Objectives
Mechanics of
breathing
Modes of ventilation
Mechanical ventilation
ABG interpretation
Mechanics of breathing
Spontaneous Breathing
Positive Pressure Breath
Overview of the respiratory system
What is the pathway that air follows?
Nose
Pharynx
Larynx
Trachea
Bronchus
Bronchioles
Alveoli
The nose
Opens at the nostrils/nares and leads into the
nasal cavities
Hairs and mucus in the nose filters the air
The nasal cavity has lot of capillaries that warm
and moisten the air
Specialized cells act as odor receptors
Tear glands drain into the nasal cavities that can
lead to a runny nose
The larynx
Triangular, cartilaginous
structure that passes air
between the pharynx
and trachea
Called the voice box and
houses vocal cords
There are 2 mucosal folds
that make up the vocal
cords with an opening in
the middle called the
glottis
The trachea
A tube, often called
the windpipe, that
connects the larynx
with the 1° bronchi
Made of connective
tissue, smooth muscle
and cartilaginous
rings
Lined with cilia and
mucus that help to
keep the lungs clean
The bronchial tree
Starts with two main bronchi that
lead from the trachea into the lungs
The bronchi continue to branch until
they are small bronchioles about
1mm in diameter with thinner walls
Bronchioles eventually lead to
elongated sacs called alveoli
The lungs
The bronchi, bronchioles and alveoli
beyond the 1° bronchi make up the lungs
The right lung has 3 lobes while the left
lung has 2 lobes that divide into lobules
Each lung is enclosed by membranes called
pleura
The alveoli
~ 300 million in the lungs
that greatly increase
surface area
Alveoli are enveloped by
blood capillaries
The alveoli and
capillaries are one layer
of epithelium to allow
exchange of gases
Alveoli are lined with
surfactant that act as a
film to keep alveoli open
Two phases of breathing/ventilation
1. Inspiration – an active process of
inhalation that brings air into the lungs
2. Expiration – usually a passive process of
exhalation that expels air from the
lungs
Inspiration
The diaphragm and
intercostal muscles
contract
The diaphragm flattens
and the rib cage moves
upward and outward
Volume of the thoracic
cavity and lungs increase
The air pressure within the
lungs decrease
Air flows into the lungs
Expiration
The diaphragm and
intercostal muscles relax
The diaphragm moves upward
and becomes dome-shape
The rib cage moves downward
and inward
Volume of the thoracic cavity
and lungs decrease
The air pressure within the
lungs increases
Air flows out of the lungs
How is breathing chemically controlled
Chemical control:
–2 sets of chemoreceptors sense the drop
in pH: one set is in the brain and the
other in the circulatory system (carotid
bodies at the bifurcation of the carotid artery, and the
central chemoreceptors located in the ventral medulla)
–Both are sensitive to carbon dioxide
levels that change blood pH due to
metabolism
Mechanical ventilation(MV)
Historical background
Modes of MV
History of MV
Andreas Wesele Veaslius: 1555
–“An opening must be attempted in the trunk of the
trachea, into which a reed or cane should be put; you
will then blow into this, so the lung may rise again
and the animal take in air.”
Heinrich Drager 1907:
Pulmotor
“The way our world will look in the
future is something that will not be
determined tomorrow, but today. “
Heinrich Dräger
Drinker & Shaw Tank
Ventilator
First widely used negative pressure
ventilator: 1929
Metal Cylinder covered patient up to
neck
Vacuum pump created negative
pressure in chamber which elevated
patient’s chest
At end of breath, pressure returned to
zero, and passive exhalation
Iron Lung
Origins of mechanical ventilation
The iron lung created negatie pressure in abdomen as well as the chest,
decreasing cardiac output.
Iron lung polio ward at Rancho Los Amigos
Hospital in 1953.
•With development of
endotracheal tubes with high
volume low pressure cuffs,
PPV replaced the iron lung.
•Invasive ventilation first used
at Massachusetts Hospital -
1955.
•The modern era of intensive
care medicine began with
positive-pressure ventilation.
Principles of Positive pressure
ventilation
Following an inspiratory trigger, a
predetermined mixture of air is forced into
the central airways and then flows into the
alveoli.
A termination signal eventually causes the
ventilator to stop forcing air into the central
airways and the central airway pressure
decreases.
Expiration follows passively, with air flowing
from the higher pressure alveoli to the lower
pressure central airways.
Types of breaths
Volume control
Volume assist
Pressure control
Pressure assist
Pressure support
Volume control
Breaths are ventilator-initiated breaths
with a set inspiratory flow rate.
Inspiration is terminated once the set
tidal volume has been delivered.
Airway pressure is determined by the
airways resistance, lung compliance,
and chest wall compliance.
Volume assist
Breaths are patient-initiated breaths
with a set inspiratory flow rate.
Inspiration is terminated once the set
tidal volume is reached
Airway pressure is determined by
airway resistance, lung and chest
compliance
Minimum minute ventilation is set
Pressure control
Breaths are ventilator-initiated breaths
with a pressure limit. Inspiration is
terminated once the set inspiratory
time has elapsed.
The tidal volume is variable and related
to compliance, airway resistance, and
tubing resistance.
A consequence of the variable tidal
volume is that a specific minute
ventilation cannot be guaranteed.
Pressure assist
Breaths are patient-initiated breaths with a
pressure limit. Inspiration is terminated once
the set inspiratory time has elapsed.
The tidal volume is variable and related to
compliance, airway resistance, and tubing
resistance
A consequence of the variable tidal volume is
that a specific minute ventilation cannot be
guaranteed.
Tidal volume
The optimal tidal volume for patients
who are mechanically ventilated for
reasons other than ALI/ARDS is
unknown
6-10ml/kg
Ventilation with lower tidal volumes as compared with traditional tidal
volumes for acute lung injury and the acute respiratory distress syndrome.
The Acute Respiratory Distress Syndrome Network.N Engl J Med. 2000
Respiratory rate(RR)
For AC the RR is set four breaths
per minute below the patient's
native rate
For SIMV the RR is set to ensure
that at least 80 percent of the
patient's total minute ventilation
is delivered by the ventilator
Monitor for auto-PEEP as the respiratory
rate is increased
In an observational study of 14 patients
receiving low tidal volume ventilation,
increasing the respiratory rate was
associated with development of a mean
auto-PEEP of 6 cmH2O
Increasing respiratory rate to improve CO2 clearance during mechanical ventilation is not a panacea
in acute respiratory failure.Vieillard-Baron A, Prin S, Augarde R, Desfonds P, Page B, Beauchet A,
Jardin F
Crit Care Med. 2002;30(7):1407
PEEP
Role is generally to mitigate
end-expiratory alveolar collapse
Initial applied PEEP is 5 cmH2O
Adverse effects includes reduced
preload, increases intracranial pressure
and plateau pressures
PEEP
Fraction of inspired oxygen (FiO2)
The lowest possible (FiO2) necessary to meet
oxygenation goals should be used.
This will decrease the likelihood that adverse
consequences of supplemental oxygen will
develop, such as absorption atelectasis,
accentuation of hypercapnia, airway injury, and
parenchymal injury.
Typical oxygenation goals include an arterial
oxygen tension (PaO2) above 60 mmHg and an
oxyhemoglobin saturation (SpO2) above 90%.
In patients with ALI/ARDS, targeting a PaO2 of 55
to 80 mmHg and a SpO2 of 88 to 95 percent is
acceptable
CMV
Minute ventilation is determined
entirely by the set RR and TV.
This may be due to pharmacologic
paralysis, heavy sedation, coma,
or lack of incentive to increase the
minute ventilation
Control Mode
AC
Minimal minute ventilation is
predetermined by setting the RR and
TV.
Patient can increase the MV by
triggering additional breaths.
Each patient-initiated breath receives
the set tidal volume from the
ventilator.
Assist/Control
SIMV
Ventilator breaths are synchronized
with patient’s inspiratory effort
Clinician determines the minimal
minute ventilation
Patients increase the minute
ventilation by spontaneous
breathing, rather than patient-
initiated ventilator breaths.
IMV – Intermittent
Mandatory Ventilation
PRESSURE-LIMITED VENTILATION
Clinician must set the inspiratory pressure level,
I:E ratio, RR, PEEP, and FiO2 .
Inspiration ends after delivery of the set
inspiratory pressure.
The TV is variable during pressure-limited
ventilation.
TV is related to inspiratory pressure level,
compliance, airway resistance, and tubing
resistance.
Peak airway pressure is constant and equal to the
sum of the set inspiratory pressure level and the
applied PEEP.
PCV—Settings
An Example
Inspiratory Pressure = 25 cm H
2
O
Rate = 10/min
Fio
2
= .40
I:E = 1:2
–This implies that there will be 6 seconds
allotted for each breath of which 2 seconds
will be for inspiration and 4 seconds will be
for expiration
Adjustments
VC Mode PCV Mode
To increase p
aO
2
Increase FiO
2
Increase PEEP
To decrease p
a
O
2
Decrease FiO
2
Decrease PEEP
To increase p
aO
2
Increase FiO
2
Increase PEEP
Decrease expiratory
time
To decrease p
aO
2
Decrease FiO
2
Decrease PEEP
Increase expiratory
time
Peak Inspiratory Pressure (PIP)
Pressure on manometer immediately at
end of inspiratory phase
Represents pressure needed to overcome
both elastic and airway resistance
Used to calculate dynamic compliance
–Cdyn = VT/Peak pressure
PEAK PRESSURE WILL CHANGE WHEN
EITHER ELASTIC OR AIRWAY RESISTANCE
CHANGES!
Plateau Pressure
Pressure on manometer after inspiration has
ended but before expiration has started
Represents pressure needed to overcome
elastic resistance only
Used to calculate static compliance
–Cstat = VT/plateau pressure
PLATEAU PRESSURE CHANGES ONLY
WHEN ELASTIC RESISTANCE CHANGES
Goal of plateau pressure and PIP is < 30
In case of increased TV and reduced lung
compliance both PIP and Plateau rises
proportionately
If PIP rises and plateau stays the same then
there is an increase in airway resistance or
flow rate
Definition..
Noninvasive ventilation is the
delivery of ventilatory support
without the need for an invasive
artificial airway
First non invasive
ventilation
‘‘And the Lord God formed man of
the dust of the ground and
breathed into his nostrils the
breath of life, and man became a
living soul. “
Genesis 2:7 (NIV bible)
Modalities of Noninvasive ventilation
Noninvasive positive-pressure ventilation ( NPPV )
a) Pressure limited
b) Volume limited
C) CPAP
d) Proportional assist ventilation (PAV)
Negative-pressure ventilation.
Abdominal displacement ventilation.
Other modes of noninvasive ventilatory assistance.
Advantages of NIV
Noninvasiveness
–Easy to implement, Easy to remove
–Allows intermittent application
–Improves patient comfort
–Reduces the need for sedation
–Oral patency (preserves speech, swallowing, and cough,
reduces the need for nasoenteric tubes)
Avoid the resistive work imposed
by the endotracheal tube
Avoids the complications of
endotracheal intubation:
–Early (local trauma, aspiration)
–Late (injury to the the hypopharynx,
larynx, and trachea, nosocomial
infections)
Disadvantages of NIV
Slower correction of gas exchange
abnormalities
Mask
–Air leakage
–Transient hypoxemia from accidental
removal
–Eye irritation
–Facial skin necrosis –most common
complication.
Complications of noninvasive positive pressure ventilation.
Respir Care 1997; 42:432.
Lack of airway access and protection
–Suctioning of secretions
–Aspiration
Increased initial time commitment
Gastric distension (occurs in <2% patients)
Prerequisite
Patient is able to cooperate
Patient can control airway and
secretions
Adequate cough reflex
Patient is able to co-ordinate
breathing with ventilator
Patient can breathe unaided for
several minutes
Haemodynamically stable
Blood pH>7.1 and PaCO2 <92 mmHg
Improvement in gas exchange, heart
rate and respiratory rate within first
two hours
Normal functioning gastrointestinal
tract
Indications
Acute respiratory failure
. Hypercapnic acute
respiratory failure
Acute exacerbation of COPD
Post extubation
Weaning difficulties
Acute respiratory failure in
Obesity hypoventilation
Syndrome
Thoracic wall deformities
Cystic fibrosis, Status
asthmaticus
Hypoxemic acute
respiratory failure
. Cardiogenic pulmonary
edema
Community acquired
pneumonia
Post traumatic respiratory
failure
ARDS
Indications cont’d
Chronic Respiratory Failure
Immunocompromised Patients
Do Not Intubate Patients (DNI)
Contraindications
Respiratory arrest
Unstable cardio respiratory status
Uncooperative patients
Unable to protect airway- impaired swallowing
and cough
Facial esophageal or gastric surgery
Craniofacial trauma/burn
Anatomic lesions of upper airway
Relative Contraindications
Extreme anxiety
Massive obesity
Copious secretions
Need for continuous or nearly
continuous ventilatory assistance
Despite evidence of efficacy, NPPV
may be underutilized among
patients with cardiogenic
pulmonary edema or hypercapnic
COPD exacerbations
Missed opportunities for noninvasive positive pressure
ventilation: a utilization review.Sweet DD, Naismith A,
Keenan SP, Sinuff T, Dodek PM J Crit Care. 2008;23(1):
Interfaces for the delivery of NIV
Interfaces are devices that connect
ventilator tubing to the face,
facilitating
the entry of pressurized
gas into the upper airway during NIV.
Currently available interfaces include
nasal mask, oronasal masks
and
mouthpieces.
Interfaces for NIPPV
Nasal
Advantages
–Less aspiration risk
–Easier secretion
clearance
–Less dead space
–Easier fit in adults
–Less claustrophobia
Disadvantages
–Mouth leak
–Higher resistance
through nasal
passages
–Nasal irritation
–Potential nasal
obstruction
Oronasal
Advantages
–Better control of
mouth leak
–Better for mouth
breathers
Disadvantages
–More dead space
–Claustrophobia
–Higher aspiration risk
–More difficulty in
speaking
Nasal mask
It is widely used for administration of CPAP
or NPPV, particularly for chronic
applications.
The
standard nasal mask is a triangular or
cone-shaped clear plastic
device that fits
over the nose and utilizes a soft cuff to form
an air seal over the skin .
Nasal masks are available
in multiple sizes
and shapes,
largely because of the demand
for such devices in the treatment
of OSA.
Nasal masks
Nasal mask (Cont..)
It exerts pressure
over the bridge of the
nose : often causing skin irritation and
redness, and occasionally
ulceration.
To minimize this
complication, use of
forehead spacers or the addition of
a
thin plastic flap that permits air sealing
with less mask pressure
on the nose.
An alternative type of nasal interface,
nasal "pillows" or "seals," consist of
soft rubber or silicone pledgets that
are inserted
directly into the nostrils.
Nasal Pillow Devices
Nasal mask (Cont..)
Nasal pillows are useful in patients
who
develop redness or ulceration on the
nasal bridge and those
with
claustrophobia, because they seem less
bulky than standard nasal
masks.
In addition, newer
"mini-masks" have
been developed that minimize the bulk
of the
mask, reducing feelings of
claustrophobia.
Straps that attach at two or as many as
five
points (More points of attachment
add to stability) on the mask have been
used, depending on the interface.
Oronasal or Full-face mask
It covers both the nose and the mouth.
They have been used mainly on patients
with acute respiratory failure but may also
be useful for chronic
applications.
During chronic use, patients may object to
having both the nose
and the mouth
covered, and asphyxia may be a concern in
patients
who are unable to remove the
mask in the event of ventilator malfunction
or power failure.
Interference with speech, eating,
and
expectoration and the risks of aspiration
and rebreathing are greater
with oronasal
than with nasal masks.
This photograph
shows a complete
headgear with a
full face mask
Arterial Blood Gases
Information Obtained from
an ABG:
Acid base status
Oxygenation
–Dissolved O2 (pO2)
–Saturation of hemoglobin
CO2 elimination
Levels of carboxyhemoglobin and
methemoglobin
Indications:
Assess the ventilatory status,
oxygenation and acid base status
Assess the response to an intervention
Contraindications:
Bleeding diathesis
AV fistula
Severe peripheral vascular disease,
absence of an arterial pulse
Infection over site
Why an ABG instead of
Pulse oximetry?
Pulse oximetry uses light absorption at
two wavelengths to determine
hemoglobin saturation.
Pulse oximetry is non-invasive and
provides immediate and continuous
data.
Evaluating Oxygenation
What is a ‘normal’ PO
2?
–Oxygenation gradually deteriorates during
life
–Several calculations available for
determining ‘normal’ based on patient
age.
PaO2 = 104.2 - (0.27 x age)
i.e., 30 year old ~ 95 mmHg
60 year old ~ 88 mmHg
pH 7.35 - 7.45
PaCO
2 35 - 45 mm Hg
PaO
2 70 - 100 mm Hg **
SaO
2 93 - 98%
HCO
3
¯ 22 - 26 mEq/L
%MetHb < 2.0%
%COHb < 3.0%
Base excess -2.0 to 2.0 mEq/L
CaO
2 16 - 22 ml O
2/dl
* At sea level, breathing ambient air
** Age-dependent
Normal Arterial Blood Gas Values*
A-a gradient
The Alveolar–arterial gradient (A–a
gradient), is a measure of the
difference between the alveolar
concentration (A) of oxygen and the
arterial (a) concentration of oxygen.
It is used in diagnosing the source
of hypoxemia
A normal A–a gradient for a young adult
non-smoker breathing air, is between 5–
10 mmHg.
Normally, the A–a gradient increases with
age. For every decade a person has lived,
their A–a gradient is expected to increase
by 1 mmHg.
(age in years/4) + 4. Thus, a 40 year old
should have an A–a gradient less than 14.
Evaluating Oxygenation
with ABGs
Check A-a
Gradient
No Yes
Is the patient hypoxic?
Hypoventilation
Normal Elevated
Check A-a
Gradient
No defect
Compensated
Defect.
i.e., patient is hyper-
ventilating or on
supplemental O
2
Other Defect
Normal
Elevated
Evaluation of Acid-Base Status:
Is the patient acidemic or alkalemic?
What is the pH?
< 7.38 >7.42
Acidemic Alkalemic
Evaluation of Acid-Base Status: Is the disorder respiratory
or metabolic?
If acidemic (pH < 7.38)
What is the PCO
2?
> 40 mmHg < 40 mmHg
Respiratory acidosis Metabolic acidosis
Evaluation of Acid-Base Status: Is the disorder
respiratory or metabolic?
If alkalemic (pH > 7.42)
What is the PCO
2?
> 40 mmHg < 40 mmHg
Metabolic alkalosis Respiratory alkalosis
For respiratory abnormalities, is
the condition acute or chronic?
Acute respiratory disturbances change
pH 0.08 units for every 10 mmHg
deviation from normal
Therefore, in acute respiratory acidosis, the
pH will fall by 0.008 x (PCO
2
– 40)
In acute respiratory alkalosis, the
pH will rise by 0.008 x (40-PCO
2
)
For respiratory abnormalities, is
the condition acute or chronic?
Chronic respiratory disturbances only
change pH 0.03 units for every 10
mmHg deviation from normal
Therefore, in chronic respiratory acidosis,
pH will fall by 0.003 x (PCO
2
– 40)
In chronic respiratory alkalosis, the
pH will rise by 0.003 x (40-PCO
2
)
Regarding Metabolic
Acidosis
It is common for patients with severe respiratory disease
to at some point develop other systemic illnesses
producing metabolic acidosis.
Patients with metabolic acidosis will attempt to
hyperventilate to correct their pH
It’s useful in patients with lung disease to determine how
successful they are in ‘blowing off their CO
2
’
Appropriateness of Respiratory Response to Metabolic
Acidosis
Predicted Change in PCO
2
= (1.5 x HCO
3
) + 8
If patient’s PCO
2
is roughly this value, his or
her response is appropriate
If patient’s PCO
2
is higher than this value, they
are failing to compensate adequately
Example 1
A 59 year old with a week of upper
respiratory symptoms followed by one day
of fever, chest pain, and dyspnea on
exertion
pH = 7.48
PCO
2
= 28 mm Hg
pO
2 = 54 mmHg
pH 7.48, PCO
2 28, PO
2 54
What is his A-a gradient?
[(760-47)x0.21] - (28/0.08) - 54 = 61 mmHg
pH 7.48, PCO
2 28, PO
2 54
Is this a respiratory or metabolic alkalosis?
pH 7.48, PCO
2 28, PO
2 54
Is this an acute or chronic abnormality?
If acute, then pH change should be 0.08 x [(40 - PCO
2)/10]
0.08 x [(40-28)/10)] = 0.09, or a pH of 7.49
If chronic, then pH change should be 0.03 x [(40-PCO
2
)/10]
0.03 x [(40-28)/10] = 0.03, or a pH of 7.43
How would you interpret
this ABG?
pH 7.48
PCO
2
28
PO
2
54
Hypoxic
Acute respiratory alkalosis
Example 2
A 47 year old woman with a 65 pack/year
history of tobacco use is being evaluated
for disability due to dyspnea
pH 7.36
PCO
2
54 mmHg
PO
2 62 mmHg
pH 7.36, PCO
2 54, PO
2 62
What is her A-a gradient?
[(760-47)x0.21] - (54/0.8) - 62 = 20 mmHg
pH 7.36, PCO
2 54, PO
2 62
Is this a respiratory or metabolic acidosis?
pH 7.36, PCO
2 54, PO
2 62
Is this an acute or chronic abnormality?
If acute, then pH change should be 0.08 x [(PCO
2
- 40)/10]
0.08 x (54-40)/10 = 0.11, or a pH of 7.29
If chronic, then pH change will be 0.03 x [(PCO
2
- 40)/10]
0.03 x (54-40)/10 = 0.04, or a pH of 7.36
How would you interpret
this ABG?
pH 7.36
PCO
2
54
PO
2
62
Hypoxic, with both a hypoventilatory and primary
oxygenation abnormality
Chronic respiratory acidosis
Case Studies :: Case Study 1
Patient in (PACU) is difficult to arouse two hours following surgery. The
nurse in the PACU has been administering Morphine Sulfate
intravenously to the client for complaints of post-surgical pain. Patient’s
RR is 7/min and is shallow.Patient does not respond to any stimuli! The
nurse assesses the ABCs (remember Airway, Breathing, Circulation!)
and obtains ABGs STAT!
The STAT results come back from the laboratory and show:
pH = 7.15
Pa C02 = 68 mmHg
HC03 = 22 mEq/L
what type of acid base disturbance is this
–Compensated Respiratory Acidosis
–Uncompensated Metabolic Acidosis
–Compensated Metabolic Alkalosis
–Uncompensated Respiratory Acidosis
Case study 2
An infant, three weeks old, is admitted to the Emergency Room. The
mother reports that the infant has been irritable, difficult to breastfeed
and has had diarrhea for the past 4 days. The infant’s respiratory rate is
elevated and the fontanels are sunken. The Emergency Room physician
orders ABGs after assessing the ABCs.
pH = 7.37
Pa C02 = 29 mmHg
HC03 = 17 mEq/L
Once you have interpreted the ABG results, click on one of the following
links
–Compensated Respiratory Alkalosis
–Uncompensated Metabolic Acidosis
–Compensated Metabolic Acidosis
–Uncompensated Respiratory Acidosis
Case study 3
A young woman, drinking beer at a party, falls and hits her
head on the ground. A friend dials "911" because the
young woman is unconscious, depressed ventilation
(shallow and slow respirations), rapid heart rate, and is
profusely bleeding from both ears.
Which primary acid-base imbalance is this young woman
at risk for if medical attention is not provided?
–metabolic acidosis
–metabolic alkalosis
–respiratory acidosis
–respiratory alkalosis
EXAMPLE ONE
ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/
Cr 5.1
Answer PH = 7.23 , HCO3 7
Acidemia
Step 2: What is the
primary disorder?
What disorder is present?pH pCO2 or HCO3
Respiratory Acidosis pH low pCO2 high
Metabolic Acidosis pH low HCO3 low
Respiratory Alkalosis pH high pCO2 low
Metabolic Alkalosis pH high HCO3 high
EXAMPLE
ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.
PH is low , CO2 is Low
PH and PCO2 are going in same directions then its
most likely primary metabolic will check to see if
there is a mixed disoder.
EXAMPLE
ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.
Winter’s formula : 17= 1.5 (7) +8 = 18.5
So correct compensation so there is only one
disorder Primary metabolic
EXAMPLE
ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.
Winter’s formula : 17= 1.5 (7) +8 = 18.5
So correct compensation so there is only one
disorder Primary metabolic
Respiratory Alkalosis
Causes of Respiratory Alkalosis
Anxiety, pain, fever
Hypoxia, CHF
Lung disease with or without hypoxia – pulmonary embolus, reactive
airway, pneumonia
CNS diseases
Drug use – salicylates, catecholamines, progesterone
Pregnancy
Sepsis, hypotension
Hepatic encephalopathy, liver failure
Mechanical ventilation
Hypothyroidism
High altitude
Respiratory Acidosis
Causes of respiratory acidosis
CNS depression – sedatives, narcotics, CVA
Neuromuscular disorders – acute or chronic
Acute airway obstruction – foreign body, tumor, reactive airway
Severe pneumonia, pulmonary edema, pleural effusion
Chest cavity problems – hemothorax, pneumothorax, flail chest
Chronic lung disease – obstructive or restrictive
Central hypoventilation, OSA
Steps for ABG analysis
1.What is the pH? Acidemic or Alkalemic?
2.What is the primary disorder present?
3.Is there appropriate compensation?
4.Is the compensation acute or chronic?
5.Is there an anion gap?
6.If there is a AG, what is the delta gap?
7.What is the differential for the clinical processes?