Hypoxic Hypoxemia - Stony Brook University School of Medicine

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Respiratory Failure in Children
Daniel Sloniewsky, MD
Associate Professor
Division of Critical Care
Department of Pediatrics
Stony Brook University Hospital
Definitions: Acute Respiratory
Failure
ARF is the inability of the respiratory system to
deliver O2 and remove CO2 at a sufficient rate to
meet the body’s metabolic demands
Can be hypoxic or hypercarbic
ABG abnormalities
– PaCO2 > 55 mm Hg (with low pH)
– PaO2 < 60 mm Hg
– SaO2 < 90% (in absence of cyanotic CHD)
Problems with Oxygenation
Hypoxemia: Decrease in tissue O2 delivery
– Hypoxic Hypoxemia -- Lung Disease
– Ischemic Hypoxemia -- Decreased Blood
Flow
-- DO2 = O2 content x Cardiac Output
– Anemic Hypoxemia -- Decreased O2-Carrying
Capacity
-- O2 Content = (1.39 x HgB x SaO2) +
(0.003)(PaO2)
Hypoxic Hypoxemia: Where is the
problem?
FIO2 (Ex. Altitude)
Decreased Air Entry
-- Sedation (Ex. Opioid Overdose)
-- Respiratory Muscle Weakness (Ex. SMA)
-- Airway Obstruction (Ex. Croup, Asthma, etc)
V/Q Mismatches (Ex. Atelectasis, ARDS)
Shunting (Ex. CHD, pulmonary hypertension)
Diffusion Abnormalities (Ex. Pulmonary Fibrosis,
ARDS)
Acute Respiratory Failure:
Problems with Ventilation
Hypercapnea (increased CO2) can be seen with:
1. Increased Dead Space (areas not involved in gas
exchange) (Ex. Asthma, Pulmonary HTN)
2. Decreased Alveolar Ventilation
- Decreased Tidal Volume or Respiratory Rate
(Ex. Coma, Overdose, MG, ARDS, etc)
3. Obstructed Airways (Ex. Asthma)
4. Increased CO2 production (Ex. Burns,Overfeeding)
CO2 diffuses easily across alveolar-capillary membrane so
diffusion problems usually do not cause hypercapnea
Acute Respiratory Failure: How to
Diagnose
Clinical Exam -- MOST IMPORTANT
1. Changes in RR and Breathing Effort:
Question - Why do infants “tire out?”
2. Changes in lung exam (stridor, wheeze, etc.)
3. Cyanosis – definition?
Flushing, tachycardia, HA, confusion – seen with
acute hypercarbia
Mental Status
Chronic Hypoxemia/Hypercarbia
Clinical signs/lab evidence of chronic
hypoxia:
-- Clubbing – seen with chronic hypoxemia
-- What might you see on abdominal
exam?
-- Labs: Polycythemia
Lab evidence of hypercarbia
Hypoxic Hypoxemia: How to
Diagnose
Pulse oximetry – How does it work? What
are its limitations?
Arterial Blood Gas – What information does
this provide that pulse-ox does not?
Pulse-oximetry: How does it work?
Current pulse-ox machines measure 2 types
of light: red (wavelength=660 nm) and
infrared (wavelength= 940 nm)
Red light is better absorbed by deoxy-Hgb,
infrared light is better absorbed by oxyHgb, so the ratio gives you the SaO2
Pulse-oximetry Problems
1. Doesn’t work well with poor perfusion
2. Other light sources (Ex. phototherapy
light) can interfere with the results
3. Abnormal Hgb can lead to overestimation
of a true SaO2 (specifically carboxy-, and
metHgb)
What laboratory test do you order in
someone with met- or carboxy-hgb
Arterial Blood Gas and
Oxygenation
ABG – can give you carboxy and metHgb
levels (if you ask); will give you cooximetry values (multiple wavelengths
measured)
-- will also give you a PaO2 which can
help you diagnose a patient with
hypoxemic hypoxia using an equation
called ………..
Alveolar Gas Equation
PAO2 = FIO2(PB-PH2O) – PCO2/R
– PAO2 = Alveolar oxygen partial pressure
– FIO2 = fraction of inspired oxygen
– PB = barometric pressure (760 mm Hg at sea
level)
– PH2O = partial pressure of water vapor (47 mm
Hg)
– PCO2 = partial pressure of CO2
– R = respiratory quotient (usually ~ 0.8)
Alveolar Gas Equation
So at room air at sea level, your PAO2
should be 100
On 100% FIO2 at sea level, your PAO2
should be 663
The difference between Alveolar (PAO2) and
arterial (PaO2) oxygen is called the A-a
gradient and should be less than 20; this
will help you figure out if this is hypoxic
hypoxemia and the degree of hypoxia
Given a PaO2, what is the SaO2
(and vice-versa)
Curve moves to right with
 Lower pH
 Higher Temperature
 Increased 2,3 DPG
Hypercarbic Respiratory Failure:
Who cares about CO2 and pH?
What makes you breathe?
Primarily pH (can be PaO2 in some patients)
What happens to you if you are too alkalotic or acidotic?
Acidosis: AMS, impaired cardiac contractility, pulmonary
vasoconstriction, metabolic abnormalities, etc.
Alkalosis: tetany (sec. to decreased iCa), arrhythmias, etc.
Does it matter what the source of the altered pH is?
Yes. For example: metabolic acidosis is worse for you than
respiratory acidosis.
Arterial Blood Gas, pH, and
Ventilation
pH < 7.35 with high CO2: respiratory
acidosis
pH > 7.35 with high CO2: compensated
respiratory acidosis
pH < 7.35 with low bicarb: metabolic
acidosis
pH > 7.35 with low bicarb: compensated
metabolic acidosis
What is a base deficit?
Base Deficit
Given a normal pCO2, how much base would
be needed to correct the pH.
Ex. 7.35/28/80/-15
Arterial Blood Gas, pH, and
Ventilation
pH > 7.45 with low CO2: respiratory alkalosis
pH < 7.45 with low CO2: compensated
respiratory alkalosis
pH > 7.45 with high bicarb: metabolic
alkalosis
pH < 7.45 with high bicarb: compensated
metabolic alkalosis
How to Approach an ABG
First – Is this an arterial or venous blood gas?
Second - does the patient have an acidosis or an
alkalosis
– Look at the pH
Third, 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
– You never overcompensate
How to Approach an ABG
Next, don’t 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
Sameer got into some of Dad’s 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 12. A blood gas is
obtained. 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 2
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.
Case 2
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 2
What is the blood gas interpretation?
1. Uncompensated respiratory acidosis with
severe hypoxia
2. Uncompensated metabolic alkalosis
3. Combined metabolic acidosis and respiratory
acidosis with severe hypoxia
4. Metabolic acidosis with respiratory
compensation
Case 3
10 year old with history of ALL and
neutropenia presents with tachypnea. He
has no O2 requirement but is breathing 30
– 40 times/minute. Lung exam (other than
the tachypnea) is normal. CXR shows no
infiltrate. An ABG is done: 7.45/30/90/22
on room air. Does this patient need a
bronchoscopy to diagnose his respiratory
compromise? Why or why not?
Case 3
Answer: No; This is a trick question
because he doesn’t have respiratory
compromise
The patient is tachypneic for some other
reason than acidosis, hypercarbia, or
hypoxia (i.e. increased intracranial
pressure, burgeoning sepsis, etc)
Other Laboratory Findings in ARF
CXR Abnormalities
Complete Blood Count (look at WBC and
Hgb, which may suggest chronic hypoxia)
Electrolyte Abnormalities (look at
bicarbonate)
Foreign Body Aspiration
Right Lung
Atelectasis
Left Lung
Pneumonia
with Effusion
Pneumothorax
ARDS
(Bilateral
Infiltrates)
Flail Chest
A Case of Hypoxia
4 yo presents to the ER with fever and cough. On examination, the patient has
the following vital signs: T 39.9, P 130, RR 32, O2 sats 87-90% on RA, Nl BP’s
PE: Lungs – tachypneic with good breathing effort, clear lung sounds,
Cardiac -- 2/6 SEM at LSB, good pulses in all extremities
Extremities -- mild clubbing of fingers and toes
Labs: WBC ct = 9.6, H/H = 14/41, platelets = 192k
Elytes normal except bicarbonate = 20; LFT’s Nl except AP = 358
CXR showed normal sized heart, possible infiltrate in hilar area
Patient is admitted to the hospital with a diagnosis of pneumonia and is
started on appropriate abx and supplemental oxygen. He defervesces after 24
hours but still has O2 saturations in the low 90’s that increase to mid-90’s on
4L NC. Physical exam remains the same and the repeat CXR is negative.
What is the cause of his hypoxia?
Clinical Scenario
Decreased O2 Availability? No
Decreased Air Entry? No
V/Q Mismatches? Possible
Shunt? Possible
Diffusion Problems? Possible
What lab test do you want to prove this?
Clinical Scenario
Arterial Blood Gas:
ABG on RA: 7.27 / 57 / 52
ABG on 100% O2: 7.29 / 60 / 69
What should his PaO2 be on RA and 100% FIO2?
RA = 78.5
100% FIO2 (through NRB) > 353
Do these ABG’s confirm our suspicions about V/Q
mismatch, shunt, or diffusion abnormalities? What role
does the high pCO2 play?
Now what tests do you want?
Clinical Scenario
Echocardiogram = no lesions
Chest CT = loss of volume in the LLL with small
consolidation, patchy atelectasis of right lung; enlarged
caliber of the pulmonary vasculature in the dependent
lung zones; rapid injection of contrast showed early filling
of the pulmonary veins
Ventilation/perfusion scan = normal ventilation; no
segmental defects in perfusion
So, what test was done to get a diagnosis?
Answer: Liver biopsy that confirmed the diagnosis of
hepatopulmonary syndrome
ARF -- Treatment
Monitoring
– invasive (ABG, PAC) or noninvasive (pulseoximeter)
Prevention
– Encourage coughing, frequent position
changes, reflux precautions, decompress
abdomen, etc.
ARF -- Treatment
Surgical: Thoracostomy tubes
Medications:
– b-agonists
– Anticholinergics
– Anti-inflammatory agents (steroids, NSAIDS)
– Surfactant
– Nitric Oxide
ARF -- Treatment
O2 Delivery Systems: Low vs. High Flow
Low Flow:
– Nasal Cannula: FIO2 < 40% (1L/min ~ 3%)
– Blow-by O2
High Flow:
– Head Hood: Flow >10 l/min
– Venturi Face Masks: FIO2 ~ 50%
– Nonrebreather Mask: FIO2 ~ 80-100%
– Bag-Mask-Valve Units: FIO2 ~ 100%
ARF -- Treatment
Continuous or Bilevel Positive Pressure
(CPAP or BIPAP) -- applied through a
tight-fitting mask
Best applied in an awake, cooperative
patient who is expected to improve in 4872 hours.
ARF – Treatment with Mechanical
Ventilation
Always Remember: Bag-mask ventilation is an
effective method to oxygenate patients: use
BMV if conditions are not ideal for intubation
Mechanical Ventilation: Indications
–
–
–
–
–
Airway Protection
Respiratory Failure
Shock
Treatment of Intracranial Hypertension
Other (for procedures, pulmonary toilet, etc.)
Mechanical Ventilation: Modes
AC – assist control
– no spontaneous breaths
– delivers full breath with any ventilator and patient
initiated effort
SIMV -- synchronized intermittent mandatory
ventilation
– ventilator breaths synchronized with patient’s own
breaths
– weaning mode
Mechanical Ventilation: Modes
Pressure Ventilation (Control)
– the size of the breath is determined by the pressure
that is set
– the tidal volume then depends on the lung compliance
(it is the dependent variable)
Volume Ventilation (Control)
– the size of the breath is determined by the volume
that is set
– the pressure is the dependent variable
Mechanical Ventilation: Goals
Your goals for gas exchange when a patient is on
a ventilator must not be so rigid as to cause
further injury to the lung when trying to obtain
them.
Oxygenation is more important than ventilation
You should try to keep the FIO2 < 60%, the PIP <
35-40 cm H20, and the TV ~6-8 cc/kg
Mechanical Ventilation:
Terminology
Mean Airway Pressure (MAP): the average
pressure over a respiratory cycle, measured at
the proximal airway
Peak Inspiratory Pressure (PIP): the maximum
amount of pressure needed to deliver a breath
Positive End Expiratory Pressure (PEEP):
pressure applied at the end of exhalation
I time: total time spent during inspiration
Mechanical Ventilation:
Terminology
Tidal Volume: the size (volume) of the breath
– goal ~ 6-10 cc/kg
Minute Ventilation: total volume of air inspired in
one minute
Compliance: relationship of volume to pressure
– C = DV / DP
Mechanical Ventilation
Oxygenation
– determined by FIO2 and Mean Airway
Pressure
– MAP is determined by PEEP, PIP, and
inspiratory time (I time)
Ventilation
– determined by rate and TV
– rate x TV = MV
Mechanical Ventilation -Supportive Care
Fluids and electrolytes: permissive
hypercapnia
Nutrition
HOB up at 30o
Suctioning/Chest PT
Mechanical Ventilation -Monitoring
ABG/VBG
Pulse-oximetry
EtCO2 -- depends on reason for respiratory
failure (not good with obstructive diseases
like asthma or if there is a big air leak
around the ETT)
Mechanical Ventilation -Weaning
Is the problem solved?
Is the patient awake?
Is the patient NPO
Is there an airleak around the ETT
What are the mode of ventilation and settings?
Mechanical Ventilation -Complications
Oxygen Toxicity: keep O2 < 60%
Barotrauma/Volutrauma: Keep PIP < 35-40 and TV < or =
to 6-8 cc/kg
Atelectasis
Ventilator Associated Pneumonia: keep HOB up at 30o
Fluid Retention
Airway Trauma: uncuffed tubes when <6 yo
ARF -- Alternate Therapies
HFOV -- High Frequency Oscillatory Ventilation:
used for problems with oxygenation, not very
good for ventilation
ECMO -- Extra-corporeal membrane oxygenation
Liquid Ventilation – oxygen dissolves well in
perfluorocarbons which can be used for gas
exchange: only used in the lab
Summary
When a patient is in respiratory failure, you
must decide the primary gas exchange
problem.
While the clinical exam is the most important
method of diagnosing someone with ARF,
an ABG can help you with the diagnosis
and can tell you the degree of hypoxia or
hypercarbia
Summary
If hypoxia is the problem, going through the
algorithm may help you decide which tests and
therapies you need
If hypercarbia is the problem, going through that
algorithm may help you manage the patient
A thoughtful, goal-directed approach to therapies
must also be used in treating respiratory failure.
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