Lecture 7: ABG Intrepretation Flashcards
O2 is either bound to Hb or dissolved in plasna
Pulse oximetry (SPo2), artierial blood gas (ABG), and venous blood gas (VBG) are all methods of assessing oxygenation, ventilation, and acid-base status, but they provide different types of information and are used in different clinical scenarios
What measure tells us the percentage of Hb in the blood that is bound to O2?
Pulse Oximetry (SPo2)
How it works: Uses light absorption at two wavelengths (red and infrared) to estimate O2 saturation in capillary BF
Spo2 correlates w/ PaO2, but is an estimate, not a direct measurement
What is normal for spo2?
* if its low what does the pt have?
95-100% = normal
< 90% = concerning (possibly hypoxia)
< 85% = Critical hypoxia (needs intervention)
When do we use Pulse oximetry (Spo2)
We use it to monitor oxygenation trends (COPD, pneumonia, ARDS, asthma)
Assessing the response to o2 therapy (so if the pt is on o2)
Quick screening tool in emergency situations
Limitations:
* Does not measure ventilation (CO2 levels) –> cannot assess for respiratory failure due to hypercapnia
Can be falsely high or low due to:
* carbon monoxide posioning (spO2 appears normal despite hypoxia) - meaning, the spo2 cannot differenitate between CO2 and O2, so it appears normal while its actually not
* severe anemia (low hb but high spo2) - so you’re hypoxia, however, the % of O2 bound to Hb remain normal, meaning that the Spo2 reads a noraml value while you’re actually hypoxic
* Poor perfusion (shock, hypothermia, dark nail polish, cold extremities)
EX: A pt w/ COPD on 6L O2 has SpO2 of 98% but is still confused –> could be CO2 retention (hypercapnia), which pulse oximetry won’t detect
* This is why artial blood gas (ABG) is needed for a full respiratory assessment
What does an artial blood gas test measure?
* How is it actually measured?
What it measures:
* pH (Acid-base balance)
* PaCO2 (Ventilation - how well CO2 is removed) - this is the partial pressure of CO2
* PaO2 (Oxygenation - direct arterial oxygen levels) - this is the partial pressure of O2
* HCO3 (Metabolic compensation) - this is bicarbonate
* Lactate (Tissue hypoxia indicator)
* SaO2 (Arterial oxygen saturation, but directly measured) - SaO₂ (arterial oxygen saturation) refers to the percentage of hemoglobin in the arterial blood that is saturated with oxygen. It is typically measured using arterial blood gas (ABG) analysis and provides a precise indication of how well oxygen is being transported in the blood. - The main difference between SaO₂ and SpO₂ is how they are measured and their accuracy: - SaO2 = taken directly out of the artery while spo2 measures it indirectly.
How it works: - note theres increased pressure in the arteries opposed to the vein, so intoducing a needle in is slightly risky. can also be painful
* Blood is drawn from an artery (usually the radial, femoral, or brachial artery)
* Directly measures arterial oxygenation and ventilation
* respiratory therapist typically does this
Before artial blood gas is tested which test is done to see if the radial nerve is good enough to draw blood from?
Allens test
* have pt clench fist while compressing both arteries
* ask pt to open hand (should appear pale)
* release ulnar artery while leaving pressure on radial)
* hand should become flushed in 5-10 seconds
* if remains pale do not puncture radial artery because it might be the only thing continuing to give blood to that hand
Arterial Blood gas (ABG) - when to use it:
* Evaluating respiratory failure (hypoxia or hypercapnia) - because pulse ox does a bad job of this)
* Assessing acid-base disorders (DKA, sepsis, kidney failure) - imbalance in the pH system in the blood
* monitoring crtically ill pts on ventilators - think people w/ COPD have a hard time forcing out their air, leading to a buildup of CO2, which the SPO2 cant detect, and they might be becoming hypoxic and you can’t tell (Co2 poisoning)
Limitations
* Painful and invasive (artial puncture)
* Cannot be performed frequently due to risk of arterial damage or thrombosis
* PaO2 is affected by O2 therapy, so FiO2 must be noted
EX:
* A COPD pt on high-flow O2 has SpO2 of 98% but is confused –> ABG shows PaCO2 = 85 mmHg, confirming Co2 retention and impending resp failure
What is our normal pH range?
* What does low indicate?
* What does high indicate?
7.35-7.45
Low = acidic
High = basic
Why do we care about pH Balance
* Maintaining pH homeostasis is critical for survival because nearly every biochemical reaction in the body depends on a stable pH environment. Even small deviation from the normal pH range (7.35-7.45) can lead to severe physiological dysfunction and in extreme cases, death
pH homeostasis is important for
1) Protein structure and enzyme function
2) Cellular metabolsm and ATP production
3) Oxygen Transport and Hb Affinity
4) Excitability of nerves and muscles
What does the buffer system do?
Immediate pH stabilization
Which buffer system is the primary pH regulator?
* do buffers work quickly?
Bicarbonate (HCO3-) buffer system
HCO3- (bicarbonate, base) neutralizes acids (H+), while carbonic acid (H2CO3) neutralizes bases
How it works: (to stop blood from becoming acidic)
* if the blood becomes acidic (lower pH, incrased H+) –> HCO3- (bicarbonate) binds H+ –> forms H2CO3, which dissociates into CO2 and H2O –> CO2 is exhaled by the lungs
* so this is basically just saying how we stop our bodies from become acidic by utilizing bicarbonate as a buffer
* so bicarbonate basically picks up those extra H+ ions
How it works: (to stop blood from becoming alkaline) - I think some of this might be wrong.
* If blood becomes alkaline (increased pH, Decreased H+) –> H2CO3 dissociates –> releases H+ to lower pH
* so the reaction basically just goes the opposite direction to release H+
* so bicarbonate is utilized either way
* So bicarbonate essentially releases more H+
equation below
Other buffer systems include the protein buffer (hemoglobin, albumin, intracellular proteins) and phosphate buffer system
Key Takeaway: Buffer systems provide immediate but limited pH corrdction
What two organs in the body react to deviations in pH
Kidneys
Lungs
Systems for Acid base balance (remember, we already talked about the buffer system doing this)
1) The lungs (CO2 Regulation - Respiratory Component)
* The lungs control pH by regulating CO2 levels
* CO2 acts as an acid (froms carbonic acid when dissolved in blood)
* Hyperventilation –> “Blows off” CO2 –> Increased pH (respiratory alkalosis)
* Hypoventilation –> Retains CO2 –> decreased pH (Respiratory Acidosis) - so think COPD where CO2 is just building up in the lungs because you can’t push it out.
* Key takeaway: The lungs provide rapid compensation - within minutes (so if you need fast adjustments the lungs do it)
2) The Kidneys (HCO3- Regulation - Metabolic Component)
* The kidneys regulate acid-base balance by:
* Excreting hydrogen ions (H+) in urine
* Reabsorbing bicarbonate (HCO3-)
* Metabolic Acidosis –> kidneys increase H+ excretion and HCO3 retention (gets rid of extra acid, retains the bicarbonate so that it can neutralize the extra H+)
* Metabolic Alkalosis –> kidneys decrease H+ excretion and excrete more HCO3- (so the add more H+ into the system and they take bicarbonate out so that it doesnt neutralize the remaining H+)
what acts faster the lungs or the kidneys to pH deviations?
Lungs
* makes sense, we can just change our breathing very quickly
Normal pH
7.35-7.45
PaCO2 (partial pressure of carbon dioxide) norms
35-45 mmHg
high = acidic (drops pH)
* think not being able to force air out of lungs so it builds up (COPD)
Low = alkaline (increases ph)
So theres an inverse relationship between the pH and the CO2. The more CO2 (which were saying is the same as H+) = decreased pH (more acidic)
Base = A base is a substance that can accept hydrogen ions (H⁺) or donate hydroxide ions (OH⁻) in a solution
* this is bicarbonate
pH has a direct relationship to bicarbonate. As one goes down the other goes down
What are the norms for bicarbonate (HCO3-)?
* What is bicarbonate regulated by (organ)
22-26 mEq/L
* Bicarbonate is regulated by the kidneys
What are the norms for PaO2? (partial pressure of O2) - so its the pressure of O2 in the blood
80-100mmHg
don’t mix up w/ SpO2/SaO2
What is the norm for SaO2?
Same as SpO2 because its essentially measuring the same value (amount of Hb bound to O2) = 95%
What is the Anion Gap and what are the norms for it?
* What doe sit help detect
8-12 mEq/L
Difference between cations and anions (helps detect metabolic acidosis)
* so its the amount of positively charged ions in blood minus negatively charged ions
Why these values matter in practice:
pH is like the pts “vital sign” for acid-base balance - if its out of range, something is wrong
PaCO2 and HCO3- tells us where the problem is - lungs or kidneys
Compensation helps determine whether the body is trying to fix the problem or if this is an acute issue
Oxygenation (PaO2, SaO2) is critical - if low, we need to intervene fast!
ABG Interpretation
Step 1: Assess pH (is the blood acidic or alkaline)
* pH < 7.35 = Acidosis (too much acid, too little base)
* pH > 7.45 = alkaline (too little acid, too much base)
* so basees are just anything that reduces the H+
* pH 7.35-7.45 –> normal (but don’t stop here! it could be a compensated disorder)
Why pH is important:
* The bodies normal pH is tightly regulated because even small changes can imapir enzyme function, hemoglobin oxygen binding, and cellular metabolism
ABG Intepretation Cont’d
Step 2: Identify the Primary Problem (Respiratory or Metabolic - meaning kidneys or lungs)
* Look at PaCo2 and HCO3- and determine the cause
PaCo2 (35-45 mmHg) –> Lungs (Respiratory Component
* High PaCO2 (>45 mmHg) –> Respiratory acidosis (hypoventilation, CO2 retention) - remember we look at CO2 and H+ the same way
* Low PaCO2 (<35 mmHg) –> respiratry alkalosis (hyperventilation [blowing CO2 out] CO2 loss)
* It makes all the sense in the world that the lungs would impact CO2 - easy to remember
HCO3- (22-26 mmHg) –> Kidneys (metabolic component)
* Low HCO3- (bicarbonate) –> Metabolic Acidosis (loss of base excess acid [can’t neutralize the acid])
* High HCO3- (>26) = metabolic alkalosis (too much bicarbonate neutralizing acid makes pH increase) (excess base loss of acid)
helpful mnemonic –> ROME - Quick way to recognize primary disorder
* Respiratory = Opposite (pH and PaCO2 move in opposite directions)
* Metabolic = Equal (pH and HCO3- move in the same direction)
**EX: Low pH and elevated CO2, bicarbonate is normal. **
* Acidosis
* CO2 high = acidic - coming from lungs
* bicarbonate = normal = kidneys are fine
* Problem = Respiratory Acidosis
* Primary respriatory acidosis because CO2 and pH are opposite directions (abnormal in opposite directions)
Respiratory acidosis (lung problem causing increased CO2) - primary causes
* **anything that causes decreased ventilation (hypoventilation, airway obstruction, or neuromuscular failure) - anything thats keeping the pt from pushing the air out
Central respiraory depression (brain not sending signals to breathe) - things acting on brain
* Opoid or sedative overdose - lowers respiratory drive
* CNS depression from stroke, trauma, brainstem injury
* Obesity hypoventilation syndrome
Airway Obstruction (Can’t get CO2 out)
* COPD Exacerbation (Air trapping –> Co2 retention)
* Severe asthma attack (bronchoconstriction prevents ventilation)
* Pneumonia or pulmonary edema (fluid or infection blocks alveolar gas exchange)
* Aspiration of foreign body (obstruction prevents CO2 exhalation)
Neuromusuclar impairment (can’t breath adequalty)
Respiratory muscle fatigue (exhaustion and CO2 buildip)
* Severe COPD exacerbation (diaphragm overworked)
* Status asthmaticus (severe prolonged asthma attack)
* Kyphoscoliosis or chest wall deformity (restricts lung expansion)
Cause Of Respiratory Alkalosis
* Anything that causes hyperventilation
* w/ hyperventilation pt is pushing CO2 out = pushing H+ out = increase pH = alkalosis
potential causes:
Anxiety and pschogenic causes
Hypoxia driven hyperventilation
* Pulmonary embolism
* Severe anemia (low O2 deliver –> increased ventilation)
* High altitude (low atmospheric O2 triggers hyperventionaltion)
* Carbon monoxide positioning (tissue hypoxia –> increased breathing rate)
Pulmonary causes (lung driven increased ventilation)
* Early pneumonia or pulmonary edema
* Interstitial lung disease (fibrosis stiffens lungs, increasing RR0
Central NS (brainstem overstimulation)
Stroke, tumor, or trauma affecting the respiroatory centers
* Meningitits, encephalits, or brainstem injury
* Fever and sepsis (increased respiratory drive due to inflammation and cytokines)
Endocrine and metabolic triggers
* Hyperthyroidism (increased metabolism increases breathing rate)
Mechanical overventulation
* Excessive ventilation or a mechanical ventilator
* Bag mask ventilation at high rates
Causes for Metabolic alkalosis
Alkalosis = increased pH = increased bicarbonate (because bicarbonate neutralizes H+, meaning its less acidic, meaning the pH will rise)
* It also has to be bicarbonate instead of CO2 because its got the word metabolic infront of it meaning its coming from the kidneys
Chloride = very helpful for letting kidneys discrte bicarbonate. So conditions are realted to low chloride vs not low chloride levels
Chloride-Responsive metabolic Alkalosis (Urine Cl- <20 mEq/L)
* Severe Vomiting (Loss of stomach acid - HCl)
* Nasogastric Suctioning (NG Tube Loss) (Removes gastric acid)
* Diuretics (Loop and Thiazides) (Lose H+ and Cl- in urine)
* Post-Hypercapniea (after Co2 retention in COPD) (Overcompensation after chronic respiratory acidosis)
* Cystric Fibrosis (Excess chloride loss through sweat)
Chloride-Resistant Metabolic Alkalosis (Urine Cl- > 20 mEq/L)
* Primary hyperaldosteronism (Conn’s syndrome) (Too much aldosterone –> H+ and K+ loss)
* Cushing’s syndrome (high cortisol) (stimulates aldosterone receptors)
* Excessive bicarbonate adminstration (overcorrection of acidosis)
ABG Interpretation:
Step 3: Check for Compensation (Is the body trying to fix it)
* If PaCO2 is the primary issue, the kidneys will try to compensate by adjusting HCO3- (because remember, they control bicarbonate, not CO2)
* If HCO3- is the primary issue, the lungs will try to compensate by adjusting PaCO2
* So if the kidneys are having issues the lungs will try and compensate and if the lungs are having issues the kidneys will try and compensate
Types of Compensation:
* Uncompensated - The opposite system (lungs or kidneys) is still normal (meaning the other system isnt even trying to help out for the failing other system)
* partially Compensated –> The opposite system is trying to fix it, but the pH is still abnormal (so its trying and failing)
* Fully Compensated –> The opposite system has corrected pH back to nomral, but PaCO2 and HCO3- are still abnormal - so they fixed the pH but one over the systems is in overdrive while the other is failing - but the pH appears normal because its sucessfully compensated
remember if its a lung problem the kidneys won’t be able to immediately compensate because they’re just slower
* so for instance if you have an acute COPD flare up, they’re going to be struggling to get air out = buildup of COPD = respiratory acidosis, however, the kidneys cannot quickly correct for this because they’re just slower (this is a common thread w/ the kdineys, think having to go through the entire RAAS system, opposed to the barareceptors which are much faster)
EX: if pt has metabolic acidosis (meaning the kidneys arent retaining enough bicarbonate) than the lungs can quickly compensate by getting rid of the excess CO2 by doing hyperventiolation (so essentially getting rid of some of that acid making the body more basic)
* so lungs can quickly compensate
ABG Intrpretation
Step 6 (skipped a couple) - Clinical correlation - What does this mean for the pt?
* What symptoms does the pt have?
* Do the ABG findings match the clinical picture
* What is the underlying cause
* What tx is needed?
EX: If you see a metabolic acidosis with an anion gap of 24, think of conditions like DKA, lactic acidosis, or toxin ingestion-now you need to order glucose, lactate, or toxicology tests!
* so she skipped the anion gap stuff so I think this is irrelavant
pt case:
* pH = 7.28 = acidosis
* PaCo2 (norm = 35-45) = 60 = high (increased CO2 = decreased pH) = lung problem - so i was able to derieve that it was a lung problem because the pH was low and the CO2 was high (we know its an inverse realtionship) meaning, I know its coming form the lungs
* Primary Respiratory acidosis (why primary?) with no compensation - this comes from elevated CO2 = COPD / neuromuscular / Central respiratory depression (think Opoids)
* Bicarbonate (norm = 22-26) = norm
Case 2: ABG results
* pH = 7.21 - acidic
* PaCO2 = 28 mmHg - low
* HCO3- = 12 mEq/L - low
* Na+ = 138 mEq/L
* Cl- = 100 mEq/L
Low bicarbonate = low pH
* Primary metabolic acidosis
* so lungs should be immediately trying to compensate - Kussmauls inspirations (lungs trying to compensate)
* DKA is the most likely cause given her hx of diabetes, hyperglycemia, and symptoms
Case 3: 54 y/o male presents w/ severe nausea and vomitting for the past 3 days after a bout of food poisioning. He feels dizzy, weak, and lightheaded. His BP is 90/60, and his labs show hypokalemia
ABG results:
* pH = 7.49 - alkolosis (basic)
* PaCO2 = 48mmHg - high (35-45) - lungs are retaining CO2 to compensate - this is off because the lungs act quickly
* HCO3- = 34 mEq/L - high
* Urine Cl- = 12 mEq/L
So primary problem is kidneys because bicarbonate is high. This is because the bicarbonate takes a while to adjust while the lungs proably adjusted quickly.
* So I think the bicarb takes priority
Primary Metabolic Alkolosis
bicarbinate is high = lower pH (because it neutralizes the acids)
NOTE: this is partial compensation because the lungs are trying to compensate but failing. pH has not come back to a normal range yet, just partially.
Case 7: A 75 year old male w/ COPD and CHF is admitted for worsening leg swelling and wt gain. He was started on high-dose furosemide (lasix). After 2 days, he becomes lethargic and confused
* likely a COPD flare up (not confusional states often represent increased CO2 - but can’t tell this by just checking pulse OX which is why we have the ABG)
ABG results:
* pH = 7.42 - normal - fully compensated
* PaCO2 = 55 mmHg - high - respiratory acidosis
* HCO3- = 34 mEq/L - high = metabolic alkolosis
High PaCO2 = increased H+ = acidosis
HCO3 high = increased pH = alkolosis
These two disorders are balancing eachother out!
