Blood Gases and Related Tests

Blood Gases and Related Tests
RET 2414 Pulmonary Function Testing Module 6.0

Objectives Describe how pH and PCO2 are used to assess acid-base balance Interpret PO2 and oxygen saturation to assess oxygenation Identify the correct procedure for obtaining an arterial blood gas specimen List situation in which pulse oximetry can be used to evaluate a patient’s oxygenation

Objectives Describe the use of capnography to assess changes in ventilatory-perfusion patterns of the lung Describe at least two limitation of pulse oximetry

Reasons for Obtaining an ABG
Assessment of ventilatory status Assessment of acid-base balance Assessment of arterial oxygenation

Acid – Base Balance The maintenance of cellular function depends on an exacting environment. One of the most important environmental factors is the hydrogen ion concentration (H+), commonly expressed as pH.

7.40 Acid – Base Balance Normal pH
The pH is a function of the relation of HCO3- (base) to PCO2 (acid) in the blood in the following fashion: pH ~ HCO3- (base) ~ metabolic component ~ kidney ~ 20 CO2 (acid) respiratory component lungs 7.40 Normal pH

Acid – Base Balance Acidemia; an acidic condition of the blood
pH < 7.35 Alkalemia; an alkaline condition of the blood pH >7.45

Acid – Base Balance Respiratory Component (PCO2) Tissues Plasma
Red Blood Cell CO2 CO2 dCO2 H2CO3

Acid – Base Balance 46 mmHg 40 mmHg
Excretion of CO2 is one of the lungs main functions PA CO2 40 mmHg PaCO2 PvCO2 46 mmHg 40 mmHg Pc CO2

“Respiratory Acidosis”
Acid – Base Balance Respiratory Component (PCO2) Ventilation PCO2 pH “Respiratory Acidosis”

“Respiratory Alkalosis”
Acid – Base Balance Respiratory Component (PCO2) Ventilation PCO2 pH “Respiratory Alkalosis”

Acid – Base Balance Metabolic Component (HCO3- and BE)
Bicarbonate (HCO3-) is the primary blood base and is regulated by the kidneys and not the lungs. Normal HCO mEq/L

Base Excess (BE) is a measure of metabolic alkalosis or metabolic acidosis expressed as the mEq of strong acid or strong alkali required to titrate one liter of blood to a pH of 7.40 Normal B.E to +2 mEq/L

HCO3- or B.E. “Metabolic Acidosis”

“Metabolic Alkalosis”
Acid – Base Balance Metabolic Component (HCO3- and BE) HCO3- or B.E. “Metabolic Alkalosis”

Acid – Base Balance Combined Respiratory / Metabolic
Respiratory and metabolic component moving toward the same acid/base status PCO HCO3- = Acidosis PCO HCO3- = Alkalosis

Acid – Base Balance Compensation HCO3- PCO2 PCO2 HCO3-
Abnormal pH is returned toward normal by altering the component NOT primarily affected, i.e., if PCO2 is high, HCO3- is retained to compensate PCO HCO3- HCO3- PCO2

Acid – Base Balance Normal metabolism produces approximately 12,000 mEq of hydrogen ions per day. Less than 1% is excreted by the kidneys, because the normal metabolite is CO2; which is excreted by the lungs.

Acid – Base Balance Acid-Base imbalance is not life-threatening for several hours to days following renal shutdown but becomes critical within minutes following cessation of breathing. WOW!

Normal Values pH PCO2 (mmHg) HCO3- (mEq/L)

Acceptable Ranges (2 SD)
pH PCO HCO3- Normal 7.35 – – Acidotic < >45 <22 Alkalotic > <35 >26

Arterial Oxygenation Tissue hypoxemia exists when cellular oxygen tensions are inadequate to meet cellular oxygen demands. PaO2 has become the primary tool for clinical evaluation of the arterial oxygenation status.

Arterial Oxygenation Hypoxemia; an arterial oxygen tension (PaO2) below an acceptable range. Arterial Oxygen Tensions for Adult and Child Normal mm Hg Acceptable Range ≥80 mm Hg (range decreases with age) Hypoxemia <80 mm Hg

Systematic Interpretation
Assessment of ventilatory status Assessment of acid-base balance Assessment of arterial oxygenation

Exercise 1 Acute ventilatory failure with hypoxemia
Acceptable Range ABG Result pH 7.26 PCO2 56 HCO3- 24 BE -4 >80 PO2 50 Acute ventilatory failure with hypoxemia (Acute respiratory acidosis with hypoxemia)

Exercise 2 Acute alveolar hyperventilation without hypoxemia
Acceptable Range ABG Result pH 7.56 PCO2 29 HCO3- 24 BE +3 >80 PO2 90 Acute alveolar hyperventilation without hypoxemia (Acute respiratory alkalosis without hypoxemia)

Uncompensated metabolic alkalosis with hypoxemia
Exercise 3 Acceptable Range ABG Result pH 7.56 PCO2 44 HCO3- 38 BE +14 >80 PO2 75 Uncompensated metabolic alkalosis with hypoxemia

Uncompensated metabolic acidosis without hypoxemia
Exercise 4 Acceptable Range ABG Result pH 7.20 PCO2 38 HCO3- 15 BE -13 >80 PO2 90 Uncompensated metabolic acidosis without hypoxemia

Exercise 5 Chronic alveolar hyperventilation without hypoxemia
Acceptable Range ABG Result pH 7.45 PCO2 20 HCO3- 16 BE -7 >80 PO2 90 Chronic alveolar hyperventilation without hypoxemia (Compensated respiratory alkalosis without hypoxemia)

Exercise 6 Chronic ventilatory failure with hypoxemia
Acceptable Range ABG Result pH 7.42 PCO2 72 HCO3- 46 BE +18 >80 PO2 45 Chronic ventilatory failure with hypoxemia (Compensated respiratory acidosis with hypoxemia)

Exercise 6 A 76-year-old man with a long history of symptomatic COPD entered the hospital with basilar pneumonia. He was alert, oriented, and cooperative. Acceptable Range ABG Result pH 7.58 PCO2 45 HCO3- 42 BE +17 >80 PO2 38

Exercise 6 Acceptable Range ABG Result pH 7.58 PCO2 45 HCO3- 42 BE +17 >80 PO2 38 Question: Is this uncompensated metabolic alkalosis with severe hypoxemia?

Exercise 6 Uncompensated metabolic alkalosis with severe hypoxemia?
Acceptable Range ABG Result pH 7.58 PCO2 45 HCO3- 42 BE +17 >80 PO2 38 Uncompensated metabolic alkalosis with severe hypoxemia?

Exercise 6 Acceptable Range ABG Result pH 7.58 PCO2 45 HCO3- 42 BE +17 >80 PO2 38 A metabolic alkalosis with hypoxemia must be clinically correlated because a disease process causing metabolic alkalosis would not be expected to produce severe hypoxemia.

Exercise 6 Correct Interpretation:
Acceptable Range ABG Result pH 7.58 PCO2 45 HCO3- 42 BE +17 >80 PO2 38 Correct Interpretation: Acute alveolar hyperventilation (respiratory alkalosis) superimposed on chronic hypercapnia (chronic ventilatory failure) with severe hypoxemia.

Exercise 7 A 67-year-old man admitted to the Emergency Department with exacerbated COPD. He was alert, oriented, and cooperative. Acceptable Range ABG Result pH 7.25 PCO2 90 HCO3- 38 BE +12 >80 PO2 34

Exercise 7 Acceptable Range ABG Result pH 7.25 PCO2 90 HCO3- 38 BE +12 >80 PO2 34 Acute ventilatory failure superimposed on chronic hypercapnia (chronic ventilatory failure) with severe hypoxemia.

Pulse Oximetry Pulse oximetry (SpO2) is the noninvasive estimation of SaO2

Pulse Oximetry SaO2

Pulse Oximetry Pulse oximetry may be used in any setting in which a noninvasive measure of oxygenation status is sufficient. O2 therapy Surgery Ventilator management Diagnostic procedures Bronchoscopy Sleep studies Stress testing Pulmonary Rehabilitation

Pulse Oximetry Pulse oximetry uses light to work out oxygen saturation. Light is emitted from light sources which goes across the pulse oximeter probe and reaches the light detector.

Pulse Oximetry If a finger is placed in between the light source and the light detector, the light will now have to pass through the finger to reach the detector. Part of the light will be absorbed by the finger and the part not absorbed reaches the light detector.

Pulse Oximetry Hemoglobin (Hb) absorbs light. The amount of light absorbed is proportional to the concentration of Hb in the blood vessel. By measuring how much light reaches the light detector, the pulse oximeter knows how much light has been absorbed. The more Hb in the finger , the more light is absorbed.

Pulse Oximetry

Pulse Oximetry The pulse oximeter uses two lights to analyze hemoglobin, red and infared, to detect the amount of oxyhemoglobin (O2Hb) and deoxyhemoglobin (rHb)

Pulse Oximetry The pulse oximeter works out the oxygen saturation by comparing how much red light and infra red light is absorbed by the blood. Depending on the amounts of oxy Hb and deoxy Hb present, the ratio of the amount of red light absorbed compared to the amount of infrared light absorbed changes.

Pulse Oximetry

Pulse Oximetry Using this ratio, the pulse oximeter can then work out the oxygen saturation.

Pulse Oximetry Pulse oximeters often show the pulsatile change in absorbance in a graphical form. This is called the "plethysmographic trace " or more conveniently, as "pleth".

Pulse Oximetry If the quality of the pulsatile signal is poor, then the calculation of the oxygen saturation may be wrong. Always look at pleth before looking at oxygen saturation.

Pulse Oximetry Never look only at oxygen saturation !

Pulse Oximetry Always look at pleth before looking at oxygen saturation!

Pulse Oximetry Interfering Substances COHb MetHb
Intravascular dyes (indocyanine green) Nail polish or coverings

Pulse Oximetry Interfering Factors Motion artifact, shivering
Bright ambient lighting Hypotension, low perfusion (sensor site) Hypothermia Vasoconstriction drugs Dark skin pigmentation

Pulse Oximetry Criteria for Acceptability
Correlation with measured SaO2 SpO2 and SaO2 should be within 2% from % Elevated levels of COHB (>3%) or MetHb (>5%) may invalidate SpO2

Adequate profusion of the sensor site as seen in the plethysmographic tracing and correlation with patient’s heart rate

Know interfering substances or agents should be eliminated, e.g., nail polishes, acrylic nails, etc. Readings should be consistent with the patient’s clinical history and presentation.

Oxygen Saturation Oxygen saturation is the ratio of either oxygenated Hb (Oxyhemoglobin or O2Hb) to total available Hb (reduced Hb or rHb + O2Hb) or total Hb (O2Hb + rHb + COHb + MetHb), depending on the instrumentation used to measure and report values

Oxygen Saturation Co – oximeters actually measures SaO2 using spectrophotometry; Ratio of oxyhemoglobin to total Hb: SaO2 = ___ O2Hb X 100 (O2Hb + rHb + COHb + MetHb) Pulse oximeters estimate the SaO2 by using a noninvasive probe that measures absorption or red and near-infrared light; Ratio of oxyhemoglobin to available Hb: SpO2 = O2Hb__ X 100 (O2Hb + rHb)

Oxygen Saturation 1 2 3 4 5 6 7 8 9 10 11 12 13 14 10 Pulse 76%
Oxyhemoglobin (O2Hb) Reduced Hb (rHb) COHb + MetHb O2Hb Pulse Oximeter 10 13 76% SpO2 Here we have a patient that has 14 grams of hemoglobin, 10 oxyhemoglobin, three deoxyhemoglobin and one dyshemoglobin. The CO-oximeter, would divide the oxyhemoglobin which is 10, by the total of oxyhemoglobin plus deoxyhemoglobin which is 14. The oxygen saturation the pulse oximeter would display is a functional hemoglobin saturation of 76%. Why? Because the pulse oximeter only has two wavelengths of light and does not see the dyshemoglobin. The co-oximeter having four wavelengths of light sees the dyshemoglobin and divides the oxyhemoglobin by 14, 10 oxyhemoglobin, plus 3 deoxyhemoglobin, plus 1 dyshemoglobin. The co-oximeter would display an fractional oxygen saturation of 71%. We will discuss this more a little later in the presentation. O2Hb + rHb O2Hb CO- Oximeter 10 14 71% SaO2 O2Hb + rHb + COHb + MetHb

Oxygen Saturation SaO2 is calculated by some blood gas analyzers based on PaO2 and PH Convenient but inaccurate! SvO2 can be measured by a reflective spectrophotometer in the pulmonary artery catheter (Swanz-Ganz)

Oxygen Saturation Normal Values SaO2 = 97% SvO2 = 75%
COHb = .5% - 2% of Total Hb MetHb = 1.5% of Total Hb Total Hb = 14 – 16 gm% (males) 13 – 15 gm% (females)

Capnography Capnography is the continuous, noninvasive monitoring or expired CO2 and analysis of the single-breath CO2 waveform

Capnography Capnography
Allows trending of changes in alveolar and dead space ventilation End-tidal PCO2 (PetCO2) is reported in mm Hg

Capnography Normal Arterial & ETCO2 Values 35 - 45 mmHg 30 - 43 mmHg
from Capnograph Arterial CO2 (PaCO2) Normal PaCO2 as measured by a blood gas, is 35 to 45 mmHg. The ABG is the gold standard. However there are several issues associated with the invasiveness of obtaining a sample, and cost. Additionally the ABG is a snapshot in time. Ten minutes later everything can change and as a clinician you know that early intervention is best. Trending PCO2 give the clinician an objective reason to do an ABG. The normal value for ETCO2 is 30 to 43 mmHg. Normal PaCO2 Values: Normal ETCO2 Values: mmHg mmHg

Capnography Arterial - End Tidal CO2 Gradient
In healthy lungs the normal PaCO2 to ETCO2 gradient is 2-5 mmHg In diseased lungs, the gradient will increase due to ventilation/perfusion mismatch

Capnography . Normal (ventilation) is 4 L of air per minute
Normal (perfusion) is 5L of blood per minute. So Normal ratio is 4/5 or 0.8 When the is higher than 0.8, it means ventilation exceeds perfusion When the is < 0.8, there is a mismatch caused by poor ventilation.

Deadspace Ventilation
Capnography Ventilation-Perfusion Relationships Relationship between ventilated alveoli and blood flow in the pulmonary capillaries Shunt perfusion Alveoli perfused but not ventilated CO2 Normal Ventilation and perfusion is matched O2 There are three scenarios that describe ventilation perfusion relations. Normal, (press down key) Shunt Perfusion (press down key) and Deadspace Ventilation. We’ll take a closer look at each of these ventilation perfusion relationships and how they effect ETCO2 and the ETCO2 to PaCO2 gradient, Lets start with normal V/Q. Deadspace Ventilation Alveoli ventilated but not perfused

. . Capnography Normal V/Q CO2 O2 ETCO2 - PaCO2 Gradient = 2 to 5 mmHg
The ventilation–perfusion ratio (V/Q) describes the relationship between air flow in the alveoli and blood flow in the pulmonary capillaries. If ventilation were perfectly matched to perfusion, then V/Q would be 1. However, even in the normal lung ventilation and perfusion are not equally matched. The normal lung has an over all V/Q of 0.8. When a normal V/Q exists the ETCO2/PaCO2 gradient is 2 to 5 mmHg. Often the cardiovascular systems are normal in patients who suffer head injuries, drug overdose, or cerebral vascular accidents. In these patients the ETCO2 to PACO2 gradient may be as little as 2 or3 mmHg. Now let take a look at what happens to the ETCO2/PaCO2 gradient when V/Q is not normal. CO2 O2

Shunt Perfusion – Low V/Q
Capnography . . Shunt Perfusion – Low V/Q Mucus plugging ET tube in right or left main stem bronchus Atelectasis Pneumonia Pulmonary edema In short anything that causes the alveoli to collapse or alveolar filling ETCO2 - PaCO2 Gradient = 4 to 10 mmHg Shunt Perfusion is commonly referred to as a Low V/Q ratio. As you can see here, in shunt perfusion the abnormality is lung related, as the alveoli are perfused by not ventilated. The ETCO2 / PaCO2 Gradient in shunt perfusion is usually larger than normal in the 4 to 10 mmHg. In Shunt Perfusion the circulatory system can often provide some compensation by moving the blood flow to where the ventilation is. Additionally, oxygenation is usually more affected than CO2 removal. Why? CO2 diffuses 19 times faster and thus has the capacity to maintain normal CO2 levels longer. No exchange of O2 or CO2

Dead Space Ventilation
Capnography Dead Space Ventilation . . ETCO2 - PaCO2 Gradient is large High V/Q Ventilation is not the problem! Deadspace ventilation occurs under conditions in which alveoli are ventilated but not perfused. This V/Q abnormality is often referred to as a high V/Q (push down key) Dead Space is not a ventilation abnormality. Perfusion is the problem. No exchange of O2 or CO2 can occur. In Dead Space Ventilation, the circulatory system cannot partially compensate like we discussed in Shunt Perfusion. There is simply not enough blood flow. In this V/Q abnormally, the ETCO2 to PaCO2 gradient is large. Why? Let take a closer look. Perfusion is the problem No exchange of O2 or CO2occurs

Dead Space Ventilation
Capnography Dead Space Ventilation ETCO2 = 33 mmHg PaCO2 = 53 mmHg Alveoli that do not take part in gas exchange will still have no CO2 – Therefore they will dilute the CO2 from the alveoli that were perfused 53 This is obviously a depiction of a very simplified alveolar sac, but we see depicted is a cluster of alveoli, and that only a few of them are perfused. In the alveoli that are perfused the ETCO2 would be the same as the PaCO2 as we can see here. If technology existed that allowed us to just measure the three alveoli that did come in contact with perfusion, then ETCO2 would match PaCO2. However this technology does not exist. Here we can see that all of the alveoli that did not come in contact with perfusion contain no CO2. During exhalation all of the alveoli eventually empty into the trachea. Alveoli that do not take part in gas exchange will still have no CO2 – Therefore they will dilute the CO2 from the of alveoli that were perfused. When we measure the exhaled CO2 at the patients airway the end result is a widened ETCO2 to PaCO2 gradient. In fact it may be as much as 20 to 25 mmHg. Now is it the patient or the capnograph that isn’t working? Clearly it is the patient, the capnograph can only measure and display the CO2 present in expired gas. The result is a widened ETCO2 to PaCO2 Gradient

Capnography Dead Space Ventilation
Disease processes that may cause Dead Space Ventilation Pulmonary embolism Hypovolemia Cardiac arrest Shock In short, anything that causes a significant drop in pulmonary blood flow The disease processes that may cause Dead Space Ventilation are of course all related to the cardiovascular system: Pulmonary embolism, Hypovolemia, Cardiac arrest, Shock. In short anything that causes a significant drop in pulmonary blood flow.

Normal Capnogram - Phase I
CO2 mmHg 50 25 During inspiration CO2 is essentially zero and thus inspiration is displayed at the zero baseline. Phase I occurs as exhalation begins, which is shown as A to B on the capnogram. The first gas to appear at the sampling point is the last gas that was inhaled into the conducting airways. This gas has not been subject to gas exchange and thus is essentially free of carbon dioxide and remains at the zero baseline as you see in blue here. What is anatomical dead space? A B Beginning of expiration = anatomical deadspace with no measurable CO2

Anatomical Dead Space Anatomical Dead Space
Internal volume of the upper airways Nose Pharynx Trachea Bronchi Anatomical Deadspace Conducting Airway - No Gas Exchange Remember, the Anatomical Dead Space is the internal volume of the upper airways were no gas exchange takes place. This includes the nose, pharynx, trachea, and bronchi.

Normal Capnogram - Phase II
CO2 mmHg 50 25 C Phase II is characterized by a rapid rise in CO2 concentration as anatomical deadspace is replaced with alveolar gas, leading to Phase III. B Mixed CO2, rapid rise in CO2 concentration

Normal Capnogram - Phase III
Alveolar Plateau, all exhaled gas took part in gas exchange CO2 mmHg 50 25 C D End Tidal CO2 value In phase III all of the gas passing by the CO2 sensor is alveolar gas which causes the capnograph to flatten out. This is often called the Alveolar Plateau. (press down key) The ETCO2 value displayed on the monitor is the highest value measured during exhalation and usually occurs just prior to inspiration. Time

Normal Capnogram - Phase IV
Inspiration starts, CO2 drops off rapidly CO2 mmHg 50 25 D Phase four is inspiration and marked by a rapid downward direction of the capnograph. This downward stroke corresponds to the fresh gas which is essentially free of carbon dioxide that passes the CO2 sensor during inspiration. The capnograph will then remain at zero baseline throughout inspiration. Now we’ve identified what the normal capnograph looks like, let take a look at some abnormal ones. E

Capnography Normal Capnogram Stable trend
The capnogram is normal and the trend is stable. The ETCO2/PaCO2 gradient is 4 mmHg. Stable trend

Capnography Hyperventilation - Decrease in ETCO2 Possible Causes:
Here we can see slow drop in ETCO2. Increase in respiratory rate, increase in tidal volume, decrease in metabolic rate, for a fall in body temperature. The difference between this and a pulmonary embolus is that the drop in ETCO2 is more gradual, and the gradient is usually not large. Possible Causes: Increase in respiratory rate Increase in tidal volume Decrease in metabolic rate Fall in body temperature

Capnography Hypoventilation - Increase in ETCO2 Possible Causes:
What could be going one here, we can see a gradual increase in CO2 both on the capnogram and on the trend. Hypoventilation will usually result in an increase ETCO2. There are may causes of increase CO2: Decrease in respiratory rate or decrease in tidal volume. An increase in metabolic rate, rapid rise in body temperature or hyperthermia. Often patients who bypass PACU and come directly to the ICU will will be cold and have decreased body temperature. ETCO2 are often in low to mid thirties. As the patient starts to warm up and wake up you see a fairly rapid increase in ETCO2. Possible Causes: Decrease in respiratory rate Decrease in tidal volume Increase in metabolic rate Rapid rise in body temperature

Capnography Rebreathing Possible Causes:
So what do you think that we have going on here? An elevated CO2 baseline indicates CO2 rebreathing. An expiatory filter that is saturated or clogged will cause resistance to exhaled flow. Neb treatments or not changing the expiratory filter often enough can cause this to occur, as well as an expiratory valve that is sticking. Inadequate inspiratory flow, or insufficient expiratory time, in short anything that causes resistance to expired flow, can result in re-breathed CO2. Possible Causes: Expiratory filter that is saturated or clogged, expiratory valve that is sticking Inadequate inspiratory flow, or insufficient expiratory time Anything that causes resistance to expired flow

Capnography Endotracheal Tube in Esophagus Possible Causes:
On this and on the following slides you can observe the CO2 waveform and CO2 trend. What do you suppose is happening here, CO2 is initially present, diminishes with each breath, then drops to zero.( Press down arrow) Did anybody say endotracheal tube in the esophagus? A normal capnogram is the best available evidence that the ET tube is correctly positioned and that proper ventilation is occurring. When the ET tube is in the esophagus, either no CO2 is sensed or only small transient waveform are present. Often because we bag the patient with a bag-mask-resuscitator prior to intubation, there is a small amount of CO2 in the esophagus. Additionally, if the patient imbibed any carbonated beverage prior to being intubated, CO2 may be present in the stomach. After several breaths, that CO2 will be washed out. After 3 to 6 breaths, if the ET tube is in the esophagus, little or no CO2 is present. Possible Causes: Missed Intubation - when the ET tube is in the esophagus, little or no CO2 is present NOTE: A normal capnogram is the best evidence that the ET tube correctly positioned.

Case Study A 29 year old male with head injury, and a compound fracture of his femur sustained in a motorcycle accident 2 weeks post trauma on mechanical ventilation with the following physiological values: PaCO2 – 42 mmHg PaO2 – 95 mmHg ETCO2 – 38 mmHg Total Rate – 14 bpm Minute Ventilation – 7 L/Min A 29 year old male with head injury and compound fracture of his femur sustained in a motorcycle accident. 2 weeks post trauma on mechanical ventilation with the following philological values: PaCO2 – 42 mmHg PaO2 – 95 mmHg ETCO2 – 38 mmHg Minute Ventilation – 12 L/Min

Case Study Normal capnogram, stable trend ETCO2/PaCO2 gradient 4 mmHg
The capnogram is normal and the trend is stable. The ETCO2/PaCO2 gradient is 4 mmHg. Normal capnogram, stable trend ETCO2/PaCO2 gradient 4 mmHg

Case Study Sudden decrease in ETCO2 from 38 mmHg to 18 mmHg
Suddenly there is a decrease in ETCO2 from 38 mmHg to 22 mmHg and it remains there remains there. The patient becomes somewhat agitated, RR increases to 24 bpm, and his minute volume increases to 12 Lpm. Sudden decrease in ETCO2 from 38 mmHg to 18 mmHg and remains there RR – increases to 24 bpm Minute Volume increases to 12 Lpm

Case Study ABG was drawn with the following results: PaCO2 38 mmHg
An ABG was drawn with the following results: PaCO mmHg, PaO mmHg, PaCO2/ETCO2 gradient increased to 18 mmHg from a previous gradient of 4 mmHg. ABG was drawn with the following results: PaCO2 38 mmHg PaO2 59 mmHg PaCO2/ETCO2 gradient 20 mmHg

Case Study Ventilation /perfusion lung scan was consistent with a pulmonary embolism A sudden drop in ETCO2, associated with a large increase in the PaCO2/ETCO2 gradient, is often associated with pulmonary embolism Ventilation /perfusion lung scan was performed and the results were consistent with a pulmonary embolism. A sudden drop in ETCO2 Associated with a large increase in the PaCO2/ETCO2 gradient, often is associated with a pulmonary embolism.

Blood Gases and Related Tests
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