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
You already know the causes of respiratory acidosis via the different mechanisms. List 5 causes of Respiratory alkalosis
CNS - Head injury, stroke, panic attacks
Pulmonary - PE, pneumonia, asthma, pulmonary oedema
!!Salicylates!
Pregnancy
Give 5 causes of metabolic acidosis with and without anion gap
No anion gap: USED CAR
Ureteral diversion
Saline infusion
Exogenous acid
Diarrhoea
Carbonic anhydrase inhibitors
Adrenal insufficiency/Addison’s disease
Renal Tubular acidosis
Anion Gap: MUDPILES
Methanol and ethanol
Uremia - Renal failure
DKA (ketones)
Propylene glycol
Isoniazid or Iron excess
Lactic acid -> dehydration
Ethylene glycol
Salicylates - Aspirin
Primary hyperaldosteronism is most likely to cause what acid-base status?
What do we expect to see in terms of serum electrolytes of K+ and Na+?
Metabolic alkalosis (H+ wasting)
K+ is also wasted => Hypokalaemia
Na+ is retained at the DCT => Hypernatraemia
Aldosterone saves sodium and Kicks out K+
A newborn with pyloric stenosis will have which acid-base disorder?
Metabolic alkalosis from vomiting => GI loss of H+
Give 4 causes of metabolic alkalosis
H+ loss: Severe vomiting, loop and thiazide diuretics, excess mineralocorticoid (primary hyperaldosteronism)
HCO3- adminstration: Post-correction of metabolic acidosis for DKA/lactic acidosis
A patient is admitted with acute kidney injury. They were subsequently treated with metformin and Oromorph
PH 7.1 / HCO3 10 / pCO2 5.3
What is the patient’s acid-base status?
Primary Metabolic Acidosis (kidney injury)
Secondary Respiratory acidosis (Metformin-associated lactic acidosis + Opiates toxicity).
What is the normal anion gap?
What is the formula?
Normal is between 8-12
Anion gap (AG) = Na - (Cl+HCO3)
* corrected would be AG +(0.25x(40-albumin) - no need to know this but know that it is corrected using albumin
B
Metabolic acidosis with partial respiratory compensation
Na – {bicarbonate + chloride} = 140.5 – 112= 28.5 or 138-112=26
High anion gap Metabolic acidosis
E
D
Metabolic acidosis, complete compensation
pH is low= acidosis
Resp or metabolic?
If it’s resp, O2 is usually abnormal, is it? No
So this looks like acidosis which is not respiratory, i.e. metabolic acidosis
If it is metabolic, HCO3 should be low? Yes it is
Compensated or not?
If decreased HCO3, the compensatory mechanism is to blow off CO2 (acid) to decrease overall acidity
Is CO2 low? Yes, so compensated
Has pH normalised? yes, so complete compensated
C
This is metabolic alkalaemia
Differential diagnosis of a metabolic alkalosis or alkalaemia:
Persistent vomiting
E.g. gastric outlet obstruction (the classic example is pyloric stenosis in a baby)
What has happened here? Why?
This is the classic picture of aspirin overdose.
Respiratory alkalosis– Salicylate directly stimulates the respiratory center, causing hyperventilation and an early decrease in the partial pressure of carbon dioxide (PaCO2) [26,41,42]. The hyperventilation protects against toxicity since alkalosis prevents salicylate distribution into the central nervous system (CNS).
●Elevated anion gap metabolic acidosis– Accumulation of organic acids, including lactic acid (from uncoupling of oxidative phosphorylation) and ketoacids (from increased catabolism), cause an elevated anion gap metabolic acidosis [42,43]. Inhibition of the tricarboxylic acid cycle also contributes to the development of metabolic acidosis [44,45]. Salicylic acid itself has only a minor impact on serum pH, since a serum concentration of 50 mg/dL (3.6 mmol/L) contributes less than 3 mEq/L of hydrogen ions. A pure metabolic acidosis is unusual in adults [42] but may be seen in children who are brought to medical care immediately after ingestion [41].
●Mixed respiratory alkalosis metabolic acidosis– Most adults develop a mixed respiratory alkalosis metabolic acidosis as the net effects of these acid-base derangements.
