HYPOXIA
THE BASICS
BY DEBORAH DEWAAY MD
ACKNOWLEDGMENT: ANTINE STENBIT MD
OBJECTIVES
• Knowledge:
Understand the difference between hypoxia and hypoxemia
Understand physiologic adaptation to hypoxia
Understand how hypoxia causes cell death
Review the different modalities of providing oxygen to a
patient
• Know the differential diagnosis of acute hypoxia in the adult
patient
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• Skills:
• Use the algorithm to determine cause of hypoxia in a particular
patient
• Attitude:
• Understand the importance of keeping the patient
comfortable when they are hypoxic
• Understand the importance of communicating
compassionately with an acutely ill patient
KEY MESSAGES
• In acute hypoxic respiratory failure, the patient
should be put on a non-rebreather.
• An ABG is crucial to the work up of hypoxia.
• It is important to continue good communication
with a patient during emergent situations like acute
respiratory failure.
DEFINITIONS
• Hypoxia: a reduction of oxygen supply to a tissue
below physiological levels despite adequate
perfusion of the tissue by blood.
• Hypoxemia: a decreased partial pressure of oxygen
in blood less than 60mmHg on room air or less than
200mmHg on 100% oxygen.
HOW O2 GETS TO TISSUES
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Inhale oxygen
Enters alveoli
Crosses alveoli/capillary membranes
Diffuses into blood
Binds to hemoglobin
Is carried to tissues
Unbinds from hemoglobin
Tissues use oxygen
DEFINITIONS
• Hypoxic hypoxia: arterial blood Po2 is reduced
• Pneumonia
• Anemic hypoxia: arterial blood Po2 is normal, but the
amount of hemoglobin is too low to meet the tissues
demands
• Sickle cell disease
• Ischemic hypoxia: arterial blood Po2 is normal, but the
blood flow is too impaired to meet the tissues demands
• STEMI, compartment syndrome
• Histotoxic hypoxia: arterial blood Po2 is normal but a toxin
is preventing the cells to utilize the O2
• Cyanide poisoning
HOW HYPOXIA RESULTS IN CELL DEATH
• When there is diminished oxygen availability, the
tissue changes to inhibit oxidative phosphorylation
and increases anaerobic glycolysis
• As a result less ATP is produced
• Less ATP leads to in adequate energy to maintain
ionic and osmotic equilibrium
• The cell swells
• Result: cell death
ADAPTATIONS TO HYPOXIA
• Hypoxia causes:
• Systemic arteriole dilatation
• Pulmonary vascular constriction
• If there is little oxygen in the alveoli  the vascular bed in
that area will constrict and send blood to better
ventilated areas
• Results in better ventilation/perfusion matching
• Results in increased pulmonary vascular resistance
• Results in increased right ventricular afterload
SO THEY HAVE ACUTE
HYPOXIA: NOW WHAT?
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Assess the patient – ABCs
Vital signs
Is the oxygen saturation monitor accurate? Wave form?
Put on at a facemask (Non-rebreather) on at least 10L
Can the patient talk? If so, get a history
Physical Exam:
• Are they wet or dry?
• Lungs: Crackles? Where is air moving?
• Extremities: edema (palpate sacrum too)
• Neck: JVD
• You will have to make an initial decision without the CXR.
• Learn to trust your exam.
• Other signs of chronic hypoxia: clubbing
• Get an ABG, basic labs, CXR, EKG stat
HOW TO GIVE THE PATIENT OXYGEN:
THE NOSE
• Nasal Cannula:
• Regular: can go up to 6L (39%). After
4L you need add humidity.
• Oxymizer: gives a more accurate
FIO2.Cannot give with humidity. Can
give up to 15L (66%)
HOW TO GIVE THE PATIENT OXYGEN:
THE MOUTH
• Ventimask: this is a “high flow” mask.
• Good for “air hunger” and mouth breather
• Very precise amount of FIO2
• 24%-50% = 1L – 10L
• Non-rebreather:
• Have flow high enough to keep bag open
• All or nothing: 50 – 66% = 10-15L
NON-INVASIVE VENTILATION
AND INVASIVE VENTILATION
• Non-invasive Ventilation:
• CPAP: Continuous Positive Airway Pressure, does not initiate
breaths
• BiPAP: Bilevel Positive Airway Pressure, gives different
pressures (high for inhalation, low for exhalation), can time
breaths. Chronic use – OSA. Acute use: Acute pulmonary
edema (CHF, HTN emergency), COPD exacerbation.
• Invasive Ventilation: the machine breaths for the
patient or supports the patients breath via a tube
that is placed through the mouth into the in the
trachea.
HYPOXIA
• If wet:
• Stop the fluids!
• Give nitroglycerin 1st to venodilate (SL or paste).
• Lasix: Dilate now, pee later. ESRD: give it anyway (dilate
now, dialyze later)
HYPOXIA
• If dry: stabilize with oxygen
• When in doubt get a spiral CT (once stable
enough).
• Throughout all of this mess, don’t forget your ABC’s,
ask RTs help with CPAP/BiPAP…
THE ART OF MULTITASKING
So you know they are
hypoxic/hypoxemic: but you need
to know
WHY
LUNG ANATOMY
V/Q - NORMAL
• Normal physiology:
• V = ventilation (How well O2 gets into alveoli)
• Q = perfusion (How well Blood gets to capillaries)
• Blood vessels and alveoli are preferential to the bases, BUT
the blood vessels > alveoli
• V/Q is highest in the apices
• V/Q is lowest in the bases
5 CAUSES OF HYPOXIA
1. Reduced inspired oxygen tension
•
not enough O2 is in the air the patient is breathing, for
example: high altitude
2. Hypoventilation
•
broken pump
3. Ventilation-Perfusion Mismatch
•
V/Q mismatch
4. Shunt
•
Really bad V/Q mismatch
5. Diffusion impairment
ON THE ABG
• “A-a O2 Gradient = [ (FiO2) * (Atmospheric
Pressure - H2O Pressure) - (PaCO2/0.8) ] - PaO2
from ABG]
• DON’T MEMORIZE THIS –
• Use the online calculators
• Can also estimate.
• If you put a “normal” person on 10L their
PaO2 should be around 300.
• A normal A-a gradient = 4 +age/4.
REDUCED INSPIRED OXYGEN TENSION
• Normal A-a gradient
• Altitude:
• Bad air - breathing air that has a low FIO2
HYPERCARBIC RESPIRATORY FAILURE
~ BROKEN PUMP ~
• There is NO difference between the Alveolar O2
and the arterial O2 [No A-a gradient] & increase
PCO2 then the problem is a matter of
HYPOVENTILATION. The air isn’t moving = Pump
failure.
• CNS depression: drugs, CNS infection, metabolic
alkalosis, stroke, hypothyroidism.
• Myopathies: diaphragm, myositis, dystrophies,
electrolytes (phosphorus).
• Neuropathies: cervical spine, phrenic nerve, GBS,
ALS, polio
• Neuro-muscular junction: Myasthenia, botulism
IF THERE IS AN A-A GRADIENT
• If there is an A-a gradient  Hypoxic respiratory
failure  V/Q problem.
• What is a V/Q mismatch? All it means is the blood
and the oxygen are not going to the same places.
• If you put the patient on oxygen and they get
better…
• “V/Q mismatch”
• DDx: airway problem (asthma, COPD), alveolar
problem (PNA, CHF), Vascular problem (PE).
IF THERE IS AN A-A GRADIENT
• If there is an A-a gradient and you give the patient
O2 and the hypoxemia doesn’t improve = “Shunt”.
• This is confusing – just remember 
Shunt = Really Bad V/Q mismatch
• DDx Shunt: Alveolar collapes (atalectasis), Alveolar
filling (CHF, PNA), RL intracardiac shunt (VSD),
intrapulmonary shunt (AVM).
DIFFUSION LIMITATION
• Usually characterized by exercised-induced or
exacerbated hypoxemia
• During exercise  less time for diffusion. Healthy lungs will
have capillary dilation to increase the surface area
available so oxygenation is not affected
• Lungs with alveolar or interstitial inflammation/fibrosis (ILD)
can’t recruit additional surface area so hypoxia occurs
• If causing acute hypoxia it is usually occurring
concurrently with V/Q mismatch
• Need PFTs to diagnose
HYPOXEMIA - RECAP
Low FIO2 (altitude)
No
Hypoventilation
A-a gradient
Yes
Corrects w/ O2?
(CNS↓, MM, Nerve, NMJ)
No
Shunt
(atalectasis, CHF, PNA
PE, intracard or intrapul shunt)
Yes
V/Q mismatch
(Asthma, COPD, PNA, CHF,PE)
***if diffusion limitation is suspected in addition to the
above, get PFTs after patient is stable
DON’T FORGET THE PATIENT
• Patients feel like they are drowning
• Give reassurance
• Don’t forget to talk to them about what is
happening and what you are going to do for them
as you try to stabilize them
• Assume they can hear you
• Give low dose IV morphine (1-2mg) if the patient is
awake and suffering to help with the “drowning”
feeling
REFERENCES
• Lung anatomy picture:
http://www.nhlbi.nih.gov/health/dci/images/lung_a
natomy.jpg
• Pocket Medicine, Sabatine, Lippincott 2008
• Uptodate.com: oxygenation and mechanisms of
hypoxemia
• Harrison’s Online: chap 35
• Ganong’s Review of Medical Physiology: chap 36