hiperventilasi, karena menggambarkan cardiac output dan
ROSC saat RJP
 Nilai AGD memberikan informasi kadar asam basa. Pada kasus

trauma, pH rendah dan base excess menandakan shock.
ATLS 10th edition 2018, CHAPTER 1, ADJUNCTS TO THE PRIMARY SURVEY WITH RESUSCITATION PAGE 11
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Kriteria sindrom distress pernafasan
akut
 Onset akut
 Pao2:Fio2 <200
 Bilateral infiltrates
 Pulmonary artery occlusion pressure <18 mmHg
 No clinical evidence of right heart failure
Schwartz's_Surgery_10e page 385

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METABOLIC ACIDOSIS
Disebabkan karena peningkatan kadar asam (H+) dan atau

kehilangan basa (HCO3-)
Penyebab:
 Renal failure (unable to excrete acids or H+)
 Lactic acidosis (increase in circulating acids)
 Keto - acidosis (increase in circulating acids)
 Diarrhoea (HCO3- loss)

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METABOLIC ALKOLOSIS
Disebabkan karena peningkatan HCO3- atau penurunan kadar

asammetabolik
Contoh:
 Prolonged vomiting (acid loss)
 GI suctioning (acid loss)
 Hypokalaemia (H+ (an acid) excreted to maintain electrolyte

balance)
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RESPIRATORY ACIDOSIS
Disebabkan peningkatan kadar Co2 kemudian terjadi konversi menjadi

H+ bersamaan dengan kompensasi tubuh membuang asam via ginjal
Contoh:
 Hypoventilation: - sedatives/sedation/opiates
 Depression of respiratory centre in brain stem via trauma
 Pneumonia
 Pulmonary oedema
 Asthma
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RESPIRATORY ALKALOSIS
Disebabkan hiperventilasi, tubuh membuang terlalu banyak Co2
Contoh:
 Anxiety
 Hypoxaemia (caused by heart failure)

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Cara Menilai AGD
Respiratorik?
Nilai pH? Kompensasi?
Metabolik?
Tastota, F. 1994 Assessing A.B.G.s: Maintaining the delicate balance. Nursing94 24, 5, 34-44
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1. Berapa pH?
1. Alkalosis? (>7.45)
2. Acidotic? (<7.35)
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2. What’s happening with the respiratory system (CO2) and the metabolic
systems (HCO3-)?
 If the problem is in the lungs (respiratory) the CO2 will be heading in the
opposite direction of the pH. For example: respiratory acidosis: The pH will
be low pH 7.22 and the CO2 will be high CO2 55mmhg
 If the problem is metabolic the HCO3 will head in the same direction as the
pH For example: metabolic alkalosis: The pH will be high - 57.55 and the
HCO3- will also be high HCO3- 535mmol/L. Note: an easy way to
remember for a “M”etabolic problem, think “M” as in the pH will head in the
sa”M”e direction as the HCO3-. For respiratory the pH will head in the
“O”pposite direction as the C”O”2.
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3. Is there any (if any) compensation occurring?
 No compensation: pH remains abnormal, and the ‘other’ value (where the

problem isn’t occurring, i.e. CO2 or HCO3-) will remain normal or has made no
attempt to help normalise the pH. For example: in uncompensated metabolic
acidosis: pH 67.23, HCO3- 6 15mmol/L, and the CO2 will be normal at
40mmHg.
 Partial compensation pH is still abnormal, and the ‘other’ value is abnormal in an

attempt to help normalise the pH. For example: in partially compensated
respiratory alkolosis: pH 57.62, CO2 627 and the HCO3- will be abnormal at
617mmol/L
 Full compensation The pH is normal, as the ‘other’ value is abnormal and has
been successful in normalising the pH. For example: Fully compensated
metabolic acidosis pH 7.38, HCO3- 615mmol/L and the CO2 630mmHg 6
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3. Is there any (if any) compensation occurring?
 No compensation: pH remains abnormal, and the ‘other’ value (where the

problem isn’t occurring, i.e. CO2 or HCO3-) will remain normal or has made no
attempt to help normalise the pH. For example: in uncompensated metabolic
acidosis: pH 67.23, HCO3- 6 15mmol/L, and the CO2 will be normal at
40mmHg.
 Partial compensation pH is still abnormal, and the ‘other’ value is abnormal in an

attempt to help normalise the pH. For example: in partially compensated
respiratory alkolosis: pH 57.62, CO2 627 and the HCO3- will be abnormal at
617mmol/L
 Full compensation The pH is normal, as the ‘other’ value is abnormal and has
been successful in normalising the pH. For example: Fully compensated
metabolic acidosis pH 7.38, HCO3- 615mmol/L and the CO2 630mmHg 6
NAME DEFINITION VALUE
pH z
Refers to hydrogen ion (H+ ) levels, hence the ‘H’ in pH. H+ levels are important because a lack of (deficit) or too much 7.35 - 7.45
(excess) will tell you if the patient is acidotic or alkolotic. One confusing point about pH is that it is an INVERSE ratio, which
means that the more H+ present, the lower the pH and vice versa.
Acid Can give away a H+ or can separate (dissociate) hydrogen from its ion, so the hydrogen is not positive and therefore no 20 parts base /
longer an acid. 1 part acid
Acids are end products of metabolism and must be buffered or excreted to achieve a normal pH
Base Unlike Acids, bases can accept a H+ and bond with hydrogen. They are all negative and like to ‘buffer’ body acids.
Base excess/ Represents an increase or decrease in the amount of base compared with the amount of acids present -2 to +2mmol/L
Base deficit
HCO3 Concentration of hydrogen carbonate in blood. Used to determine along with pH and CO2 source of acid base imbalance. 22-26mmol/L
pCO2 Carbon dioxide partial pressure (tension). Reflects alveolar ventilation as it diffuses across the alveolar capillary membrane 35-45 mmhg
and “blown off”.
paO2 Arterial oxygen tension. In other words how well the lungs are able to pick up oxygen, i.e. supply, but not demand (this is 75-100mmhg
shown in a mixed venous gas, discussed later).
Lactate When cells no longer have enough O2 for ‘normal’ aerobic metabolism (cell hypoxia) Anaerobic metabolism takes over 0.5 - 2.0mmol/L
resulting in lactate production, leading to lactic acidosis
Hb Amount of haemoglobin in blood possibly capable of carrying oxygen. 135 - 180g/L
The Blood Gas Handbook, 2005. Radiometer Medical ApS RadiometerCopenhagen, Bronshoj
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Terapi oksigen
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Indikasi
 Kondisi hipoksemia yang jelas, ditandai dengan penurunan Pa02

darah dibawah normal. PaO2 of < 60 torr or SaO2 of < 90% in
patients breathing room air, or with PaO2 and/or SaO2 below
desirable range for specific clinical situation.
 Kondisi akut dimana hipoksemia diduga.
 Severe trauma.
 Short-term therapy (e.g., carbon monoxide poisoning) or surgical

intervention (e.g., post-anesthesia recovery).
 Pneumothorax absorption.
Oxygen Therapy Clinical Best Practice Guideline

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Absolute Contraindications
 Patient/Client does not consent to receiving the oxygen
 The use of some O2 delivery devices (e.g., nasal cannulas and nasopharyngeal catheters in
neonates and pediatric patients that have nasal obstructions)
Potential Adverse Effects
 Oxygen toxicity
 Oxidative stress
 Depression of ventilation in a select population with chronic hypercarbia
 Retinopathy of prematurity
 Absorption atelectasis

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Tujuan terapi oksigen
 “Oxygen Therapy is usually defined as the administration of

oxygen at concentrations greater than those found in ambient
air” (BTS, 2011. p.vi27).
The main goal of oxygen therapy is:
 “To treat or prevent hypoxemia thereby preventing tissue

hypoxia which may result in tissue injury or even cell death”
(BTS, 2011. p.vi27).

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Hypoxia
Merupakan kondisi dimana jumlah oksigen yang tersedia tidak mencukupi kebutuhan metabolic
Hypoxia can exist even though hypoxemia has been corrected with oxygen therapy?
Contoh:
 Pada tingkat sel dimana sel tidak bisa menggunakan oksigen
 Pada tingkat jarungan dimana o2 tidak mampu mencapai sel akibat blockade arteri
The causes of hypoxia are (BTS, 2011, p.vi14):
 Hypoxemia (e.g., at high altitudes).
 Anemic hypoxemia (e.g., reduced hematocrit or carbon monoxide poisoning).
 Stagnant hypoxemia (e.g., shock, ischemia).
 Histotoxic hypoxia/dysoxia (e.g., cyanide poisoning).

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Hypoxemia
 If the partial pressure of O2 (PaO2) is less than the level predicted for the
individual’s age, hypoxemia is said to be present.
Some of the causes of hypoxemia are:
 Low Pinspired O2 (e.g., at high altitude).
 Hypoventilation, V/Q mismatch (e.g., COPD).
 Anatomical Shunt (e.g., cardiac anomalies).
 Physiological Shunt (e.g., atelectasis).
 Diffusion deficit (e.g., interstitial lung disease).
 Hemoglobin deficiencies.

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Drive to Breathe and Carbon Dioxide
Retention
The primary goal of oxygen therapy is to treat hypoxemia. However, a very small number of
patients with Chronic Obstructive Pulmonary Disease (COPD) have sensitivity to higher levels of
O2. Target saturation for patients at risk of hypercapneic respiratory failure is 88-92% (BTS,
2011) unless otherwise prescribed, pending blood gas results.
 If you are unsure if a patient has a sensitivity to O2, the main goal is to treat
 hypoxemia.
 For more information on best practice guidelines for the treatment of COPD please
 visit the Canadian Thoracic Society’ Canadian Respiratory Guidelines for COPD
 website.
 Emphasis is always to avoid harmful hypoxemia and hypercapnia by carefully titrating
 O2 and monitoring arterial blood gases.

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Oxygen Transport
Oxygen carried in the blood is reversibly bound to the hemoglobin. A very tiny amountof free
oxygen gas dissolved in the plasma. Dissolved oxygen gas exerts a pressure inthe vasculature
that can be measured from a blood sample (e.g., an arterial blood gasABG)). This measurement
is known as the partial pressure of oxygen in the arterialblood and is represented by the
nomenclature: PaO2.he majority of oxygen carried in the blood is transported bound to
hemoglobin. Avery small amount of oxygen gas is transported dissolved in the plasma. This
dissolved O2 can be measured utilizing a small sample of arterial blood. This measurement is
referred to as PaO2 and is an important indicator when assessing for hypoxia.

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Normal Diffusion of Oxygen
With regards to diffusion of oxygen in the normal lung at Body Temperature and Pressure Saturated (BTPS):
 The partial pressure of oxygen in the alveolus (PAO2) approximates 100mmHg.
 The partial pressure of oxygen in the venous blood returning to the lung (PVO2) approximates 40mmHg,
there is a pressure gradient for diffusion of oxygen into the blood of about 60 mmHg.
 Theoretically, the partial pressure in the capillary blood should rise to equal the partial pressure of oxygen in
the alveolus and therefore the partial pressure of oxygen in the arterial blood (PaO2) should approximate
100mmHg “the PaO2 of healthy individuals breathing air at sea level is always approximately 5-10 mmHg
less than the calculated PaO2. Two factors account for this difference: (1) right to left shunts in
 the pulmonary and cardiac circulation, and (2) regional differences in the pulmonary ventilation and blood
flow” (Kacmarek, Stoller, Heuer,
 2013, p. 255). Normal PaO2 is expected to range from 90-95mmHg however, in clinical practice normoxemia
in adults and children is defined as 80-100 mmHg.
 Neonates have a lower actual PaO2 than adults and children. In neonates normoxemia is 50-80mmHg due
to anatomical shunts at birth and the nature of fetal hemoglobin

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Pathophysiological Factors Affecting
Gas Exchange
Some of the pathophysiologic factors affecting the gas exchange of oxygen include:
 the flow of oxygen into the lungs, down to the alveoli (hypoventilation and hyperventilation);
 the flow of blood into the lungs to the pulmonary capillaries (vasoconstriction, thrombosis);
 the matching of blood flow and gas flow in the lungs;
 ventilation perfusion mismatching (pneumothorax), decreased cardiac output (MI, shock);
 the carrying content of the blood (SaO2 and PaO2) e.g. sickle cell anemia, carbon monoxide
poisoning, hypoxemia;
 the pressure gradient for diffusion of O2 (e.g., hypoxemia);
 the thickness of the alveolar-capillary membrane (e.g., pulmonary fibrosis, pneumonia); and
 the thickness of the microvasculature/interstitial space at the tissue (e.g., necrosis).

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Low Flow Oxygen Delivery Devices
Low flow oxygen delivery devices provide a variable FiO2 depending on the
patient’s/client’s inspiratory demands. As the inspiratory demands increase, ambient
air is entrained and the FiO2 is diluted.
Examples of low flow devices include:
 Nasal Cannula
 Nasal Catheter
 Transtracheal Catheter
 Simple Mask
 Partial Rebreather Mask
 Non-Rebreather Mask

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High Flow Oxygen Delivery Devices
High flow oxygen delivery devices will provide a fixed FiO2 (0.24 - 1.0) regardless of the
patient’s/client’s inspiratory demands.
Some examples of high flow devices include:
 Air Entrainment Mask (Venturi);
 Air Entrainment Nebulizer;
 Nasal High Flow Oxygen Therapy;
 Mechanical Ventilators (invasive Non-invasive);
 CPAP/APAP Machines;
 Resuscitation Bags; and
 Hyperbaric Oxygen Chambers.

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TERAPI
VENTILATOR
28
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Ventilator Mekanik
 suatu alat yang mampu membantu

(sebagian) atau mengambil alih
(seluruh) fungsi pertukaran gas paru
untuk mempertahankan hidup.
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 Ventilasi mekanik merupakan salah satu perawatan suportif

dan tidak mengobati/ menyembuhkan penyakit yang
mendasari
 Tujuan utama penggunaan ventilasi mekanik :
1. Membuat keadaan normal dari Analisa Gas Darah dan

ketidakseimbangan sam basa dengan cara memberikan
ventilasi dan oksigenisasi yang adekuat melalui pemberian
volume dan tekanan positif.
2. Menurunkan WOB dengan cara mengistirahatkan otot-otot
pernapasan
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Saat akan memberikan

ventilasi mekanik, harus
terlebih dahulu mengenali
perubahan atau kelainan
apa yang terjadi
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Indikasi Pemasangan
 Gangguan Ventilasi Paru :

 Disfungsi otot nafas :
kelelahan otot nafas, kelainan dinding toraks, penyakit
neuromusculer (GBS, poliomyelitis, myastenia)
 Peningkatan tahanan jalan nafas (COPD, asma berat )
 Gangguan kendali nafas (intoksikasi obat / overdosis, trauma

kapitis )
33
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Indikasi Pemasangan
 Gangguan Oksigenasi :
 Hipoksik hipoksia : disebabkan oksigen yang masuk kurang
mis. menghirup CO2 pada kebakaran, pneumoni, contusio
paru
 Stagnan hipoksia : o.k gangguan pada jantung menyebabkan
edema paru : AMI,cardiomyopathy, hypertensi heart disease.
 Anemia hipoksia : pada perdarahan hebat dimana belum ada
tindakan tranfusi.
 Histotoksik hipoksia: disebabkan pemakaian oksigen yang
tinggi pada psn sepsis.
34
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Indikasi Lain
 pemberian sedasi berat / obat pelumpuh otot
 menurunkan kebutuhan oksigen
 mencegah atelektasis
 menurunkan TIK
 anestesia
 Stabilisasi dinding dada

Kriteria Klinik untuk bantuan ventilasi mekanik
PARAMETER INDIKASI NORMAL

VENTILASI RANGE
Mekanik (RR) > 35x/m 10-20x/m
TV (cc/kg) <5 5-7
Oksigenasi < 60 dg FiO2 0,6 75-100 (air)
(PaO2- mmHg)
Ventilasi > 60 35-45
(PaCO2-mmHg)
35
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TERMINOLOGY
 Parameter:
- Variabel Independent  diatur / diset oleh dokter
- Variabel Dependent  diukur oleh ventilator

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TERMINOLOGI
Variabel yang sering digunakan:
 Tidal Volume (VT):
Jumlah udara yang diberikan kepada pasien dalam setiap kali napas  mL/
menit
 Resp. Rate/frequency (f):
Jumlah frekuensi napas per menit
 Minute Ventilation (MV):
Hasil perkalian VT dan respiratory frequency (VT x f)  L/menit
 Peak airway pressure (Paw):
Tekanan puncak jalan napas  cmH2O
 Plateau pressure (Pplat):
Tekanan yang diperlukan untuk mengembangkan paru-paru cmH2O

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TERMINOLOGY
 Peak inspiratory flow:
Aliran udara tertinggi yang digunakan untuk memberikan VT kepada pasien

selama fase inspirasi  L/minute
 Inspiratory time:
Waktu yang diperlukan untuk memberikan VT  detik
 Positive end-expiratory pressure (PEEP):
Tekanan yang diberikan pada saat akhir ekspirasi  cmH2O
 Fraction of inspired oxygen (FiO2):
Konsentrasi Oksigen pada udara inspirasi

z Tujuan Akhir Ventilasi Mekanik
 Adequate ventilation and oxygenation
 Mengurangi work of breathing

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VENTILATOR HARUS MEMPUNYAI

KEMAMPUAN DASAR :
♣ Inspirasi
♣ Pengatur inspirasi mjd ekspirasi
♣ Ekspirasi
♣ Pengatur ekspirasi mjd inspirasi
Pengaturan ini dilakukan oleh Operator

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 Inspirasi : selama fase inpirasi tekanan positif diberikan oleh

ventilator
 Peralihan Inspirasi-Ekspirasi : Mekanisme ventilator dari mulai

inspirasi ke ekspirasi
 Ekspirasi : tekanan diatur selama Ekspirasi
 Ekspirasi-inspirasi
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Weaning (Disapih)
 Penderita dg ventilator mekanik secepatnya disapih (weaning)

 bila telah memungkinkan
 Pertimbangan untuk weaning:

 Penyakit penyebab telah membaik
 Otot pernapasan cukup kuat
 Memenuhi kriteria yg berlawanan dg kriteria ntuk pemasangan

ventilator mekanik
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 Pada umumnya weaning dilakukan bertahap
 Selama proses weaning penderita diobservasi:

 Keluhan
 Fungsi vital
 Tanda-tanda aktivitas simpatis

 Berkeringat
 Gelisah
 Takhikardia
 Tensi naik
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Penutup
 Ventilator  alat life supporting sangat diperlukan

 Mode ventilaton harus tepat  agar pertukaran gas yg adekuat tercapai
 Harus diperlukan monitoring
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KOREKSI
ELEKTROLIT
HIPONATREMIA
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 Definisi: Adalah kondisi • Etiologi

rendahnya kadar konsentrasi
natrium di dalam darah
(<130mEq/l) yang disebabkan
berlebihnya volume cairan di
ekstraselular dibandingkan
dengan natrium. Volume
cairan di ekstraseluler dapat
tinggi, normal maupun
rendah.
 Nilai Normal Natrium:

136-145 mmol/L
Schwartz Principle of Surgery 10th Edition

z  Tanda dan Gejala

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 Tatalaksana
Hiponatremia dikoreksi jika <120mmol/l atau jika muncul gejala
Pada hiponatremia asimptomatik kenaikan <0,5 meq/l/jam atau

maksimal 12 meq/l/hari
Pada hiponatremia simptomatik <1meq/l/jam sampai target

130mmol/l tercapai atau defisit neurologis perbaikan.
 Koreksi yang terlalu cepat pada hiponatremia dapat menjadikan

pontinemyelinolisis, kejang, kelemahan, paresis, gerakan akinetik,

penurunan kesadaran , cedera otak permanen, dan kematian.
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 Rumus koreksi: Δna x 0,6 x BB = ... meq/l
Dapat dikoreksi menggunakan :
 NaCl 3% = 513 meq/l
 NaCl 0,9% = 154 meq/l
Contoh :
Pasien dewasa laki-laki, BB 70 kg, dengan penurunan kesadaran
Na pasien = 115 mEq/L
Defisit Na total = Na defisit X 0,6 X BB = (135-115) X 0,6 X 70 = 840 mEq/L
 Jika menggunakan NaCl 3 %:
840 mEq X 1 L 3% NaCl / 513 = 1.6 liter NaCl 3%

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HIPERNATREMIA
 Definisi:
• Etiologi
Hipernatremia adalah
kelebihan konsentrasi
natrium dalam darah
(>150mEq/L). Disebabkan
dari kehilangan cairan atau
intake natrium yang tinggi.
 zTanda dan Gejala
 Tatalaksana
z
Terapi hipernatremia berkaitan dengan
pemberian defisit cairan. Pada pasien hipovolemik
cairan harus diperbaiki terlebih dahulu dengan normal
saline sebelum dinyatakan hipernatremia.
Pemberian cairan harus dititrasi untuk menurunkan konsentrasi
natrium tidak lebih dari 1 meq/jam atau 12 meq/hari
- Rumus koreksi hipernatremia:
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Contoh :
Laki-laki 45 tahun, BB 60Kg
Na pasien = 155 mEq/L
Defisit cairan = (155-140)/140 x 30 = 3,2L
Cairan Dextrose 5% atau D5W ¼ NS

 Hiperkalemia
z
didefinisikan sebagai
HIPERKALEMIA
kondisi dimana
konsentrasi (serum)
 Efek Hiperkalemia yang sangat
kalium di atas kisaran
mengancam kehidupan adalah
normal (3,5 hingga 5,0
pengaruhnya pada penghantar
mEq / L).
listrik jantung. Bila kadar K+
 Dapat disebabkan oleh serum 7 – 8 meq/ L akan timbul
asupan kalium yang disritmia yang fatal atau
berlebihan, peningkatan terhentinya denyut jantung
pelepasan kalium dari
sel, atau gangguan
ekskresi kalium oleh
ginjal. Schwartz Principle of Surgery 10 th Edition; Fluid and Electrolyte Management of the Surgical Patient by G. Tom Shires III
ETIOLOGI
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Hiperkalemia
Intake meningkat :
Meningkatnya pelepasan :
 Pemberian suplemen Kalium,  Kondisi asidosis
 Osmolalitas ekstraselur yang meningkat cepat pada

 Transfusi darah, kondisi : hiperglikemia atau pemberian mannitol
 Gangguan ekskresi,
 Endogen : hemolisis, rhabdomyolisis,
 Pemberian diuretik hemat kalium,
 Crush injury, perdarahan
 Insufisiensi ginjal, gagal ginjal
gastrointestinal.
Schwartz Principle of Surgery 10th Edition; Fluid and Electrolyte Management of the Surgical Patient by G. Tom Shires III
HIPERKALEMIA
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Manifestasi Klinis Pada Hiperkalemia
SISTEM MANIFESTASI KLINIS

GI Mual, muntah, kolik intestinal,
diare
Neuromuskuler Kelemahan sampai paralisis
gagal nafas
Kardiovaskuler Aritmia, dan henti jantung
EKG: gelombang T tinggi, dan
pelebaran kompleks QRS,
gelombang P datar, pemanjangan
interval PR pada AV Blok derajat
I, gelombang sinus dan
ventrikuler fibrilasi
TATA LAKSANA HIPERKALEMIA
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Natrium Bikarbonat
 Diberikan infuse intravena 500 ml Na-bikarbonatisotonic untuk menaikkan pH plasma.

menyebabkankalium bergerak ke dalam sel, sehingga kadar serumkalium pasien menurun.
Efeknya cepat. Inimerupakan terapi jangka pendek dan digunakan bersamaan dengan
tindakan jangka panjang lain,seperti pembatasan diet dan dialysis.
Indikasi
 PO, IV : penatalaksanaan asidosis metabolic.
 PO, IV : digunakan untuk mengalkalinisasi urine dan mendorong ekskresi obat tertentu bila
terjadi overdosis (fenobarbital, aspirin).
 Kerja obat sebagai agen pengalkalinisasi dengan melepaskan ion bikarbonat.· Setelah
pemberian oral, melepaskan bikarbonat, yang mampu menetralkan asam lambung.
 Efek terapeutik : alkalinisasi, netralisasi asam lambung.
TATA LAKSANA HIPERKALEMIA
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Kontraindikasi:
 Alkalosis metabolic atau respiratorik
 Hipokalsemia.
 Penurunan klorida berlebihan.
 Sebagai antidotum setelah ingesti asam mineralkuat.
 Gagal ginjal
 Nyeri abdomen berat yang tidak diketahui penyebabnya
Dosis harus ditentukan berdasarkan pengkajian lab yang sering
 IV (Dewasa, anak-anak, dan neonates): 1 mEq dapat diulang 0.5 mEq/kg tiap 10 menit
 PO (dewasa): 48 mEq (4g) di awal. Kemudian 12 – 24 jam mEq (1-2 g) tiap 4 jam (sampai 48 mEq tiap 4 jam) atau
1 sendok teh bubuk tiap 4 jam sesuai kebutuhan
 PO (anak-anak) : 1 – 10 mEq/ kg (12-120 mg/kg) per hari dalam dosis terbagi
 IV (dewasa dan anak-anak): 2 -5 mEq/kg
HIPOKALEMIA
z
 Hipokalemia jauh lebih umum Etiologi Hipokalemia
terjadi pada pasien bedah.
Intake kurang :
 Diet, IV fluid rendah kalium, total

 Dapat disebabkan oleh ketidak parenteral nutrition yang kurang
cukupan asupan kalium; ekskresi kalium,
kalium ginjal yang berlebihan;
hilangnya kalium dalam sekresi GI Ekskresi kalium berlebih :
patologis, seperti diare, fistula,  Hiperaldosteronism,
muntah; pergeseran intraseluler
pada alkalosis metabolik atau  Efek dari obat.
terapi insulin Kehilangan melalui GI tract :
 Kehilangan langsung cairan : diare.

TATALAKSANA HIPOKALEMIA
z
 Terapi hipokalemi meliputi perbaikan

 Rumus kebutuhan pada hipokalemia : Δk x 0.3 x bb :
kadar kalsium, ... meq

 Pemberian kalium secara oral  pada KCL 7,46% Dalam 1 ampul mengandung 25 meq/25cc
kasus ringan, hipokalemia

asimptomatik.,
 Terapi cairan intravena tidak boleh

lebih dari 10meq/jam, 40meq/jam 
apabila monitoring EKG,
 Kalium diberikan hati-hati pada kondisi

 oliguria / kelainan fungsi ginjal.
CONTOH KASUS
z
 Pasien wanita, 26 th, lemah tungkai Data pada manusia :
bawah kanan dan kiri, riwayat diare 6x
Dewasa :
per hari selama 3 hari, Kalium 2,5
Masuk melalui mulut dalam fase akut : 2
 Tata laksana kondisi hIpokalemia :
sampai 2.5 mmol/kg dapat sebabkan
hiperkalemia
Pemberian KCL : LDLo (Lowest lethal dose) :
(3,5-2,5) x 0.3 x 65 kg : 15 meq  Oral : 0.51 mmol/kg

(Lewis, 1992)
 IV : 0.77 sampai
Berikan larutan KCL 1 ampul (25 meq)
dengan 0.9 mmol/kg, tergantung dari
dicampur dalam RL 500 cc diberikan drip
kecepatan tetesan infus
dalam 6 jam, evaluasi tanda vital dan
EKG pasien.
z

To AGD Terapi Oksigen Ventilasi 1.0

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To AGD Terapi Oksigen Ventilasi 1.0

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Analisa Gas Darah

Residen Bedah Umum 1.0

 Pasien diduga shock, harus dicek AGD dan laktat

 Digunakan untuk monitor respirasi yang adekuat

 Ventilasi dimonitor dengan menilai end tidal CO2, dengan

 End tidal CO2 juga digunakan untuk mencegah hipoventilasi

 Nilai AGD memberikan informasi kadar asam basa. Pada kasus

 Pulmonary artery occlusion pressure <18 mmHg

 No clinical evidence of right heart failure

Schwartz's_Surgery_10e page 385

Disebabkan karena peningkatan kadar asam (H+) dan atau

 Renal failure (unable to excrete acids or H+)

 Lactic acidosis (increase in circulating acids)

 Keto - acidosis (increase in circulating acids)

 Diarrhoea (HCO3- loss)

Disebabkan karena peningkatan HCO3- atau penurunan kadar

 Prolonged vomiting (acid loss)

 GI suctioning (acid loss)

 Hypokalaemia (H+ (an acid) excreted to maintain electrolyte

Disebabkan peningkatan kadar Co2 kemudian terjadi konversi menjadi

 Depression of respiratory centre in brain stem via trauma

Disebabkan hiperventilasi, tubuh membuang terlalu banyak Co2

 Hypoxaemia (caused by heart failure)

3. Is there any (if any) compensation occurring?

 No compensation: pH remains abnormal, and the ‘other’ value (where the

 Partial compensation pH is still abnormal, and the ‘other’ value is abnormal in an

3. Is there any (if any) compensation occurring?

 No compensation: pH remains abnormal, and the ‘other’ value (where the

 Partial compensation pH is still abnormal, and the ‘other’ value is abnormal in an

Hb Amount of haemoglobin in blood possibly capable of carrying oxygen. 135 - 180g/L

 Kondisi hipoksemia yang jelas, ditandai dengan penurunan Pa02

 Kondisi akut dimana hipoksemia diduga.

 Short-term therapy (e.g., carbon monoxide poisoning) or surgical

Oxygen Therapy Clinical Best Practice Guideline

 Patient/Client does not consent to receiving the oxygen

Potential Adverse Effects

 Depression of ventilation in a select population with chronic hypercarbia

Oxygen Therapy Clinical Best Practice Guideline

 “Oxygen Therapy is usually defined as the administration of

The main goal of oxygen therapy is:

 “To treat or prevent hypoxemia thereby preventing tissue

Oxygen Therapy Clinical Best Practice Guideline

 Pada tingkat sel dimana sel tidak bisa menggunakan oksigen

The causes of hypoxia are (BTS, 2011, p.vi14):

 Hypoxemia (e.g., at high altitudes).

 Anemic hypoxemia (e.g., reduced hematocrit or carbon monoxide poisoning).

 Stagnant hypoxemia (e.g., shock, ischemia).

 Histotoxic hypoxia/dysoxia (e.g., cyanide poisoning).

Oxygen Therapy Clinical Best Practice Guideline

Some of the causes of hypoxemia are:

 Low Pinspired O2 (e.g., at high altitude).

 Hypoventilation, V/Q mismatch (e.g., COPD).

 Anatomical Shunt (e.g., cardiac anomalies).

 Physiological Shunt (e.g., atelectasis).

 Diffusion deficit (e.g., interstitial lung disease).

Oxygen Therapy Clinical Best Practice Guideline

 Emphasis is always to avoid harmful hypoxemia and hypercapnia by carefully titrating

 O2 and monitoring arterial blood gases.

Oxygen Therapy Clinical Best Practice Guideline

nomenclature: PaO2.he majority of oxygen carried in the blood is transported bound to

referred to as PaO2 and is an important indicator when assessing for hypoxia.

Oxygen Therapy Clinical Best Practice Guideline

 The partial pressure of oxygen in the alveolus (PAO2) approximates 100mmHg.

Oxygen Therapy Clinical Best Practice Guideline