OXYGENATION AND ACID-BASE EVALUATION

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Presentation transcript:

OXYGENATION AND ACID-BASE EVALUATION Chapter 1

MECHANICAL VENTILATION Used when patients are unable to sustain the level of ventilation necessary to maintain the gas exchange functions Artificial support of lung function The Roman physician Galen may have been the first to describe mechanical ventilation: "If you take a dead animal and blow air through its larynx [through a reed], you will fill its bronchi and watch its lungs attain the greatest distention.“ Andreas Vesalius (founder of modern human anatomy) also describes ventilation by inserting a reed or cane into the trachea of animals..

INDICATIONS Ventilatory Failure Oxygenation Failure Failure of both oxygenation and ventilation Pathophysiological Factors Increased airway resistance Changes in lung compliance Hypoventilation V/Q mismatch Intrapulmonary shunting Diffusion defect

VENTILATION DELIVERY Available for: Performed by: Interface Short term Long term Acute care Extended home care Interface ETT Tracheostomy Mask LMA Performed by: Hand Machine

GAS EXCHANGE

ARTERIAL BLOOD GAS REVIEW Provides valuable information about a patient’s oxygenation, ventilation, and acid-base status Vital part of the assessment and management of a mechanically ventilated patient Should be used with caution – represents one point in time A series of ABG results should be compared to see if “trends” are present Avoid excessive or curiosity sampling Interpretation in the context of the clinical setting/ patient status

OXYGENATION PaO2 SaO2 CaO2 P(A-a)O2 PvO2 C(a-v) O2 VO2 DO2 Qs/Qt - - .

CLINICAL ROUNDS 1-1 A 40 year old patient has a P(A-a)O2 of 15mmHg. Is this in the normal range for this patient? At age 20 the normal P(A-a)O2 is about 5mmHg; it increases 4mmHg per decade. At age 40 this would represent an increase of 8mmHg or a value of 13mmHg. The value of 15 is reasonably close to normal.

LOW OXYGEN LEVELS: Hypoxia Hypoxemia Lower than normal oxygen pressure in the tissues or alveoli Types/Causes Hypoxemic Anemic Circulatory/stagnant Histotoxic Affinity Hypoxemia Low arterial blood oxygen pressure Causes Hypoventilation Decreased PiO2 Shunt Diffusion defects Poor distribution of ventilation

TRANSFER AND UPTAKE OF O2 FROM THE ALVEOLI P(A-a)O2: ability of lungs to bring in and transfer oxygen Increased gradient demonstrates a decreased transfer, due to: Age Lung disease V/Q mismatch Shunt Diffusion defects

TRANSFER AND UPTAKE OF O2 FROM THE ALVEOLI PaO2/PAO2: fraction of oxygen that is transferred to the artery Stable with changes in FiO2 Normal 0.9 (90%) Less than 75% indicates a problem

TRANSFER AND UPTAKE OF O2 FROM THE ALVEOLI PaO2 /FiO2: P to F ratio Amount of oxygen moving into the blood in relation to the inspired oxygen Used to describe the degree of lung injury Normal 380-476mmHg Lower values indicate disorders <200 ARDS 200-300 ALI

OXYHEMOGLOBIN DISSOCIATION CURVE S-shaped curve, relationship of plasma PO2 and O2 bound to Hb (SO2) Flat portion: minor changes in PO2 have little effect on SO2 Strong Affinity! Steep portion: small drop in PO2 causes a large drop in SO2 Weak Affinity!

OXYGEN CONTENT AND OXYGEN DELIVERY Together these determine the amount of oxygen available for utilization at the tissues Considers oxygen, hemoglobin and cardiac output CaO2 = (1.34xHbxSaO2) + (PaO2x0.003) DO2= CaO2xCO

CLINICAL ROUNDS 1-2 A patient has a measured PaO2 of 80mmHg and an SaO2 of 97%. The Hb is 10gm%. Does this patient have a normal oxygenation status? Although the PaO2 and SaO2 are normal the low hemoglobin will cause a reduction in this patient’s CaO2. Therefore this patient does not have a normal oxygenation status.

ALVEOLAR VENTILATION Normal: 4-5L/min VA= Vt-VD VA= (Vt-VD)x f ↑ VA = ↓PaCO2, ↑PaO2 Hyperventilation ↓VA = ↑PaCO2,↓PaO2 Hypoventilation Alveolar air equation As PaCO2 ↑ by 1mmHg, PaO2 ↓ by 1.25mmHg . . .

CLINICAL ROUNDS 1-3 A patient has a PaO2 of 50mmHg and a PaCO2 of 80mmHg. If the PaCO2 were to decrease to a normal of 40mmHg, what would you expect the PaO2 to be after the change (assuming the PaO2 changes were due to the PaCO2 changes alone and not to lung pathology A change in PaCO2 from 80 to 40mmHg is a 40 mmHg difference; 40 X 1.25 = 50mmHg. The PaO2 would be expected to increase by about 50mmHg to approximately 100mmHg.

PaCO2 = VCO2 x 0.863 VA Relationship between the amount of CO2 produced from cellular metabolism and how well the CO2 is removed from the lungs . .

HENDERSON-HASSELBALCH EQUATION Simplified to : H+ = 24 x PaCO2 HCO3- Requires knowing the hydrogen ion concentration for a given pH Verification of pH/PaCO2 relationship Buffers make it more difficult for the blood to become acidotic, CO2 must increase more to change the pH than compared to how much it decreases to raise the pH

CLINICAL ROUNDS 1-4 A patient has a PaCO2 of 78mmHg and a pH of 7.20. What would be an estimate of the patient’s bicarbonate level? HCO3- = 24 x 78 = 28.8 65 29mEq/L

ABG INTERPRETATION Degree of compensation Acid-base balance Cause: respiratory, metabolic, mixed Oxygenation – degree of hypoxemia Must interpret in the context of the clinical picture!! Requires ventilation status History, signs, symptoms Acute changes versus chronic