ABG + Acid-Base Flashcards
ABG shows a very low O2
level but the pt appears well
and is sitting up chatting. What is the most likely cause?
VBG instead of ABG by accident
ABG shows normal O2 levels
but the pt is clearly unwell & in
respiratory distress?
Patient on oxygen but not written on ABG as it should be
What is the normal PO2?
What PO2 would be considered hypoxaemic?
Normal PO2 is 11-13
Hypoxaemia is <8kPa
What is considered normal PCO2?
What PCO2 would be considered hypercapnic?
Normal PCO2 is 4.7-6kPa
Hypercapnia >6.7kPa
What is considered normal pH?
7.35-7.45
What is considered normal HCO3?
22-28 mEq/L
What are the classifications of Acute Resp Failure (3) with the definition (cutoffs) of each
Acute Type 1: Hypoxia without hypercapnia (PaO2 <8, normal/low CO2 (hyperventilation), pH normal)
Acute type 2: Hypoxia with hypercapnia (PaO2 <8, PaCO2 >6.7, pH <7.35)
Chronic Type 2: Hypoxia with hypercapnia (PaO2 <8, PaCO2 >6.7, Ph normal)
If a patient is receiving 28% FiO2 from a Venturi mask, what would you expect the PO2 to be in a healthy individual?
General rule: PO2 should be about 10kPa less than the FiO2 (%) => PO2 should be about 18kPa
What are the top 4 causes of hypoxaemia?
Give 1 example for each
Reduced PiO2/FiO2: High altitude
Hypoventilation: CNS depression, morbid obesity
Diffusion limitation: Emphysema, ILD
V/Q mismatch: PE, pneumonia
Indicate the effect of each of the following mechanisms of hypoxaemia on the A-a gradient:
Reduced inspired O2 (PiO2/FiO2):
Hypoventilation:
Diffusion limitation:
V/Q mismatch:
Reduced inspired O2 (PiO2/FiO2): Normal
Hypoventilation: Normal
Diffusion limitation: Increased
V/Q mismatch: Increased
Indicate the effect of each of the following mechanisms of hypoxaemia on the A-a gradient:
Pulmonary Embolism:
Pneumonia:
High altitude:
CNS depression:
Morbid obesity:
Emphysema:
ILD:
Pulmonary Embolism: Increased
Pneumonia: Increased
High altitude: Normal
CNS depression: Normal
Morbid obesity: Normal
Emphysema: Increased
ILD: Increased
List the causes of type 1 and type 2 ARF (5 each)
Common: Acute COPD and ARDS (more likely type 2)
Type 1: Acute Asthma, Pulmonary fibrosis, ILD, pneumothorax, pulmonary embolism!!, Congenital HD (shunt), Bronchiectasis, !pneumonia,
Type 2: Severe asthma, pulmonary oedema, opioid/sedative overdose, Neuromuscle disorders (myasthenia gravis), CNS depression, Chest wall deformities, polyneuropathy, cervical cord injury, !obestiy hypoventilation syndrome!
A 45-year-old man with no known medical conditions
comes to the emergency department due to severe
dyspnoea and chest discomfort that began earlier in the day. The dyspnoea has been worsening throughout the day and is now present at rest. Temperature is 36.7 C, blood pressure is 110/60 mmHg, and pulse is 96/min. Respiratory
rate at time of assessment is 24 breaths/min.
What is the most likely diagnosis?
What do you expect to find on ABG?
PE
Hypoxia without hypercapnia => T1RF
Acute-onset dyspnoea and chest discomfort - acute
pulmonary embolism
* PE leads to a ventilation/perfusion (V/Q) mismatch & causes hypoxaemia
* The acute hypoxaemia triggers an increase in respiratory drive and hyperventilation
In a case of PE, what would you expect the CO2 levels to be?
If treatment of a PE was not promptly performed, what can happen?
- Increased ventilation rate -> increased expiration of
CO2 -> hypocapnia -> respiratory alkalosis
an acute V/Q mismatch (e.g. PE) frequently
results in hypocapnia, respiratory alkalosis and persistent hypoxaemia
*prolonged hyperventilation -> respiratory muscle fatigue -> hypoventilation -> hypercapnia and respiratory acidosis
Arterial blood gas drawn on room air shows an arterial partial pressure of oxygen (pO2) of 7.4 kPa and an arterial partial pressure of carbon dioxide (pCO2) of 3.4 kPa.
Is this type 1 or type 2 respiratory failure?
1
A 43-year-old man is brought to the emergency
department after being found drowsy by his wife. She says he was in his usual state of health when she left home a few hours ago. The patient has a history of depression and type 2 diabetes mellitus. He was recently laid off from work. Blood pressure is 100/60 mmHg and pulse is 64/min
Arterial blood gas analysis reveals the following:
pH 7.22
PaCO2 8.4 kPa
HCO3− 24 mEq/L
What is the most likely current acid base status in this patient?
Is this an acute or chronic process? why?
Respiratory acidosis without compensation
This is an acute process since although pH is low, HCO3 is within the normal range => acute
Causes of respiratory acidosis without compensation
include any disorder that causes acute hypoventilation (such as, in this case, opioid/sedative overdose with depression of respiratory drive)
And remember as in the anaesthetic notes, that hypoventilation is a process that leads to hypoxaemia and hypercapnia
A 60-year-old woman with known COPD comes to the emergency department due to shortness of breath and productive cough. The patient has a 30-pack-year smoking history. Oxygen saturation is 88% on room air. She is started on high-flow oxygen supplementation. Shortly afterward, she becomes increasingly lethargic and confused.
What is the most likely cause of his in-hospital decline
This patient’s clinical presentation is consistent with an exacerbation of COPD
* Supplemental oxygen may be warranted in patients with COPD who have significant hypoxemia; however one must be cautious in doing so
* Excessive O2 administration in patients with COPD can lead to oxygen-induced hypercapnia, resulting in
confusion and a depressed level of consciousness
* This is largely due to V/Q mismatch and the Haldane effect
What is the Haldane effect in COPD
1) In COPD, the respiratory drive is often more dependent on hypoxemia than hypercapnia. Supplemental oxygen can blunt this drive leading to hypoventilation
2) When giving a COPD patient supplemental oxygen, Hb becomes more oxygenated => reduced affinity to CO2 (as per the oxygen dissociation curve). => Hb will dissociate from CO2 and release it into the blood stream. The body is much less efficient in removing CO2 from the blood => hypercapnia, confusion, and lethargy. Buffering systems is the way to clear the CO2 in the blood by binding with H2O to form H2CO3
A 74-year-old man with advanced COPD and
bronchiectasis is brought to the ED. He is lethargic and difficult to rouse. A collateral history reveals worsening dyspnoea, increased cough and sputum purulence over the previous 4 days. Oxygen saturation is 86% on room air. An ABG is performed prior to initiation of therapy, and venous blood samples are also taken for routine biochemistry.
Results show a pH of 7.29, PaO2 of 7.8 kPa and PaCO2 of 12.7 kPa.
HCO3− is 38 mEq/L.
What is your interpretation of these results?
Hx suggests an exacerbation of COPD/ bronchiectasis +
features of CO2 retention
* The patient is in type 2 respiratory failure
pO2 is low pCO2 is high
* HCO3− is ++ elevated, the pH is decreased
* This suggests that the patient is a chronic CO2 retainer, and the bicarbonate is likely elevated at baseline
Resp acidosis with baseline bicarb raised
Although this is an acute exacerbation, COPD patients have impaired chemoreceptor sensitivity to PCO2 => their baseline bicarb is elevated
At what GCS score is NIV contraindicated?
Why?
GCS<8
Inability to protect airway
What are the contraindications for NIV? (5)
Urgent need for intubation (cardiac/pulmonary arrest, organ failure),
altered conciousness GCS <8
Pneumothorax,
Fixed upper airway obstruction,
Severe facial deformity or facial burns
Active vomiting
A 43-year-old woman with borderline personality disorder is brought to the emergency department at midday after taking an undetermined number of pills earlier than morning. She is lethargic but rousable. Blood pressure is 110/60 mmHg and heart rate is 120/min and regular. Pertinent blood results are as follows:
pH 7.46
PaO2 11.2 kPa
PaCO2 2.9 kPa
HCO3− 13 mEq/L
Sodium 139 mEq/L
Potassium 3.3 mEq/L
Chloride 98 mEq/L
Haemoglobin 12 g/dL
Calculate the anion gap
The patient also describes tinnitus. Based on the available data, which of the following medications did she likely overdose on?
A. Amitriptyline
B. Alprazolam
C. Aspirin
D. Lorazepam
E. Morphine
Can you explain what is going on with this patient?
Recall that in all cases of metabolic acidosis, an anion
gap should be calculated
* In this instance, the anion gap is [(139 +3) − (98 + 13) = 31], which is high
* Salicylate poisoning is a recognized cause of mixed primary acid-base disturbance, and typically presents with a primary respiratory alkalosis followed by a primary high-anion gap metabolic acidosis
C. Aspirin
This patient’s elevated pH and low pCO2 are suggestive of primary respiratory alkalosis
* Although we would expect a decrease in HCO3
− to ensue, the magnitude of the decrease in HCO3
− is far greater than would be expected in such a short time frame
* This indicates a second primary acid-base disorder,
specifically a concomitant metabolic acidosis
What is the expected pH in salicylate overdose?
What drives acid-base disturbances in salicylate overdose?
In salicylate overdose, the pH is typically near or within normal range due to the opposing influences of the respiratory alkalosis and metabolic acidosis
– However, the pH being near-normal does not mean these patients are well
– Effects are dose-related, and potentially fatal
Primary respiratory alkalosis is due to direct stimulation of the medullary respiratory center by excess salicylate, resulting in both an increased respiratory rate and tidal volume (increasing minute
ventilation) => Hypocapnia
* Primary metabolic acidosis occurs mostly because salicylate uncouples oxidative phosphorylation, which results in increased production of lactic acid and ketoacids in peripheral tissues
How is a salicylate overdose managed generally?
Rehydration
Alkalinisation of urine using sodium bicarb NaCHO3
Dialysis in cases of substantial ingestion
