Acid base balance
Professor/mohammed Ahmed Bamashmos
• Pathophysiology
• Definition Of Acid-Base Balance:
• This regulation of the extracellular fluid environment involves the ratio of acid to base,
measured clinically as pH.
• Physiologically all positively charged ions are called acids, and all negatively charged ions are bases.
• Physiological changes in the concentration of H+
ions in the blood lead to acid-base
balance.
• A systemic increase in the H+
ions concentration is called acidosis.
• A systemic decrease in the H+
ions is called alkalosis.
• The acid-base must be regulated within a narrow range for the body to function normally.
• A very slight change in the pH will affect the body.
• H+
ions are needed for:
• To maintain the integrity of the membrane.
• Speed of the metabolic reactions.
• Any change in the pH will lead to harmful effects than other diseases.
• The symbol pH represents the power of H+
.
• When pH changes one unit like 7.0 to 6.0 = [H+
] [H+
] = H+
ions concentration changes 10 folds.
• Body acids are formed from end products of:
• Metabolism of proteins.
• Metabolism of Carbohydrates.
• Metabolism of fats.
• This must be balanced by the number of basic substances in the body to maintain the
normal pH.
• Lungs, kidneys, and bones are the major organs involved in the regulation of acid-base balance
• Body acids are formed from end products of:
• Metabolism of proteins.
• Metabolism of Carbohydrates.
• Metabolism of fats.
• This must be balanced by the number of basic substances in the body to maintain the normal pH.
• Lungs, kidneys, and bones are the major organs involved in the regulation of acid-base balance.
• Body acids are of two types:
• Volatile acids:
• Carbonic acid (H2CO3) is a week acid, and it does not easily release the H+
ions.
• In the presence of carbonic anhydrase enzyme can eliminate CO 2 gas and water H2O.
• CO 2 is eliminated through the lungs.
• Nonvolatile acids:
• These are sulfuric acid, phosphoric acid, and other organic acids that are eliminated through the kidneys.
• These are the strong acids and readily give up their H+
ions.
• Nonvolatile acids are secreted into the urine by the renal tubules.
• These acids are about 150 meq/L of H+ ions per day or about 1 meq/kg body weight
• Buffer Systems Of The Acid-Base Balance:
• The buffer systems become active in response to change in the pH of the
body as acid-base balance.
• Functions of the buffer system:
• Prevent the significant change in pH.
• Buffer can absorb the excess of the H+
ions (acid).
• Buffer system can absorb OH–
ions, Hydroxyl (base).
• The buffer system is present in the intracellular fluid (ICF) and extracellular fluid (ECF).
• The most buffer system is:
• Carbonic acid-bicarbonate system.
• Hemoglobin system.
• Phosphate and protein are the most important intracellular buffers (ICF
• Renal buffering system:The distle tubule of the kidneys regulates acid-base
balance by secreting the H+
ions in the urine and reabsorbs the HCO3–
.
• Dibasic phosphate (HPO4—
) and ammonia (NH3) are two important renal buffer.
• The renal buffering of H+ ions requires CO2 and water (H2O) to form the
H2CO3.
• The enzyme carbonic anhydrase catalyzes the reaction.
• H+ ions are secreted from the tubular cells and buffer in the lumen by PO4
—
and NH3 = H2PO–
3 + NH4+
.
• The rest of HCO3–
is reabsorbed.
• Carbonic acid-bicarbonate buffering system:This buffer system operates
both in the lungs and kidneys.
• This is the major extracellular buffer system.
• Lungs can decrease the carbonic acid by blowing out the CO2 and leaving
water behind.
• Kidneys can reabsorb HCO3- or regenerate new HCO3- from CO 2 and water.
• Normal bicarbonate (24 meq/L) and normal carbonic acid (1.2 meq/L),
producing a 20:1 relation and maintain the pH of 7.4
• Both the systems are very efficient because:
• HCO3–
is easily reabsorbed or regenerated by the kidneys.
• The lungs adjust acid concentration
• Protein buffering system:Hemoglobin (Hb) is the best
intracellular buffer system, and it combines with H+
and forming
HHb and CO2, forming the HHbCO2 complex.
• When Hb combines with H+
ions becomes weak acid.
• Venous blood Hb is a better to buffer system than arterial blood
Hb.
• Acid-base balance:
• H+ ions and electrolytes disturbances may be:
• Acute.
• Chronic.
• Modest or severe.
• Simple or mixed.
• When there is an accumulation of H+ ions is called acidosis.
• When blood pH is declining below 7.3, this process is called acidemia.
• When there is a deficiency of H+ ions is called alkalosis.
• Blood pH rises above 7.45 is called alkalemia.
• There are conditions related to the respiratory system that leads to respiratory acidosis or
alkalosis.
• There are metabolic conditions related to kidneys, and abnormality of intake/output leads to
metabolic acidosis/alkalosis.
• The blood pH is normally maintained at 7.38 to 7.42. Any deviation
from this range indicates a change in the H+
ions concentration.
• Blood pH is a negative logarithm of [H+
] as shown in the following equation:
• pH = log10 [H+
]
• This equation shows that an increase in the H+
ions will lead to a fall in the blood pH is
called acidemia.
• So a decrease in the H+
ions will lead to an increase in the pH of the blood
called alkalemia.
• The conditions which cause the change in the pH are called acidosis and alkalosis.
• The following diagram can explain how pH is maintained by the arterial
carbon dioxide tension (pCO2) and plasma bicarbonate (HCO3–
).
• Plasma HCO3–
decrease in the plasma caused by
gastrointestinal or renal losses will increase H+
ions and lowers
the pH.
• Metabolic acidosis
• Definition:
• Metabolic acidosis occurs whenever there is a primary decrease in the HCO3¯ in the blood.
• This may occur due to:
• Exogenous acid administration.
• Endogenous acid production.
• Impaired renal H+ secretion.
• HCO3–
losses from the kidney or in the gastrointestinal secretions.
• Anion gap:
• Definition of the anion gap:
• Anion gap referred to anions usually not measured in the laboratory like sulfate, phosphate, and
lactate. The anions usually measured are Chloride (Cl-) and bicarbonate (HCO3-). The sum of the
anions is subtracted from the sum of cations (Na+
and +
); there is a gap around 10 to 12 meq/L, which
is called an anion gap. An elevated anion gap gives clues for acidosis.
• The importance of the anion gap is to identify the etiology of metabolic acidosis.
• The anion gap is measured in meq/L.
• Definition of anion gap: This is the difference between the plasma concentration of
major cation sodium (Na+
) and other anions are HCO3–
and Cl–
.
• Anion gap = [Na+
] – ([HCO3–
] + [Cl–
])
• The normal anion gap is 3 to 13 meq/L, and the mean is 10 meq/L.
• This is dependant mainly on the plasma protein, primarily albumin.
• 2.5 meq/L falls for every 1 gram/dl of albumin concentration in the blood.
• H+
ions changes in the blood lead to acid-base imbalance.
• A systemic increase in the H+ ions is called acidosis.
• In the case of acidemia pH of the arterial blood is <7.4.
• While in alkalemia, the pH of the arterial blood is >7.4.There is a
systemic decrease in the H+ ions in the systemic blood is called
alkalosis.
• Causes Of Metabolic Acidosis:
• In metabolic acidosis, noncarbonic acid increases, or HCO3¯ is lost from the extracellular space.
• The buffering system becomes active and maintains the pH.
• In case of the buffering system’s failure, the anion gap HCO3¯: H2CO3 = 20:1 changes.
• Increased noncarbonic acid with an elevated anion gap and Increased H+ load:
• Diabetes mellitus with ketoacidosis. There is a production of acetoacetic acid and β-hydroxybutyric acid in
diabetic acidosis.
• In the case of starvation.
• Lactic acidosis in shock and hypoxemia. There is the production of lactic acid.
• Ingestion of drugs like NH4CL, salicylates, methanol, ethylene glycol, and paraldehyde.
• Decreased H+ ions excretion was seen in:
• Uremia.
• Distal renal tubular acidosis (decreased renal H+ secretion).
• There is an accumulation of the acid that consumes the bicarbonate (HCO3¯).
• Causes Of A High Anion Gap (>12 Meq/L):
• Methanol toxicity.
• Uremia due to renal failure.
• Starvation.
• Diabetes mellitus (ketoacidosis).
• Lactic acidosis.
• Salicylates toxicity.
• Ethyl alcohol toxicity.
• Isoniazid toxicity.
• Iron toxicity.
• Causes Of Decreased Anion Gap (<6 Meq/L):
• Hypoalbuminemia.
• Plasma cell disorders.
• Bromide intoxication.
• Causes Of A High Anion Gap (>12 Meq/L):
• Methanol toxicity.
• Uremia due to renal failure.
• Starvation.
• Diabetes mellitus (ketoacidosis).
• Lactic acidosis.
• Salicylates toxicity.
• Ethyl alcohol toxicity.
• Isoniazid toxicity.
• Iron toxicity.
• Causes Of Decreased Anion Gap (<6 Meq/L):
• Hypoalbuminemia.
• Plasma cell disorders.
• Bromide intoxication.
• Respiratory acidosis
• Definition:
• With respiratory failure, CO2 accumulates (hypercapnia). This
state will raise the pCO2 and causes the pH to drop, and lead to
acidosis.
• This is a decrease in alveolar ventilation in relation to the
metabolic production of the CO2 produces respiratory acidosis
by the increase in the carbonic acid.
• Pathophysiology:Alveolar ventilation provides the necessary
oxygen for oxidative metabolism and eliminates the CO2
produced by these metabolic processes.
• There is a depression in the ventilation, resulting in excess of
CO2 (hypercapnia) in the blood circulation.
• A decrease in alveolar ventilation in relation to the metabolic
production of CO2 produces respiratory acidosis by an increase
in H2CO3 acid.
• The arterial CO2 tension (or pressure) PaCO2 is >45 mm Hg.
• This is seen in respiratory failure, where CO2 accumulates, called hypercapnia.
• This condition will raise the pCO2 and causes the pH to drop.
• To compensate, the HCO3–
will increase, but this is not sufficient to restore the pH to a
normal level.
• CO2 level rises, and this retained CO2 combines with water and form H2CO3.
• H2CO3 dissociates to release H+
and HCO3–
ions.
• Increased paCO2 and free H+
ions stimulate the medulla to increase the respiratory rate and expel the
CO2.
• As the pH falls, 2.3, diphosphoglycerate accumulates in the RBCs, where it will alter the Hb
(hemoglobin) to release the O2 (oxygen).
• Hb picks up H+
ions and CO2 and removes both from the blood circulation.
• If the respiratory mechanism fails, rising paCO2 stimulates the kidneys, retains HCO3–
and Na+
(sodium)
ions, and starts excreting H+
ions.
• Total CO2 may rise to a very high level of chronic respiratory acidosis
• Signs And Symptoms:
• There is often breathlessness.
• The patient is restless.
• There is headache, dyspnoea, and tachypnea.
• There is apprehension followed by lethargy.
• The patient will have disorientation.
• There are muscle twitching and tremors.
• Skin will be warm and flushed due to raised CO2 causes vasodilatation.
• There may be hypertension or hypotension.
• There are atrial and ventricular arrhythmias.
• The patient will have convulsions and ultimately goes into a coma.
• Lab diagnosis:
• pH = <7.35 to 7.45.
• paCO2 = >45 mm Hg.
• HCO3–
= Normal (in the acute stage).
• HCO3–
= Increased (in the chronic stage
• Treatment
• Treatment of the pulmonary causes:
• If there is obstruction by the foreign body, remove that immediately.
• There may be a need for mechanical ventilators.
• Give bronchodilators.
• If there is pneumonia, then start antibiotics.
• If there is pneumothorax, then put chest tube.
• In the case of pulmonary embolism, start thrombolytic and anticoagulants.
• Remove the secretions by bronchoscopy.
• Treatment of chronic obstructive pulmonary disease (COPD):
• Give O2 at a slow rate.
• Start bronchodilators.
• Start corticosteroids.
• You can also give I/V sodium bicarbonate.
• Other drugs are needed for the treatment of the cause.
• cause.
• Causes Of Respiratory Acidosis:
• Acute respiratory acidosis:
• This occurs with sudden obstruction to:
• The airway.
• Chest trauma that damages the respiratory muscles.
• Acute paralysis or depression of CNS respiratory center.
• HCO3–
rises 1 meq/L for each 10 mmHg rise in pCO2.
• Chronic respiratory acidosis:
• This chronic respiratory acidosis is difficult to treat as compared to acute respiratory acidosis.
• This will take place by:
• Chronic obstructive pulmonary diseases like bronchitis, emphysema, pulmonary fibrosis, or scarring.
• Accumulation of the CO2 lasting days, weeks, or months will provoke a sustained increase in HCO3–
generation and leads to
enhanced renal excretion of the H+ ions with chronic CO 2 retention.
• HCO3–
rises 3.5 meq/L for each 10 mm Hg rise in pCO 2.
• The serum level of Na+
and K+
may be normal or mildly raised.
• Suppression of the medullary respiratory center:
• Sleep apnea.
• Sedation medicines.
• Cardiopulmonary arrest.
• Upper respiratory obstruction:
• Laryngospasm.
• Aspiration of the foreign body or vomitus.
• Obstruction in sleep apnea.
• Defective respiratory muscle function:
• Myasthenia gravis.
• Guillain-barre syndrome.
• Botulism.
• Hypokalemia (severe).
• Poliomyelitis.
• Myxedema.
• Amyotrophic lateral sclerosis.
• Defect in the pulmonary gas exchange:
• Acute respiratory distress syndrome.
• Pneumothorax.
• Hemothorax.
• Severe asthma.
• Severe pneumonia.
• Chronic obstructive pulmonary disease
• Respiratory Alkalosis
• Definition:
• This is due to over-breathing, causing excessive CO2 excretion, leading to
a rise in blood pH.
• Pathophysiology:
• Overbreathing causes excessive CO2 exhaled out and causing the blood
pH to rise.
• Acute respiratory alkalosis interacts with intracellular and protein buffers before affecting
the HCO3–
system.
• After the adjustment, blood HCO3–
drops 5 meq/L for every 10 mmHg decline in pCO2.
• Alkalosis causes plasma proteins to have a more negative charge that in turn binds more
ionized Ca++.
• This hypocalcemia increases neuromuscular excitability and leads to tetany.
• Respiratory alkalosis occurs when there are alveolar hyperventilation and
excessive reduction in plasma CO2 levels. This is called hypocapnia.
• In the case of initial hypoxemia, there is increased ventilation mostly
mediated by the chemoreceptors in the carotid body; these are located near
the carotid artery’s bifurcation.
• Kidneys compensate by decreasing H+ excretion and HCO3¯
reabsorption.
• The PaCO2 is <35 mm Hg.
• Causes Of Respiratory Alkalosis:
• Pulmonary diseases due to hypoxemia:
• Pneumonia.
• Pulmonary embolism.
• Pulmonary edema.
• High-altitude syndrome.
• Severe anemia.
• Congestive heart failure.
• Stimulation of the medullary (respiratory) center:
• Hepatic encephalopathy.
• Sepsis with fever.
• Salicylates toxication.
• Hyperventilation syndrome.
• Pregnancy when there is increased progesterone.
• Cerebrovascular accidents.
• Pontine tumors.
• Hypermetabolic conditions:Fever.
• Anemia.
• Thyrotoxicosis.
• Hysteria.
• Cirrhosis.
• Gram-negative sepsis.
• Pregnancy.
• Signs And Symptoms:
• The central and peripheral nervous system is stimulated, leading to:
• There is light-headedness or Dizziness.
• The patient may be agitated.
• Confusion.
• Tingling of the extremities appears first around the mouth and in the fingers and toes, called
circumoral and peripheral paresthesia.
• There is a carpopedal spasm, twitching, and muscle weakness.
• Light-headedness and weakness may occur and progress to unconsciousness.
• Convulsions.
• Ultimately the patient goes into a coma.
• Deep and rapid respirations are the primary symptoms that cause respiratory alkalosis.
• Diagnosis:
• Diagnosis:
• The blood pH is >7.42.
• Decreased pCO2.
• HCO3: H2CO3 = 20:0.5
• Decreased H2CO3 level.
• HCO3–
= Normal in acute stage
• HCO3–
= Less than normal in the chronic stage.
• Treatment:
• If there is intoxication like salicylates, then induce emesis or use gastric lavage.
• May need treatment for fever or sepsis.
• O2-therapy for acute hypoxemia.
• In the case of CNs disease, treat those diseases.
• Ask the patient to breathe in the paper bags.
• Ventilators are needed.
• Treatment is mostly not needed.
• It is important to diagnose the cause and treat the underlying disease.

Types and diagnosis and treatment of acid base balance

  • 1.
  • 3.
    • Pathophysiology • DefinitionOf Acid-Base Balance: • This regulation of the extracellular fluid environment involves the ratio of acid to base, measured clinically as pH. • Physiologically all positively charged ions are called acids, and all negatively charged ions are bases. • Physiological changes in the concentration of H+ ions in the blood lead to acid-base balance. • A systemic increase in the H+ ions concentration is called acidosis. • A systemic decrease in the H+ ions is called alkalosis. • The acid-base must be regulated within a narrow range for the body to function normally. • A very slight change in the pH will affect the body.
  • 4.
    • H+ ions areneeded for: • To maintain the integrity of the membrane. • Speed of the metabolic reactions. • Any change in the pH will lead to harmful effects than other diseases. • The symbol pH represents the power of H+ . • When pH changes one unit like 7.0 to 6.0 = [H+ ] [H+ ] = H+ ions concentration changes 10 folds. • Body acids are formed from end products of: • Metabolism of proteins. • Metabolism of Carbohydrates. • Metabolism of fats. • This must be balanced by the number of basic substances in the body to maintain the normal pH. • Lungs, kidneys, and bones are the major organs involved in the regulation of acid-base balance
  • 5.
    • Body acidsare formed from end products of: • Metabolism of proteins. • Metabolism of Carbohydrates. • Metabolism of fats. • This must be balanced by the number of basic substances in the body to maintain the normal pH. • Lungs, kidneys, and bones are the major organs involved in the regulation of acid-base balance. • Body acids are of two types: • Volatile acids: • Carbonic acid (H2CO3) is a week acid, and it does not easily release the H+ ions. • In the presence of carbonic anhydrase enzyme can eliminate CO 2 gas and water H2O. • CO 2 is eliminated through the lungs. • Nonvolatile acids: • These are sulfuric acid, phosphoric acid, and other organic acids that are eliminated through the kidneys. • These are the strong acids and readily give up their H+ ions. • Nonvolatile acids are secreted into the urine by the renal tubules. • These acids are about 150 meq/L of H+ ions per day or about 1 meq/kg body weight
  • 6.
    • Buffer SystemsOf The Acid-Base Balance: • The buffer systems become active in response to change in the pH of the body as acid-base balance. • Functions of the buffer system: • Prevent the significant change in pH. • Buffer can absorb the excess of the H+ ions (acid). • Buffer system can absorb OH– ions, Hydroxyl (base). • The buffer system is present in the intracellular fluid (ICF) and extracellular fluid (ECF). • The most buffer system is: • Carbonic acid-bicarbonate system. • Hemoglobin system. • Phosphate and protein are the most important intracellular buffers (ICF
  • 7.
    • Renal bufferingsystem:The distle tubule of the kidneys regulates acid-base balance by secreting the H+ ions in the urine and reabsorbs the HCO3– . • Dibasic phosphate (HPO4— ) and ammonia (NH3) are two important renal buffer. • The renal buffering of H+ ions requires CO2 and water (H2O) to form the H2CO3. • The enzyme carbonic anhydrase catalyzes the reaction. • H+ ions are secreted from the tubular cells and buffer in the lumen by PO4 — and NH3 = H2PO– 3 + NH4+ . • The rest of HCO3– is reabsorbed.
  • 9.
    • Carbonic acid-bicarbonatebuffering system:This buffer system operates both in the lungs and kidneys. • This is the major extracellular buffer system. • Lungs can decrease the carbonic acid by blowing out the CO2 and leaving water behind. • Kidneys can reabsorb HCO3- or regenerate new HCO3- from CO 2 and water. • Normal bicarbonate (24 meq/L) and normal carbonic acid (1.2 meq/L), producing a 20:1 relation and maintain the pH of 7.4 • Both the systems are very efficient because: • HCO3– is easily reabsorbed or regenerated by the kidneys. • The lungs adjust acid concentration
  • 10.
    • Protein bufferingsystem:Hemoglobin (Hb) is the best intracellular buffer system, and it combines with H+ and forming HHb and CO2, forming the HHbCO2 complex. • When Hb combines with H+ ions becomes weak acid. • Venous blood Hb is a better to buffer system than arterial blood Hb.
  • 15.
    • Acid-base balance: •H+ ions and electrolytes disturbances may be: • Acute. • Chronic. • Modest or severe. • Simple or mixed. • When there is an accumulation of H+ ions is called acidosis. • When blood pH is declining below 7.3, this process is called acidemia. • When there is a deficiency of H+ ions is called alkalosis. • Blood pH rises above 7.45 is called alkalemia. • There are conditions related to the respiratory system that leads to respiratory acidosis or alkalosis. • There are metabolic conditions related to kidneys, and abnormality of intake/output leads to metabolic acidosis/alkalosis.
  • 16.
    • The bloodpH is normally maintained at 7.38 to 7.42. Any deviation from this range indicates a change in the H+ ions concentration. • Blood pH is a negative logarithm of [H+ ] as shown in the following equation: • pH = log10 [H+ ] • This equation shows that an increase in the H+ ions will lead to a fall in the blood pH is called acidemia. • So a decrease in the H+ ions will lead to an increase in the pH of the blood called alkalemia. • The conditions which cause the change in the pH are called acidosis and alkalosis. • The following diagram can explain how pH is maintained by the arterial carbon dioxide tension (pCO2) and plasma bicarbonate (HCO3– ).
  • 18.
    • Plasma HCO3– decreasein the plasma caused by gastrointestinal or renal losses will increase H+ ions and lowers the pH.
  • 23.
    • Metabolic acidosis •Definition: • Metabolic acidosis occurs whenever there is a primary decrease in the HCO3¯ in the blood. • This may occur due to: • Exogenous acid administration. • Endogenous acid production. • Impaired renal H+ secretion. • HCO3– losses from the kidney or in the gastrointestinal secretions. • Anion gap: • Definition of the anion gap: • Anion gap referred to anions usually not measured in the laboratory like sulfate, phosphate, and lactate. The anions usually measured are Chloride (Cl-) and bicarbonate (HCO3-). The sum of the anions is subtracted from the sum of cations (Na+ and + ); there is a gap around 10 to 12 meq/L, which is called an anion gap. An elevated anion gap gives clues for acidosis.
  • 24.
    • The importanceof the anion gap is to identify the etiology of metabolic acidosis. • The anion gap is measured in meq/L. • Definition of anion gap: This is the difference between the plasma concentration of major cation sodium (Na+ ) and other anions are HCO3– and Cl– . • Anion gap = [Na+ ] – ([HCO3– ] + [Cl– ]) • The normal anion gap is 3 to 13 meq/L, and the mean is 10 meq/L. • This is dependant mainly on the plasma protein, primarily albumin. • 2.5 meq/L falls for every 1 gram/dl of albumin concentration in the blood. • H+ ions changes in the blood lead to acid-base imbalance. • A systemic increase in the H+ ions is called acidosis. • In the case of acidemia pH of the arterial blood is <7.4.
  • 25.
    • While inalkalemia, the pH of the arterial blood is >7.4.There is a systemic decrease in the H+ ions in the systemic blood is called alkalosis.
  • 29.
    • Causes OfMetabolic Acidosis: • In metabolic acidosis, noncarbonic acid increases, or HCO3¯ is lost from the extracellular space. • The buffering system becomes active and maintains the pH. • In case of the buffering system’s failure, the anion gap HCO3¯: H2CO3 = 20:1 changes. • Increased noncarbonic acid with an elevated anion gap and Increased H+ load: • Diabetes mellitus with ketoacidosis. There is a production of acetoacetic acid and β-hydroxybutyric acid in diabetic acidosis. • In the case of starvation. • Lactic acidosis in shock and hypoxemia. There is the production of lactic acid. • Ingestion of drugs like NH4CL, salicylates, methanol, ethylene glycol, and paraldehyde. • Decreased H+ ions excretion was seen in: • Uremia. • Distal renal tubular acidosis (decreased renal H+ secretion). • There is an accumulation of the acid that consumes the bicarbonate (HCO3¯).
  • 30.
    • Causes OfA High Anion Gap (>12 Meq/L): • Methanol toxicity. • Uremia due to renal failure. • Starvation. • Diabetes mellitus (ketoacidosis). • Lactic acidosis. • Salicylates toxicity. • Ethyl alcohol toxicity. • Isoniazid toxicity. • Iron toxicity. • Causes Of Decreased Anion Gap (<6 Meq/L): • Hypoalbuminemia. • Plasma cell disorders. • Bromide intoxication.
  • 31.
    • Causes OfA High Anion Gap (>12 Meq/L): • Methanol toxicity. • Uremia due to renal failure. • Starvation. • Diabetes mellitus (ketoacidosis). • Lactic acidosis. • Salicylates toxicity. • Ethyl alcohol toxicity. • Isoniazid toxicity. • Iron toxicity. • Causes Of Decreased Anion Gap (<6 Meq/L): • Hypoalbuminemia. • Plasma cell disorders. • Bromide intoxication.
  • 32.
    • Respiratory acidosis •Definition: • With respiratory failure, CO2 accumulates (hypercapnia). This state will raise the pCO2 and causes the pH to drop, and lead to acidosis. • This is a decrease in alveolar ventilation in relation to the metabolic production of the CO2 produces respiratory acidosis by the increase in the carbonic acid.
  • 34.
    • Pathophysiology:Alveolar ventilationprovides the necessary oxygen for oxidative metabolism and eliminates the CO2 produced by these metabolic processes. • There is a depression in the ventilation, resulting in excess of CO2 (hypercapnia) in the blood circulation. • A decrease in alveolar ventilation in relation to the metabolic production of CO2 produces respiratory acidosis by an increase in H2CO3 acid. • The arterial CO2 tension (or pressure) PaCO2 is >45 mm Hg.
  • 36.
    • This isseen in respiratory failure, where CO2 accumulates, called hypercapnia. • This condition will raise the pCO2 and causes the pH to drop. • To compensate, the HCO3– will increase, but this is not sufficient to restore the pH to a normal level. • CO2 level rises, and this retained CO2 combines with water and form H2CO3. • H2CO3 dissociates to release H+ and HCO3– ions. • Increased paCO2 and free H+ ions stimulate the medulla to increase the respiratory rate and expel the CO2. • As the pH falls, 2.3, diphosphoglycerate accumulates in the RBCs, where it will alter the Hb (hemoglobin) to release the O2 (oxygen). • Hb picks up H+ ions and CO2 and removes both from the blood circulation. • If the respiratory mechanism fails, rising paCO2 stimulates the kidneys, retains HCO3– and Na+ (sodium) ions, and starts excreting H+ ions. • Total CO2 may rise to a very high level of chronic respiratory acidosis
  • 38.
    • Signs AndSymptoms: • There is often breathlessness. • The patient is restless. • There is headache, dyspnoea, and tachypnea. • There is apprehension followed by lethargy. • The patient will have disorientation. • There are muscle twitching and tremors. • Skin will be warm and flushed due to raised CO2 causes vasodilatation. • There may be hypertension or hypotension. • There are atrial and ventricular arrhythmias. • The patient will have convulsions and ultimately goes into a coma.
  • 39.
    • Lab diagnosis: •pH = <7.35 to 7.45. • paCO2 = >45 mm Hg. • HCO3– = Normal (in the acute stage). • HCO3– = Increased (in the chronic stage
  • 41.
    • Treatment • Treatmentof the pulmonary causes: • If there is obstruction by the foreign body, remove that immediately. • There may be a need for mechanical ventilators. • Give bronchodilators. • If there is pneumonia, then start antibiotics. • If there is pneumothorax, then put chest tube. • In the case of pulmonary embolism, start thrombolytic and anticoagulants. • Remove the secretions by bronchoscopy. • Treatment of chronic obstructive pulmonary disease (COPD): • Give O2 at a slow rate. • Start bronchodilators. • Start corticosteroids. • You can also give I/V sodium bicarbonate. • Other drugs are needed for the treatment of the cause.
  • 42.
    • cause. • CausesOf Respiratory Acidosis: • Acute respiratory acidosis: • This occurs with sudden obstruction to: • The airway. • Chest trauma that damages the respiratory muscles. • Acute paralysis or depression of CNS respiratory center. • HCO3– rises 1 meq/L for each 10 mmHg rise in pCO2. • Chronic respiratory acidosis: • This chronic respiratory acidosis is difficult to treat as compared to acute respiratory acidosis. • This will take place by: • Chronic obstructive pulmonary diseases like bronchitis, emphysema, pulmonary fibrosis, or scarring. • Accumulation of the CO2 lasting days, weeks, or months will provoke a sustained increase in HCO3– generation and leads to enhanced renal excretion of the H+ ions with chronic CO 2 retention. • HCO3– rises 3.5 meq/L for each 10 mm Hg rise in pCO 2. • The serum level of Na+ and K+ may be normal or mildly raised.
  • 43.
    • Suppression ofthe medullary respiratory center: • Sleep apnea. • Sedation medicines. • Cardiopulmonary arrest. • Upper respiratory obstruction: • Laryngospasm. • Aspiration of the foreign body or vomitus. • Obstruction in sleep apnea. • Defective respiratory muscle function: • Myasthenia gravis. • Guillain-barre syndrome. • Botulism. • Hypokalemia (severe). • Poliomyelitis. • Myxedema. • Amyotrophic lateral sclerosis. • Defect in the pulmonary gas exchange: • Acute respiratory distress syndrome. • Pneumothorax. • Hemothorax. • Severe asthma. • Severe pneumonia. • Chronic obstructive pulmonary disease
  • 44.
    • Respiratory Alkalosis •Definition: • This is due to over-breathing, causing excessive CO2 excretion, leading to a rise in blood pH. • Pathophysiology: • Overbreathing causes excessive CO2 exhaled out and causing the blood pH to rise.
  • 46.
    • Acute respiratoryalkalosis interacts with intracellular and protein buffers before affecting the HCO3– system. • After the adjustment, blood HCO3– drops 5 meq/L for every 10 mmHg decline in pCO2. • Alkalosis causes plasma proteins to have a more negative charge that in turn binds more ionized Ca++. • This hypocalcemia increases neuromuscular excitability and leads to tetany. • Respiratory alkalosis occurs when there are alveolar hyperventilation and excessive reduction in plasma CO2 levels. This is called hypocapnia. • In the case of initial hypoxemia, there is increased ventilation mostly mediated by the chemoreceptors in the carotid body; these are located near the carotid artery’s bifurcation.
  • 47.
    • Kidneys compensateby decreasing H+ excretion and HCO3¯ reabsorption. • The PaCO2 is <35 mm Hg.
  • 48.
    • Causes OfRespiratory Alkalosis: • Pulmonary diseases due to hypoxemia: • Pneumonia. • Pulmonary embolism. • Pulmonary edema. • High-altitude syndrome. • Severe anemia. • Congestive heart failure. • Stimulation of the medullary (respiratory) center: • Hepatic encephalopathy. • Sepsis with fever. • Salicylates toxication. • Hyperventilation syndrome. • Pregnancy when there is increased progesterone. • Cerebrovascular accidents. • Pontine tumors.
  • 49.
    • Hypermetabolic conditions:Fever. •Anemia. • Thyrotoxicosis. • Hysteria. • Cirrhosis. • Gram-negative sepsis. • Pregnancy.
  • 50.
    • Signs AndSymptoms: • The central and peripheral nervous system is stimulated, leading to: • There is light-headedness or Dizziness. • The patient may be agitated. • Confusion. • Tingling of the extremities appears first around the mouth and in the fingers and toes, called circumoral and peripheral paresthesia. • There is a carpopedal spasm, twitching, and muscle weakness. • Light-headedness and weakness may occur and progress to unconsciousness. • Convulsions. • Ultimately the patient goes into a coma. • Deep and rapid respirations are the primary symptoms that cause respiratory alkalosis. • Diagnosis:
  • 51.
    • Diagnosis: • Theblood pH is >7.42. • Decreased pCO2. • HCO3: H2CO3 = 20:0.5 • Decreased H2CO3 level. • HCO3– = Normal in acute stage • HCO3– = Less than normal in the chronic stage.
  • 53.
    • Treatment: • Ifthere is intoxication like salicylates, then induce emesis or use gastric lavage. • May need treatment for fever or sepsis. • O2-therapy for acute hypoxemia. • In the case of CNs disease, treat those diseases. • Ask the patient to breathe in the paper bags. • Ventilators are needed. • Treatment is mostly not needed. • It is important to diagnose the cause and treat the underlying disease.