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PH2501- pharmacology > Lec 11- Arterial blood gases > Flashcards

Lec 11- Arterial blood gases Flashcards

1
Q

whats the point of knowing this

A
  • Patient with acute asthmatic crisis arrives at ED. Present severe crisis after cleaning house and important dust exposure
  • pH= 7.25
  • PaCO2= 76 mmHg
  • PaO2= 58 mmHg
  • HCO3= 33 mmol/L
  • SaO2= 85%
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2
Q

Arterial blood gases

A
  • Blood gas measurements are used to evaluate the severity of an O2/CO2 or pH imbalance
  • The tests are ordered for patients who: Respiratory disease; Metabolic condition; Kidney disease; Diabetic ketoacidosis; Undergoing surgery and prolonged anaesthesia
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3
Q

The procedure

A

-The procedure involves drawing blood from usually the radial artery from a patient’s non-dominant hand -Heparinised self-filling

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4
Q

The basics

A
  • RESPIRATORY: CO2 produced from breathing, combines with H2O to give H2CO3, thus H+
  • METABOLIC: problem with oxidative metabolism, accumulation of lactic acid, uric acid, more H+. Also, CO2 from metabolism
  • Think about the fact we split them into 4 groups respiratory acidosis and alkalosis and metabolic acidosis and alkalosis
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5
Q

Control of plasma pH

A
  • The normal value of pH 7.35
  • Immediate control by the blood buffers: extracellular; intracellular -
  • Long-term control:

1st Respiratory system; 2nd-Renal system

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6
Q

Metabolic acid and Base production

A
  • VOLATILE ACID: CO2
  • NON-VOLATILE: Metabolic acids e.g. lactic acid, keto acids and uric acid
  • BICARBONATE:
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7
Q

Physiological buffers

A
  • EXTRACELLULAR FLUID: Carbonic acid buffer
  • INTRACELLULAR BUFFER: proteins

+Blood stream: Hb buffer

  • Renal tubule: Phosphate and ammonia
  • Buffer definition- a buffer solution resists changes in pH when small quantities of an acid or an alkali are added to it

NB- A buffer solution cannot buffer itself

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8
Q

Acids and Bases

A
  • Bronsted-Lowry- Acid a substance capable of donating a proton; base a substance capable of accepting a proton
  • Lewis acid- electron acceptor; base- electron donor
  • Corresponding acid and base are a conjugate pair
  • The strength of an acid is measured by the ability to donate protons
  • Water is amphiprotic solvent: Can accept or donate protons
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9
Q

Carbonic acid

A

Remeber Henderson hasselbalch equation

pH= pKa + log [HCO3-]/[H2CO3]

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10
Q

Influence of carbon dioxide

A

pH=pKa + [HCO3-]/[CO2]

  • Carbonic anhydrase
  • Bicarbonate and carbonic acid buffer
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11
Q

pH and the bicarbonate buffer

A

-The bicarbonate buffer works by having 20:1 (base: acid)

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12
Q

The Phosphate buffer

A
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13
Q

Blood buffers: Hb

A
  • Hb carries O2 from the lungs to the muscles through the blood
  • The muscle produces CO2 and H+
  • The buffering action of Hb picks up the extra H+ and CO2
  • If Hb buffer is exceeded, the pH of the blood is lowered, causing acidosis
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14
Q

The ideal buffer

A
  • pKa =pH+log(base/acid)
  • if pKa=pH then log(base/acid)=0 and base/acid=1 –> this means [base]=[acid]
  • Equal capacity for acid and base buffering
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15
Q

Treatment of respiratory acid/base disorders

A

Respiratory alkalosis: -Resolve underlying cause -Reduced blood CO2 Strategies to be used: Oxygen therapy; Reassurance; Diuretics; Breath holding techniques; Positive end-expiratory pressure (hold the inspiratory phase abit longer)

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16
Q

The isohydric principle

A
  • H+= Ka1[HA1]/[A1] = Ka2[HA2]/[A2] = Ka3 etc = Ka4 etc
  • Where multiple acid pairs in solution will be in equilibrium with one another, tied together by their common reagent: H+ and hence, the pH of the solution
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17
Q

Respiratory Regulation of pH

A
  • Central chemoreceptors - 70-80% of drive- lungs
  • Peripheral Chemoreceptors- 20-30% of drive- muscles
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18
Q

Renal regulation of pH

A
  • Reabsorption of bicarbonate HCO3-
  • Secretion of protons
  • Facilitated by carbonic anhydrase
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19
Q

Early PCT Na+ reabsorption

A

-

20
Q

Intercalated cells

A
  • Generation of new bicarbonate i.e. H+ secretion not linked to HCO3- reabsorption
  • H+ secretion into the lumen is favoured by -ve potential difference in the lumen
  • Active proton secretion in tubular fluid
  • Secretion NOT by importer Na+/H+
  • But is enhanced by increase Na+ absorption by principal cells (Generates a favourable lumen -ve potential)
  • Secretion H+ must be buffered in tubular fluid (Secretion limit tubular pH of 4.5)
  • Affected by K+ homeostasis
21
Q

Ammonium buffer

A
  • Glutamine -(Glutaminase) –> Glutamic acid + NH3
  • NH3 + H+= NH4+
  • The ammonium ion is Quaternary highly charged and has very low lipid solubility so is trapped in the tubular fluid
22
Q

Normal pH status

A
  • pH= 7.35-7.45
  • PaCO2= 4.7-6.0 kPa (35-45 mmHg)
  • PaO2= 10-13 kPa (70-100 mmHg)
  • [HCO3]= 22-26 mmol/L
  • Base excess= -2 to +2

Sa02= 96-98% (Change in high altitude to

23
Q

Types of acid/base disorder

A

-Acidosis- pH falls below 7.35

+So increasing [H+] from either too much pCO2 or too little HCO3-

-Alkalosis- pH rises above 7.45

+Vice-versa i.e. decreasing H+ from reduced PCO2 or increased HCO3-

24
Q

Terminology

A
  • PaCO2= partial pressure of carbon dioxide is a measurement of CO2 in the blood- which reflects alveolar ventilation. If the pH and PaCO2 change in opposite directions, the primary disorder is respiratory
  • PaO2= Partial pressure of O2- is the amount of oxygen dissolved in the blood and represents gas exchange in the blood
  • SaO2= oxygen saturation- the ratio of oxygen bound to Hb
  • pH= Determines the [H+] found in arterial blood
25
Q

Terminology 2

A
  • HCO3-, Bicarbonate is the metabolic component in an ABG and represents the concentration of hydrogen carbonate in the blood. If the CO3- and the pH changes in the same direction, the primary disorder is of the metabolic component
  • Base excess- another measure used to determine the metabolic component of an acid-base disturbance and all bases are measured. It is calculated using blood pH and PaCO2. It increases in metabolic alkalosis and decreases in metabolic acidosis
26
Q

Types of acid/base disorder

A
  • Metabolic disorder- involves non-volatile acid or altered HCO3-
  • Respiratory disorder- Primary change is in plasma CO2 (volatile acid)
  • Plasma Buffers- more effective in acidosis than alkalosis (remember 20:1)
27
Q

Causes of metabolic acidosis

A

1)Increased metabolic acid production:

Lactic acidosis; Ketoacidosis- uncontrolled diabetes mellitus; Ingestion of acidic material e.g. aspirin

2)Decreased acid secretion:

Renal failure; Type 1 renal tubular acidosis (DCT); Hypoaldosteronism (Type 4 renal tubular acidosis)

3)Loss of bicarbonate-

Diarrhoea and loss of intestinal bicarbonate; Type 2 renal tubular acidosis (PCT)

28
Q

Metabolic acidosis- causes, signs and symptoms

A

CAUSES:

Ketoacidosis; shock; severe diarrhoea; impaired renal function

WARNING SIGNS AND SYMPTOMS

Headache; lethargy; anorexia; deep rapid respiration; nausea; diarrhoea; abdominal discomfort; coma

29
Q

Metabolic acidosis

A
  • 1st correction: Intracellular/extracellular buffering (Use respiratory compensation when you have a metabolic disorder)
  • Respiratory compensation: decreased pH= hyperventilation moves [HCO3-]/pCO2 -> 20:1
  • Renal correction: delayed by resporatory compensation
30
Q

Causes of metabolic alkalosis

A
  • GI H+ loss: loss of gastric secretion e.g. vomiting
  • Urinary loss of H+: loop of thiazide diuretics; hyperaldosteronism
  • Movement of H+ into cells: Hypokalaemia
  • Administration of bicarbonate or an organic ion metabolised to bicarbonate (e.g. citrate)
31
Q

Metabolic alkalosis

A
  • Primary condition: increase pH; increase [HCO3-]; +VE base
  • First correction: intracellular and extracellular buffering
  • Respiratory compensation: due to decrease CO2 and increase pH. Hypoventilation moves [HCO3-]/ pCO2 -> 20:1
  • Renal correction: delayed by respiratory compensation
32
Q

Metabolic alkalosis- signs and symptoms

A

SIGNS AND SYMPTOMS

-Confusion; increased irritability; dysrhythmias (tachycardia from decreased K+); compensatory hyperventilation; nausea; vomiting; diarrhoea; anxiety; seizures; tremors, muscle cramps (Decreased serum Ca2+)

33
Q

Respiratory acidosis

A

Cause: Increased plasma CO2 (hypercapnia)

  • Primary condition: increased pCO2, decreased pH, increase HCO3-
  • First correction: intracellular buffering
  • Renal compensation: increased H+ excretion and bicarbonate reabsorption (almost complete); At full compensation both buffer components are elevated and there is positive base excess
34
Q

Respiratory acidosis

A

Causes: Lung disorder

-COPD (emphysema, bronchitis); Severe asthma; pneumonia; pneumothorax

Causes: Neuromuscular causes

-Diaphragm dysfunction and paralysis; Guillian-Barre syndrome; myasthenia gravis

Causes: chest wall

-Severe kyphoscoliosis; flail chest

Causes: Drugs that cause respiratory depression

-Opioids, narcotics, barbiturates, benzodiazepine and other CNS depressants

35
Q

Respiratory acidosis- Signs and symptoms

A

Signs and symptoms

-Hypoventilation (hypoxia); rapid shallow breathing; decreased BP with vasodilation; dyspnea; headache; hyperkalaemia; dysrhythmias (increased K); Drowsiness; muscle weakness

Causes

-Decreased respiratory stimuli (anaesthesia drug overdose); COPD; Pneumonia; atelectasis

36
Q

Respiratory alkalosis

A
  • Primary condition: Decreased pCO2, increased pH, decreased HCO3-
  • Renal compensation: reduced H+ excretion and bicarbonate reabsorption; At full compensation both buffer and components are depressed and there is positive base excess
37
Q

Respiratory alkalosis- Causes

A

CNS

-Head injury; Cardiovascular accident (CVA); anxiety (Hyperventilation); supra-tentorial (pain, fear, stress); pyrexia; chronic liver failure

38
Q

Metabolic alkalosis- signs and symptoms

A

Signs and symptoms

-Hyperventilation (Loss of CO2); tachycardia; decreased or normal BP; hypokalemia; hyper reflexes and muscle cramping; seizures; increased anxiety and irritability

Causes

-Hyperventilation (Anxiety, PE, fear) Mechanical ventilation

39
Q

Arterial blood sample: pH= <7.35

A
40
Q

Disorders of acid/base- effects

A

Altered neuronal excitability

  • CNS changes. Acidosis decrease excitability, disorientation eventually coma; Alkalosis increased excitability- early ‘pins and needles’, later muscle twitch then spams. Respiratory can cause death
  • Changes in metabolic activity- enzyme systems
  • Changes in [K+]- DCT secretion, If H+ increases K+ falls and vice versa
41
Q

Treatment of metabolic Acid/Base disorder

A

METABOLIC ACIDOSIS

  • Ideally correct the underlying cause
  • Infusion of sodium bicarbonate. 1.26% is isotonic, strengths up to 8.4% may be used but slow infusion

METABOLIC ALKALOSIS

  • Correct underlying cause
  • Infusion of 0.9% NaCl- rehydration
  • Ammonium chloride orally- in severe cases
42
Q

Treatment of Respiratory Acidosis

A
  • Primary treatment focus- address the underlying cause or pathophysiological process
  • Depending on severity- the patient may require artificial ventilation
  • Treatments may include (depending on PMR)
  • Bronchodilators
  • Antibiotics
  • O2 therapy to reduce hypoxia

Non-invasive positive pressure ventilation

43
Q

Treatment of respiratory Acid/base disorders

A
  • Resolve the underlying cause
  • Reduce blood CO2
  • Strategies that may be used:
  • O2 therapy
  • Reassurance
  • Diuretics
  • Breath holding techniques
  • Positive end-expiratory pressure- to hold the inspiratory phase a little longer
44
Q

Treatment cheat sheet

A
45
Q
A

PH2501- pharmacology (47 decks)

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