Ketrampilan Modalitas

Seting Gawat darurat

Opening and Maintaining an

Airway

Head tilt/Chin Lift

Modified Jaw Thrust (C-spine immobilization)
Oropharyngeal Airway (OPA)
Nasopharyngeal Airway (NPA)

Head Tilt/Chin Lift Procedure

The tongue is the most
common cause of
airway obstruction
One hand on patients
forehead, fingers of
opposite hand under
bony part of the chin
Lift the chin forward
and support the jaw,
helping to tilt the head
back

Modified Jaw Thrust

Used when possibility
of C-spine injury
exists
Grasp the angles of the
patients lower jaw
and lift with both
hands, displacing the
mandible forward
If the lips close, retreat
the lower lip with
thumb

Oral Airways
are designed to keep the
tongue from falling back
and blocking the upper
airway
easily available in six to
nine sizes
are only used in
unresponsive patients
without a gag reflex
do not eliminate the need
to monitor airway for
patency

Oral Airway Sizing

To choose the
proper size, hold
the airway against
the side of the
patients face. It
should extend from
the corner of the
patients mouth to
the angle of the
jaw.

Oral Airway Insertion

Open mouth with cross finger
technique. Insert airway with
tip pointing up to avoid
pushing tongue backward.
Rotate airway tip slowly
downward until its curve
matches the curve of the
tongue.
The flange of the airway
should rest against the
patients lips.

Nasopharyngeal Airways
Curved, flexible rubber or plastic tubes
inserted into the patients nostril
Use on responsive patients who need an
airway assist

Nasopharyngeal Airway Sizing

Measure length from tip of patients nose to earlobe
Diameter of airway should fit patients nostril
without excessive tightness

Nasopharyngeal Airway Insertion

Lubricate with sterile,
water soluble lubricant
and insert into nostril
that appears most open
Insert until flange is
against the nostril
opening
Check to ensure flow

PAK ... BANGUN PAK ..

APAKAH BAPAK
BAIK-BAIK SAJA ?????

TOLONG !!!!
HUBUNGI DOKTER

CEK RESPON PASIEN

ADA RESPON
TIDAK ADA
RESPON

APAKAH ADA NAFAS ?

ADA NAFAS
TIDAK ADA NAFAS

Raba selama 5 detik

APAKAH TERABA NADI ?

TERABA ADA NADI

TIDAK TERABA
ADA NADI

JARI MENELUSURI BAWAH IGA

PAKAI 2 JARI

MENELUSURI SAMPAI
UJUNG TULANG DADA

LETAKAN TELAPAK TANGAN

SATUNYA DIATAS 2 JARI
TANGAN YG MENELUSURI

PERGUNAKAN PANGKAL
TELAPAK TANGAN
JARI TIDAK MENYENTUH
PASIEN

Pijat jantung dengan cara

Badan naik turun menekan
Tulang dada 4 5 cm
(pasien dewasa)

Gerakan
Naik
Turun

Lengan tetap
lurus

Pinggul dan kaki posisi

Tetap tidak bergerak

TIUP 2 KALI
PIJAT JANTUNG 30 KALI

TIUP 2 KALI
PIJAT JANTUNG 30 KALI

TIUP 2 KALI
PIJAT JANTUNG 30 KALI

TIUP 2 KALI
PIJAT JANTUNG 30 KALI

RESUSITASI
JANTUNG PARU
SATU SIKLUS

APAKAH TERABA NADI ?

TERABA NADI
TIDAK TERABA NADI

TERABA NADI
JANTUNG PASIEN BERDENYUT
HENTIKAN RESUSITASI JANTUNG PARU
POSISIKAN PASIEN DENGAN POSISI
MANTAP
PASIEN MEMERLUKAN PENANGANAN
LEBIH LANJUT
BAWA PASIEN KE PETUGAS KESEHATAN

ADA RESPON

PASIEN SADAR
PASIEN MEMERLUKAN
PEMERIKSAAN LEBIH
LANJUT
BAWA PASIEN KE
PETUGAS KESEHATAN

ADA NAFAS

PASIEN BERNAFAS DENGAN

SPONTAN
PERTAHANKAN JALAN NAFAS
TETAP TERBUKA
PASIEN MEMERLUKAN
PEMERIKSAAN LEBIH LANJUT
BAWA PASIEN KE PETUGAS
KESEHATAN

TERABA NADI
JANTUNG MASIH BERDENYUT
PERTAHANKAN JALAN NAFAS TETAP
TERBUKA
BERIKAN NAFAS BANTUAN 16 20
KALI/PERMENIT
PASIEN MEMERLUKAN PENANGANAN
LEBIH LANJUT
TETAP BERIKAN NAFAS BANTUAN BILA
MEMUNGKINKAN
BAWA KE PETUGAS KESEHATAN

KAPAN RESUSITASI
DIHENTIKAN
PASIEN ADA TANDA-TANDA SADAR :
REFLEK BATUK, NADI TERABA
BANTUAN PETUGAS KESEHATAN
DATANG ; RESUSITASI DILANJUTKAN
OLEH PETUGAS KESEHATAN
YANG MELAKUKAN RESUSITASI
KELELAHAN DAN TIDAK ADA
PENGGANTINYA
TIDAK ADA TANDA TANDA PERBAIKAN
SETELAH DILAKUKAN LEBIH DARI 30
MENIT

Pemasangan Neck Collar

Pemasangan Neck Collar

Imobilisasi Tulang Belakang

Spinal Board

Imobilisasi Tulang Belakang

Spinal Board

Imobilisasi Tulang
Belakang
Spinal Board

Imobilisasi Tulang
Belakang
Kendriks Extrication
Device

Rapid Extrication

Imobilisasi Tulang Belakang

Log Roll

Mengangkat Tandu
1. Dekati tandu dan ketahui jumlah berat yang akan kita
angkat.
2. Bila jumlah berat yang kita angkat untuk berdua sesuai dengan
kemampuan kita maka kita akan lakukan. Tetapi kalau tidak maka
kita memerlukan teman yang lain.
3 . Mulai mengangkat dengan menjaga kelurusan tulang belakang

Ada 2 Cara Untuk Mengangkat Tandu

1. Power Lift Position adalah untuk yang lemah daerah lutut dan otot quadriceps. Dimana dia hanya bisa
membengkokan lututnya setengah.
A. Letakan kaki kita pada jarak yang baik
B. Tegakan tulang belakang dan gunakan otot perut untuk menjaga kelurusan tulang belakang.
C. Pertahankan kaki tetap lurus di lantai
D. Distribusikan beban tubuh anda pada kaki dengan merata
E. Pada saat anda beridiri anda pastikan bahwa anda menjaga kelurusan tulang belakang

Cara Untuk Mengangkat Tandu

1. Pegangan Yang Kuat adalah untuk memegang pengangan strecher harus memegang dengan seimbang.

A. Gunakan gengaman yang kuat untuk menahan tekanan yang kuat Letakan kaki yang lemah pada bagian
depan
B. Letakan gengaman tangan pada jarak 10 inc (25 cm) dengan tangan yang lain.
C. Pada saat anda beridiri anda pastikan bahwa anda menjaga kelurusan tulang belakang

Cara Untuk Mengangkat Tandu

Jangan Pernah Lakukan Hal Ini !!!!

Pengangkatan Dengan Tandu

(Scoop Stretcher)
Langkah 1. Atur & sesuaikan panjang
tandu
Langkah 2. Buka pengunci tandu,
pisahkan tandu menjadi dua

Langkah 3. Secara perlahan,

posisikan belahan tandu ke bawah
pasien dengan digeser

Pengangkatan Dengan Tandu

(Scoop Stretcher)
Langkah 4. Masukkan belahan yang
satu ke bawah badan pasien; hati-hati
saat memasukkan, badan pasien sedikit
dimiringkan
Langkah 5. Pertemukan kedua belahan
dan satukan dengan cara menguncinya
Langkah 6. Angkat tandu, dengan
mengangkat pada masing-masing ujung

Selalu Jaga Kelurusan

Punggung Anda !!!

RAGAM TANDU

RAGAM TANDU

RAGAM TANDU

RAGAM TANDU

Pengangkatan Tanpa Alat

(Gawat Darurat)

Memindah
Korban
Menarik Dengan
Selimut
SELALU JAGA KELURUSAN PUNGGUNG ANDA !!!

Memindah
Korban
Menarik Lengan

Memindah
Korban
Menarik Baju

Pengangkatan Tanpa Alat

(Dari Lantai Ke Tandu)
Langkah 1. Atur tubuh pasien lurus

Langkah 2. Letakkan seluruh lengan

bawah anda di bawah badan pasien
Langkah 3. Angkat tubuh pasien di
atas paha anda
Langkah 4. Bawa tubuh korban ke
arah badan pengangkat
(Memeluk/merangkul)
Langkah 5. Kemudian pindahkan ke
tandu
SELALU JAGA KELURUSAN
PUNGGUNG ANDA!!!

Pengangkatan Tanpa Alat

(Dari Lantai Ke Tandu)
Langkah 1. Satu orang
meletakkan tangan di bawah
lengan korban & pegang
pergelangangan. Lainnya
meletakkan tangan di bawah
lutut
Langkah 2. Badan pengangkat
merunduk kemudian bersama sama berdiri lalu pindahkan
pasien ke tandu

Selalu Jaga Kelurusan

Punggung Anda !!!

Pengangkatan Tanpa Alat

(Dari Tempat Tidur Ke Tandu)
Langkah 1. Letakkan tangan dibawah
badan pasien, geser sedikit badan
korban ke arah pinggir tempat tidur
Langkah 2. Angkat dan dekap badan
korban kearah badan anda
Langkah 3. Angkat dan bawa pasien
ke tandu
Langkah 4. Letakkan pasien di atas
tandu

Selalu Jaga Kelurusan

Punggung Anda !!!

Pengangkatan Tanpa Alat

(Dari Tempat Tidur Ke Tandu)

Langkah 1. Rapatkan
tandu ke tempat tidur
Langkah 2. Raih &
pegang ujung sprei

Langkah 3. Geser
perlahan ke arah
stretcher
Langkah 4. Atur Pasien di
atas tandu
Kelurusan

Selalu Jaga
Punggung Anda !!!

The
EsophagealTracheal
Combitube
(ETC)
Class IIa

Combitube - Technique

100 ml of air
into blue cuff

Insert until teeth are

between black lines

Insert 15 ml of
air into white
cuff

Combitube - Technique
If ventilation is
inadequate
change to the
other port

Begin with
longer or port
closer to you

Its in the esothink EOA

In the tracheaits an ETT

Bag-Valve-Mask (BVM)
Ventilation
Oxygen delivery

Bag-Valve-Mask (BVM)
Ventilation
Oxygen delivery

Bag-Valve-Mask (BVM)
Ventilation
Oxygen delivery

Stylet

ET Intubation Technique
If trauma is not
suspected, place
patients head in
sniffing position
Aligns axes of mouth, pharynx,
and trachea

ET Intubation Technique
Advance the laryngoscope
blade until the distal end
reaches the base of the
tongue

ET Intubation Technique
Lift the laryngoscope to
elevate the mandible without
putting pressure on the front
teeth
Visualize the epiglottis
Suction the
laryngopharynx as
necessary
Identify the vocal cords
Place the blade in proper
position

 The straight blade is

advanced under the
epiglottis.

The blade is then lifted

anteriorly, directly
exposing the vocal cords.

ET Intubation - Complications
Bleeding
Laryngospasm

Occlusion caused by patient

biting tube or secretions
Laryngeal or tracheal edema

Vocal cord damage

Tube occlusion

Mucosal necrosis

Inability to talk

Barotrauma

Hypoxia due to prolonged or

unsuccessful intubation

Aspiration

Cuff leak

Dysrhythmias

Esophageal intubation

Trauma to lips, teeth, tongue, or

soft tissues of oropharynx

Right mainstem intubation

Increased intracranial pressure

ET Intubation - Technique
Secure ET tube with
commercial tubeholder (preferred) or
tape
Provide ventilatory
support with
supplemental oxygen
After securing the tube,
observe and record
tube depth at the
patients teeth

Confirming ET Tube Placement

Primary methods
Visualizing passage of ET tube between the vocal cords
Auscultating presence of bilateral breath sounds
Confirming absence of sounds over epigastrium during ventilation
Adequate chest rise with each ventilation
Absence of vocal sounds after placement of ET tube
Secondary methods

Monitoring for changes in the color (colorimetric device) or

number (digital device) on an end-tidal CO2 detector
Verification by an esophageal detector device
Chest x-ray

What About?
Condensation within the tube as an indicator
In this model, condensation on the inner surface of the
endotracheal tube was common after placement within
the esophagus. If these results are confirmed in human
studies, the presence of a vapor trial should not be used
as a clinical indicator of correct endotracheal tube
placement
Ann Emerg Med. 1998 May;31(5):575-8.Related Articles, Links

Use of tube condensation as an indicator of endotracheal tube

placement.

 Tube migration?
How to secure the tube?

IV FLUIDS AND VASCULAR

ACCESS DEVICES
Rick Slaven
NREMT-P Critical Care
Claiborne County EMS

Reasons for IV Infusion

Life sustaining fluids

Electrolytes
Route for medication administration
Immediate results
Predictable therapeutic effects
There are more than 200 types of
commercially prepared IV fluids

Types of Solutions

CRYSTALLOIDS
Isotonic
Hypotonic
Hypertonic

COLLOIDS
Always hypertonic

Crystalloids
Solutions with small molecules that flow
easily from the bloodstream into cells and
tissues.

Crystalloid Solutions
Isotonic solutions have a concentration of
dissolved particles equal to that of intracellular
fluid.
Hypertonic solutions have a greater concentration
of dissolved particles than does intracellular
fluid.Fluid is pulled from cells
Hypotonic solutions have less particles than does
intracellular fluid.Fluid flows into cells

SO WHAT!!!!
The wrong fluid for the wrong patient
can make a critical difference in their
outcome. Dont depend on the
physician. KNOW YOUR FLIUDS

OSMOSIS and DIFFUSION

In Osmosis, fluid
moves passively from
areas with more fluid
to areas with less fluid
FLUID MOVES

In Diffusion,
solutes(particles)
move from an area of
high concentration to
an area of lesser
concentration.
PARTICLES MOVE

ISOTONIC FLUIDS
Osmotic pressure is the same both inside
and outside the cell.
Cells neither shrink nor swell with fluid
movement.
Same tonicity as plasma

Hypotonic Solutions
Osmotic pressure is less than intracellular fluid
Water is drawn into the cells from the extracellular
fluid causing them to swell
Inappropriate use can result in increased ICP and
cardiovascular collapse from volume depletion.
May cause blood cells to burst
Volume Depletion?

Hypertonic Solutions
Osmotic pressure is greater than that of
intracellular fluid. Hypertonic solutions have a
large concentration of solutes(particles).
Water is drawn from the cells to equalize the
concentration, which causes the cells to shrink.
Inappropriate use can cause fluid overload and
pulmonary edema

Isotonic Fluids
0.9% Sodium Chloride ( Normal Saline )
Lactated Ringers
Dextrose 5% in Water (D5W)

Normal Saline
Uses

Shock
Resuscitation
Fluid challenges
Blood transfusions
Metabolic alkalosis
Hyponatremia
DKA

Special
considerations
Use with caution in
patients with heart
failure, edema, or
hypernatremia
Can lead to overload

Lactated Ringers

Uses
Dehydration
Burns
GI tract fluid loss
Acute blood loss
Hypovolemia

Special Considerations
Contains Potassium, can
cause hyperkalemia in
renal patients
Patients with liver disease
cannot metabolize lactate
Lactate is converted into
bicarb by liver

D5W
Uses
Fluid loss and
dehydration
Hypernatremia

Special Considerations
Solution becomes
Hypotonic when
dextrose is
metabolized
Do not use for
resuscitation
Use cautiously in renal
and cardiac patients

Hypotonic Solutions
0.45% Sodium Chloride (1/2 normal saline)

0.45% Sodium Chloride

Uses
Gastric fluid loss
Cellular dehydration
from excessive
diuresis
Hypertonic
dehydration
Slow rehydration

Special Considerations
Do not give to patients
at risk for ICP
Not for rapid
rehydration
Electrolyte
disturbances can occur

Hypertonic Solutions
5% Dextrose in 0.9% Sodium
Chloride(D5NS)
5% Dextrose in Lactated Ringers (D5LR)
5% Dextrose in 0.45% Sodium Chloride
(D51/2NS)

D5NS

Uses
Heat related disorders
Fresh water drowning
Peritonitis

Special Considerations
Should not be given to
patients with impaired
cardiac or renal
function
Draw blood before
administering to
diabetics

D5LR

Uses
Hypovolemic Shock
Hemorrhagic Shock
Certain cases of
acidosis

Special Considerations
Do not administer in
patients with cardiac
or renal dysfunction
Monitor for
circulatory overload

D5 1/2NS

Uses
Heat exhaustion
Diabetic disorders
TKO solution in
patients with renal or
cardiac dysfunction

Special Considerations
Not for rapid fluid
replacement

Colloids

Albumin
Plasma Protein fraction
Dextran
Hetastarch
Colloids are made up of much larger solutes
than are crystalloids

Colloids
Plasma Expander
Used if crystalloids do not improve blood
volume
Colloids pull fluid into the bloodstream,
remember they are always Hypertonic
Watch for increased BP, Dyspnea, and
bounding pulse

VASCULAR ACCESS DEVICES

Short-Term
Mid-Term
Long-Term
Tunneled or Non-Tunneled

Tunneled Vs Nontunneled
Groshong, Broviac,
and Hickman
Single or multi lumen
Tunneled through
tissue for several
inches to the
cannulated vein
Used for intermittent
or continued therapy

Single or multi lumen

Inserted
peripherally(PICC) or
centrally(central
line)directly into
vasculature
Short term
therapy(analgesics,TPN,fl
uids,meds)CVP
monitoring through distal
port

Short Term Devices

Standard IV access
Heplock or saline lock
Short term central catheters(i.e.: triple
lumen, Swan-Ganz)
Quinton catheter

Swan-Ganz Catheter
The Swan - Ganz is a long
plastic tube with several
openings.Its purpose is to
measure the pressures in
the heart and vessels going
to the lungs.After
placement, a monitor is
attached that displays
numbers and wave forms
that help to assess heart
and lung function.

 Proximal Port (Blue) - Monitors RA

pressure. Port for blood samples. Meds and
fluids.
Distal Port (Yellow) - Monitors PA
pressure. Monitors PCWP.
Thermistor Port (Square White Box) Cardiac output port.
Inflation Port (Balloon Port)

Multi Lumen Devices

Central catheters
Enter in subclavian
and are advanced into
right atrium
Used for medication
administration, blood
draws, CVP
monitoring, fluid
administration,cardiac
pacing

Quinton Catheter
Temporary
hemodialysis access
2 lumens, one for
intake and one for
venous return
Infection risk is high.

Mid-Term Devices
Peripherally Inserted Central Catheter
Mid Line Catheter

PICC
Can be single or multi
lumen.
Used for extended home
TPN
Home health care use
Administration of meds
and fluids
Used when repeated IV
sticks would be necessary

Midline Catheter
Similar to a PICC but
not a true central line
Catheter is advanced
only into the upper
arm
Not used when caustic
agents such as chemo
will be needed

Long Term Devices

Hickman-Broviac Catheter
Groshong Catheter
Implantable Venous Access Devices(Port-acath)
Hohn Catheter
Long term catheters are almost always
tunneled and the scar tissue serves to anchor
the catheter

Hickman-Broviac
Tunneled from chest wall
to subclavian vein and
continues to superior vena
cava
Good as long as line is
patented and not
infected(months-years)
Commonly used for
oncology
Broviac is smaller and
generally used in peds

Groshong
Similar to Hickman
however catheter is closed
when not in use
Requires only a saline
flush weekly
Used in patients where
heparin is undesirable due
to low platlet count
Good for long periods

Groshong

IVADs
Portacath-Inserted in the
chest below the
clavicle.Access is gained
by puncturing the skin
then the synthetic port
Permacath-Lasts
longer.Up to a year
Passport-Placed in the arm
instead of chest.Cheapest

Hohn Catheter
Similar to Hickman
but it lies just under
the insertion point
rather than up the
subcutaneous portion
of the catheter body

REMEMBER
Many of these vascular access
devices are sealed with a heparin
solution. Some contain as much as
5000U - 7500U. You can
significantly anticoagulate your
patient if this heparin is not drawn
off before administering fluids or
medications

QUESTIONS

ACLS and arrhythmias

Dr. Jason Waechter
Feb/04

ACLS

Advanced Cardiac Life Support

algorithms (plans) for organized treatment
all Canadian anesthesiologists take ACLS
good for teamwork
good for patient treatment
good for staff safety

ACLS
ACLS is mostly CPR, but with
extras:
drugs
electricity

ACLS

For ALL PATIENTS

manage airway as clinically indicated
perform CPR ALWAYS when no pulse
a non-breathing or pulseless patient will not
survive without O2 and CPR!

Dysrhythmias
Brady- or tachy- cardia

Ventricular tachycardia (VT)

Ventricular fibrillation (VF)

Asystole

Tachycardia
sudden onset of rapid heart rate
what do you do?

Tachycardia
ALWAYS CHECK THE PATIENT FIRST
1. Check for a pulse
2. Check the blood pressure
3. Make a diagnosis

Tachycardia
Case 1
On ward, sudden onset of palpitations
Does the patient have a pulse? Yes
2. What is the blood pressure? 60/20
1.

Is the patient stable or unstable?

Definition of Unstable
presence of any one of:
1.
2.
3.
4.
5.

Low blood pressure

Short of Breath
Chest pain
Lightheaded
CHF

Unstable Tachycardia
DISCLAIMER: in the OR, it is different
Bleeding unstable tachycardia
treat with a blood transfusion!!
This algorithm is for non sinus rhythm

Unstable Tachycardia

goal is to slow down rate or

convert to sinus rhythm
drugs or electrical cardioversion is used
usually cardioversion if unstable

Electrical Shock

defibrillation or
cardioversion (= synchronized)
action: resets all activity to zero
good for tachycardia (non-sinus)
good for ventricular fibrillation (VF)

Electrical Shock

defibrillation or
cardioversion (= synchronized)
NOT USED FOR:
sinus rhythm
bradycardia
asystole

Case #2
Alarm on ECG monitor makes noise!!

Case #2

Patient is awake and talking

Diagnosis?
ECG lead is disconnected
ECG shows artifact

Case #3
Alarm on ECG monitor makes noise!!

Case #2

Try to wake up. Does not wake up

Check for breathing. No breathing.
Check for pulse. No pulse.
What is the diagnosis?
What do you do?

Ventricular Fibrillation (VF)

What is the cure for VF?

DEFIBRILLATION
EARLY defib. has higher success
SHOCK SOON, SHOCK OFTEN

VF

Drugs
improve success of defibrillation (the cure)
do NOT cure VF

lidocaine
procainamide
amiodarone

VF
What is the cardiac output in VF?
Zero. There is no circulation
What MUST occur at all times?
CPR unless defib. is happening.
How do you manage ventilation?
bag-mask and early intubation

VF Summary

Start CPR and only stop to shock

Intubate
Defibrillation is the most important!!!
Drug
shock
drug
shock

VF Easy Algorythm:
CPR

Shock, shock, shock

Drug
Shock
Drug
Shock
Drug
Shock

Case #4
BP 60/30

Diagnosis?
Treatment?

Case #4: Sinus Bradycardia

Treatment: increase heart rate!
Methods:
1. atropine (probably successful)
2. pacing (thoracic skin paddles)
3. dopamine infusion

Case #5
BP 60/30

Diagnosis?
Treatment?

3rd Degree Block (Bradycardia)

Treatment: increase heart rate!
Methods:
1. atropine (probably NOT successful)
2. pacing (thoracic skin paddles)
3. dopamine infusion

Questions?

Note: ACLS in Canada is mandatory

ACLS saves lives
You must learn the algorithms

Another Case report!

70 yr. old woman for neurosurgery

hx. of asthma, and HTN
Hb 13.0 pre-op

And this is the ECG:

after 3 hours, blood loss is 500 cc.
BP is 90/50 and HR 94

What is your diagnosis?

How will you treat it?

Ischemia = supply < demand

decrease HR
increase BP
check Hb

Phenylephrine 100g given

Fluid IV given (500 cc)

And this is the ECG:

4 minutes later

ST Segments are almost normal

The Hb was 10.1
Liandiolol infusion started

ABG INTERPRETATION
Marc D. Berg, MD DeVos Childrens Hospital
Rita R. Ongjoco, DO Sinai Hospital of Baltimore

ABG Interpretation
First, does the patient have an acidosis or an
alkalosis
Second, what is the primary problem
metabolic or respiratory
Third, is there any compensation by the
patient respiratory compensation is
immediate while renal compensation takes
time

ABG Interpretation
It would be extremely unusual for either the
respiratory or renal system to
overcompensate
The pH determines the primary problem
After determining the primary and
compensatory acid/base balance, evaluate
the effectiveness of oxygenation

Normal Values
pH 7.35 to 7.45
paCO2 36 to 44 mm Hg
HCO3 22 to 26 meq/L

Abnormal Values
pH < 7.35
Acidosis (metabolic
and/or respiratory)
pH > 7.45
Alkalosis (metabolic
and/or respiratory)
paCO2 > 44 mm Hg
Respiratory acidosis
(alveolar hypoventilation)

paCO2 < 36 mm Hg
Respiratory alkalosis
(alveolar hyperventilation)
HCO3 < 22 meq/L
Metabolic acidosis
HCO3 > 26 meq/L
Metabolic alkalosis

Putting It Together - Respiratory

So
paCO2 > 44 with a pH < 7.35 represents a respiratory
acidosis
paCO2 < 36 with a pH > 7.45 represents a respiratory
alkalosis
For a primary respiratory problem, pH and paCO2
move in the opposite direction
For each deviation in paCO2 of 10 mm Hg in either
direction, 0. 08 pH units change in the opposite
direction

Putting It Together - Metabolic

And
HCO3 < 22 with a pH < 7.35 represents a
metabolic acidosis
HCO3 > 26 with a pH > 7.45 represents a
metabolic alkalosis
For a primary metabolic problem, pH and
HCO3 are in the same direction, and paCO2
is also in the same direction

Compensation
The bodys attempt to return the acid/base
status to normal (i.e. pH closer to 7.4)
Primary Problem Compensation
respiratory acidosis metabolic alkalosis
respiratory alkalosis metabolic acidosis
metabolic acidosis
respiratory alkalosis
metabolic alkalosis respiratory acidosis

Expected Compensation
Respiratory acidosis
Acute the pH decreases 0.008 units for
every 1 mm Hg increase in paCO2; HCO3
0.1-1 mEq/liter per 10 mm Hg paCO2
Chronic the pH decreases 0.003 units for
every 1 mm Hg increase in paCO2; HCO3
1.1-3.5 mEq/liter per 10 mm Hg paCO2

Expected Compensation
Respiratory alkalosis
Acute the pH increases 0.008 units for
every 1 mm Hg decrease in paCO2; HCO3
0-2 mEq/liter per 10 mm Hg paCO2
Chronic - the pH increases 0.017 units for
every 1 mm Hg decrease in paCO2; HCO3
2.1-5 mEq/liter per 10 mm Hg paCO2

Expected Compensation
Metabolic acidosis
paCO2 = 1.5(HCO3) + 8 (2)
paCO2 1-1.5 per 1 mEq/liter HCO3
Metabolic alkalosis
paCO2 = 0.7(HCO3) + 20 (1.5)
paCO2 0.5-1.0 per 1 mEq/liter HCO3

Classification of primary acid-base

disturbances and compensation
Acceptable ventilatory and metabolic acid-base
status
Respiratory acidosis (alveolar hypoventilation) acute, chronic
Respiratory alkalosis (alveolar hyperventilation) acute, chronic
Metabolic acidosis uncompensated,
compensated
Metabolic alkalosis uncompensated, partially
compensated

Acute Respiratory Acidosis

paCO2 is elevated and pH is acidotic
The decrease in pH is accounted for entirely
by the increase in paCO2
Bicarbonate and base excess will be in the
normal range because the kidneys have not
had adequate time to establish effective
compensatory mechanisms

Acute Respiratory Acidosis

Causes
Respiratory pathophysiology - airway
obstruction, severe pneumonia, chest
trauma/pneumothorax
Acute drug intoxication (narcotics, sedatives)
Residual neuromuscular blockade
CNS disease (head trauma)

Chronic Respiratory Acidosis

paCO2 is elevated with a pH in the
acceptable range
Renal mechanisms increase the excretion of
H+ within 24 hours and may correct the
resulting acidosis caused by chronic
retention of CO2 to a certain extent

Chronic Respiratory Acidosis

Causes

Chronic lung disease (BPD, COPD)

Neuromuscular disease
Extreme obesity
Chest wall deformity

Acute Respiratory Alkalosis

paCO2 is low and the pH is alkalotic
The increase in pH is accounted for entirely
by the decrease in paCO2
Bicarbonate and base excess will be in the
normal range because the kidneys have not
had sufficient time to establish effective
compensatory mechanisms

Respiratory Alkalosis
Causes

Pain
Anxiety
Hypoxemia
Restrictive lung
disease
Severe congestive
heart failure
Pulmonary emboli

Drugs
Sepsis
Fever
Thyrotoxicosis
Pregnancy
Overaggressive
mechanical ventilation
Hepatic failure

Uncompensated Metabolic
Acidosis
Normal paCO2, low HCO3, and a pH less
than 7.30
Occurs as a result of increased production
of acids and/or failure to eliminate these
acids
Respiratory system is not compensating by
increasing alveolar ventilation
(hyperventilation)

Compensated Metabolic Acidosis

paCO2 less than 30, low HCO3, with a pH
of 7.3-7.4
Patients with chronic metabolic acidosis are
unable to hyperventilate sufficiently to
lower paCO2 for complete compensation to
7.4

Elevated AG
Metabolic Acidosis
Causes
Ketoacidosis - diabetic, alcoholic, starvation
Lactic acidosis - hypoxia, shock, sepsis,
seizures
Toxic ingestion - methanol, ethylene glycol,
ethanol, isopropyl alcohol, paraldehyde,
toluene
Renal failure - uremia

Normal AG Metabolic Acidosis

Causes
Renal tubular acidosis
Post respiratory
alkalosis
Hypoaldosteronism
Potassium sparing
diuretics
Pancreatic loss of
bicarbonate

Diarrhea
Carbonic anhydrase
inhibitors
Acid administration
(HCl, NH4Cl, arginine
HCl)
Sulfamylon
Cholestyramine
Ureteral diversions

Effectiveness of Oxygenation
Further evaluation of the arterial blood gas
requires assessment of the effectiveness of
oxygenation of the blood
Hypoxemia decreased oxygen content of blood paO2 less than 60 mm Hg and the saturation is less
than 90%
Hypoxia inadequate amount of oxygen available
to or used by tissues for metabolic needs

Mechanisms of Hypoxemia
Inadequate inspiratory partial pressure of
oxygen
Hypoventilation
Right to left shunt
Ventilation-perfusion mismatch
Incomplete diffusion equilibrium

Assessment of Gas Exchange

Alveolar-arterial O2 tension difference
A-a gradient
PAO2-PaO2
PAO2 = FIO2(PB - PH2O) - PaCO2/RQ*

arterial-Alveolar O2 tension ratio

PaO2/PAO2

arterial-inspired O2 ratio
PaO2/FIO2
P/F ratio
*RQ=respiratory quotient= 0.8

Assessment of Gas Exchange

Low FIO2
Alveolar hypoventilation
Altered gas exchange
Regional V/Q mismatch
Intrapulmonary R to L shunt
Impaired diffusion
Anatomical R to L shunt
(intrapulmonary or intracardiac)
* N=normal

ABG
PaO2

PaCO2

A-a grad
RA
100%
N*
N
N
N

/N/
N/
N/

N/

N/

Summary
First, does the patient have an acidosis or an
alkalosis
Look at the pH

Second, what is the primary problem metabolic

or respiratory
Look at the pCO2
If the pCO2 change is in the opposite direction of the
pH change, the primary problem is respiratory

Summary
Third, is there any compensation by the
patient - do the calculations
For a primary respiratory problem, is the pH
change completely accounted for by the change
in pCO2
if yes, then there is no metabolic compensation
if not, then there is either partial compensation or
concomitant metabolic problem

Summary
For a metabolic problem, calculate the expected
pCO2
if equal to calculated, then there is appropriate
respiratory compensation
if higher than calculated, there is concomitant
respiratory acidosis
if lower than calculated, there is concomitant
respiratory alkalosis

Summary
Next, dont forget to look at the
effectiveness of oxygenation, (and look at
the patient)
your patient may have a significantly increased
work of breathing in order to maintain a
normal blood gas
metabolic acidosis with a concomitant
respiratory acidosis is concerning

Case 1
Little Billy got into some of dads
barbiturates. He suffers a significant
depression of mental status and respiration.
You see him in the ER 3 hours after
ingestion with a respiratory rate of 4. A
blood gas is obtained (after doing the
ABCs, of course). It shows pH = 7.16,
pCO2 = 70, HCO3 = 22

Case 1
What is the acid/base abnormality?
1. Uncompensated metabolic acidosis
2. Compensated respiratory acidosis
3. Uncompensated respiratory acidosis
4. Compensated metabolic alkalosis

Case 1
Uncompensated respiratory acidosis
There has not been time for metabolic
compensation to occur. As the barbiturate
toxicity took hold, this child slowed his
respirations significantly, pCO2 built up in
the blood, and an acidosis ensued.

Case 2
Little Suzie has had vomiting and diarrhea for
3 days. In her moms words, She cant
keep anything down and shes runnin out.
She has had 1 wet diaper in the last 24
hours. She appears lethargic and cool to
touch with a prolonged capillary refill time.
After addressing her ABCs, her blood gas
reveals: pH=7.34, pCO2=26, HCO3=12

Case 2
What is the acid/base abnormality?
1. Uncompensated metabolic acidosis
2. Compensated respiratory alkalosis
3. Uncompensated respiratory acidosis
4. Compensated metabolic acidosis

Case 2
Compensated metabolic acidosis
The prolong history of fluid loss through diarrhea
has caused a metabolic acidosis. The mechanisms
probably are twofold. First there is lactic acid
production from the hypovolemia and tissue
hypoperfusion. Second, there may be significant
bicarbonate losses in the stool. The body has
compensated by blowing off the CO2 with
increased respirations.

Case 3
You are evaluating a 15 year old female in the ER who was brought in by
EMS from school because of abdominal pain and vomiting. Review of
system is negative except for a 10 lb. weight loss over the past 2
months and polyuria for the past 2 weeks. She has no other medical
problems and denies any sexual activity or drug use. On exam, she is
alert and oriented, afebrile, HR 115, RR 26 and regular, BP 114/75,
pulse ox 95% on RA. Exam is unremarkable except for mild
abdominal tenderness on palpation in the midepigastric region and
capillary refill time of 3 seconds. The nurse has already seen the
patient and has sent off routine blood work. She hands you the
result of the blood gas. pH = 7.21 pCO2= 24 pO2 = 45 HCO3 = 10
BE = -10 saturation = 72%

Case 3
What is the blood gas interpretation?
Uncompensated respiratory acidosis with severe
hypoxia
Uncompensated metabolic alkalosis
Combined metabolic acidosis and respiratory
acidosis with severe hypoxia
Metabolic acidosis with respiratory compensation

Case 3
Metabolic acidosis with respiratory compensation
This is a patient with new onset diabetes mellitus
in ketoacidosis. Her pulse oximetry saturation and
clinical examination do not reveal any respiratory
problems except for tachypnea which is her
compensatory mechanism for the metabolic
acidosis. The nurse obtained the blood gas sample
from the venous stick when she sent off the other
labs.