Assessment and Disorders of Acid Base Balance Flashcards

Question

What systemic effects of respiratory Acidosis?

Answer 1

**Hypoxaemia:** * Breathlessness, cyanosis, drowsiness **Neurological (Hypercapnia):** * Headache, papilloedema, extensor plantar responses, myoclonus (chronic) * Anxiety, confusion, impaired consciousness **Effects of acidosis (as for metabolic) e.g. Bohr shift, hyperkalaemia, etc.**

Answer 2

**Buffering** * Limited buffering by haemoglobin (rapid) * Other intracellular buffers important in chronic acidosis **Respiratory Compensation** * Increase PCO2 stimulates respiratory centre (hyperventilation) but underlying disease prevents adequate response ***Renal Compensation (2-5 days)\**** * Maximal bicarbonate reabsorption * Almost all phosphate excreted as H2PO4- * Marked increase in urinary ammonium * Increased Na+/H+ exchange

Answer 3

* Treat underlying cause if possible * Maintain adequate arterial PO2, avoid loss of hypoxic stimulus to respiration * Avoid rapid correction of PCO2 (risk of alkalosis due to persistence of compensation) * Bronchodilators (e.g. salbutamol in COPD)

Answer 4

* pH - High * [H+] - Low * [HCO3-] - High * PaCO2 - Normal or High * K+ - Low

Answer 5

* U&Es (Na+, K+, Cl-, urea, creatinine) * Calcium and albumin * Magnesium * Urine pH\* * Urine chloride (spot urine) * Blood pressure

Answer 6

**Saline responsive (urine Cl- \< 20 mmol/L)** * **Gastrointestinal:** Vomiting / Pyloric stenosis (common), Gastric drainage, Congenital Cl-losing diarrhoea * **Exogenous alkali administration:** Sodium bicarbonate (IV), Lactate, Citrate (transfusion), Acetate (especially if ¯GFR), Milk alkali syndrome (rare) * **Other exogenous:** Diuretics (Common), Diuretic administration post PCO2, Poorly reabsorpable anion therapy (e.g. penicillin, carbenicillin) **Saline unresponsive (urine Cl- \> 20 mmol/L)** * **Association with hypertension (mineralocorticoid excess):** Primary hyperaldosteronism (Conn’s), Secondary hyperaldosteronism, Cushing’s Syndrome, 11-β-hydroxylase and 17-α-hydroxylase deficiencies (CAH), Carbenoxalone and Liquorice (glycrrhizic acid) * **Other:** Barter’s syndrome, Gitelman’s syndrome, Refeeding syndrome, Severe potassium depletion, Magnesium deficiency, Extreme hypercalcemia

Answer 7

* Gastric Loss of [Cl-], [Na+], [K+], [H+] * Loss of [Cl-] leads to retention of [HCO3-] so increased [HCO3-] * Loss of [Na+], [K+], [H+] leads to rention of [Na+], [K+] at the expenses of [H+]. This leads to low [H+] * This can lead to metabolic alkalosis

Answer 8

Generally opposite to those of acidosis. Less pronounced CV effects and no apparent bone effects * Impaired O2 delivery to tissues * Potassium depletion, which sustains alkalosis and may manifest as muscle weakness. * Neuromuscular hyperexcitability (acute): parasthesia, muscle cramps, tetany, convulsions. This is due binding of H+ to albumin increases Ca2+binding, lowering ionised calcium)

Answer 9

**Buffering** * Release of buffered H+, with increased HCO3- **Respiratory Compensation (24 – 36h)\*** * Decreased stimulation of chemoreceptors but self-limiting as PCO2 stimulates ventilation (maximal pCO2 ~ 8 kPa) * Hypoxic stimulus also overrides decreased H+ stimulus at respiratory centre. **Renal Compensation** * Inappropriate reabsorption of HCO3- due to decreased GFR/increased tubular function. * If decreased ECF volume associated with [Cl-] deficiency, obligatory increased [HCO3-] reabsorption which exacerbates alkalosis. * Potassium deficiency contributes to persistence of alkalosis. Increased mineralocorticoid activity promotes distal tubular Na+ (with increased K+ and H+ excretion)

Answer 10

* **Treat underlying cause** * **Treat factors that sustain alkalosis:** Volume expansion (saline responsive), Potassium replacement, Magnesium replacement * **Dangerous to give saline in saline-unresponsive causes (e.g. sodium excess)** * **Spironolactone or amiloride (hyperaldosteronism)**

Answer 11

* pH - High * [H+] - Low * [HCO3-] - Normal/Low * PaCO2 - Low * K+ - Low * Phos - Low

Answer 12

* LFTs * Salicylate * FBC (? Sepsis (WCC), ?anaemia). Possibly cultures. * Chest radiograph * Lung function tests

Answer 13

**Non-pulmonary stimulation of respiratory centre** * **Cortical influences (common):** Pain, Fever, Anxiety * **Drugs / toxins:** Salicylate, Catecholamines, Progesterone, Theophylline, Thyroxine * **Endogenous compounds:** Hepatic failure (toxins), Pregnancy (progesterone), Sepsis (cytokines), Thyroid crisis * **CNS lesions:** Encephalitis, Meningitis, SAH, Tumours, Trauma / Head injury, Stroke * **Hypoxia:** High altitude, Severe anaemia, Right-to-left shunts **Hyperventilation** * **Voluntary** * **Mechanical** **Pulmonary disorders** * **Pneumonia** * **Pulmonary oedema (all types)** * **Lung fibrosis** * **Pneumothorax** * **Pulmonary embolism** * **Asthma** * **Interstitial lung disease** * **Chronic bronchitis**

Answer 14

* Manifestations of underlying disease predominate * Acute hypocapnia decreases cerebral blood flow causing light-headedness, confusion, etc. * Perioral and peripheral parasthesia (¯ionised calcium) * Cardiovascular: increased heart rate, tightening of chest, angina * Mild hypokalaemia * Hypophosphataemia

Answer 15

**Buffering** * Release of H+ from non-bicarbonate buffers * New steady state achieved quickly. Persists for up to 6 hours (when renal compensation becomes evident) **Respiratory Compensation** * Inhibitory effect of ¯PCO2 on respiration overwhelmed by primary cause which stimulates hyperventilation **Renal Compensation (2-5 days)\*** * Decreased renal generation of bicarbonate (CO2is substrate). Decreased urinary acidification.

Answer 16

* Treat underlying cause * Rapid symptomatic relief by re-breathing from paper bag * Sedation or prevention of hyperventilation by mechanical hyperventilation (in severe cases)

Answer 17

* Hypoventilation e.g. Head injury, drugs (morphine or barbiturates), respiratory muscle weakness, chest trauma, COPD, obesity, etc. * Diffusion impairment e.g. Lung Fibrosis * Ventilation-perfusion mis-matching * Right-to-left shunt * Low inspired pO2 e.g. high altitude

Answer 18

* Non-invasive, transcutaneous estimation of arterial oxygen saturation (SaO2). Differential light absorption by haemoglobin and oxyhaemoglobin sensed through a pulsatile signal * SaO2 may be normal if tissue hypoxia caused by Low cardiac output states, Anaemia, Failure of tissue oxygen use, Severe hypoxia in a single organ.

Answer 19

* Bright light (pulsatile waveforms and saturation). * Dyes and pigments e.g. nail varnish (artificially low). * Abnormal haemoglobins e.g. methaemoglobinaemia. * Carboxyhaemoglobin in CO poisoning (saturation since oxyhaemoglobin and carboxyhaemoglobin cannot be distinguished). * Cardiac arrhythmias (interfere with detection of pulsatile signal). * Vasoconstriction / hypothermia (desaturation, failure to register signal due to reduced perfusion). * Movement e.g. shivering. * Saturations \< 75%

Answer 20

**[H+] = K ([pCO2]/[HCO3])** ## Footnote **K** – embraces dissociation constants and solubility coefficient of carbon dioxide **K** – 180 when H+ in nmol/L, HCO3 in mmol/L and pCO2 kPa