Alterations in acid-base balance: respiratory and metabolic acidosis and alkalosis

By Cristiano Antonino On Apr 11, 2023

Let’s talk about alterations in acid-base balance: the pH of arterial blood is maintained within normal limits (7.38-7.42; i.e. 7.40 ± 0.02) by the contribution of buffer systems

The most important of these is the bicarbonate-carbonic acid system, whose ratio is 20:1.

Maintaining this ratio depends largely on lung ventilation, which regulates the CO2 tension in the blood.

Schematically, it can be said that H+ ions produced in the body and released into the extracellular fluids are immediately buffered and excreted:

CO2 through the lungs (blood pCO2 is normally maintained between 36 and 44 mmHg)
Non-volatile acids through the kidney => eliminated in the form of titratable acids (mainly phosphates) and NH+4; at the same time, the kidney reabsorbs the filtered bicarbonates
Bicarbonates in the blood are maintained between 22 and 25 mEq/l plasma.

Acid-base balance: pathophysiology

Acidosis or alkalosis occurs when the normal acid-base balance is disturbed.

The respective lowering and raising of the pH can be prevented by compensation mechanisms.

The distinction between metabolic and respiratory indicates conditions in which there is a disturbance in the regulation of bicarbonates or CO2, which constitute the metabolic and respiratory components of the acid-base balance respectively.

If the pH does not change => acidosis or compensated alkalosis

If the pH changes => decompensated acidosis or alkalosis

Examples:

Simple disorders of acid-base balance: metabolic due to reduced plasma bicarbonates in ketoacidotic diabetes.

Mixed disorders (metabolic and respiratory): reduced plasma bicarbonates from ketoacidosis + increased pCO2 from alveolar hypoventilation.

Haemogasanalysis (arterial blood sampling from humeral, radial or femoral arteries): quantification of gases, pH and bicarbonates.

METABOLIC ACIDOSIS

Definition Tendency to: reduced blood pH, decreased plasma HCO3- (bicarbonate) and presence of compensatory hyperventilation (attempting to lower pCO2 levels).

Metabolic acidosis, causes by anion gap:

In plasma normally the sum of cations (positively charged ions, mainly represented by Na+) subtracted from that of anions (negatively charged ions: Cl- and HCO3-), i.e: Na – (Cl + HCO3) = anion gap = 8-16 m mol/L;

On this basis, acidosis can be divided into 2 groups:

With NORMAL ANION GAP: the value of the anion gap above is not changed.

proximal, distal, from diuretics and mixed: proximal-distal: no acidification of urine; usually associated with: nephrolithiasis and nephrocalcinosis; renal tubular acidosis

use of carbonic anhydrase inhibitors;

profuse diarrhoea;

With INCREASED ANION GAP: the anion gap value is increased

lactic acidosis in the case of: hypotension, arteriovenous shunts, acute arterial occlusion, prolonged exercise;

keto-acidosis during diabetes mellitus;

intoxication, by: methanol or salicylates;

RENAL INSUFFICIENCY

Signs and symptoms: hyperpnoea with Kussmaul’s breathing (typical of acute onset forms), drowsiness obnubilation of the sensorium up to coma in the worst cases.

Then we also have nausea, vomiting, risk of arrhythmias in an already compromised heart, hypotension up to cardiogenic shock.

To the above-mentioned signs and symptoms must be added those characteristic of each of the aetiological forms mentioned.

Note: Long-lasting acidosis (such as that from CRI) is usually well tolerated and there may only be polypnoea.

Laboratory data

pH ≤ 7.36
pCO2 normal or decreased
HCO3- < 22 mEq/l
acid urine

Metabolic acidosis: the body’s response to acidosis

Buffering:

extracellular buffering: extracellular distribution of acid valences;
intracellular buffering

Respiratory buffering:

Stimulation of lung respiration in an attempt to reduce PCO2.
Renal response: (1) excretion of ammonium and titratable acids, (2) reabsorption and generation of new bicarbonates.

Metabolic acidosis therapy:

administration of sodium bicarbonate;
correction of the underlying cause:

If there is use of carbonic anhydrase inhibitors, discontinuation is necessary.

If diarrhoea is present: hydroelectrolyte replenishment and use of loperamide (anti-diarrhoeal) is preferable

in lactic acidosis, hypotension must be resolved
in keto acidosis administration of insulin
in intoxication: induction of vomiting and gastric lavage
in renal insufficiency: use of ACE inhibitors and sartans; in advanced chronic renal insufficiency: dialysis.

RESPIRATORY ACIDOSIS (acute or chronic)

Definition: tendency to decrease pH due to decreased ventilation, with accumulation of CO2 and elevation of pCO2.

2 forms:

acute: not compensated by renal mechanisms
chronic: compensated by the kidney

Causes of alveolar hypoventilation

Pulmonary:

pneumonia
emphysema
acute pulmonary oedema
trauma
airway obstruction

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Extra-pulmonary

obesity
kyphoscoliosis
CNS lesions

Signs and Symptoms: headache, dyspnoea, cyanosis and hypertension; mental confusion

Laboratory data:

increased pCO2 (> 44 mmHg)
pH normal or < 7.40 (if compensated forms < 7.36)
increased total CO2
HCO3- normal or decreased in decompensated forms
Acidic urine, especially in decompensated acidosis
Decreased serum Cl-

Compensation during respiratory acidosis:

– Acute: tissue buffer (with bicarbonate production)

– Chronic: renal

Therapy: of the underlying disease that caused the acidosis.

ACID-BASE BALANCE: METABOLIC ALKALOSIS

Definition: tendency for pH to rise, due to increased plasma bicarbonates and compensatory pulmonary hypoventilation (attempting to increase pCO2).

It is generally considered a benign condition, but must be corrected.

Causes:

Gastrointestinal H+ loss forms: profuse vomiting and naso-gastric drainage, and high Cl- diarrhoea (the latter: from villous adenoma or congenital diarrhoea);
Renal H+ loss forms: diuretics (except: carbonic anhydrase inhibitors and K+ spares); renal tubular diseases;
Extracellular volume expansion forms: Primary and secondary hyperaldosteronism, Cushing’s S;
Ingestion of alkaline salts;

So there are 2 forms of alkalosis:

– Hypokalemic alkalosis: typically from primary hyperaldosteronism

– Hypochloremic alkalosis: typically from high Cl- diarrhoea.

Signs and symptoms: slow and shallow breathing, neuromuscular hyperexcitability; to these must be added the signs and symptoms characteristic of each triggering cause (incoercible vomiting, dehydration, asthenia, confusion, etc.)

Laboratory data:

pH ≥ 7.42
pCO2 ≥ 44 mmHg
HCO3- > 25 mEq/l

Alkaline urine

Treatment of metabolic alkalosis: administration of solutions of: NaCl and K+ salts

In desperate conditions: administration of acids.

As a last resort: dialysis.

ACID-BASE BALANCE: RESPIRATORY ALKALOSIS

Definition: tendency for blood pH levels to rise with hyperventilation and increased elimination of CO2 with exhaled air.

2 forms:

acute: not compensated by renal mechanisms
chronic: compensated by the kidney

Causes:

Hyperventilation of pulmonary origin: pneumopathies

Hyperventilation of extra-pulmonary origin:

Organic diseases: encephalitis and meningitis, neoplasms, hyperthyroidism and anaemia
Mental disorders: neurosis and excessive anxiety
Symptomatic alterations: development of fever and pain
Traumatic conditions: trauma, disorders due to high altitude, state of pregnancy
Drug intake: salicylates in primis

Signs and symptoms: the symptomatology is generally masked by that of the basic pathology; however we have hyperventilation, tachypnoea and polypnoea; but also: nausea, vomiting, paresthesias, arrhythmias; possible evolution into coma.

Complications of alkalosis => hypocalcaemia and therefore: tetany, spasms, paresthesias; palpitations and cardiac extrasystoles.

Laboratory data: