PULMONOLOGY, MED II - 3RD YEAR
ventilation.
RESPIRATORY FAILURE
(DR CONSTANTINO TRANS FINALS APRIL 2017)
Acute Respiratory Failure pertains to: Failure of gas exchange due
to inadequate function of one or more essential components of
the respiratory system. So you remember, we have several parts.
We have the central controller, the lung and the chest wall, and
the nerves also. Clinically, respiratory failure may manifest either
as hypoxemia, hypercarbia, or a combination of both.
PATHOPHYSIOLOGY
 Normal respiration requires the integrated function of five
separate components of normal respiratory function
 A better understanding of the underlying pathophysiology
and potential treatment strategies can be gained
considering the individual components of the respiratory
system that are required for effective function under
physiologic conditions
FIVE COMPONENT OF NORMAL RESPIRATORY FUNCTION
1. Nervous System (controller dysfunction)
2. Musculature (pump dysfunction)
3. Airways (Airway system dysfunction)
4. Alveolar units (alveolar component dysfunction)
5. Vasculature (Pulmonary vascular dysfunction)
Dysfunction may cause the respiratory failure.
NERVOUS SYSTEM
The control system consists of:
 Medullary respiratory control group of neurons:
Dorsal (DRG) – integration site of changes in pH, PCO2, PO2
– changes whether increased or decreased levels in pH,
CO2, and oxygen are processed in the DRG, and
corresponding adjustments in terms of respiration are
decided on this site.
Ventral (VRG) – active expiration
 Afferent & efferent neural pathways
 Cerebral cortex – exercises voluntary control of respiration.
Voluntary because you try to stop or inhibit respiration only
for a certain extent. You can hold your breath but after a
while when the pCO2 elevates or pO2 decreases at a
certain level, the involuntary control takes over. So the
brainstem would take over. That is the reason why you
cannot kill yourself by holding your breath.
MUSCULATURE
 Primary muscle of respiration – diaphragm – It is very
important so much so that weakness in the diaphragm can
often lead to respiratory failure.
 Accessory muscles – internal intercostal muscles,
suprasternal muscles and stendocleidomastoid muscle
AIRWAYS
- A complex conduit system for the bulk delivery of gases so it
comprises the trachea, major bronchi and the segmental &
subsegmental bronchi up to the respiratory bronchioles.
ALVEOLAR UNITS
- Consists of the respiratory bronchioles, alveolar ducts &
alveoli so this is where gas exchange takes place
VASCULATURE:
Consist of:
 Pulmonary capillary network
 Pulmonary membrane system wherein you have actual
exchange of oxygen and carbon dioxide.
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First priority is to establish adequate oxygenation &
CLINICAL EVALUATION OF RESPIRATORY FAILURE BASED ON
PHYSIOLOGIC PRINCIPLES:
(1) CONTROLLER DYSFUNCTION:
 Least common primary cause of respiratory failure
 Most common cause of controller dysfunction is due to
medications that impair respiratory drive so drugs that
would inhibit ventilatory drive would be through controller
dysfunction so what are the example of these drugs?
Barbiturates, anesthetic agents, alcohol. These drugs would
lead to hypoventilation by inhibiting the respiratory center in
the brainstem.
 Defect in regulatory drive – No elevations in respiratory rate
and no use of accessory muscles of respiration, inspite of
CAYRAPF – MED II, PULMONOLOGY - APRIL 2017, 2ND SEMESTER
significant hypercarbia or hypoxemia – that is the reason
why the patient does not feel dyspneic. There are several
causes of defects in the regulatory drive. It could be a
defect in the metabolic control system so they usually have
 A normal AaDO2 - a normal arterial oxygen gradient
 Diagnostic aid to test respiratory drive:
1. Carbon dioxide challenge test – inhalation of 5% CO2
& 15% of O2 (normal response is an increase of RR to at
least 25/min) – you are inhaling less oxygen but if you
have impairment of a regulatory control mechanism,
you do not a manifest an increase in the respiratory
rate.
2. PO2.1 test – measuring the pressure generated 0.1 s
after the start of inhalation
(2) PUMP DYSFUNCTION:
 Common cause of respiratory failure in ICU and is usually
multifactorial – this is the most common cause
 Conditions that affect the respiratory muscles
1. Prolonged periods of mechanical ventilation
2. Polyradiculopathy associated with critical illness
3. Respiratory muscle fatigue
 Sign of respiratory muscle weakness – the most important
would be abdominal (paradoxical) breathing in this case
the abdomen will collapse during inspiration
 Measurement of muscle strength – VC & MIP – the best
measure of muscle strength is actually the MIP or muscle
inspiratory pressure or the peak negative pressure that is
generated on inspiration. You measure that using a
negative pressure manometer. You inhale through a
mouthpiece connected to the device and it measure the
negative pressure you can generate in the airways. Usually it
is minus 30 and above. (>-30)
 Other breathing indices:
- RSBI (rr/Vt) rapid spontaneous breathing index which is
the ratio of the respiratory rate over the tidal volume
this is also called the weaning index
- Trans-diaphragmatic pressure measurement
- EMG & nerve conduction study – to assess the integrity
of the respiratory muscle function
- Respiratory muscle insufficiency indicated by: a
decrease in the vital capacity VC <10 ml/kg; and the
maximal inspiratory pressure is MIP <- 20 cmH2O
Clinical Evaluation
 Initial Assessment & Stabilization of respiratory failure
- Upper airway patency – If there is an obstruction in the
upper airway so keep the airway open.
- Cyanosis – the PO2 is about 40 mmHg so that is ½ of the
normal and at that level, you are beginning to have
permanent damage to your vital organs
 - Respiratory rate & pattern of respiration – tachypnea
would be the early sign of hypoxemia; if you have
bradypnea the patient already has respiratory failure
- Respiratory distress – flaring of ala nasi, pursed lip
breathing & use of accessory muscles of respiration –
what is the purpose of pursed lip breathing? COPD or
Emphysema. Why do they do that? You prolong
expiratory time so you are able to remove the trapped
air inside because you prolong expiratory time. You
also generate positive pressure when you compress the
lung for adequate expiration.
- Shape of chest wall and movement – Is it symmetrical?
Does the patient have a barrel chest or a flail chest?
- Palpation & auscultation of the chest
- ABG - Check the blood gases because this is very
important. Assessment of the respiratory function of the
patient based on the grounds is often very dangerous
- ABG to detect hypoxemia
- Chest X-ray – to determine the cause of pulmonary
vascular dysfunction. Also on Chest X-ray, you can see
signs of pulmonary hypertension. So what are those
signs? Makikita yan sa embolism. Ano ang radiologic
signs ng Pulmonary Embolism? Diba may Westermark’s
Sign, Humpton’s Sign. Ano yung Pulmonary
Hypertension? Enlargement of the Pulmonary Artery,
the Right Descending Artery. Dalawa iyon eh – Palla’s
Sign and the other is Fleisher’s Sign. Both are pulmonary
vessel enlargement. Bilis niyo naman makalimot.
Nabasa ko iyan ng Grade 1 ako naalala ko! Haha!
- 2D Echo – show right ventricular hypertrophy or
dilatation.
- Right heart catheterization – dilatations of the pressures
in the right side of the heart
- Contrast enhanced CT scan of the chest – of course,

CAYRAPF – MED II, PULMONOLOGY - APRIL 2017, 2ND SEMESTER

because sometimes you may detect the hypoxemia or again, the dilatations of the right ventricular
the hypercarbia when it is too late already. hypertrophy and the enlarged pulmonary vessels

(3) AIRWAY DYSFUNCTION METHODS FOR ASSESSING CONTROLLER, PUMP, AIRWAY,

 PE findings of airway obstruction: ALVEOLAR COMPARTEMENT & VASCULAR DYSFUNCTION AT THE
1. Stridor – do not mistake them for wheezes; BEDSIDE
2. Ronchi – produced by the vibration of air against a Type of Test Method of Findings
liquid surface in a large airway; it means you have a lot Dysfunction determination consistent
of secretion in your bronchi; it is like scratching the back with
dysfunction
of your ear with your fingernail (not your fingertip!)
3. Wheezes Controller Respiratory Clinical < 12/min in
Rate observation in presence of
4. Dynamic hyperinflation – What is dynamic spontaneously hypoxemia or
hyperinflation? That is due to air trapping. The more you breathing hypercarbia &
inhale, the more air you will trap, so the more patient acidosis
hyperinflation you will have. It is dynamic because it is Pump Vital Capacity Bedside Presence of
ever-changing and that can only be relieved by & Inspiratory measurement in paradoxical
prolonging expiration or increasing ventilation. Force awake patient respiratory
motions
5. Increased airway resistance – What are the examples
VC<20 ml/kg;
of your increased airway resistance? Wheezes. MIF <-20
Anong signs ng dynamic hyperinflation? Decreased breath cmH2O
sounds kasi konti nalang pumapasok na air. And then you have RSBI > 105
barrel chest. Also, hyperresonance on percussion kasi puro air na Airway Wheezing or Physical exam Presence of
yung nasa loob ng chest. ronchi on Bedside wheezing
auscultation Measurement Raw > 20
In intubated patient airway resistance can be estimated by measurement in cm H2O/L
determining the plateau pressure & dividing it by the end Clinical cooperative per second
inspiratory flow rates (normal value – 3 to 8 cmH2O) evidence of or sedated Presence of
auto-PEEP patient auto-PEEP
 Pneumotachography – measures lung impedance, airway Ausculatation
resistance, and dynamic compliance or bedside
measurement
(4) ALVEOLAR COMPARTMENT in sedated
 Chest X-ray – show you if you have infiltrates, if you have patient
hyperlucent lung because of air trapping, or if you have Alveolar ABG Arterial blood Exam
atelectasis everything is seen in the X-ray Respiratory sample suggestive of -
 ABG – you can determine the pCO2 & the pO2 levels, system Bedside consolidation
assess the function of the alveolar compartment compliance measurement in - Abnormal
Chest X-ray sedated patient P/F or
 Lung Compliance – normal value 35-50 ml/cmH2O. Values Besdised X-ray ↑PaCO2; -
<30 during conventional tidal volume inflation (7-12 ml/kg) Crs> 30
indicates increased stiffness of the lung, chest wall or both – cmH2O
so you have decreases in compliance. The lung is not able - Alveolar
to expand fully. infiltrates
Pulmonary Assessment of JVP – central Elevation
(5) PULMONARY VASCULAR DYSFUNCTION: vasculature right Heart venous pressure Right Heart
function ECG Strain or RBBB
 Sign of right heart dysfunction because if you have right
If you have a controller dysfunction, check the respiratory rate by
heart dysfunction, you will have pulmonary hypertension:
observing the patient. Findings consistent with controller dysfunction
- Distended jugular veins
would be hypoventilation <12/min, RR in the presence of hypoxemia
- Prolong or delayed pulmonic component of S2 or hypercarbia and respiratory acidosis.
- Right sided S3
- Murmur of tricuspid regurgitation because of right For pump dysfunction, you check the vital capacity and the inspiratory
ventricular dilatation so this is a functional murmur force or maximal inspiratory pressure so this is done as bedside
 Ancillary Procedures: measurements. Findings include the presence of paradoxical
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respiratory motions – abdominal breathing, the vital capacity is less botulism. Because of paralysis of the respiratory muscles, you will
than 20ml/kg, the maximum inspiratory force or maximal inspiratory have hypoventilation, you will develop hypercarbia. You need to
pressure is less than -20 cmH2O, the respiratory spontaneous breathing review the medical history. Myopathy, again, you have paralysis
index is more than 105. of respiratory muscles, you will have hypercarbia. You evaluate
these by doing strength testing, EMG, or nerve conduction
For airway dysfunction, wheezing, ronchi and signs of airway velocity studies. For myositis, because you affect respiratory
resistance and also clinical evidence of auto-PEEP. Auto-PEEP is the
muscle function, you will have hypercarbia.
same as dynamic hyperinflation. You generate positive end expiratory
pressure automatically so the cause there is expiratory outflow
Type of Specific Predominant Additional
obstruction. Physical examination findings would determine the
Dysfunction Representative Gas Testing/
causes. So you have presence of wheezing, airway resistance more Condition Exchange Evaluation
than 10 cmH2O/second and the presence of auto-PEEP as Abnormality
determined by signs of hyperinflation. Maybe, hypotension also. Pump Metabolic abnormality Hypercarbia TSH;
Hypothyroidism Serum
Again, for alveolar dysfunction, you can check for the blood gases, Hypophosphatemia phosphate
respiratory system compliance, and x-ray. Findings consistent of Myasthenia gravis Hypercarbia EMG/NCV
alveolar dysfunction include x-ray signs of consolidation, abnormal studies
P/FiO2 ratio or increase in pCO2, compliance of more than 30 cmH2O Tensilon test

CAYRAPF – MED II, PULMONOLOGY - APRIL 2017, 2ND SEMESTER

or the presence of alveolar infiltrates will show you alveolar Guillain-Barre Hypercarbia Clinical
dysfunction. syndrome evaluation
EMG/NCV
Dysfunction of the pulmonary vasculature is by assessing the right heart studies
function by measuring the jugular venous pressure or central venous Paraneoplastic Hypercarbia Clinical
pressure. We have evidences of right heart strain or right bundle Syndrome Evaluation
branch block on the ECG. EMG/NCV
studies

CLINICAL SYNDROME ASSOCIATED WITH DYSFUNCTION OF Polyradiculopathy of Hypercarbia Clinical

THE COMPARTMENTS OF THE RESPIRATORY SYSTEM critical illness evaluation
EMG/NCV
Type of Specific Predominant Additional
studies
Dysfunction Representative Gas Exchange Testing
Condition Abnormality Evalutation Other conditions that will lead to pump dysfunction, you will have
Controller Sedative Hypercarbia Review of metabolic abnormalities, like hypothyroidism and
medication medication hypophosphatemia or hypokalemia. Again, because of
COPD or Hypoxemia + Hx of daytime weakness of respiratory muscles, hypoventilation, hypercarbia.
Interstitial Lung Hypercarbia somnolence, Myasthenia gravis, also hypoventilation, hypercarbia. You check
Disease lung function that using EMG/NCV studies or the Tensilon Test. GBS you will have
Toxic overdose Hypoxemia + Toxicology
hypercarbia, again. That will be diagnosed using a history in PE
Hypercarbia screen
and EMG/NCV studies. Other causes of pump dysfunction
Hypothermia Hypercarbia Measurement
post-operatively of core body paraneoplastic syndromes, because of neuromyopathies, you will
temperature have hypercarbia. Polyradiculopathy of critical illness, again
Brainstem stroke Hypercarbia Head CT/ MRI hypercarbia because of respiratory muscle weakness.
scan
Depending on the cause, you will have changes in your blood gas. Type of Specific Predominant Gas Additional
Like for controller dysfunction, if you use sedative medications, you Dysfunctio Represent Exchange Abnormality Testing/
depress the respiratory drive, you will have hypercarbia so you try to n ative Evaluation
review the medications. For COPD or Interstitial Lung Disease, you can Condition
have both hypoxemia and hypercarbia. For toxic overdoses, you
inhibit the respiratory drive, you have both hypoxemia and
Airways Asthma Mild: Hypoxemia + PFT;
hypercarbia so you do toxicology screens. For Hypothermia, you have Hypocarbia response to
hypercarbia due to hypoventilation, you draw back into a very low Severe: Hypoxemia + bronchodila
metabolic state so you measure core body temperature to determine Hypercarbia tor
hypothermia. For brainstem strokes, you have hypercarbia due to
hypoventilation due to involvement of the respiratory center in the COPD Hypoxemia + Hypercarbia PFT; Chest X-
brainstem so you do a CT scan/MRI. ray

Type of Specific Predominant Additional

Dysfunction Representative Gas Exchange Testing/ For airway dysfunction like Asthma, you will have mild hypoxemia
Condition Abnormality Evaluation and hypocarbia during the early stages like in mild asthma but
Pump Medication/Toxins Hypercarbia Review of during attacks or late stages, you will have hypoxemia and
paralytic medical hypercarbia because you have already developed respiratory
Aminoglycosides history muscle fatigue so you test for asthma by doing pulmonary
Steroids
function testing with response to bronchodilators. Paano niyo
Botulism
iinterpret ang spirometry with post bronchodilator for asthma? You
Myopathy Hypercarbia Strength
testing have increases in the FEV1 postbronchodilator by how much?
EMG/ NCV How many percent? How many mL? 12% or more or 200 ml
studies increase. For COPD, it is more of chronic so you have hypoxemia
Myositis HypercarbiaClinical and hypocarbia so you have pulmonary function testing and
exam; CXR. You have CXR finding of Emphysema, ano yun? Hyperlucent
serum CK & lung fields diba? Ano pa! What would be the most indicative of
aldolase Emphysema? Bullae. Ano pa? Narrowed intercostal spaces,
For pump dysfunction, you can have medications or toxins that flattened diaphragm, tapos mesocardic heart position.
will paralyze the respiratory muscles, yung glycosides, steroids,
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 Type of Specific Predominant Addition TYPES OF ARF
Dysfunction Representative Gas Exchange Testing/ Blood Gas Abnormality Pathophysiologic Derangement
Condition Abnormality Evaluation - Type 1 - Type 1
Airways Bronchiolitis Hypoxemia + PFT; chest x-ray
- Type 2 - Type 2
Hypercarbia Lung biopsy
- Type 3
Endobranchial variable PFT
tumor, mass or Ct imaging - Type 6
stricture Bronchoscopy What are the types of ARF? Here we are dealing with acute
Airway dysfunction again, for bronchiolitis, you have hypoxemia respiratory failure, not chronic respiratory failure. In chronic
and hypercarbia. In this case, you may have fluid in the respiratory failure, you have compensation already so it means
bronchioles, do pulmonary function testing, CXR & lung biopsy. For your pH will be normal or near normal even if you have marked
the endobronchial tumors, masses or strictures, the findings would arrangements of your PCO2 levels. And then, your bicarbonate
be variable, you may have normal blood gases or hypoxemia. In also will have changed.
the more severe stages you may have hypercarbia also.
Pulmonary function testing, CT imaging or bronchoscopy to So you have 2 major types of ARF base on that gas abnormality.
diagnose the problem. We have Type 1 ARF, which is hypoxemic therapeutic failure. You
have Type 2 ARF which is hypercarbic,respiratory failure with or
without hypoxemia. Again,

CAYRAPF – MED II, PULMONOLOGY - APRIL 2017, 2ND SEMESTER

So Pneumonia, obviously, hypoxemia because you have fluid in
the alveoli and hypercarbia also.
Type 1 – hypoxemia
Pulmonary edema, hypoxemia and hypercarbia. Type 2 – hypercarbia with normal PO2 or decreased PO2
So remember that. Major disorder is the PCO2 in type 2 respiratory
Pulmonary hemorrhage, hypoxemia and hypercarbia. This would failure.
be secondary to severe hypoxemia leading to respiratory muscle
fatigue with hypercarbia. X-rays are very important. RESPIRATORY FAILURE CATEGORIZED MECHANICALLY, BASED ON
PATHOPHYSIOLOGICAL DERANGEMENT
Type of Specific Predominant Addition  Type I or Acute Hypoxemic Respiratory Failure
Dysfunction Representative Gas Exchange Testing/ - Occurs when there is alveolar flooding so you have fluid in
Condition Abnormality Evaluation the alveoli so it can be due to (pulmonary edema,
Alveolar ARDS Hypoxemia + Chest X-ray pneumonia, or alveolar hemorrhage)
Hypercarbia ABG - In this case you have an Intrapulmonary shunt physiology
Pulmonary Hypoxemia + Chest wall
occurs which means you have the absence of the
Contusion Hypercarbia pain;
Chest X-ray
ventilation with intact perfusion. Walang ventilation kasi
Drug reaction Hypoxemia + Drug hindi na makakapasok yung air sa alveoli kasi it is filled with
Hypercarbia exposure; fluid so you do not have gas exchange. So you have
Toxicology hypoxemia. Hypoxemia here is refractory to oxygen therapy
screen meaning it will not respond until you give high fractions of
ARDS, practically the same, hypoxemia, hypercarbia. Pulmonary inspired oxygen more than 60% FiO2.
contusion would have the same findings or manifestations as
ARDS. Drug reaction, also, hypoxemia and hypercarbia.  Type II Respiratory Failure Hypercarbic RF with or without
Hypoxemia
Type of Specific Predominant Addition - Occurs as a result of alveolar hypoventilation and results in
Dysfunction Representative Gas Exchange Testing/ the inability to effectively eliminate carbon dioxide so you
Condition Abnormality Evaluation cannot blow off the CO2 that is inside the lung. So you have
Pulmonary Acute New onset V/Q Scan, CT
elevations in blood PCO2 and subsequently you may have
Vasculature Pulmonary hypoxemia pulmonary
Embolus with or without emboli study hypoxemia because you are not breathing adequately.
hypercarbia
Pulmonary Exertional 2D Echo, R Mechanism by which this occurs are categorized as:
Hypertension Hypoxemia heart 1. Impaired central nervous system (CNS) drive to breath (drug
catheterization overdose, brainstem injury because that’s where you have
AV Hypoxemia 2D Echo with the respiratory center, sleep-disordered breathing &
malformation or that is bubble study; hypothyroidism)
intra-cardiac refractory to HRCT scan
2. Impaired muscle strength with failure of neuromuscular
shunt O2
function in the respiratory system
For Pulmonary vasculature, you have acute pulmonary embolism.
- Impaired neuromuscular transmission – Myasthenia
You have new onset hypoxemia with or without hypercarbia. This
Gravis, Guillain-Barre syndrome, ALS, phrenic nerve
would depend on the presence or absence of concomitant
injury
respiratory muscle fatigue. Testing for this you have ventilation
- Impaired strength with respiratory muscle weakness –
perfusion scan, CT angiography. Actually, the gold standard for
myopathy, electrolyte derangement like hypokalemia,
pulmonary embolism is pulmonary angiography but because of
fatigue when you have increased the work of
the advent of CT angiography which is much easier to do. This is
breathing to the point where the respiratory muscles will
now commonly done than pulmonary angiography. Pulmonary
develop fatigue.
hypertension, exertional hypoxemia. You can do 2D Echo or right
3. Increased load on the respiratory system so this would
heart catheterization to measure pressures in the right side of the
increase the work of breathing
heart. You can have AV malformation or intracardiac shunts.
- You may have an increase in the Resistive load –
Because of shunts, you have hypoxemia that is refractory to
bronchospasm due to increased resistance in the
oxygen therapy so 2D echo, or HRCT (high resolution CT scan) so
airways
that they will be able to diagnose the problem.
- Reduced lung compliance preventing lung expansion
– alveolar edema, atelectasis, intrinsic PEEP

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 - Reduced chest wall compliance – pneumothorax,
pleural effusion, abdominal distention & this will prevent
chest wall expansion
- Load due to increased minute ventilation requirements
– pulmonary embolus with ↑dead space fraction
(when you have dead space, it is the portion of air in
the airways that does not participate in ventilation or
gas exchange so with pulmonary embolism since you
have occlusion of the pulmonary vessels, you have
ventilation but not perfusion so you do not have gas
exchange. That is the reason why you have increase in
the dead space fraction with pulmonary embolism),
sepsis
Type III Respiratory Failure
 Occurs as a result of lung atelectasis
 Because atelectasis occurs commonly in the peri-operative
period, this is also called peri-operative respiratory failure
 So you have decreased ventilation due to the Effect of
anesthesia & pain. So anesthesia the patient is not
breathing normally or ventilating properly. Pain restricts
chest wall expansion diba so again the patient will
hypoventilate.
Type IV Respiratory Failure
 Occurs because of hypoperfusion of respiratory muscles in
patients in shock. This is the type of respiratory failure that
would be due to shock.
 Normally, the respiratory muscles consume <5% of the total
cardiac output and oxygen delivery during normal
conditions
 Patient in shock often suffer respiratory distress due to
pulmonary edema, lactic acidosis, and anemia so you have
increased work of breathing. In this setting, up to 40% of the
cardiac output may be redistributed to the respiratory
muscles. The problem is you have shock so you do not have
adequate cardiac output so you have hypoperfusion of the
respiratory muscle and that will lead to respiratory
dysfunction so you will have respiratory failure. Clear ba
yun? Again, type 4 respiratory failure due to shock will lead
to hypoperfusion of respiratory muscles.
CLINICAL EVALUATION
INITIAL ASSESSMENT
- Determine upper airway patency because that is
where the problem may be located. Always check the
airway.
- Look for cyanosis which means you may have severe
hypoxemia already when it is present.
- Determine RR & Respiratory pattern. Tachypnea would
mean that the patient may be hypoxemic and the
respiratory pattern may determine the cause of the
failure. Like if you have Kussmaul’s breathing, it may be
due to metabolic acidosis or due to brainstem
hemorrhage.
- Also look for signs of respiratory distress. Like
supraclavicular or intercostal retractions, flaring of ala
nasi. Ano pa?
- Look for abnormalities of chest wall & its movement
because you may have kyphoscoliosis, for example, or
flail chest
- ABG very important for objective measurement of
PCO2, PO2 and the blood pH
Signs of respiratory distress
1. Flaring of ala nasi
2. Pursed lip breathing
3. Use of accessory muscles of respiration
CLINICAL MANIFESTATION
 HYPOXEMIA
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- Agitation, restlessness, “air hunger”
In hypoxemia, the patient is medyo malikot. They may
be even trying to sit up in the bed, sucking in air. That is
how hypoxemia would present.
- Initially may be euphoric/confused because of
decreased perfusion to the brain or decreased
oxygenation of the brain. Some of the patients will even
tell you they do not need oxygen tinatanggal nila ang
oxygen tapos after a few minutes they will have
cardiac arrest.
 CVS
- Tachycardia, dysrhythmias, hypotension
 HYPERCARBIA: would present as the opposite of hypoxemia
- Lethargy, drowsiness, stupor → COMA
I think I told you this before when I was in training, yung
patient na emphysema sabi ng nurse binigyan niya ng
oxygen natutulog. Binigyan niya ng oxygen nilagay niya sa
CAYRAPF – MED II, PULMONOLOGY - APRIL 2017, 2ND SEMESTER
6L. Ang requirement ng patient is only 2 liters. Patients with
emphysema when you give them too much oxygen, that will
inhibit the respiratory drive. They will develop hypoventilation,
PCO2 retention and they will go into coma. So pagpunta mo
sa patient tulog na, hindi mo na magising. Tapos pag binlood
gas mo ang PCO2 100 so you need to intubate the patient
and place them on a respirator. This is a very common
occurrence. That is the reason why in COPD patients you
have to compute for the desired fraction of inspired oxygen
based on the target oxygen requirement of the patient. Kasi
in Emphysema, you will only need to get a PO2 of 60-65 with
an O2 saturation of 90% at least in order for them to be
properly oxygenated. You do not need to go for a ** which
is normal kasi di naman sila normal eh.
For oxygenation you need to compute for the target PO2
based on the age kasi when you grow older, your lung will
also age and your PO2 will diminish with aging so if you are
70 years old hindi mo kailangan ang PO2 na 100. Pag 70, 70.
Kasi there is a shortcut computation for that. You subtract 40
from the age of the patient. Kunwari, 70 years old yung
patient so -40 = 30. Yung 30 you subtract from 100%. So 100%
- 30% = 70. Bakit 40 ang sinusubtract sa age ng patient? 40 is
the time you develop a decline in lung function. Wala sa libro
yan eh. Naisip ko lang. Hindi ko alam kung totoo yun. But I
think that is the logical explanation why 40 kasi mga libro
naman di naman nag eexplain. Haha!
STABILIZATION OF PATIENTS
 Adequate airway protection
 Oxygenation
 Ventilation
So you stabilize the patient by giving adequate airway
protection. So if you need to intubate the patient, you have to
intubate and provide oxygenation based on the requirements
for oxygenation and also for ventilation. It can be invasive or
non-invasive.
MANAGEMENT OF ARF
 Determine the type of ARF because management will be
somewhat different.
 Determine the etiology & treat appropriately because you
cannot relieve the respiratoryt failure without treating the
cause.
 Invasive or noninvasive ventilation
QUESTION
Ito anong type ito ng respiratory failure? ALCOHOL! Type 2,
alcohol kasi nadepress yung respiratory drive.
-LIGHT-
Please do not rely on this. Double check for any mistakes. Read
the book and study well. God bless, doctors! Thank you.