STUDY - Technical - New Dacian's Medicine
Acidosis
and Alkalosis (3)
Translation Draft
If I'm done with acidosis, obviously it's the turn of the alkalosis.
If I'm done with acidosis, obviously it's the turn of the alkalosis.
And I'm going to start
with metabolic alkalosis. This is manifested by increased
arterial pH, an increase in HCO3-seric and an increase in PaCO2
as a result of compensatory alveolar hypoventilation.
It is often associated with hypochloremia and hypopotasemia. Patients with high and low HCO3 and Cl have either metabolic alkalose or chronic respiratory acidosis. PaCO2 increases by 6 mmHg for every 10 mmoli/ l increase in HCO3- above normal. Set differently, relative to HCO3- between 10-40 mmoli/ l, the predicted PaCO2 is approximately equal to HCO3- +15. Arterial pH establishes the diagnosis, as it is increased in metabolic alkalose and decreased or normal in respiratory acidosis. Metabolic alkalose commonly occurs in combination with other conditions, such as acidosis or respiratory alkalose or metabolic acidosis.
From the point of view of pathogenesis, metabolic alkalose occurs as a result of a net gain of HCO3- or loss of nonvolatile acids (common HCl through vomiting) from extracellular fluid. Since alkali intake in the body is not common, the condition involves a stage of generation, in which acid loss frequently causes alkalose and a maintenance stage in which the kidneys are unable to compensate for alkalose by excretion of HCO3- due to volemy decrease, low RFG or cl- or K+ dislet.
Under normal conditions, the kidneys have an impressive excretion capacity of HCO3 in a common manner. In order for HCO3 to be extra in the extracellular fluid, it must be administered exogenously or be synthesized endogenously, in part or entirely by the kidneys. The kidneys will retain, rather than secrete, excess alkalis and thus maintain alkalose if one or both of the following mechanisms are operative: 1. Cl- deficiency (by decreasing extracellular fluids) exists at the same time as the deficiency of K+, the decrease of RFG and/ or the increase in the reabsorption of the proximal fraction of HCO3-. This combination of conditions causes secondary hyperaldosteronism and stimulates the secretion of H+ in the collector duct. Alkalose is corrected by administration of NaCl and KCl; 2. Hyperaldosteronism and hypokalemia are autonomous and non-responsive to increasing the volume of extracellular fluids.
Increased distal secretion of H+ is sufficient to reabsorb the increased amount of filtered HCO3 and overcome the low proximal reabsorption of HCO3- due to the expansion of extracellular fluids. To reduce alkalose in these situations it is necessary to inhibit the secretion or action of aldosterone or to surgically remove the secretory adrenal adenoma of aldosterone.
Let's now proceed to small presentations about differential diagnosis. In order to determine the cause of metabolic alkalose it is necessary to evaluate the status of extracellular volume (VEC), blood pressure in clino and orthostatism, serum K+ and the renin-aldosterone system. For example, the presence of hypertension and hypopotasemia in a patient with alkalose suggests an excess of mineralocorticoids, or a hypertensive patient receiving diuretics. Low activity of plasma renin and normal Na+ and Cl-values in urine in a patient who does not take diuretics indicates a primary excess syndrome of mineralocorticoid.
Combining hipposemia with alkalose in a normotensive, nonedematos patient may be given by Bartter syndrome, magnesium deficiency, vomiting, exogenous alkalis or diuretic ingestion. Determination of primary electrolytes (especially Cl-urinary) and urine screening for diuretics may be useful. if urine is alkaline, with Increased Na+ and K+, but with low Cl, the diagnosis is vomiting (recognized or hidden) or ingestion of alkalis. if urine is relatively acidic and has a low concentration of Na+, K+ and Cl-, it is highly likely that there are previous vomiting, a posthypercapinic situation or a previous ingestion of diuretics. If, on the other hand, urinary concentrations of Na+, K+ or Cl- are not low, a magnesium deficiency, Bartter syndrome or a routine ingestion of diuretics should be taken into account.
Chronic alkali administration in patients with normal renal function causes at most a minimum alkalose. However, alkalose in patients with chronic renal impairment may develop following the administration of alkalis when the normal excretion capacity of HCO3 is exceeded, or when coexisting hemodynamic disorders cause increased fractional reabsorption of HCO3-. These patients are represented by those receiving HCO3- orally or intravenously, acetate (parenteral hyperfood solutions), citrate (transfusions) or antacids and cation-changing resins (aluminum hydroxide and sodium polystyrene sulfonate).
A rare cause is long-term ingestion of excess milk and antacids. Both hypercalcemia and excess vitamin D may increase renal reabsorption of HCO3- and cause nephrocalcinosis, renal failure or metabolic alkalose. Stopping ingestion or administration of alkalis is frequently sufficient to correct alkalose.
Metabolic alkalose associated with vfEC decrease, K+ deletation and secondary hyperreinemic hyperaldosteronism has several origins. In the case of gastrointestinal origin, vomiting and gastric aspiration, gastrointestinal losses of H+ cause the retention of HCO3-. The increase in H+ losses through gastric secretions can be determined by vomiting, gastric aspiration or gastric fistula. Loss of fluids and NaCl pri vomiting or nasogastric suction causes decreasein volume of extracellular fluids (VFEC) and increased secretion of renin and aldosterone. The decrease in volume causes a decrease in RFG and an increase in the ability of renal tubules to reabsorb HCO3-.
During vomiting, a continuous plasma intake of HCO3- is achieved by exchange with Cl-, and plasma HCO3- exceeds the reabsorption capacity of the proximal tube. Excess NaHCO3 reaches the distal tube, where part of Na+ will be exchanged for K+ through an aldosterone-mediated process. Due to the decrease in VFEC and hypochloremia, Cl- is preserved by the kidneys.
After stopping vomiting, Plasma HCO3 decreases to the threshold of renal elimination of HCO3-, which is increased due to the effects of decreased VFEC, hypokalemia and hyperaldosteronism. Alkalose is less severe than in the active vomiting phase and urine is relatively acidic with low levels of Na+, Cl- and HCO3-. The correction of the VfEC value with NaCl may be sufficient to restore normal blood pH, even without covering the K+ deficiency. However, the practice also dictates the restoration of K+. Metabolic alkalose has also been described in cases of vilos adenoma and is given rather by a potassium deplation.
In the case of renal origin (diuretics), drugs that cause chloresis without bicarbonate, such as thiazides and anse diuretics (furosemid, bumetanide, torsamid, etacrinic acid), acutely decrease VFEC without altering the total bicarbonate content of the body. HCO3- serum increases. PaCO2 does not increase proportionally and results in a decrease in alkalose. The degree of alkalose is usually low, due to cellular and nonHCO3 pads.
Chronic administration of diuretics tends to generate alkalose by increasing distal sodium delivery (Na+) and consequently stimulating the secretion of K+ and H+. Diuretics, by blocking the reabsorption of Cl- in the distal tube or by increasing the activity of the proton pump, can stimulate the distal secretion of H+, evidenced by increased net acid excretion. Alkalose is maintained by the persistence of decreased VFEC, secondary hyperaldosteronism, K+ deficiency and the direct effect of diuretics (as long as diuretics continue). The control of alkalose is carried out by the administration of isotone solutions to correct the deficiency of VFEC.
In posthypercapnia, prolonged CO2 retention with chronic respiratory acidosis increases renal absorption of HCO3- and generates new HCO3 (increasing net acid excretion). If PaCO2 returns to normal, metabolic alkalose is given by consistently elevated levels of HCO3-. Alkalose develops immediately if the increased PaCO2 is rapidly reduced to normal by a change in controlled mechanical ventilation and the acute bicarbonate response is proportional to the PaCO2 changes.
The associated cation is predominantly K+ (especially if K+ in the diet is not limited) with natrium as proportional to salt intake. Secondary hyperaldosteronism in chronic states of hypercapnia may be responsible for this type of response. The associated vfFEC decrease does not allow a complete correction of alkalose only by correcting PaCO2 and alkalose persists until an additional with Cl-. Increased proximal acidification, as a result of a previous hypercapnice-induced situation, may also contribute to posthypercapic alkalosis.
After the treatment of lactic acidosis and ketoacidosis, when an underlying stimulus for the generation of lactic acid or ketoacidis is rapidly removed by restoring circulation or insulin therapy, lactate or ketones are metabolized producing an equivalent amount of HCO3-, H+ being consumed by metabolism by organic anions, with the release of an equivalent amount of HCO3-. This process will regenerate HCO3- if organic acids are metabolized to HCO3- before their renal excretion. This production is partly compensated by urinary loss of organic ions.
Other sources of new HCO3 are additives with the initial amount generated by the metabolism of organic anions, producing an excess of HCO3-. These sources include: 1. HCO3- newly added to the blood by the kidneys as a result of increased acid excretion over the pre-existing period of acidosis and 2. alkaline therapy during acidosis treatment. The acidosis-induced decrease in VFEC and The deficiency of K+ work to support alkalose.
In the case of non-resorbable anions and magnesium deficiency, the administration of small amounts of non-resorbable anions, such as penicillin or carbenicillin, may increase distal acidification and k+ secretion by increasing the light difference of potential. Mg2+ deficiency causes hypopotasemic alkalose by increasing distal acidification as a result of stimulation of renin and thus aldosterone secretion.
Pure potassium (K+) deletion causes modest metabolic alkalose, increasing urinary acid elimination in the form of NH4+ and also increasing the reabsorption of HCO3-. Alkalose is moderate due to the fact that the Devenletion of K+ also causes the NaCl balance to be positive, with or without the administration of mineralocorticoid. Salt retention, by contrast, decreases alkalose. When access to NaCl and K+ is restricted, alkalose is more severe. Alkalose associated with severe K+ deletis is resistant to salt administration, while recovery of K+ deficiency corrects alkalose.
Let's see what's with metabolic alkalosis associated with VFEC expansion, hypertension and hyperaldosteronism! The administration of mineralocortidoid or its excess production (primary aldosteronism in Cushig syndrome and enzymatic cortico-adrenal defects) increases the net secretion of acid and may produce a metabolic alkalosis that may be accentuated by the association of K+ deficiency. The expansion of VFEC by salt retention causes hypertension and antagonizes the reduction of RFG and/ or increases tubular acidification induced by aldosterone and K+ deficiency. Kaliuresis persists and causes a continuous deplation of K+ with polydipsia, inability to concentrate urine and polyuria.
The increase in aldosterone levels may be the result of an autonomic primary adrenal overproduction or a secondary release of aldosterone caused by renal renin overproduction. In both cases, the normal feedback of VFEC on net aldosterone production is affected and hypertension may result in volume retention hypertension. Liddle syndrome results from increased activity of the Na+ channels of the collector duct and is a cause of volemy expansion and hypopotasic alkalosis with normal levels of aldosterone.
Symptoms that occur include functional disorders in the central and peripheral nervous system similar to those caused by hypocalcemia: mental confusion, obnubilation, predisposition to seizures, paresthesia, muscle cramps, tetanus, worsening of arrhythmias and hypoxemia in chronic obstructive pulmonary disease. Associated electrolyte abnormalities include hypopotasemia and hypophosphatemia.
Treatment is mainly directed on the correction of the underlying stimuli that generate HCO3-. If primary aldosteronism is present, correction of the underlying causes will correct and alkalose. The loss of H+ in the stomach or kidney may be reduced by the use of H2 receptor blockers or the discontinuation of diuretics. The second aspect of treatment is to remove factors that support the reabsorption of HCO3-, such as decreased VFEC or K+ deficiency.
Although K+ deficiency needs to be corrected, NaCl therapy is usually sufficient to correct alkalose, given the decrease in VFEC, which is evidenced by low Cl in the urine. In some cases, known as salt resistance, there is an association with a high deficiency of K+, Mg2+ deficiency, Bartter syndrome or with an autonomous primary secretion of mineralocorticoid. Under these conditions, therapy should be directed at underlying physiopathological problems.
If the associated situations exclude salt administration, renal losses of HCO3- can be accelerated by the administration of acetazolamide, a carbonic anhydrase inhibitor, which is consistently effective in patients with adequate renal function, but which may increase the loss of K+. Diluted hydrochloric acid is also effective, but can cause hemolysis. The administration of amino acids such as amginin hydrochloride is safe and effective. Acidification can also be done with Oral NH4Cl, which should be avoided in the presence of liver disease. Finally, hemodialysis performed with a dialysis with low-HCO3 and high Cl- may be effective when renal function is impaired.
Respiratory acidosis can be caused by severe lung disease, respiratory muscle fatigue or abnormalities in ventilation control and is caused by increased PaCO2. In acute respiratory acidosis, there is an immediate compensatory increase (through cellular buffer mechanisms) of HCO3-, which increases by one mmol/l for every 10 mmHg increase in PaCO2. In chronic respiratory acidosis (more than 24 hours), renal adaptation occurs and HCO3- increases by 4 mmol/ l for every 10 mmHg increase in PaCO2. HCO3- serum does not normally increase above 38 mmoli/ l.
Renal compensation (increased reabsorption of HCO3-) begins within the first 12-24 hours and is complete after 5 days. Clinical manifestations vary depending on the severity and duration of respiratory acidosis, underlying diseases and hypoxemia, when it exists. A rapid increase in PaCO2 can cause anxiety, dyspnoea, confusion, psychosis, hallucinations and, finally, coma. In less advanced stages, chronic hypercapnia includes sleep disorders, memory loss, daytime sleepiness, personality disorders, coordination disorders and motor disorders such as tremors, myoclonia, asterixis.
Headache and other signs such as papillary edema, abnormal reflexes, focal muscle weakness are caused by vasoconstriction secondary to the loss of vasodilating effects of CO2. Depression of the respiratory centers through a variety of drugs, trauma or diseases, can produce respiratory acidosis.
It can occur acutely in general anesthesia, administration of sedatives, brain trauma or chronic in the administration of sedatives, alcohol, intracerebral tumors and in syndromes of respiratory disorders during sleep, which include primary alveolar impairment syndrome and hyperventilation syndrome from obesity.
Anomalies or disorders of motor neurons, neuromuscular junctions or skeletal muscles may cause hypoventilation through fatigue of the respiratory muscles. Mechanical ventilation, when not properly adapted and supervised, can cause respiratory acidosis, especially if CO2 production increases sharply (due to fever, agitation, sepsis or oversupply) or if alveolar ventilation decreases due to deterioration of lung function. Increased levels of positive pressure at the end of exhalation in the presence of low heart rate may cause hypercapnia as a result of large increases in dead alveolar space.
Acute hypercapnia is often the consequence of obstruction of the upper airways or generalized bronchospasm, such as in severe asthma, anaphylaxis, inhalation of hot air or toxins. Chronic hypercapnia and respiratory acidosis occur at the stage of an obstructive pulmonary disease. Restrictive conditions including both the chest wall and lungs can cause respiratory acidosis due to a high metabolic breathing effort, which causes fatigue of the respiratory muscles.
Advanced studies of intra and extrapulmonary restrictive diseases are presented as chronic respiratory acidosis. Diagnosis of respiratory acidosis requires, by definition, measurements of PaCO2 and arterial pH. A detailed anamnesis and a careful objective examination often indicate the cause. Lung function studies, including spirometry, carbon monoxide diffusion capacity, lung volumes, PaCO2 blood pressure and O2 saturation usually indicate whether respiratory acidosis is secondary to lung disease.
The study of nonpulmonary causes should include a detailed history of drug intake, measurement of hematocrit and assessment of the upper airways, chest wall, pleura and neuromuscular function.
Treatment of respiratory acidosis depends on its onset and severity. Acute respiratory acidosis can be life-threatening, and measures taken to remove the underlying causes should be associated with adequate alveolar ventilation. This may mean tracheal intubation and assisted mechanical ventilation. Oxygen should be administered with care in patients with severe obstructive pulmonary disease and chronic CO2 retention who are breathing spontaneously. When oxygen is administered properly, these patients may have progressive respiratory acidosis.
Rapid and aggressive correction of hypercapnia should be avoided because parco2 decrease can cause the same complications in acute respiratory alkalosis (e.g. cardiac arrhythmias, decreased brain infusion and seizures). PaCO2 should be gradually decreased in chronic respiratory acidosis to basic levels of PaCO2, while taking enough Cl- and K+ to increase renal excretion of HCO3-.
Chronic respiratory acidosis is often difficult to correct, but measures taken to improve lung function, such as stopping smoking, using oxygen, bronchodilators, glucocorticoids, diuretics and physiotherapy can help some patients and prevent damage to lung function in most. The use of respiratory stimulants may be useful in selected patients, especially if hypercapnia is exaggerated in relation to lung damage.
Now, in the end of this long post, I'm going to tackle respiratory alkalosis. Alveolar hyperventilation decreases PaCO2, so the pH increases. Non-bicarbonate cell buffer systems responding to the consumption of HCO3-. Hypocapnia develops when sufficiently strong fan stimuli cause a greater release of CO2 in the lung than its metabolic production at the tissue level. Plasma pH and HCO3- vary proportionally to PaCO2 when it is between 15 and 40 mmHg. The relationship between the arterial concentration of hydrogen ions and PaCO2 is 0.7 mmoli/ l/ mmHg (or 0.01 pH/mmHg units) and for HCO3-plasma is 0.2 mmol/ l/ mmHg.
Sustained hypocapnia for more than 2-6 hours is compensated by a decrease in renal ammonium and titrable acidity excretion, as well as by a reduction in the reabsorption of Filtered HCO3. Complete renal adaptation to respiratory alkalose is done within a few days under conditions of a volemic status and normal renal function. Kidneys seem to respond directly to low PaCO2 rather than to the alkalose itself. A decrease of 1 mmHg of PaCO2 results in a decrease of 0.4-0.5 mmol/ l of HCO3- and 0.3 mmol/ l of H+ (or a 0.003 pH increase).
The effects of respiratory alkalosis vary depending on its duration and severity, but are mainly represented by those related to the underlying conditions. Decreased cerebral blood flow as a result of rapid decrease in PaCO2 can cause dizziness, mental confusion and seizures even in the absence of hypoxemia.
Cardiovascular effects of acute hypocapnia are generally minimal in conscious patients, but in patients anesthetized or mechanically ventilated, heart rate and blood pressure may decrease due to the depressing effect of anesthesia and ventilation with positive pressure on heart rate, systemic resistance and venous return. Heart arrhythmias may occur in patients with heart disease as a result of decreased oxygen loading of the blood and left shift of the hemoglobin-oxygen dissociation curve (Bohr effect). Acute respiratory alkalose causes intracellular exchanges of Na+, K+ and PO4- and decreases Ca2+ freely by increasing the protein-related fraction. Hypocapnia induces hipposemia, usually minor.
Respiratory alkalose is the most common acid-base imbalance in patients with serious conditions and, when severe, has a poor prognosis. Several cardiopulmonary disorders are manifested by respiratory alkalosis in the initial and middle stages and the discovery of normocapnia and hypoxemia in patients with hyperventilation may mean the onset of rapid respiratory failure, requiring prompt evaluation to determine whether the patient becomes exhausted. Respiratory alkalose is common during mechanical ventilation.
Hyperventilation syndrome can be disabling. Paresthesia, circumoral numbness, tightness or chest pain, dizziness, inability to breathe properly and rarely tetanus may be sufficient to perpetuate the disorder. Analysis of arterial gases demonstrates acute or chronic respiratory alkalosis, often with hypocapnia between 15-30 mmHg and without hypoxemia. Damage to the central nervous system through disease or trauma can produce several models of hyperventilation and a PaCO2 between 20 and 30 mmHg.
Hyperthyroidism, high caloric load and physical exertion increase the rate of basal metabolism with proportional increase in ventilation, thus without changes in blood gases and without the development of respiratory alkalose. Salicilations are the most common cause of drug-induced respiratory alkalosis, arising as a result of direct stimulation of medullary chemoreceptors. Methylxanthins, theophylline and aminophilin stimulate ventilation and increase fan response to CO2. Progesterone increases ventilation and increases fan response to CO2.
Progesterone increases ventilation and decreases PaCO2 to 5-10 mmHg. So respiratory alkalose is a common feature of pregnancy. Respiratory alkalose is also present in liver failure and its severity correlates with the degree of liver failure. Respiratory alkalose is commonly found in the early stages of gram-negative septicaemia, before fever, hypoxemia or hypotension.
The diagnosis of respiratory alkalosis depends on the values of arterial pH and PaCO2. Plasma K+ is often low and Cl- increased. In the acute phase, respiratory alkalose is not associated with increased renal excretion of HCO3-, but within a few hours net acid excretion is low. In general, the concentration of HCO3- decreases by 2 mmoli/ l for each 10 mmHg decrease in PaCO2.
Chronic hypocapnia reduces HCO3-serial by 5 mmoli/ l for every 10 mmHg decrease in PaCO2. It is unusual to observe a serum HCO3 greater than 2 mmol/ l as a result of pure respiratory alkalose. When the diagnosis of respiratory alkalosis is made, the causes that caused it should be investigated. Diagnosis of hyperventilation syndrome is a diagnosis of exclusion. In difficult cases, it is important to exclude other conditions, such as pulmonary embolism, coronary artery disease and hyperthyroidism.
Treatment of respiratory alkalosis is directed towards the elimination of underlying causes. If respiratory alkalose complicates ventilation control, changes in dead space, current volume and respiratory frequency may reduce hypocapnia. Patients with hyperventilation syndrome may benefit from encouragement, breathing in a paper bag during symptomatic attacks and observation of underlying psychological stress. Antidepressants and sedatives are not recommended, although beta-adrenergic blockers may improve peripheral manifestations of hyperadrenergic status.
All right, I've been able to complete this series of posts... Another victory of mine.
It is often associated with hypochloremia and hypopotasemia. Patients with high and low HCO3 and Cl have either metabolic alkalose or chronic respiratory acidosis. PaCO2 increases by 6 mmHg for every 10 mmoli/ l increase in HCO3- above normal. Set differently, relative to HCO3- between 10-40 mmoli/ l, the predicted PaCO2 is approximately equal to HCO3- +15. Arterial pH establishes the diagnosis, as it is increased in metabolic alkalose and decreased or normal in respiratory acidosis. Metabolic alkalose commonly occurs in combination with other conditions, such as acidosis or respiratory alkalose or metabolic acidosis.
From the point of view of pathogenesis, metabolic alkalose occurs as a result of a net gain of HCO3- or loss of nonvolatile acids (common HCl through vomiting) from extracellular fluid. Since alkali intake in the body is not common, the condition involves a stage of generation, in which acid loss frequently causes alkalose and a maintenance stage in which the kidneys are unable to compensate for alkalose by excretion of HCO3- due to volemy decrease, low RFG or cl- or K+ dislet.
Under normal conditions, the kidneys have an impressive excretion capacity of HCO3 in a common manner. In order for HCO3 to be extra in the extracellular fluid, it must be administered exogenously or be synthesized endogenously, in part or entirely by the kidneys. The kidneys will retain, rather than secrete, excess alkalis and thus maintain alkalose if one or both of the following mechanisms are operative: 1. Cl- deficiency (by decreasing extracellular fluids) exists at the same time as the deficiency of K+, the decrease of RFG and/ or the increase in the reabsorption of the proximal fraction of HCO3-. This combination of conditions causes secondary hyperaldosteronism and stimulates the secretion of H+ in the collector duct. Alkalose is corrected by administration of NaCl and KCl; 2. Hyperaldosteronism and hypokalemia are autonomous and non-responsive to increasing the volume of extracellular fluids.
Increased distal secretion of H+ is sufficient to reabsorb the increased amount of filtered HCO3 and overcome the low proximal reabsorption of HCO3- due to the expansion of extracellular fluids. To reduce alkalose in these situations it is necessary to inhibit the secretion or action of aldosterone or to surgically remove the secretory adrenal adenoma of aldosterone.
Let's now proceed to small presentations about differential diagnosis. In order to determine the cause of metabolic alkalose it is necessary to evaluate the status of extracellular volume (VEC), blood pressure in clino and orthostatism, serum K+ and the renin-aldosterone system. For example, the presence of hypertension and hypopotasemia in a patient with alkalose suggests an excess of mineralocorticoids, or a hypertensive patient receiving diuretics. Low activity of plasma renin and normal Na+ and Cl-values in urine in a patient who does not take diuretics indicates a primary excess syndrome of mineralocorticoid.
Combining hipposemia with alkalose in a normotensive, nonedematos patient may be given by Bartter syndrome, magnesium deficiency, vomiting, exogenous alkalis or diuretic ingestion. Determination of primary electrolytes (especially Cl-urinary) and urine screening for diuretics may be useful. if urine is alkaline, with Increased Na+ and K+, but with low Cl, the diagnosis is vomiting (recognized or hidden) or ingestion of alkalis. if urine is relatively acidic and has a low concentration of Na+, K+ and Cl-, it is highly likely that there are previous vomiting, a posthypercapinic situation or a previous ingestion of diuretics. If, on the other hand, urinary concentrations of Na+, K+ or Cl- are not low, a magnesium deficiency, Bartter syndrome or a routine ingestion of diuretics should be taken into account.
Chronic alkali administration in patients with normal renal function causes at most a minimum alkalose. However, alkalose in patients with chronic renal impairment may develop following the administration of alkalis when the normal excretion capacity of HCO3 is exceeded, or when coexisting hemodynamic disorders cause increased fractional reabsorption of HCO3-. These patients are represented by those receiving HCO3- orally or intravenously, acetate (parenteral hyperfood solutions), citrate (transfusions) or antacids and cation-changing resins (aluminum hydroxide and sodium polystyrene sulfonate).
A rare cause is long-term ingestion of excess milk and antacids. Both hypercalcemia and excess vitamin D may increase renal reabsorption of HCO3- and cause nephrocalcinosis, renal failure or metabolic alkalose. Stopping ingestion or administration of alkalis is frequently sufficient to correct alkalose.
Metabolic alkalose associated with vfEC decrease, K+ deletation and secondary hyperreinemic hyperaldosteronism has several origins. In the case of gastrointestinal origin, vomiting and gastric aspiration, gastrointestinal losses of H+ cause the retention of HCO3-. The increase in H+ losses through gastric secretions can be determined by vomiting, gastric aspiration or gastric fistula. Loss of fluids and NaCl pri vomiting or nasogastric suction causes decreasein volume of extracellular fluids (VFEC) and increased secretion of renin and aldosterone. The decrease in volume causes a decrease in RFG and an increase in the ability of renal tubules to reabsorb HCO3-.
During vomiting, a continuous plasma intake of HCO3- is achieved by exchange with Cl-, and plasma HCO3- exceeds the reabsorption capacity of the proximal tube. Excess NaHCO3 reaches the distal tube, where part of Na+ will be exchanged for K+ through an aldosterone-mediated process. Due to the decrease in VFEC and hypochloremia, Cl- is preserved by the kidneys.
After stopping vomiting, Plasma HCO3 decreases to the threshold of renal elimination of HCO3-, which is increased due to the effects of decreased VFEC, hypokalemia and hyperaldosteronism. Alkalose is less severe than in the active vomiting phase and urine is relatively acidic with low levels of Na+, Cl- and HCO3-. The correction of the VfEC value with NaCl may be sufficient to restore normal blood pH, even without covering the K+ deficiency. However, the practice also dictates the restoration of K+. Metabolic alkalose has also been described in cases of vilos adenoma and is given rather by a potassium deplation.
In the case of renal origin (diuretics), drugs that cause chloresis without bicarbonate, such as thiazides and anse diuretics (furosemid, bumetanide, torsamid, etacrinic acid), acutely decrease VFEC without altering the total bicarbonate content of the body. HCO3- serum increases. PaCO2 does not increase proportionally and results in a decrease in alkalose. The degree of alkalose is usually low, due to cellular and nonHCO3 pads.
Chronic administration of diuretics tends to generate alkalose by increasing distal sodium delivery (Na+) and consequently stimulating the secretion of K+ and H+. Diuretics, by blocking the reabsorption of Cl- in the distal tube or by increasing the activity of the proton pump, can stimulate the distal secretion of H+, evidenced by increased net acid excretion. Alkalose is maintained by the persistence of decreased VFEC, secondary hyperaldosteronism, K+ deficiency and the direct effect of diuretics (as long as diuretics continue). The control of alkalose is carried out by the administration of isotone solutions to correct the deficiency of VFEC.
In posthypercapnia, prolonged CO2 retention with chronic respiratory acidosis increases renal absorption of HCO3- and generates new HCO3 (increasing net acid excretion). If PaCO2 returns to normal, metabolic alkalose is given by consistently elevated levels of HCO3-. Alkalose develops immediately if the increased PaCO2 is rapidly reduced to normal by a change in controlled mechanical ventilation and the acute bicarbonate response is proportional to the PaCO2 changes.
The associated cation is predominantly K+ (especially if K+ in the diet is not limited) with natrium as proportional to salt intake. Secondary hyperaldosteronism in chronic states of hypercapnia may be responsible for this type of response. The associated vfFEC decrease does not allow a complete correction of alkalose only by correcting PaCO2 and alkalose persists until an additional with Cl-. Increased proximal acidification, as a result of a previous hypercapnice-induced situation, may also contribute to posthypercapic alkalosis.
After the treatment of lactic acidosis and ketoacidosis, when an underlying stimulus for the generation of lactic acid or ketoacidis is rapidly removed by restoring circulation or insulin therapy, lactate or ketones are metabolized producing an equivalent amount of HCO3-, H+ being consumed by metabolism by organic anions, with the release of an equivalent amount of HCO3-. This process will regenerate HCO3- if organic acids are metabolized to HCO3- before their renal excretion. This production is partly compensated by urinary loss of organic ions.
Other sources of new HCO3 are additives with the initial amount generated by the metabolism of organic anions, producing an excess of HCO3-. These sources include: 1. HCO3- newly added to the blood by the kidneys as a result of increased acid excretion over the pre-existing period of acidosis and 2. alkaline therapy during acidosis treatment. The acidosis-induced decrease in VFEC and The deficiency of K+ work to support alkalose.
In the case of non-resorbable anions and magnesium deficiency, the administration of small amounts of non-resorbable anions, such as penicillin or carbenicillin, may increase distal acidification and k+ secretion by increasing the light difference of potential. Mg2+ deficiency causes hypopotasemic alkalose by increasing distal acidification as a result of stimulation of renin and thus aldosterone secretion.
Pure potassium (K+) deletion causes modest metabolic alkalose, increasing urinary acid elimination in the form of NH4+ and also increasing the reabsorption of HCO3-. Alkalose is moderate due to the fact that the Devenletion of K+ also causes the NaCl balance to be positive, with or without the administration of mineralocorticoid. Salt retention, by contrast, decreases alkalose. When access to NaCl and K+ is restricted, alkalose is more severe. Alkalose associated with severe K+ deletis is resistant to salt administration, while recovery of K+ deficiency corrects alkalose.
Let's see what's with metabolic alkalosis associated with VFEC expansion, hypertension and hyperaldosteronism! The administration of mineralocortidoid or its excess production (primary aldosteronism in Cushig syndrome and enzymatic cortico-adrenal defects) increases the net secretion of acid and may produce a metabolic alkalosis that may be accentuated by the association of K+ deficiency. The expansion of VFEC by salt retention causes hypertension and antagonizes the reduction of RFG and/ or increases tubular acidification induced by aldosterone and K+ deficiency. Kaliuresis persists and causes a continuous deplation of K+ with polydipsia, inability to concentrate urine and polyuria.
The increase in aldosterone levels may be the result of an autonomic primary adrenal overproduction or a secondary release of aldosterone caused by renal renin overproduction. In both cases, the normal feedback of VFEC on net aldosterone production is affected and hypertension may result in volume retention hypertension. Liddle syndrome results from increased activity of the Na+ channels of the collector duct and is a cause of volemy expansion and hypopotasic alkalosis with normal levels of aldosterone.
Symptoms that occur include functional disorders in the central and peripheral nervous system similar to those caused by hypocalcemia: mental confusion, obnubilation, predisposition to seizures, paresthesia, muscle cramps, tetanus, worsening of arrhythmias and hypoxemia in chronic obstructive pulmonary disease. Associated electrolyte abnormalities include hypopotasemia and hypophosphatemia.
Treatment is mainly directed on the correction of the underlying stimuli that generate HCO3-. If primary aldosteronism is present, correction of the underlying causes will correct and alkalose. The loss of H+ in the stomach or kidney may be reduced by the use of H2 receptor blockers or the discontinuation of diuretics. The second aspect of treatment is to remove factors that support the reabsorption of HCO3-, such as decreased VFEC or K+ deficiency.
Although K+ deficiency needs to be corrected, NaCl therapy is usually sufficient to correct alkalose, given the decrease in VFEC, which is evidenced by low Cl in the urine. In some cases, known as salt resistance, there is an association with a high deficiency of K+, Mg2+ deficiency, Bartter syndrome or with an autonomous primary secretion of mineralocorticoid. Under these conditions, therapy should be directed at underlying physiopathological problems.
If the associated situations exclude salt administration, renal losses of HCO3- can be accelerated by the administration of acetazolamide, a carbonic anhydrase inhibitor, which is consistently effective in patients with adequate renal function, but which may increase the loss of K+. Diluted hydrochloric acid is also effective, but can cause hemolysis. The administration of amino acids such as amginin hydrochloride is safe and effective. Acidification can also be done with Oral NH4Cl, which should be avoided in the presence of liver disease. Finally, hemodialysis performed with a dialysis with low-HCO3 and high Cl- may be effective when renal function is impaired.
Respiratory acidosis can be caused by severe lung disease, respiratory muscle fatigue or abnormalities in ventilation control and is caused by increased PaCO2. In acute respiratory acidosis, there is an immediate compensatory increase (through cellular buffer mechanisms) of HCO3-, which increases by one mmol/l for every 10 mmHg increase in PaCO2. In chronic respiratory acidosis (more than 24 hours), renal adaptation occurs and HCO3- increases by 4 mmol/ l for every 10 mmHg increase in PaCO2. HCO3- serum does not normally increase above 38 mmoli/ l.
Renal compensation (increased reabsorption of HCO3-) begins within the first 12-24 hours and is complete after 5 days. Clinical manifestations vary depending on the severity and duration of respiratory acidosis, underlying diseases and hypoxemia, when it exists. A rapid increase in PaCO2 can cause anxiety, dyspnoea, confusion, psychosis, hallucinations and, finally, coma. In less advanced stages, chronic hypercapnia includes sleep disorders, memory loss, daytime sleepiness, personality disorders, coordination disorders and motor disorders such as tremors, myoclonia, asterixis.
Headache and other signs such as papillary edema, abnormal reflexes, focal muscle weakness are caused by vasoconstriction secondary to the loss of vasodilating effects of CO2. Depression of the respiratory centers through a variety of drugs, trauma or diseases, can produce respiratory acidosis.
It can occur acutely in general anesthesia, administration of sedatives, brain trauma or chronic in the administration of sedatives, alcohol, intracerebral tumors and in syndromes of respiratory disorders during sleep, which include primary alveolar impairment syndrome and hyperventilation syndrome from obesity.
Anomalies or disorders of motor neurons, neuromuscular junctions or skeletal muscles may cause hypoventilation through fatigue of the respiratory muscles. Mechanical ventilation, when not properly adapted and supervised, can cause respiratory acidosis, especially if CO2 production increases sharply (due to fever, agitation, sepsis or oversupply) or if alveolar ventilation decreases due to deterioration of lung function. Increased levels of positive pressure at the end of exhalation in the presence of low heart rate may cause hypercapnia as a result of large increases in dead alveolar space.
Acute hypercapnia is often the consequence of obstruction of the upper airways or generalized bronchospasm, such as in severe asthma, anaphylaxis, inhalation of hot air or toxins. Chronic hypercapnia and respiratory acidosis occur at the stage of an obstructive pulmonary disease. Restrictive conditions including both the chest wall and lungs can cause respiratory acidosis due to a high metabolic breathing effort, which causes fatigue of the respiratory muscles.
Advanced studies of intra and extrapulmonary restrictive diseases are presented as chronic respiratory acidosis. Diagnosis of respiratory acidosis requires, by definition, measurements of PaCO2 and arterial pH. A detailed anamnesis and a careful objective examination often indicate the cause. Lung function studies, including spirometry, carbon monoxide diffusion capacity, lung volumes, PaCO2 blood pressure and O2 saturation usually indicate whether respiratory acidosis is secondary to lung disease.
The study of nonpulmonary causes should include a detailed history of drug intake, measurement of hematocrit and assessment of the upper airways, chest wall, pleura and neuromuscular function.
Treatment of respiratory acidosis depends on its onset and severity. Acute respiratory acidosis can be life-threatening, and measures taken to remove the underlying causes should be associated with adequate alveolar ventilation. This may mean tracheal intubation and assisted mechanical ventilation. Oxygen should be administered with care in patients with severe obstructive pulmonary disease and chronic CO2 retention who are breathing spontaneously. When oxygen is administered properly, these patients may have progressive respiratory acidosis.
Rapid and aggressive correction of hypercapnia should be avoided because parco2 decrease can cause the same complications in acute respiratory alkalosis (e.g. cardiac arrhythmias, decreased brain infusion and seizures). PaCO2 should be gradually decreased in chronic respiratory acidosis to basic levels of PaCO2, while taking enough Cl- and K+ to increase renal excretion of HCO3-.
Chronic respiratory acidosis is often difficult to correct, but measures taken to improve lung function, such as stopping smoking, using oxygen, bronchodilators, glucocorticoids, diuretics and physiotherapy can help some patients and prevent damage to lung function in most. The use of respiratory stimulants may be useful in selected patients, especially if hypercapnia is exaggerated in relation to lung damage.
Now, in the end of this long post, I'm going to tackle respiratory alkalosis. Alveolar hyperventilation decreases PaCO2, so the pH increases. Non-bicarbonate cell buffer systems responding to the consumption of HCO3-. Hypocapnia develops when sufficiently strong fan stimuli cause a greater release of CO2 in the lung than its metabolic production at the tissue level. Plasma pH and HCO3- vary proportionally to PaCO2 when it is between 15 and 40 mmHg. The relationship between the arterial concentration of hydrogen ions and PaCO2 is 0.7 mmoli/ l/ mmHg (or 0.01 pH/mmHg units) and for HCO3-plasma is 0.2 mmol/ l/ mmHg.
Sustained hypocapnia for more than 2-6 hours is compensated by a decrease in renal ammonium and titrable acidity excretion, as well as by a reduction in the reabsorption of Filtered HCO3. Complete renal adaptation to respiratory alkalose is done within a few days under conditions of a volemic status and normal renal function. Kidneys seem to respond directly to low PaCO2 rather than to the alkalose itself. A decrease of 1 mmHg of PaCO2 results in a decrease of 0.4-0.5 mmol/ l of HCO3- and 0.3 mmol/ l of H+ (or a 0.003 pH increase).
The effects of respiratory alkalosis vary depending on its duration and severity, but are mainly represented by those related to the underlying conditions. Decreased cerebral blood flow as a result of rapid decrease in PaCO2 can cause dizziness, mental confusion and seizures even in the absence of hypoxemia.
Cardiovascular effects of acute hypocapnia are generally minimal in conscious patients, but in patients anesthetized or mechanically ventilated, heart rate and blood pressure may decrease due to the depressing effect of anesthesia and ventilation with positive pressure on heart rate, systemic resistance and venous return. Heart arrhythmias may occur in patients with heart disease as a result of decreased oxygen loading of the blood and left shift of the hemoglobin-oxygen dissociation curve (Bohr effect). Acute respiratory alkalose causes intracellular exchanges of Na+, K+ and PO4- and decreases Ca2+ freely by increasing the protein-related fraction. Hypocapnia induces hipposemia, usually minor.
Respiratory alkalose is the most common acid-base imbalance in patients with serious conditions and, when severe, has a poor prognosis. Several cardiopulmonary disorders are manifested by respiratory alkalosis in the initial and middle stages and the discovery of normocapnia and hypoxemia in patients with hyperventilation may mean the onset of rapid respiratory failure, requiring prompt evaluation to determine whether the patient becomes exhausted. Respiratory alkalose is common during mechanical ventilation.
Hyperventilation syndrome can be disabling. Paresthesia, circumoral numbness, tightness or chest pain, dizziness, inability to breathe properly and rarely tetanus may be sufficient to perpetuate the disorder. Analysis of arterial gases demonstrates acute or chronic respiratory alkalosis, often with hypocapnia between 15-30 mmHg and without hypoxemia. Damage to the central nervous system through disease or trauma can produce several models of hyperventilation and a PaCO2 between 20 and 30 mmHg.
Hyperthyroidism, high caloric load and physical exertion increase the rate of basal metabolism with proportional increase in ventilation, thus without changes in blood gases and without the development of respiratory alkalose. Salicilations are the most common cause of drug-induced respiratory alkalosis, arising as a result of direct stimulation of medullary chemoreceptors. Methylxanthins, theophylline and aminophilin stimulate ventilation and increase fan response to CO2. Progesterone increases ventilation and increases fan response to CO2.
Progesterone increases ventilation and decreases PaCO2 to 5-10 mmHg. So respiratory alkalose is a common feature of pregnancy. Respiratory alkalose is also present in liver failure and its severity correlates with the degree of liver failure. Respiratory alkalose is commonly found in the early stages of gram-negative septicaemia, before fever, hypoxemia or hypotension.
The diagnosis of respiratory alkalosis depends on the values of arterial pH and PaCO2. Plasma K+ is often low and Cl- increased. In the acute phase, respiratory alkalose is not associated with increased renal excretion of HCO3-, but within a few hours net acid excretion is low. In general, the concentration of HCO3- decreases by 2 mmoli/ l for each 10 mmHg decrease in PaCO2.
Chronic hypocapnia reduces HCO3-serial by 5 mmoli/ l for every 10 mmHg decrease in PaCO2. It is unusual to observe a serum HCO3 greater than 2 mmol/ l as a result of pure respiratory alkalose. When the diagnosis of respiratory alkalosis is made, the causes that caused it should be investigated. Diagnosis of hyperventilation syndrome is a diagnosis of exclusion. In difficult cases, it is important to exclude other conditions, such as pulmonary embolism, coronary artery disease and hyperthyroidism.
Treatment of respiratory alkalosis is directed towards the elimination of underlying causes. If respiratory alkalose complicates ventilation control, changes in dead space, current volume and respiratory frequency may reduce hypocapnia. Patients with hyperventilation syndrome may benefit from encouragement, breathing in a paper bag during symptomatic attacks and observation of underlying psychological stress. Antidepressants and sedatives are not recommended, although beta-adrenergic blockers may improve peripheral manifestations of hyperadrenergic status.
All right, I've been able to complete this series of posts... Another victory of mine.
Have a good day!
Dorin, Merticaru