Disorders of Acid-Base Flashcards

1
Q

Why do we care about acid-base homeostasis?

A
  • Critical to life
  • Must be tightly controlled for proteins
  • Metabolic processes produce acid= cellular respiration (CO2), other processes produce non-volatile acids (ketones and lactate)
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2
Q

How do our bodies maintain acid-base homeostasis?

A
-Buffers
=Bind H+ ions to reduce acidity
=Proteins- haemoglobin
=Bicarbonate
-Lungs 
=Remove CO2 from cellular respiration and non-volatile acid by shifting equilibrium (limited by bicarbonate reserves)
-Kidneys
=excrete H+ into urine, recover and regenerate bicarbonate
=24-48hrs to maximum efficiency
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3
Q

How can pathology lead to respiratory acid-base disorders?

A
  • Acidosis= lung disease (COPD), airway obstruction, neurological problems resulting in reduced respiratory rate (head injury, opiate overdose)
  • Alkalosis= panic attack, reaction to pain, acute asthma exacerbation (increased RR)
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4
Q

How can pathology lead to metabolic acidosis?

A

-Overproduction of acid
=lactic acidosis from inadequate oxygen supply to tissues (hypovolaemia, severe anaemia, damage to major arteries or cardio-respiratory arrest_
=Ketoacidosis secondary to inadequate cellular glucose supply (Type 1 diabetes, starvation, alcohol intoxication)

-Impaired excretion of H+ by kidneys
=Global loss of renal function (severe acute kidney injury/ end-stage chronic kidney disease)
=Specific impairment of renal tubule’s ability to excrete acid (renal tubular acidosis)

-Losing large amounts of bicarbonate
=Severe diarrhoea, surgical formation of fistula in small bowel, kidney via renal tubular acidosis

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5
Q

How can pathology lead to metabolic alkalosis?

A

-Unusual loss of H+ ions
=protracted vomiting
=sever hypokalaemia and hyperaldosteronism
=reabsorption of sodium in exchange for H+ ions (given low availability of K+ ions) causes H+ ions to be excreted

-Ingesting unusual quantity of bicarbonate (overdose of sodium bicarbonate)

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6
Q

What indicates acidaemia or alkalaemia?

A

-H+ ion concentration (usually measured from a blood sample)
=Outside the reference range
-pH in terms of blood concentrations of CO2 or bicarbonate
=caused by underlying pathology
=body compensation for acid-base disturbance

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7
Q

Describe metabolic correction of respiratory disturbances

A
  • Acidosis= kidneys regenerate bicarbonate

- Alkalosis= tends to be too acute for kidneys to react

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8
Q

Describe correction for metabolic disturbances

A
  • Acidosis= rapid and deep breathing (Kussmaul) and regenerate bicarbonate
  • Alkalosis= marginal, hypoventilation limited by need for oxygen, few severe metabolic alkaloses
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9
Q

How do we assess an acid-base disorder?

A
  • History = respiratory, fluid balance, intoxication, drug therapy, inadequate blood supply to tissues
  • Physical examination= GCS, pupil reactivity, RR, oxygen saturation, heart rate, bp, temperature (sepsis)
  • Blood gas (arterial/ venous)
  • Venous bicarbonate (total CO2)
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10
Q

How does a blood gas analyser work?

A
  • Uses electrochemistry to measure concentrations of oxygen, CO2 and H+ ions
  • Bicarbonate result calculated
  • Henderson-Hasselbalch equation (water concentration constant so K)
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11
Q

How is total CO2 measured?

A

-Measured by enzymatic reaction

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12
Q

How is blood for blood gas analysis collected?

A

-Radial artery
=Compared to venous collection, painful and risk of damage to artery thus compromising supply to hand
=In an arrest- femoral artery
-Collected into syringe with anti-coagulant (heparin)
=presence of bubbles reduces stability as air exchanges with oxygen and CO2 in blood
=Pod systems to send blood pressurised and affects pO2 and pCO2 values

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13
Q

What are the 4 parameters of blood gas analysis?

A

-pH
-pO2
-pCO2
-Bicarbonate
(Calculate standardised bicarbonate, base excess, anion gap)

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14
Q

What questions are asked to interpret the gas?

A

-• Is your patient adequately oxygenated? Does your pO2 fall within the reference range and given their “fraction of inspired” oxygen is that pO2 what you’d expect. Lastly what’s their [Hb]? As even if their pO2 is encouraging, if their [Hb} is very low they may not be delivering enough oxygen to their body.
• What is the pH? Reference range, low or high?
• Next – how did the pH get to where it is? Is it reflected in a derangement of CO2? Or bicarbonate? Or perhaps both? And which one of the changes in pCO2 or bicarbonate is caused by pathology, and which one is the body’s attempt at restoring acid-base homeostasis?

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15
Q

What is base excess?

A

Base excess is defined as the concentration of H+ required to return pH to reference range assuming a specific pCO2 of 5.3. It should therefore only be deranged in a metabolic disorder, and is negative in metabolic acidosis and positive in metabolic alkalosis.

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16
Q

What is standardised bicarbonate?

A

It represents what we would expect the bicarbonate concentration to be if pCO2 were in the reference range. So it should be within reference range for a purely respiratory disorder, about the same as the actual bicarbonate in a metabolic disorder…. but quite different to the actual bicarbonate where there are both respiratory and metabolic disorders.

17
Q

How are the blood gas parameters visualised?

A
  • Plots on graph

- Can be helpful where one or more pathologies simultaneously driving acid-base disorders (mixed)

18
Q

What are the main underlying causes of metabolic acidosis?

A

-Excess acid production
=Ketoacidosis (diabetic, starvation, alcoholic)
=lactic acidosis (tissue hypoxia from sepsis, anaemia, major haemorrhage, cardio-resp arrest, peripheral vasculature disease)
-Poisoning
=Aspirin, screen-wash, methanol, salicylate
-Inherited (produces acidic metabolites)
-Reduced excretion of acid
=global renal impairment (AKI, CKD), defect in tubular function (Types 1 and 4)
=Nephrocalcinosis, myeloma, heavy metal poisoning
-Bicarbonate loss
=bowel (small)
=specific renal tubular dysfunction (type 2)

19
Q

What is the anion gap?

A

-Theoretical construct
-Difference between the most abundant positively charged ions and most abundant negatively charged ions
-Helps narrow differential diagnosis (elevated in some, normal in others)
-Plasma chloride levels static or increase
=Hyperchloraemic acidosis with normal anion gap in severe diarrhoea, RTA, high fistula output
=Elevated= replaced with anions corresponding to lactate and keto-acids

20
Q

What are the clinical effects of significant metabolic acidosis?

A
  • Negative inotropic effects (cardiovascular)
  • Changes to the way Hb binds to oxygen
  • Impaired consciousness
  • Cellular K+ may leak into the plasma and be lost renally… such that prolonged acidosis can result in total body potassium depletion
  • Similarly, calcium will be more readily freed from bony tissue, and therefore chronic acidosis may lead to bony demineralisation/ decalcification
21
Q

What are the clinical effects of significant respiratory acidosis?

A
  • Hypercapnia
  • SOB, raised RR (although this may be blunted in chronic CO2 retention)
  • A variety of neurological effects (anxiety, coma, headache, extensor plantars, myoclonus)
  • Systemic vasodilatation
22
Q

What can cause respiratory alkalosis?

A
  • Asthma exacerbation
  • Other acute respiratory pathologies (COPD exacerbation, pulmonary embolism)
  • Things that might stimulate raised RR like pain or anxiety
  • Over-ventilation in intubated patients (iatrogenic)
  • Raised RR in altitude sickness
  • Inappropriate stimulation of the respiratory centre in the brain stem (head injury, raised ICP, local tumour, hepatic encephalopathy, poisoning)
  • mild chronic respiratory alkalosis= pregnancy (compensated through mild renally-mediated metabolic acidosis)
23
Q

What are the clinical effects of respiratory alkalosis?

A
  • Stemming from acute hypocapnia
  • Cerebral vasoconstriction (light-headedness, confusion, syncope, fits)
  • Fall in ionised calcium (less soluble in alkaline conditions, perioral, peripheral paraesthesia)
  • Cardiovascular= increased HR, vasoconstriction (chest tightness/ angina with background of coronary artery disease)
24
Q

What can lead to hypokalaemia?

A
  • Vomiting (gastric fluid rich in potassium)
  • Liver cirrhosis (fluid loss from intravascular space as ascites= hyperaldosteronism= stimulates kidney to retain sodium in exchange for excreting K+)
  • Alkalaemia causes K+ ions to move from plasma into cells
25
Q

How does hypokalaemia worsen alkalaemia?

A

-Relative to absence of K+ ions, Na+ ions may be exchanged by the kidney for the excretion of H+ ions instead

26
Q

What are the causes of metabolic alkalosis?

A
  • Vomiting
  • Hypokalaemia
  • Hyperaldosteronism
  • Loop/ thiazide diuretics
  • Over-treatment with sodium bicarbonate
27
Q

Describe the steps to diagnosis using gas results

A

1) What is the pO2? Is it what you would expect given any known respiratory disease, and given the fraction of inspired oxygen? Thinking about how the oxygen gets to tissues, is there adequate levels of properly functioning haemoglobin… because if not there will almost inevitably be a lactic acidosis.
2) Does the patient have a reference range H+ level, or does it indicate acidaemic or alkalaemia? And then turn your thoughts to how we arrived at that H+ level.
3) Was it via a disturbance in either pCO2 or bicarbonate levels? And thinking about these two influences, what does the clinical context indicate as being the primary disorder?
4) Usually the primary disturbance will match both the suspected cause from the clinical details, and the direction of any change in H+ ion levels

28
Q

What are the causes of respiratory acidosis?

A
-Acute
=Airway obstruction, cardio-resp arrest
=Infective exacerbation COPD, pneumonia
=Neurological: opiate toxicity, Guillain-Barre syndrome, myasthenia gravis
-Chronic
=COPD
=Obstructive= obesity
=Restrictive= pulmonary fibrosis
=Neurological= MND, myopathy
29
Q

Why does IV sodium bicarbonate have to be given slowly to CKD patients?

A
  • Metabolic acidosis common in CKD

- Acute fall in acidity may reduce solubility of calcium slats and increase risk of systemic calcification