HyPoxia the basics

BY DEBORAH DEWAAY MDMEDICAL UNIVERS ITY OF SOUTH CAROL INA

MAY 29 , 2012

A C K N O W L E D G M E N T: A N T I N E S T E N B I T M D

HYPOXIATHE BASICS

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• 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

• 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?

• 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 VENTILATIONAND 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 altitude2. 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), RL 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 A-a gradient Hypoventilation Yes(CNS↓, MM, Nerve, NMJ) Corrects w/ O2?

No Yes

Shunt V/Q mismatch(atalectasis, CHF, PNA (Asthma, COPD, PNA, CHF,PE)PE, intracard or intrapul shunt)

***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_anatomy.jpg• Pocket Medicine, Sabatine, Lippincott 2008• Uptodate.com: oxygenation and mechanisms of h

ypoxemia• Harrison’s Online: chap 35• Ganong’s Review of Medical Physiology: chap 36