BY DEBORAH DEWAAY MD ACKNOWLEDGMENT: ANTINE STENBIT MD HYPOXIA THE 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

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 O 2 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 Po 2 is reduced Pneumonia Anemic hypoxia: arterial blood Po 2 is normal, but the amount of hemoglobin is too low to meet the tissues demands Sickle cell disease Ischemic hypoxia: arterial blood Po 2 is normal, but the blood flow is too impaired to meet the tissues demands STEMI, compartment syndrome Histotoxic hypoxia: arterial blood Po 2 is normal but a toxin is preventing the cells to utilize the O 2 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: re they wet or dry? Are they wet or dry? Lungs: Crackles? Where is air moving? Lungs: Crackles? Where is air moving? Extremities: edema (palpate sacrum too) Extremities: edema (palpate sacrum too) Neck: JVD Neck: JVD You will have to make an initial decision without the CXR. You will have to make an initial decision without the CXR. Learn to trust your exam. 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: If wet: Stop the fluids! Stop the fluids! Give nitroglycerin 1 st to venodilate (SL or paste). Give nitroglycerin 1 st to venodilate (SL or paste). Lasix: Dilate now, pee later. ESRD: give it anyway (dilate now, dialyze later) Lasix: Dilate now, pee later. ESRD: give it anyway (dilate now, dialyze later)

HYPOXIA If dry: stabilize with oxygen If dry: stabilize with oxygen When in doubt get a spiral CT (once stable enough). 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… 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 = [ (Fi O2 ) * (Atmospheric Pressure - H 2 O Pressure) - (Pa CO2 /0.8) ] - Pa O2 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 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: natomy.jpg natomy.jpg Pocket Medicine, Sabatine, Lippincott 2008 Uptodate.com: oxygenation and mechanisms of hypoxemia Uptodate.com: oxygenation and mechanisms of hypoxemia Harrison’s Online: chap 35 Ganong’s Review of Medical Physiology: chap 36