MONITOREO DE AVES PLAYERAS MIGRATORIAS EN LAS LAGUNAS COSTERAS DE SONORA Y SINALOA

• pH of a solution is defined as the negative logarithm of the hydrogen ion concentration. As it is “negative log”, so pH decreases as H⁺ concentration increases.

Normal pH of blood is 7.4 (range 7.36-7.44).

• A unit change in pH means 10 times change in hydrogen ion concentration. Hence, although pH change appears small, it is sufficiently large in terms of H⁺ concentration.

• A buffer is a mixture of a weak acid and its conjugate base or salt. The buffers maintain the pH of body fluids within normal limits.

• K_A is called dissociation constant of the acid and it tells about degree of dissociation (strength) of the acid. Strong acids are completely dissociated.

Therefore, larger the value of K_A, more dissociated or stronger the acid.

• Henderson Hasselbalch equation relates pH of buffer solution to pKa of its weak acid and the ratio of molar concentration of the weak acid and its salt.

A

[Base/salt]

pH = pK + log

Acid

• When a strong acid is added to a buffer solution it reacts with the salt part of the buffer pair. This neutralizes the added acid generating an equivalent amount of the buffer acid. In this way a strong acid is replaced by a weak acid and pH is maintained.

Box 9.12: Comparison between crystalloid and colloid

Crystalloid Colloid Composition Water + electrolytes High mol wt

substance Pressure Osmotic pressure Oncotic pressure Distribution Extravascular space Intravascular

space Volume 3 times of loss Equal to loss requirement

Cross-matching No effect Interfere

Cause edema Yes No

Anaphylaxis No Do occur

Cost Economic Costly

Comparison between crystalloid and colloid is given in Box 9.12.

• Different acids generated in body can be divided into three groups.

 Carbonic acid: It is formed by hydration of CO_2.

 Fixed acids: The examples are H₂SO₄ and H₃PO₄. Since these acids are not volatile, hence called as fixed acids.

 Organic acids: The examples are lactic acid, acetoacetic acid, β-hydroxy butyric acid, uric acid, etc.

• A large change in pH is not compatible with proper functioning of tissues. A proper pH is necessary for structural and functional integrity of proteins (including enzymes), nucleic acids and membranes.

A large change in pH alters ionization of certain groups of amino acids (and proteins), purine and pyramidine bases and certain components of phospholipids. Concentration of certain free ions like Ca⁺⁺ depends on pH of our body fluids. These free ions are important in regulation of excitability of excitable tissues like muscle and nervous tissue.

• Buffers form the first line of defense against incoming acids or alkalis. A useful buffer should keep pH of body fluids close to 7.4, should be present in high concentration and the pKa value of its weak acid should be close to 7.4.

• Important buffers of the body are:

 Hemoglobin and protein buffers

 Phosphate buffer

 Bicarbonate buffer

• The bicarbonate buffer is most important buffer of the body. It has bicarbonate (HCO₃) and carbonic acid (H₂CO₃) as two components and their normal ratio is 20 : 1. Alteration in this ratio alters the pH regardless of absolute values of HCO₃ and H₂CO₃. A decrease in ratio leads to acidosis while increase leads to alkalosis. The bicarbonate level can be altered by metabolic factors while carbonic acid level is regulated by respiratory factors. Alteration in one is automatically followed by compensation by the other thus maintaining their ratio and therefore pH of blood tends to remain constant. The excess of H₂CO₃ is eliminated as CO₂ by lungs while HCO₃ is regulated by the kidneys.

Acid Base Disorders

Acid base disorders are classified according to changes in components of bicarbonate-carbonic acid buffer, since

Compensation in Acid Base Disorders Respiratory regulation:

• Respiratory regulation is important in metabolic acidosis and alkalosis.

• In metabolic acidosis, because of decrease in bicarbonate, the ratio HCO₃/H₂CO₃ is reduced and accordingly pH is reduced. This stimulates chemoreceptors and causes reflex hyperventilation leading to CO₂ wash-off. This reduces H₂CO₃ and tends to normalize pH. It may however be pointed out that although ratio is normalized, the actual concentrations of both HCO₃ and H₂CO₃ are reduced. These concentrations are then normalized by the renal regulatory processes.

• In metabolic alkalosis the ratio HCO₃/H₂CO₃ is increased because of increase of HCO₃. pH is, accordingly, increased. This reduces chemoreceptor stimulation, resulting in hypoventilation and consequent CO₂ retention. This increases H₂CO₃ thereby tending to normalize the HCO₃/H₂CO₃ ratio.

This tends to normalize pH, although, the actual HCO₃ and H₂CO₃ concentrations are both increased. These concentrations are then normalized by the renal regulatory processes.

Box 9.13: Compensatory changes in acid base disorders Primary disorder Primary Compensation

abnormality

Metabolic acidosis ↓ HCO3→ ↓ pH Respiratory (↓ pCO2 ) Metabolic alkalosis ↑ HCO3→ ↑ pH Respiratory

(↑ pCO2) Respiratory acidosis ↑ pCO2→ ↓ pH Renal (↑ HCO3 ) Respiratory alkalosis ↓ pCO2→ ↑ pH Renal (↓ HCO3) these can be easily evaluated. The three components (pH, HCO₃ and pCO₂) of this buffer are related as follows (the Henderson-Hasselbalch equation):

pH= pK+ log [HCO₃] / [H₂CO₃]

= pK+ log [HCO₃] /pCO₂ as [H₂CO₃] can be replaced by pCO_{2 .}

Whenever there is disturbance in acid base balance in the body, the changes are labeled as primary disorders. In order to correct these changes and to normalize the pH, certain compensatory changes occur (Box 9.13).

• It should be remembered that the pulmonary response in normalization of the ratio HCO₃/H₂CO₃ is incomplete and therefore, pH is not completely normalized. This is because the effect of pH in respiratory response is opposed by the prevailing pCO₂. For example, in acidosis reduced pH stimulates respiration while reduced pCO₂ opposes the response. Similarly in alkalosis the raised pH depresses respiration but increase in pCO₂ tends to stimulate respiration.

• In metabolic acidosis and alkalosis the pulmonary compensation is rapid and uncompensated cases are not seen. For example, in metabolic acidosis one will always find reduced HCO₃ (primary disorder) and reduced pCO₂ or reduced H₂CO₃ (pulmonary compensation). Similarly in metabolic alkalosis one will find increased HCO₃ (primary disorder) and increased H₂CO₃ or increased pCO₂ (pulmonary compensation).

Renal regulation:

• Renal regulation is important both in metabolic acid base disorders as well as respiratory acid base disorders.

• In respiratory acidosis the ratio HCO₃/H₂CO₃ is reduced because of retention of CO₂ and increase of H₂CO₃.To normalize pH renal excretion of HCO₃ is reduced and generation of new HCO₃is increased.

This will normalize HCO₃/H₂CO₃ ratio, although, the actual amounts of both the components are increased. These can only be normalized by removal of primary pulmonary disorder.

• Similarly in respiratory alkalosis the ratio HCO₃/ H₂CO₃ is increased because of excessive loss of CO₂ (and reduction of H₂CO_3.). To normalize pH, renal excretion of HCO₃ is increased and generation of new HCO₃ reduced. pH is thus normalized by restoration of HCO₃/H₂CO₃ ratio, although, the actual amounts of both components are reduced.

The actual amount can not be normalized unless the causative pulmonary disorder is treated.

• In respiratory acid base disorders the renal compen-sation is a slow process and therefore both uncompensated (acute disorder) and compensated (chronic disorder) cases are seen. In acute cases of respiratory acidosis one may find increased pCO₂ (or H₂CO₃ ) and normal HCO₃ while in chronic cases both the components are increased. Similarly

in acute respiratory alkalosis only pCO₂ (H₂CO₃) is reduced while in chronic cases both the components are reduced. It may also be realized that normaliza-tion of pH in respiratory disorders will only occur when the slow renal response has produced the desired effect on HCO₃component of the buffer.

There are four primary acid base disorders:

• Metabolic acidosis

• Metabolic alkalosis

• Respiratory acidosis

• Respiratory alkalosis.

Metabolic Acidosis

• It is a condition in which there is deficit of base or excess of any acid other than carbonic acid.

• Primary change is ↓ HCO3 or ↑ H⁺ → ↓ pH

a. Increase in fixed acid

 Ketoacidosis in diabetes, starvation

 Lactic acidosis due to tissue hypoxia and anaerobic metabolism in hypovolemia, septic shock, cardiac arrest, etc.

 Renal failure

 Salicylate poisoning.

b. Loss of base

 Prolonged Ryle’s tube aspiration

 High intestinal fistula

 Ulcerative colitis

 Prolonged diarrhea.

Clinical features

• Rapid, deep, noisy respiration due to stimulation of respiratory centers (Kussmaul’s respiration).

• Tachycardia and hypotension in patients of septicemia.

• Central nervous system depression (fatigue, confusion, stupor).

• Oliguria with strongly acidic urine.

BGA report

• ↓ pH

• ↓ HCO3

• A typical BGA report will be as follows:

Metabolic acidosis pH 7.3 pCO₂ 20 HCO₃ 9 Treatment

• To correct hypoxia, restore adequate tissue perfusion by rapid infusion of ringer lactate solution.

• Administration of sodabicarb solution should not be done routinely (Box 9.14 ).

• Sodabicrb should only be given in cases of severe acidosis (pH<7.2) or cases with base deficit.

• Calculating dose of HCO₃:

 1 ml sodabicarb (7.5%) contains 0.9 mmol of HCO₃.

 HCO₃ requirement (mmol/lit) = 0.3 × body weight (kg) × base deficit (mmol/lit).

 Initially give only half of the required dose of sodabicarb IV slowly and repeat only if required based on blood pH value.

Box 9.14: Harmful effects of excessive and rapid HCO₃ administration

1. Hypokalemic cardiac toxicity if patient is K⁺ depleted 2. Tetany in a patient of renal failure or having

hypo-calcemia

3. Congestive heart failure or worsening of hypertension due to excessive intake of Na⁺

4. In acidosis there is hyperventilation as respiratory center (RC) is stimulated (from acid pH of both blood and cerebrospinal fluid). As plasma HCO₃ is corrected RC shall remain stimulated as CSF HCO₃ does not quickly equilibrate with plasma HCO₃.It may result in respiratory alkalosis

Anion Gap

• There are unmeasured anions in blood (proteins, PO₄^–, SO₄^–) = 23 mmol/L.

• There are unmeasured cations in blood (Ca⁺⁺, K⁺, Mg⁺⁺ ) = 11 mmol/L.

• The anions are more than cations and the difference is called anion gap. The normal anion gap = 12-18 mmol /L.

• When organic acids increase (lactic acid, ketoacids), there is increase in anion gap (>20 mmol/L)

• Anion gap is used for evaluation of patients with metabolic acidosis.

• Accumulation of H⁺ (e.g. lactic acidosis) leads to high anion gap.

• Anion gap remains unchanged in cases of metabolic acidosis due to loss of HCO₃ ions (e.g. intestinal obstruction_, intestinal fistula) because lost HCO₃ is replaced with chloride ions (hyperchloremic acidosis).

• This helps in diagnosis of cause of acidosis. In most of the cases, however, careful history may be enough and study of the anion gap may not be required.

Metabolic Alkalosis

• It is a condition in which there is excess of base or deficit of any acid other than carbonic acid.

• The alkalosis due to loss of acid is almost always associated with hypokalemia.

• Primary change is ↑ HCO3 or ↓ H⁺ → ↑ pH.

• For each ↑ in HCO3 of 7-7.5 mEq/L–pH ↑ by 0.1.

• Respiratory compensation

 ↑ pCO2

 ↑ HCO3 excretion by kidneys (alkaline urine)

• Expected pCO₂ in metabolic alkalosis = 0.7 × HCO₃ + 21 ( + 2).

Causes—two types a. Chloride responsive

 Loss of acid from stomach, e.g. vomiting, prolonged Ryle’s tube aspiration

 Volume depletion (Chloride loosing diarrhea)

 Diuretics (long-term use) b. Chloride nonresponsive

 Potassium depletion (low serum K)

 Diuretics (recent use)

 Corticoid excess (over administration, Cushing’s disease).

BGA report

• ↑ pH

• ↑ HCO3

• A typical BGA report will be as follows:

Metabolic alkalosis pH 7.55 pCO₂ 50 HCO₃ 42 Clinical features

• Cheyne-Stokes’ respiration with apnoic spells (cessation of breathing) of 5-30 sec.

• Tetany.

• Associated features of hypokalemia, e.g. lethargy, muscle weakness.

Treatment

• Saline infusion for chloride responsive.

 Chloride deficit (mEq/L) = 0.3 × wt. (in kg) × (100 – Plasma chloride)

 Volume of isotonic saline (L) = Chloride deficit/

154.

• For chloride nonresponsive—correct hypokalemia, correct corticoid excess.

• Compensatory change is ↑ HCO3.

 Acute respiratory acidosis: For each 10 mm Hg

↑ pCO₂, HCO₃ ↑ by 1 mEq/L.

 Chronic respiratory acidosis: For each 10 mm Hg

↑ pCO₂, HCO₃ ↑ by 3 mEq/L.

Causes

• Inadequate ventilation of anesthetized patient.

• Incomplete reversal of muscle relaxants at extubation following general anesthesia.

• Surgery in patients with underlying lung disease, e.g.

COPD, severe acute asthma.

• Others (fever, anxiety, hyperthyroidism, pulmonary edema, cirrhosis).

BGA report

• ↓ pH

• ↑ pCO2

• A typical BGA report will be as follows:

Respiratory acidosis pH 7.1 pCO₂ 90 HCO₃ 30 Clinical features: The features are primarily of underlying problem.

Treatment

• Correction of underlying pathology.

• Oxygenation.

• Ventilatory support.

Respiratory Alkalosis

• It is a condition in which pCO₂ is below normal range.

• Primary change is ↓ pCO2 → ↑ pH.

• For each 10 mm Hg ↓ pCO2 – pH ↑ by 0.1.

• Compensatory change is ↓ HCO3 by increased renal excretion of HCO₃.

 Acute respiratory alkalosis: For each 10 mm Hg

↓ pCO₂, HCO₃ ↓ by 2 mEq/L .

 Chronic respiratory alkalosis: For each 10 mm Hg ↓ pCO2, HCO₃ ↓ by 4-5 mEq/L.

Causes

• Hyperventilation under anesthesia

• Hyperpyerexia

• Head injury (Hypothalamic lesion)

• High altitude

• Hysteria

• Anxiety

• Sepsis.

Clinical features

• The features are primarily of underlying problem.

• During anesthesia, alkalosis is accompanied with pallor and fall of BP.

BGA report

• ↑ pH

• ↓ PCO2

• A typical BGA report will be as follows:

Respiratory alkalosis pH 7.55 pCO₂ 20 HCO₃ 22

Treatment CO₂ rebreathing.

How to Read an ABG Report ?

An arterial blood sample is taken from the femoral or radial artery and subjected to blood gas analysis. The acid base disorders can be recognized by interpreting the ABG (Arterial Blood Gas) report (Box 9.15 ).

Box 9.15: Normal ABG report

pH : 7.40 (7.35-7.45)

• pO₂ is measurement of partial pressure of oxygen in blood.

• pCO₂ is measurement of partial pressure of CO₂ in blood.

• HCO₃ (standard bicarbonate) is concentration of serum bicarbonate after fully oxygenated blood has been equilibrated with CO₂ at 40 mm Hg.

• BE (Base excess or deficit) is total of buffer anions present in the blood in excess or deficit of normal.

Base excess or deficit multiplied by 0.3 of body weight in kg gives the total extracellular excess or deficit of base in mmol.

• Anion gap is discussed above.

Calculating Acid Base Status from ABG Report:

Step 1: First look at pH

• ↓ pH(<7.35)—acidosis

• ↑ pH (>7.45)—alkalosis

• Normal pH (7.35-7.45).

Step 2: Look at pCO₂

• pH ↓ and pCO2 ↑ = Primary Respiratory Acidosis

• pH ↑ and pCO2 ↓ = Primary Respiratory Alkalosis.

An easy way to remember is that if change in pH and pCO₂ occurs in opposite directions (one increasing and other decreasing), the problem is respiratory.

Step 3: Look at HCO₃

• pH ↓ and HCO3 ↓= Primary Metabolic Acidosis

• pH ↑ and HCO3 ↑ = Primary Metabolic Alkalosis An easy way to remember is that if change in pH and HCO₃ occurs in same directions (both increasing or both decreasing), the problem is metabolic.

If both PaCO₂ and HCO₃ are out of normal range and pH is also out of range, such a disturbance is called Mixed disorder.

Step 4: Study compensation

• In Metabolic Disorders, the respiratory compen-sation causing retention or removal of CO₂ occurs in few minutes to few hours. Calculate difference between measured and expected pCO₂ using formulae given in Box 9.16.

• If measured pCO₂ is greater than the expected pCO₂, it implies that the respiratory system is not compensating for the metabolic acidosis and respiratory acidosis is also present.

• In respiratory disorders, first determine change in pH and HCO₃ to decide whether it is acute or chronic problem. Then calculate difference between measured and expected pH using formulae given in Box 9.17

Box 9.17: Formulae for evaluation of compensation in respiratory disorders

Respiratory disorder Expected pH Respiratory acidosis

Acute 7.4 – [(observed pCO₂–40) × 0.008]

Chronic 7.4 – [(observed pCO₂–40) × 0.003]

Respiratory alkalosis

Acute 7.4 + [(40–observed pCO₂) × 0.008]

Chronic 7.4 + [(40–observed pCO₂) × 0.001]

Step 5: Anion gap estimation

If metabolic acidosis is diagnosed—check anion gap to find the cause of acidosis.

Step 6: Assessment of oxygenation

• The value of pO₂ depends upon inspired oxygen concentration (FiO₂).

• The expected pO₂ of a person can be estimated with the formula:

Expected pO₂ = FiO₂% × 5

For example, if a person is given 25% oxygen, his expected pO₂ is 25 × 5= 125 mm Hg

• pO₂ < 80 mm Hg is hypoxemia.

• pO₂ < 60 mm Hg is life threatening.

• The relation between pO₂ and FiO₂ is given in Box 9.18.

Box 9.18: Relation between pO₂ and FiO₂

Clinical condition pO₂ / FiO₂

Normal > 5

Some oxygenation problem 3-5

Acute lung injury 2-3

ARDS < 2

Box 9.16: Formulae for evaluation of compensation in metabolic disorders

Metabolic disorder Expected pCO₂ Metabolic acidosis 1.5 × HCO₃ +8 (+2) Metabolic alkalosis 0.7 × HCO₃ + 21 (+2)

In document TÉRMINOS DE REFERENCIA DE LOS CONCEPTOS DE APOYO DEL PROGRAMA DE MONITOREO BIOLÓGICO (PROMOBI), EJERCICICO FISCAL 2015 (página 28-31)