Lec 11- Arterial blood gases Flashcards
whats the point of knowing this
- 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%
Arterial blood gases
- 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
The procedure
-The procedure involves drawing blood from usually the radial artery from a patient’s non-dominant hand -Heparinised self-filling
The basics
- 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
Control of plasma pH
- The normal value of pH 7.35
- Immediate control by the blood buffers: extracellular; intracellular -
- Long-term control:
1st Respiratory system; 2nd-Renal system
Metabolic acid and Base production
- VOLATILE ACID: CO2
- NON-VOLATILE: Metabolic acids e.g. lactic acid, keto acids and uric acid
- BICARBONATE:
Physiological buffers
- 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
Acids and Bases
- 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
Carbonic acid
Remeber Henderson hasselbalch equation
pH= pKa + log [HCO3-]/[H2CO3]
Influence of carbon dioxide
pH=pKa + [HCO3-]/[CO2]
- Carbonic anhydrase
- Bicarbonate and carbonic acid buffer
pH and the bicarbonate buffer
-The bicarbonate buffer works by having 20:1 (base: acid)
The Phosphate buffer
Blood buffers: Hb
- 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
The ideal buffer
- 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
Treatment of respiratory acid/base disorders
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)
The isohydric principle
- 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
Respiratory Regulation of pH
- Central chemoreceptors - 70-80% of drive- lungs
- Peripheral Chemoreceptors- 20-30% of drive- muscles
Renal regulation of pH
- Reabsorption of bicarbonate HCO3-
- Secretion of protons
- Facilitated by carbonic anhydrase
Early PCT Na+ reabsorption
-
Intercalated cells
- 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
Ammonium buffer
- 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
Normal pH status
- 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
Types of acid/base disorder
-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-
Terminology
- 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
Terminology 2
- 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
Types of acid/base disorder
- 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)
Causes of metabolic acidosis
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)
Metabolic acidosis- causes, signs and symptoms
CAUSES:
Ketoacidosis; shock; severe diarrhoea; impaired renal function
WARNING SIGNS AND SYMPTOMS
Headache; lethargy; anorexia; deep rapid respiration; nausea; diarrhoea; abdominal discomfort; coma
Metabolic acidosis
- 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
Causes of metabolic alkalosis
- 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)
Metabolic alkalosis
- 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
Metabolic alkalosis- signs and symptoms
SIGNS AND SYMPTOMS
-Confusion; increased irritability; dysrhythmias (tachycardia from decreased K+); compensatory hyperventilation; nausea; vomiting; diarrhoea; anxiety; seizures; tremors, muscle cramps (Decreased serum Ca2+)
Respiratory acidosis
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
Respiratory acidosis
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
Respiratory acidosis- Signs and symptoms
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
Respiratory alkalosis
- 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
Respiratory alkalosis- Causes
CNS
-Head injury; Cardiovascular accident (CVA); anxiety (Hyperventilation); supra-tentorial (pain, fear, stress); pyrexia; chronic liver failure
Metabolic alkalosis- signs and symptoms
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
Arterial blood sample: pH= <7.35
Disorders of acid/base- effects
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
Treatment of metabolic Acid/Base disorder
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
Treatment of Respiratory Acidosis
- 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
Treatment of respiratory Acid/base disorders
- 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
Treatment cheat sheet
