Mechanical_ventilation[_fellow[1][1][1][1].ppt

Mechanical ventilation
By
Theodora Fynn (MD)

Objectives
 Mechanics of
breathing
 Modes of ventilation
 Mechanical ventilation
 ABG interpretation

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

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.

Settings
 The trigger mode
and sensitivity
 Respiratory rate
 Tidal volume
 Positive end-
expiratory
pressure(PEEP)
 Flow rate
 Flow pattern
 Fraction of inspired
oxygen.

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

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

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.

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 H2O
 Rate = 10/min
 Fio2 = .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 paO2
 Increase FiO2
 Increase PEEP
To decrease paO2
 Decrease FiO2
 Decrease PEEP
To increase paO2
 Increase FiO2
 Increase PEEP
 Decrease expiratory
time
To decrease paO2
 Decrease FiO2
 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

 Initial Values
– Peak = 31
cmH2O
– Plateau = 25
cmH2O
 2 Hours Later
– Peak = 40
cmH2O
– Plateau = 25
cmH2O

–Increased airway resistance
–? increased flow rate
–? mucus plug

Non invasive Mechanical
Ventilation

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 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 inserteddirectly into the nostrils.

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
patientswho 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

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’ PO2?
– 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
PaCO2 35 - 45 mm Hg
PaO2 70 - 100 mm Hg **
SaO2 93 - 98%
HCO3
¯ 22 - 26 mEq/L
%MetHb < 2.0%
%COHb < 3.0%
Base excess -2.0 to 2.0 mEq/L
CaO2 16 - 22 ml O2/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 O2
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 PCO2?
> 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 PCO2?
> 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 (PCO2 – 40)
In acute respiratory alkalosis, the
pH will rise by 0.008 x (40-PCO2)

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 (PCO2 – 40)
In chronic respiratory alkalosis, the
pH will rise by 0.003 x (40-PCO2)

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 CO2’

Appropriateness of Respiratory Response to Metabolic
Acidosis
Predicted Change in PCO2 = (1.5 x HCO3) + 8
If patient’s PCO2 is roughly this value, his or
her response is appropriate
If patient’s PCO2 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
PCO2 = 28 mm Hg
pO2 = 54 mmHg

pH 7.48, PCO2 28, PO2 54
What is his A-a gradient?
[(760-47)x0.21] - (28/0.08) - 54 = 61 mmHg

pH 7.48, PCO2 28, PO2 54
Is this a respiratory or metabolic alkalosis?

pH 7.48, PCO2 28, PO2 54
Is this an acute or chronic abnormality?
If acute, then pH change should be 0.08 x [(40 - PCO2)/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-PCO2)/10]
0.03 x [(40-28)/10] = 0.03, or a pH of 7.43

How would you interpret
this ABG?
pH 7.48
PCO2 28
PO2 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
PCO2 54 mmHg
PO2 62 mmHg

pH 7.36, PCO2 54, PO2 62
What is her A-a gradient?
[(760-47)x0.21] - (54/0.8) - 62 = 20 mmHg

pH 7.36, PCO2 54, PO2 62
Is this a respiratory or metabolic acidosis?

pH 7.36, PCO2 54, PO2 62
Is this an acute or chronic abnormality?
If acute, then pH change should be 0.08 x [(PCO2 - 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 [(PCO2 - 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
PCO2 54
PO2 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
–

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

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?

Mechanical_ventilation[_fellow[1][1][1][1].ppt

Mechanical_ventilation[_fellow[1][1][1][1].ppt

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Editor's Notes