15/03/2018

VENTILASI MEKANIK &

ANALISA GAS DARAH

Ninuk Dian Kurniawati

Analisa Gas Darah

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ARTERIAL BLOOD GASES

• ARTERIAL SAMPLING:
• Common sites include:
– 1) radial, 30-45
– 2) femoral, 45-90
– 3) brachial, 45-60
– 4) dorsalis pedis, or
– 5) axillary artery
• the radial artery is used most often because it is
– accessible,
– easily positioned, and
– more comfortable for the patient than the alternative
sites

ARTERIAL BLOOD GASES

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ARTERIAL BLOOD GASES

ARTERIAL BLOOD GASES

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ARTERIAL BLOOD GASES

ARTERIAL BLOOD GASES

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ARTERIAL BLOOD GASES

ARTERIAL BLOOD GASES

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ARTERIAL BLOOD GASES

ARTERIAL BLOOD GASES

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ARTERIAL BLOOD GASES

ARTERIAL BLOOD GASES

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ARTERIAL BLOOD GASES

"Oxygenation and mechanisms of
hypoxemia“
MEASURES OF OXYGENATION:
1) Arterial oxygen saturation (SaO2)
2) Arterial oxygen tension (PaO2)
3) A-a oxygen gradient
4) PaO2/FiO2 ratio a-
5) A oxygen ratio
6) Oxygenation index

ARTERIAL BLOOD GASES

A -a
(alveolar) (arteriol) oxygen gradient

A-a oxygen gradient = PAO2 - PaO2

A-a gradient = 2.5 + 0.21 x age in years

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ARTERIAL BLOOD GASES

PaO2/FiO2 ratio
A normal PaO2/FiO2 ratio is 300 to 500
mmHg
less than 300 mmHg indicating
abnormal gas exchange
less than 200 mmHg indicates severe
hypoxemia

Normal Values
• pH = 7.35 – 7.45
• pCO2 = 35 – 45 mmHg lungs
(Reference Value = 40)

• HCO3 = 22 – 26 mmol/L kidneys

(Reference value = 24)

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

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Example # 1 Example # 2 Example # 3

PH – 7.34 PH – 7.34 PH – 7.38
pCO2 – 52 pCO2 – 50 pCO2 – 24
HCO3 - 19 HCO3 - 31 HCO3 - 19

Example # 4 Example # 5 Example # 6

PH – 7.46 PH – 7.39 PH – 7.41
pCO2 – 42 pCO2 – 41 pCO2 – 51
HCO3 - 31 HCO3 - 25 HCO3 - 33

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Normal Values
(Harrisons)

CHECK THE
COMPENSATORY RESPONSE

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MIXED DISORDER
• difficult and it is important to look at all the parameters
• If compensation calculations are not compatible with one
primary disorderr
• if the respiratory and metabolic parameters are both changed
in the same direction (acidic, alkaline),
• if the pH is changed in the opposite direction from what is
expected for a primary disorder (eg, the lactate is high but the
pH is alkaline), or when pCO2 and HCO3- change in opposite
directions from what is predicted

ANION GAP
Na – (HCO3 + Cl) = 10-12 mmol/L
Atau 12-14 mEq/L

Na = 135 HCO3 = 15
Cl = 97 RBS = 100 mg%

AG = 135 – 112 = 23

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ANION GAP
Na – (HCO3 + Cl) = 10-12

Na = 135 HCO3 = 15
Cl = 97 RBS = 500 mg%

Corrected AG = Na + RBS mg% -100 x 1.4

100

AG = 135 + 5.6 – 112 = 28.6

ANION GAP

AG = Na+ - (Cl- + CO2)

12 mEq/L

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ANIONS CATIONS

Proteins 15 Calcium 5
ANIONS CATIONS
Organic acids 5 Magnesium 1.5 Cl- + HCO3- =
Na+ = 140
128
Phosphates 2 Potassium 4.5

Bicarbonate 24 Sodium 140

Sulfates 1

Difference (cations -
Chloride 104 anions) = 140 - 128 = 12
TOTAL 151 TOTAL 151

Bicarbonate gap = delta AG - delta

CO2
where
delta AG = patient's AG - 12 mEq/L
delta CO2 = 27 mEq/L - patient's CO2

#normal venous CO2 of 27 mEq/L

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There is a 1-to-1 correlation between the rise in

anion gap and the fall in bicarbonate (measured
as serum CO2); that is, the normal difference
between rise in AG and fall in serum CO2 should
be zero. For example, if AG goes up by 10 mEq/L
(to 24 mEq/L) then serum CO2 should go down by
10 mEq/L (to 17 mEq/L); in this case delta AG -
delta CO2 = 10 - 10 = 0 bicarbonate gap.

Elevated AG with a significant variation of

bicarbonate gap from zero, either + or -,
suggests the patient has a mixed acid-base
disorder: anion gap acidosis plus another
disorder, such as metabolic alkalosis (+
bicarbonate gap) or hyperchloremic metabolic
acidosis (- bicarbonate gap)

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• PREDICTION OF COMPENSATORY RESPONSES

ON SIMPLE ACID BASE DISORDERS
• Metabolic Acidosis PaCO2 = (1.5 X HCO3) + 8

• Metabolic Alkalosis PaCO2 will increase 0.75 mmHg per meq/L increase in
HCO3

• Respiratory Acidosis
Acute HCO3 will increase 1 meql/L per 10 mmHg increase in
PaCO2
Chronic HCO3 will increase 4 meq/L per 10 mmHg increase in
PaCO2
• Respiratory Alkalosis
Acute HCO3 will decrease 2 meq/L per 10 mmHg decrease in
PaCO2
Chronic HCO3 will decrease 4 meq/L per 10 mmHg decrease in
PaCO2

COMPENSATORY RESPONSE

METABOLIC ACIDOSIS
PaCO2 = (1.5 X HCO3) + 8

HCO3 =12 pCO2 =1.5 X 12 + 8 = 26

HCO3 =7 pCO2 = 1.5 X 7 + 8 = 18.5

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COMPENSATORY RESPONSE

METABOLIC ALKALOSIS
PaCO2 will increase 0.75 mmHg per
meq/L increase in HCO3

HCO3 =35 pCO2 =11 X 0.75 = 8.25

= 8.25 + 40 = 48
HCO3 =40 pCO2 = 52

COMPENSATORY RESPONSE

ACUTE RESPIRATORY ACIDOSIS

HCO3 will increase 1 meq/L per 10 mmHg
increase in PaCO2

pCO2 =55 HCO3 = 25.5

pCO2 =80 HCO3 = 28

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COMPENSATORY RESPONSE

RESPIRATORY ALKALOSIS
Acute: HCO3 will decrease 2 meq/L per 10 mmHg
decrease in PaCO2

Check for Secondary Acid Base

Disorders
Primary Acid Base Compensation Secondary Base Disorder
Disorder

Metabolic Acidosis Actual reduction of pC02 from Secondary RESPIRATORY

baseline is HIGHER than that of ALKALOSIS is present
calculated compensation

Actual reduction of pC02 from Secondary RESPIRATORY

baseline is LESS than that of ACIDOSIS is present
calculated compensation

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Check for Secondary Acid Base

Disorders
Primary Acid Base Compensation Secondary Base Disorder
Disorder

Metabolic Alkalosis Actual increase of Pc02 from Secondary RESPIRATORY

baseline is HIGHER than that of ACIDOSIS is present
calculated compensation

Actual reduction of pC02 from Secondary RESPIRATORY

baseline is LESS than that of ACIDOSIS is present
calculated compensation

Check for Secondary Acid Base

Disorders
Primary Acid Base Compensation Secondary Base Disorder
Disorder

Respiratory Actual increase of Hc03 from Secondary Metabolic Alkalosis

Acidosis baseline is HIGHER than that of is present
calculated compensation

Actual increase of Hc03 from Secondary METABOLIC

baseline is LESS than that of ACIDOSIS is present
calculated compensation

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Check for Secondary Acid Base

Disorders
Primary Acid Base Compensation Secondary Base Disorder
Disorder

Respiratory Actual decrease of Hc03 from Secondary Metabolic Acidosis

Alkalosis baseline is HIGHER than that of is present
calculated compensation

Actual decrease of Hc03 from Secondary METABOLIC

baseline is LESS than that of Alkalosis is present
calculated compensation

DETERMINE CLUES
FROM THE
CLINICAL SETTING

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CLUES FROM CLINICAL SETTING

HIGH ANION GAP METABOLIC ACIDOSIS
(HAGMA)
M Methanol

U Uremia

D Diabetic Ketoacidosis

P Paraldehyde

I Isoniazid, Iron

L Lactic Acidosis

E Ethylene Glycol, Ethanol

S Salicylates

CLUES FROM CLINICAL SETTING

NORMAL ANION GAP METABOLIC ACIDOSIS
(NAGMA)
H Hyperalimentation

A Acetazolamide

R Renal Tubular Acidosis

D Diarrhea

U Ureteropelvic shunt

P Post Hypocapnia

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CLUES FROM CLINICAL SETTING

METABOLIC ALKALOSIS
Vomiting Remote
diuretic use Post
hypercapnea
Chronic diarrhea
Cystic fibrosis
Acute alkali administration

CLUES FROM CLINICAL SETTING

METABOLIC ALKALOSIS
Bartter’s syndrome Severe
potassium depletion
Current diuretic use
Hypercalcemia
Hyperaldosteronism
Cushing’s syndrome
Gastric aspiration

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CLUES FROM CLINICAL SETTING

RESPIRATORY ACIDOSIS
CHRONIC: COPD, intracranial tumors
ACUTE: pneumonia, head trauma, general
anesthetics, sedatives

RESPIRATORY ALKALOSIS
Hyperventilation, Pregnancy, Liver failure,
Methylxanthines

CASE 1
56F with vomiting and diarrhea 3 days ago
despite intake of loperamide. Her last urine
output was 12 hours ago.

PE showed BP = 80/60, HR = 110, RR = 28. There

is poor skin turgor.

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CASE 1
serum Na = 130 pH = 7.30
K = 2.5 pCO2 = 30
Cl = 105 HCO3 = 15
BUN = 42 pO2 = 90
crea = 2.0
RBS = 100

BCR = BUN / crea = 21 PRE-RENAL

CASE 1
serum Na = 130 pH = 7.30
K = 2.5 pCO2 = 30
Cl = 105 HCO3 = 15
BUN = 42 pO2 = 90
crea = 2.0
RBS = 100

pH = acidosis, pCO2 =alk, Metabolic

HCO3 = acidosis Acidosis

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CASE 1
serum Na = 130 pH = 7.30
K = 2.5 pCO2 = 30
Cl = 105 HCO3 = 15
BUN = 42 pO2 = 90
crea = 2.0
RBS = 100
Compensated
pCO2 = 15 x 1.5 + 8 = 30.5 Metabolic
Acidosis

CASE 1
serum Na = 130 pH = 7.30
K = 2.5 pCO2 = 30
Cl = 105 HCO3 = 15
BUN = 42 pO2 = 90
crea = 2.0
RBS = 100

AG= 130 – (105+15) = 10 NAGMA

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CASE 2
19F, fashion model, is surprised to find her K=2.7
mmol/L because she was normokalemic 6
months ago. She admits to being on a diet of
fruit and vegetables but denies vomiting and
the use of diuretics or laxatives. She is
asymptomatic. BP = 90/55 with subtle signs of
volume contraction.

CASE 2
Plasma Urine
serum Na 138 63
K Cl 2.7 34
HCO3 96 0
pH 30 0
pCO2 7.45 5.6
45

pH = alk, pCO2 =acidosis Metabolic

HCO3 = alkalosis Alkalosis

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COMPENSATORY RESPONSE

METABOLIC ALKALOSIS
PaCO2 will increase 0.75 mmHg per
mmol/L increase in HCO3

HCO3 =35 pCO2 =11 X 0.75 = 8.25

= 8.25 + 40 = 48
HCO3 =40 pCO2 = 52

VENTILATOR

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Pengertian
Pemberian oksigen kejalan nafas pasien melalui
mesin:
• Invasif(Ventilator)
• Non Invasif(NIV)

• Merupakan alat penunjang pernafasan

• Bukan terapi/kuratif

Invasive

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Jenis Ventilasi mekanik yang

digunakan di rumah sakit

Evita

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Savina

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Galileo

Raphael

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Servo

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dan masih banyak model lain

Tahapan melakukan ventilasi mekanik

 Indikasi
 Persiapan: obat, alat
 Intubasi/NIV
 Setting awal ventilasi mekanik
 Evaluasi: fisiologis, klinis
 Penyesuaian (adjustment)

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Indikasi Pemasangan
• Gangguan Ventilasi Paru :
– Disfungsi otot nafas :
kelelahan otot nafas, kelainan dinding torax, penyakit
neuromusculer (GBS, poliomyelitis, myastenia)
– Peningkatan tahanan jalan nafas (COPD, severe astma)
– Gangguan kendali nafas (intoxikasi obat / overdosis,
trauma capitis )
– ARDS/ALI
– Pneumonia/infeksi

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Indikasi Pemasangan
• Gangguan Oksigenasi :
– Hypercapnic Respiratory Failure: PaCO2 > 50 mmHg
– Hypoxemic Respiratory Failure: PaO2 < 60 mmHg
– 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.
78

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Indikasi Lain
• pemberian sedasi berat / obat pelumpuh otot
• menurunkan kebutuhan oksigen
• mencegah atelektasis
• menurunkan TIK
• anestesia
• Stabilisasi dinding dada

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Tujuan pemberian ventilasi mekanik

Fisiologis
Memperbaiki pertukaran gas di paru-paru
•Ventilasi alveoli : PaCO2, pH
•Oksigenasi arteri: PaO2, SaO2, CaO2

Penambahan volume paru

•Pengembangan paru akhir inspirasi
•FRC

MenurunkanWOB
•Tidak meningkatkan beban otot-otot pernapasan

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Tujuan ventilasi Mekanik

KLINIS:
_Mengatasi hipoksia
–Mengatasi Respiratorik asidosis
–Menghilangkan distress napas
–Mencegah/ mengatasi atelektasis
–Mencegah fatigue otot pernapasan
–Bila diperlukan sedasi berat, obat pelumpuh otot
–Menurunkan kebutuhan Oksigen otot jantung atau
sistemik
–Menurunkan Tekanan Intra Kranial
–Stabilisasi dinding thorak

Kriteria Klinik untuk bantuan

ventilasi mekanik
PARAMETER INDIKASI NORMAL RANGE
VENTILASI
Mekanik (RR) > 35x/m 10-20x/m
TV (cc/kg) <5 5-7
Oksigenasi < 60 dg FiO2 0,6 75-100 (air)
(PaO2- mmHg)
P(A-a DO2) mmHg, Alveolar- > 450 25-65(FiO2 1.0)
arterial oxygen difference
PAO2 = 150 - PaCO2 x 1.25A-
10-25 (FiO2 0,21)
aDO2=PAO2-PaO2 A-aDO2 = 2.5 + 0.21 x
umur (th)
Ventilasi > 60 35-45
(PaCO2-mmHg)
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Jenis Jenis Ventilator

pembagian berdasarkan cara penghentian
inspirasi :
a. Time Cycle
b. Pressure Cycle : sering u/ pediatrik dan
neonatus
c. Volume Cycle : paling banyak di ICU
Ekspirasi bersifat pasif

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Ventilator Settings Terminology

•A/C: Assist-Control
•IMV: Intermittent Mandatory Ventilation
•SIMV: Synchronized Intermittent
Mandatory Ventilation
•Bi-level/Biphasic: Non-inversed Pressure Ventilation
with Pressure Support (consists of 2 levels of
pressure)

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Ventilator Settings Terminology (con’t)

•PRVC: Pressure Regulated Volume Control

•PEEP: Positive End Expiratory Pressure
•CPAP: Continuous Positive Airway
Pressure
•PSV: Pressure Support Ventilation
•NIPPV: Non-Invasive Positive Pressure Ventilation

Komponen Setting Ventilator

• FiO2 : fraksi oksigen
• Volume Tidal : 6-10cc/kgBB
• Frekuensi Napas : 10 – 12 x/mnt
• I : E Ratio (Rasio Inspirasi : Ekspirasi)
• PEEP : Positive End Exspiracy Pressure, (3 – 5
cmH2O)

86

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Starting mechanical ventilation simple

method
• Set the FiO2 to 100 %
• Set a tidal volume of 6 ml / Kg
• Set a rate of 14 breaths / min
• Use Pressure control
• Set PEEP to 10 cmH2O or best PEEP
( need a P-V curve )
• Set I:E ratio = 1 : 1,5 or 1 : 2
• Arterial blood gas after 15 minute
• Adjust FiO2 , Rate , Pressure to target

Setting ventilasi yang tidak tepat

• Hypoxemia
• Surfactant depletion
• Cytokine release
• Bacterial transmigration
• Atelectasis
• Barotrauma - volutrauma

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MODES of VENTILATION

Control Mode
Delivers pre-set volumes at a pre-set rate and
a pre-set flow rate.
The patient CANNOT generate spontaneous
breaths, volumes, or flow rates in this mode.

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Control Mode

Assist/Control Mode
•Delivers pre-set volumes at a pre-set rate and a pre-
set flow rate.
•The patient CANNOT generate spontaneous
volumes, or flow rates in this mode.
•Each patient generated respiratory effort over and
above the set rate are delivered at the set volume
and flow rate.

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Assist-control

Ingento EP & Drazen J: Mechanical Ventilators, in Hall JB, Scmidt GA, &
Wood LDH(eds.): Principles of Critical Care

A/C cont.

Negative deflection,
triggering assisted
breath

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SYCHRONIZED INTERMITTENT
MANDATORY VENTILATION
(SIMV):

Delivers a pre-set number of breaths at a

set volume and flow rate.
Allows the patient to generate
spontaneous breaths, volumes, and flow
rates between the set breaths.
Detects a patient’s spontaneous breath
attempt and doesn’t initiate a ventilatory
breath – prevents breath stacking

IMV

Ingento EP & Drazen J: Mechanical Ventilators, in Hall JB, Scmidt GA, &
Wood LDH(eds.): Principles of Critical Care

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SIMV

SIMV

Ingento EP & Drazen J: Mechanical Ventilators, in Hall JB, Scmidt GA, &
Wood LDH(eds.): Principles of Critical Care

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SIMV cont.

Machine Breaths
Spontaneous Breaths

PRESSURE REGULATED VOLUME

CONTROL (PRVC):

• This is a volume targeted, pressure limited

mode. (available in SIMV or AC)
• Each breath is delivered at a set volume
with a variable flow rate and an absolute
pressure limit.
• The vent delivers this pre-set volume at the
LOWEST required peak pressure and adjust
with each breath.

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PRVC

POSITIVE END EXPIRATORY

PRESSURE (PEEP):

• This is NOT a specific mode, but is rather an adjunct

to any of the vent modes.
• PEEP is the amount of pressure remaining in the
lung at the END of the expiratory phase.
• Utilized to keep otherwise collapsing lung units
open while hopefully also improving oxygenation.

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PEEP cont.

Pressure above zero

PEEP is the
amount of
pressure
remaining in the
lung at the END
of the expiratory
phase.

Continuous Positive Airway

Pressure (CPAP):

• This IS a mode and simply means that a pre-set

pressure is present in the circuit and lungs
throughout both the inspiratory and expiratory
phases of the breath.
• CPAP serves to keep alveoli from collapsing,
resulting in better oxygenation and less WOB.
• The CPAP mode is very commonly used as a mode
to evaluate the patients readiness for extubation.

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HIGH FREQUENCY
VENTILATION

TROUBLESHOOTING
 Anxious Patient and/or dis-synchrony on the ventilator:
 Could be secondary to overall discomfort
 Increase sedation
 Can be due to a malfunction of the ventilator
 Patient may need to be suctioned
 Could be secondary to feelings of air hunger
 Options include increasing tidal volume, increasing flow rate,
adjusting I:E ratio, increasing sedation

• Attempt to fix the problem

• Call your RT/MD

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Low Pressure Alarm

• Usually due to a leak in the circuit.

– Attempt to quickly find the problem

– Bag the patient and call your RT/MD.

High Pressure Alarm

• Usually caused by:

– A blockage in the circuit (water
condensation)
– Patient biting his ETT
– Mucus plug in the ETT

– You can attempt to quickly fix the problem

– Bag the patient and call for your RT/MD.

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High Peak Pressure

• If peak pressures are increasing:
– Check plateau pressures by allowing for an
inspiratory pause (this gives you the pressure in
the lung itself without the addition of resistance)
– If peak pressures are high and plateau pressures
are low then you have an obstruction
– If both peak pressures and plateau pressures are
high then you have a lung compliance issue

High Peak Pressures High Peak Pressures

Low Plateau Pressures High Plateau Pressures

Mucus Plug ARDS

Bronchospasm Pulmonary Edema

ET tube blockage Pneumothorax

Biting ET tube migration to a

single bronchus

Effusion

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Trouble Shooting the Vent

• If you have a patient with history of
COPD/asthma with worsening oxygen
saturation and increasing hypercapnia
differential includes:
– Given the nature of the disease process, patients have difficultly with
expiration (blowing off all the tidal volume)
– Must be concern with breath stacking or auto- PEEP
– Management options include:
Decrease respiratory rate Decrease tidal volume
Adjust flow rate for quicker Increase sedation
inspiratory rate
Adjust I:E ratio

Trouble shooting the vent

• If you are concern for acute respiratory
distress syndrome (ARDS)
– Correlate clinically with HPI and radiologic findings
of diffuse patchy infiltrate on CXR
– Obtain a PaO2/FiO2 ratio (if < 200 likely ARDS)
– Begin ARDSnet protocol:
• Low tidal volumes
• Increase PEEP rather than FiO2
• Consider increasing sedation to promote synchrony
with ventilator

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Low Minute Volume Alarm

• Usually caused by:

– Apnea of your patient (CPAP)
– Disconnection of the patient from the
ventilator

– You can attempt to quickly fix the

problem
– Bag the patient and call for your
RT/MD.

Accidental Extubation
• Role of the Nurse:

– Ensure the BVM is attached to the oxygen

flow meter and it is on!
– Attach the face mask to the BVM and after
ensuring a good seal on the patient’s face;
supply the patient with ventilation.

– Bag the patient and call for your

RT/MD.

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OTHER

• Anytime you have concerns, alarms,

ventilator changes or any other
problem with your ventilated
patient.

–Call for your RT/MD

–NEVER hit the silence button!

Mechanically ventilated with ETT or

VAP Tracheostomy tube
Prolonged MV - MV > 48 hours
. Number of intubations, reintubations
A nosocomial pneumonia that occurs NGT or Orogastric tube
at 1.
least Device
2 days afterrelated
a patient is Use of humidifier
Most plausible mechanism and
intubated (CDC GUIDELINES)
source:
Now 2.Leakage
Health
considered care
a PREVENTABLE
around the ETT cuff Improper hand washing
HEALTHCARE ERROR
personnel related
(primary route)… aspiration of Failure to change gloves between
bacteria of the ET-tubes leads
The presence contacts with pts
to3.VAP Host
High theofrelated
rate
(not the oropharyngeal or
ventilator) Failure to wear personal protective
tracheobronchial colonization equipment when required
(gram neg bacilli)
VAP rate increases with the # of days
Bacteria
High ratefrom
on• mechanical the
ventilation
of the tongue
oropharyngeal or tracheobronchial colonization (gram neg bacilli)
Bacteriafrom
• Bacteria fromthe environment:
tongue
caregivers’
Medical
Mortality /varies hand,
surgical air, water,
disease,
according the dust
toImmunosuppression,
type Malnutrition (Alb<2.2g/dl)
Contaminated
ofAdvanced
organisms age equipment
Pt’s (ventilator tubing, aerosol, etc.)
position (supine)
, Suctioning
delirium, coma equipment
Multi-resistant organisms have a
Medications
higher mortality– sedation, steroids, previous antibiotic use, NM blockers
Number of intubations- reintubations

Critical Care Med 2012 vol.40, no. 118

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VAP DIAGNOSIS-CPIS

VAP BUNDLE
1. Elevation of HOB to between 30-
45° (RN / RT)
2. Daily sedative interruption and
daily assessment of readiness to
extubate (RN / RT /MD)
3. DVT prophylaxis (MD / RN /
Pharmacy)
4. Stress ulcer disease prophylaxis –
including initiation of safe enteral
nutrition within 24-48 hours of ICU
admission (MD / RN / Pharmacy)
5. Daily oral care and
decontamination with
Chlorhexidine (added in 2010) (RT /
RN / MD)

Munro & Ruggiero,

AACN Advanced Critical Care (2014), 25(2): 163-175

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Additional Evidence-Based Component of Care:

HANDWASHING

• Single most important and

easiest method for reducing
the transmission of pathogens
• Waterless antiseptic:
acceptable and may increase
compliance

Libatkan pasien

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HOB 30-45°
Adverse efffects
• HOB 30-45° unless Meta analysis: 45° :
venous stasis,
contraindicated hemodynamic
instability-
• Especially inconclusive

recommended for
Neuro population 
• To prevent aspiration
during enteral feeding

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Daily sedative interruption and daily assessment of readiness to

extubate

OVERSEDATION
predisposes pts to: OVERSEDATION predisposes
pts to:
• Thromboemboli
• Pressure ulcers • Difficulty in monitoring
• Gastric neuro status
regurgitation and • Increased use of diagnostic
aspiration procedures
• VAP
• Increased ventilator days
• Sepsis
• Prolonged ICU and Hospital
stay

Daily Wake-up
• Every pt must be awakened
daily unless contraindicated
• Daily weaning assessments
reduce the duration of MV
• If pt becomes symptomatic
– rebolus and restart
infusion at lower dose than
original dose
• Goal is to decrease
sedation

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Stress Ulcer Prophylaxis

• Sucralfate, H2
receptor blocker and
proton pump
inhibitor – increases
gastric ph and
minimize bacterial
colonization and
reduces risk of VAP

Enteral Feedings
• Initiation of safe
enteral nutrition within
24-48 hours of ICU
admission
• Early initiation
decreases bacterial
colonization
• HOB 30-45°
• Routinely + PRN
verification tube
placement

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Additional Evidence-Based
Component of Care:
Deep venous
thrombosis (DVT)
prophylaxis (unless
contraindicated)
• TED stockings
• SCD machine
• Heparin S/C

Deep venous Thrombosis Prophylaxis

and early mobility practices
• Pt turning every
2hours increase
pulmonary drainage
and decreases risk VAP
• Early mobilization:
improves muscle pump

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Daily Oral care

• Oral assessment every
shift
• Brushing teeth, tongue
and gums with a soft
toothbrush (minimally
twice daily)
• Swabs are not effective
at removing plaques

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Daily Oral care

• Moisturizing agent for
mouth
• Antiseptic rinse
• Chlorhexidine
decontamination of
mouth

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Daily Oral care

• Routine suctioning of Suction oropharyngeal secretions Q 2hours,
before repositionning, before suctionning
mouth to manage oral ETT, before mobilizing patient and PRN
secretions and Gently follow tongue to suction back of
throat
minimize risk of Use yankauer suction
aspiration

Oral suction devices (Yankauer)

Follow policy for use and storage
?Harbor potentially pathogenic
bacteria within 24 hours
Date and change Q day
Rinse with sterile water after each use
Allow to air dry

ET Tube Care
• Cuff pressure
(between 20-30cm
H2O)

• Oral intubation
preferred
• Pengaman ETT

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ET Tube Care
• Continuous or intermittent sub-glottic
aspiration
• Avoid unnecessary
disconnection of MV
circuit

Prevent micro-aspiration of secretions

• 100-150ml of oral
secretion can
accumulate in patient
mouth in 24hrs
• Mouth can colonize as
quickly as 24hr after
admission
• Intermittent and
continuous subglottic
suctioning
• Suctioning of the mouth
before position change

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• Integrated suction
line
Subglottal Suctioning • Increased pressure
distribution and
effective sealing
Should be done using a
14 French sterile
suction catheter
• Prior to ETT
suctionning
• Prior to pt change of
position
Subglottic
secretions
• Prior to extubation
* Continuous subglottic
ETT with dedicated
lumen above cuff may
reduce risk of VAP

ET Tube Care
• Open vs close
suctioning… benefits
is not demonstrated
yet

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Prevent contamination of equipment

• Heat and moisture
exchangers (green filters)
are preferred over
humidifiers (CDC B-II)

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Prevent contamination of equipment

• Ventilator tubing
• Be careful with the
tubing of the
ventilator when you
suction patient…
• Remove
contaminated
condensate from
ventilator circuit
(CDC, A-II)

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Evaluasi-monitoring
• Look at the patient
• Listen to the patient
• SpO2–SaO2
• AnalisaGas Darah
• End Tidal CO2
• CXR
• Ventilator : PIP, VT, exp, Alarm.

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Physical examination &

image
• HR
– Tachycardia or bradycardia in
hypoxia patient
• BP
– Hypoxia, hypercapnia, changes in
circulating blood volume
• Inspection (symmetric?)
• Auscultation
• Chest X-Ray
• Ultra sound
– Fluid
– Heart function

Waveforms Analysis
• Scalars are waveform representations of pressure,
flow or volume on the y axis vs time on the x axis
• Loops are representations of pressure vs
volume or flow vs volume

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Scalar Waveforms

Loop

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Common problems
that can be diagnosed
by analyzing
Ventilator waveforms

Abnormal ventilatory Patient-ventilator

Ventilatory circuit related
Parameters/ Interactions E.g. problems
lung mechanics E.g.. flow starvation,
E.g. auto cycling and
Overdistension, Auto Double triggering, Secretion build up in the
PEEP Wasted efforts
Ventilatory circuit
COPD Active expiration

Lung Mechanics
• Use Scalar
• Pressure Time Waveform with a square wave
flow pattern

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Recognizing Lung Overdistension

Flow-time waveform
• Flow-time waveform has both an inspiratory and an expiratory
arm.

• The shape of the expiratory arm is determined by:

– the elastic recoil of the lungs
– the airways resistance
– and any respiratory muscle effort made by the patient during
expiration (due to patient-ventilator interaction/dys=synchrony)

• It should always be looked at as part of any waveform analysis

and can be diagnostic of various conditions like COPD, auto-
PEEP, wasted efforts, overdistention etc.

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Recognizing lung overdistension

Suspect this when:

There are high peak and plateau

Pressures…

Accompanied by high expiratory

flow rates

PEARL: Think of
low lung compliance (e.g. ARDS),
excessive tidal volumes,
right mainstem intubation etc

The Stress Index

• In AC volume ventilation using a
constant flow waveform observe the
pressure time scalar. flow

• Normal, linear change in airway

pressure Stress index =1
Paw

• Upward concavity indicates decreased

compliance and lung overdistension
Stress index > 1

• Downward concavity indicates

increased compliance and potential
alveolar recruitment
Stress index < 1

time
Note: Patient effort must be absent

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The Stress Index

Pressure-volume loop

Compliance (C)
is markedly reduced in the
injured lung on the right as
compared to the normal lung
Normal
on the left
lung

Upper inflection point (UIP)

above this pressure,
additional alveolar recruitment
requires disproportionate
increases in applied
airway pressure
ARDS

Lower inflection point (LIP)

Can be thought of as the
minimum baseline pressure
(PEEP)
needed for optimal
alveolar recruitment

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Overdistension

Peak
inspiratory
pressure

Upper
inflection
point

Note: During normal ventilation the LIP cannot be assessed due to the effect of
the inspiratory flow which shifts the curve to the right

Recognizing Auto-PEEP

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Dynamic Hyperinflation (Gas Trapping)

• Dynamic hyperexpansion, defined as premature
termination of exhalation, often occurs when respiratory
• rate, inspiratory time, or both have been increased.
By not permitting exhalation to finish, an increase in mean
• airway pressure results.
• Gas trapping may occur leading to an elevation in PCO2.
Careful attention must be paid to dynamic hyperexpansion
in patients with obstructive lung disease whose long time
constants and slow emptying can result in progressive air
trapping, hypercarbia, and eventually decreased cardiac
output.

Expiratory flow continues and fails to return to the

baseline prior to the new inspiratory cycle

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Detecting Auto-PEEP

Recognize
Auto-PEEP
when

Expiratory flow continues

and fails to return to
the baseline prior to the new
inspiratory cycle

The development of auto- PEEP over several

breaths in a simulation

Notice how the expiratory flow fails

to return to the baseline indicating
air trapping (AutoPEEP)

Also notice how air trapping causes

an increase in airway pressure due
to increasing end expiratory
pressure and end inspiratory
lung volume.

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Understanding how flow rates affect I/E ratios and

the development of auto PEEP

Decreasing the flow rate

Increase the inspiratory time

and consequently decrease the
expiratory time
(decreased I/E ratio)

Thus allowing incomplete emptying

of the lung and the development of
air trapping and auto-PEEP

Lluis Blanch MD, PhD et al: Respiratory Care Jan 2005 Vol 50 No 1

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Understanding how inspiratory time affect I/E

ratios and the development of auto-PEEP

• In a similar fashion, an increase in inspiratory time

can also cause a decrease in the I: E ratio and favor
the development of auto-PEEP by not allowing
enough time for complete lung emptying between
breaths.

Recognizing Expiratory Flow

Limitation
(e.g. COPD, asthma)

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Recognizing prolonged expiration (air trapping)

Recognize
airway obstruction
when

Expiratory flow quickly tapers off

and then enters a prolonged
low-flow state without returning to
baseline (auto- PEEP)

This is classic for the flow

limitation and decreased lung
elastance characteristic of COPD
or status asthmaticus

PATIENT-VENTILATOR INTERACTIONS

Wasted efforts
Double triggering
Flow starvation
Active expiration

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Ventilator Dyssynchrony: Inaccurate Sensing

of Patient’s Effort
• Many modern ventilators sense patient effort
– by detecting decreases in airway pressure or
– flow between the inspiratory and expiratory limbs of the circuit.
• Inadequate sensing of patient effort leads to tachypnea, increased
work of breathing, ventilator dyssynchrony, and patient discomfort.
• Flow triggering is often used in children, as it is very sensitive to
patients with minimal respiratory effort and small endotracheal
tubes.
•
Dyssynchrony also occurs when an air leak leads to loss of PEEP,
• resulting in excessive ventilator triggering (auto cycling).
The unstable pressure baseline that occurs due to leak may be
misinterpreted as patient effort by the ventilator.

Recognizing ineffective/wasted patient effort

Patient inspiratory effort

fails to trigger vent
resulting in a wasted effort

Results in fatigue, tachycardia,

increased metabolic needs,
fever etc

Causes: High AutoPEEP,

respiratory muscle weakness,
inappropriate sensitivity settings

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Recognizing double triggering

High peak airway
pressures and
double the inspiratory
volume

Continued patient inspiratory effort

through the end of a delivered
breath causes the ventilator to trigger again
and deliver a 2nd breath immediately after
the first breath.

This results in high lung volumes and pressures.

Causes: patient flow or volume demand exceeds

ventilator settings
Consider: Increasing tidal volume, switching
modes i.e. pressure support, increasing sedation
or neuromuscular paralysis as appropriate

Ventilator Dyssynchrony: Inadequate Ventilatory

Support
• Inadequate ventilatory support occurs when patient effort is not
satiated by the inspiratory flow of the mechanical breath.
• As a result, patients attempt to initiate breaths during a mechanical
breath.
• This phenomenon is seen as a reduction of airway pressure, seen as
a decrease in airway pressure tracing during inspiration (flow
• dyssynchrony).
In volume-limited ventilation a reduction of the inspiratory pressure
as a result of dyssynchronous patient effort can translate into a
• higher PIP.
Titration of flow rate, decreasing inspiratory time, or changing the
mode of ventilation can help meet a patient’s inspiratory demand.

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Another example of double triggering

Recognizing flow starvation

Look at the pressure-time

waveform

If you see this kind of

scooping or distortion instead
of a smooth rise in the
pressure curve….

Diagnose flow starvation

in the setting of patient
discomfort, fatigue,
dyspnea, etc on the vent

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Recognizing active expiration

Look at the flow-time

& pressure-time
waveform

Notice the high and variable

expiratory flow rates due to
varying expiratory muscle effort

The patient’s active expiratory efforts

during the inspiratory
phase causes a pressure spike.

PEARL: This is a high drive state where increased sedation/paralysis and mode
change may be appropriate for lung protection.

Recognizing
Airway Secretions
&
Ventilator Auto-Cycling

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Recognizing airway or tubing secretions

Flow volume loop
Normal flow-volume showing a ‘saw tooth’
loop pattern typical of
retained secretions

Characteristic scalars due to secretion

build up in the tubing circuit

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Recognizing ventilator auto-cycling

• Think about auto-cycling when
– the respiratory rate increases suddenly without any patient input and
– if the exhaled tidal volume and minute ventilation suddenly decrease.
• Typically occurs because of a leak anywhere in the system starting
from the ventilator right up to the patients lungs
– e.g. leaks in the circuit, ET tube cuff leak, lungs (pneumothorax)
• May also result from condensate in the circuit
• The exhaled tidal volume will be lower than the set parameters and
this may set off a ventilator alarm for low exhaled tidal volume, low
minute ventilation, circuit disconnect or rapid respiratory rate.

Pulse Oximetry
• A non-invasive method of measuring arterial
oxygen saturation
• Monitor sharp fall in PaO2
– Accurate in mild to moderate hypoxia
– SaO2<75%not reliable
– Other conditions
• Vasoconstriction
• Poor peripheral perfusion
• Severe hypotension
• shock

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Airway CO2 monitoring

• End-tidal pressure of CO2: PETCO2(via Endo/catheter)
• PETCO2PACO2PaCO2
– ↑: high CO2 production, alveolar hypoventilation
– ↓:hyperventilation
• When V/Q mismatch
– PETCO2high V/Q ratio unit, dead space
– PaO2low V/Q ratio unit, shunt
• In CPR patients
– Poor PETCO2 indicates poor venous return to heart

Specific Respiratory and

Hemodynamics parameters
• Tidal volume (VT), respiratory frequency (f)
and minute ventilation (VE) should be
monitored in ventilatory failure patient and
who are to be weaned off ventilator support.
• f/ VT >100 don’t wean
• VT >5 ml/kg and VC>10ml/kg wean

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Alarm
• Lakukan kaliberasi
• •Test lung
• •Setting alarm –periksa setiap 4 –6 jam
• •Periksa parameter, apakah frekwensi, volume
atau tekanan yang ditetapkan sudah sesuai.
• •Fungsi humidifier
• •Sirkuit / pipa pernapasan ( breathing circuit ):
kebocoran, timbunan air, letak.

alarm
•Butuh perhatian segera
•Lihat pasien: ABC: airway, tubing connect, dada
naik turun? Warna pasien? Saturasi?
•Pasien distress, masalah tidak ditemukan,
disconnect, ventilasi di berikan secara manual
•Jika pasien stabil, lihat ventilator

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Terimakasih

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