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Acid Base Balance

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Acid Base Balance
ACID BASE IMBALENCE

INTRODUCTION The body normally maintains a steady balance between acids, produced during metabolism and bases that neutralize and promote the excretion of the acids.Many health problems may lead to acid base imbalance.Patients with Diabetis mellitus ,COPD,and kidney disease frequently frequently develop acid base imbalences. Vomiting and diarrhea may also cause acid base imbalance.The kidneys are an essential buffer system for acids and in the older adults the kidneys are less able to compensate for an acid load. The older adult also has decreased respiratory function leading to impaired compensation for acid base imbalences. In addition tissue hypoxia from any cause may alter acid base balance. The must always consider the possibility of acid base imbalence in patients with serious illnesses.

pH and hydrogen ion concentration The acidity and alkalinity of a solution depends on its hydrogen ion (H+)
Concentration. An increase in H+ concentration leads to acidity ,a decreased leads to alkalinity . acids are produced by the body daily.H+ concentration of body fluid is small(0.0004meq/l).H+ ion concentration is usually expressed as a negative logarithm(symbolized as pH) rather than in milliequivalents. The use of the negative logarithm means that the lower the pH ,the higher the H+ concentration. In contrast to a pH of 7 ,a pH of 8 represents a 10 fold decrease in H+ ion concentration. The pH of a chemical solution may range from 1to 14 . A solution with pH of 7 is considered as neutral. An acid solution has a pH less than 7 and an alkaline solution has a pH greater than 7. Blood is slightly alkaline(pH 7.35 to 7.45);yet if it drops below 7.35 the person has acidosis,even though the blood may never become truly acidic. If the blood pH is greater than 7.45 the person has alkalosis

ACID BASE REGULATION The body’s metabolic processes constantly produce acids. these acids must be neutralized and excreted to maintain acid base imbalance. Normally the body has three mechanisms by which it regulates the acid base balance to maintain the arterial pH between 7.35 and 7.45. these mechanisms are the buffer systems,the respiratory system,and the renal system. The regulatory mechanisms react at different speeds. Buffers react immediately, the respiratory system responds in minutes and reaches maximum effectiveness in hours,the renal responds takes 2-3 days to respond maximally,but the kidneys can maintain balance indefinitely in chronic imbalences.
BUFFER SYSTEM Buffer system is the fastest acting system and the primary regulator of acid base imbalance.Buffers are the substances act chemically to change strong acids into weaker acids or to bind acids to neutralize their effect. The buffers in the body include carbonic acid- bicarbonate,monohydrogen-dihydrogen phosphate,intracellular and plasma protein and hemoglobin buffers. Buffer consists of a weakly ionized acid or a base and its salts. Buffers action is to minimize the effect of acids on blood pH until they can be excreted from the body. The carbonic acid (H2CO3)-bicarbonate(HCO3) buffer system neutralizes hydrochloric acid(HCL) in the following manner; HCI (strong acid)+NAH2CO3( strong base ) NaCl(salt) +H2CO3(weak acid)

In this way an acid is prevented from making a large changes in the blood’s pH,and more H2CO3 is formed. The carbonic acid in turn broaken down in to H2O and CO2. The CO2 is excreted through the lungs. In this process the buffer system maintains normal ratio between bicarbonate and carbonic acid and the normal pH. The sodium buffer system is composed of sodium and other cations in combination with monohydrogen phosphate or dihydrogen phosphate. This intracellular buffer system will act in the same manner as the bicarbonate system. Strong acids are neutralized to form NaCl and sodium biphosphate,a weak acid that can be excreted through urine. When a strong base such as sodium hydroxide is added to the system it can be neutralized by sodium dihydrogen phosphate to a weak base and water. Intracellular and extracellular proteins are an effective buffering system throughout the body. The protein buffering system acts like bicarbonate system. Some of the aminoacids of protein contain free radicals(-COOH) which can dissociate into CO2 and H+ ion. Other aminoacids have basic radicals (-NH3OH or ammonium hydroxide), which can dissociate in to NH3(ammonia) an OH-(hydroxide). The hydroxide can combine with an H+ to form H2O.Hemoglobin is a protein that assists in the regulation of pH by shifting chloride in and out of RBCs in exchange for bicarbonate. The cell can also act as a buffer by shifting hydrogen in and out of the cells.with an accumulation of H+ in the ECF,the cells can accept H+ in exchange for another cation(k+) The body buffers an acid load better than it neutralizes base excess.Buffers cannot maintain pH without the adequate functioning of the respiratory and renal system s.

REPIRATORY SYSTEM The lungs help maintain a normal pH by excreting CO2 and water ,which are by products of cellular metabolism. Which are by products of cellular metabolism.
When released in to circulation ,CO2 enters RBCs and combines with water to form H2CO3. This carbonic acid dissociates into hydrogen ions and bicarbonate. The free hydrogen is buffered
By hemoglobin molecules and the bicarbonate diffuses in to plasma. In the pulmonary capillaries this process is reversed and CO2 is formed and excreted by the lungs. The overall reversible reaction is expressed as the following; CO2+H2O H2CO3 H+ +HCO3- The rate of excretion CO2 is controlled by the respiratory centre in the medulla in the brain stem. If increased amount of CO2 and H+ are present the respiratory centre stimulate an increased rate and depth of breathing. Respirations are inhibited if the centre senses low H+ or CO2 levels. If a respiratory problem is the cause of an acid base imbalance the respiratory system loses its ability to correct a pH alteration.

RENAL SYSTEM Under normal conditions ,the kidneys reabsorb and conserve all of the bicarbonate they filter. The kidneys can generate additional bicarbonate and eliminate excess H+
As compensation for acidosis. The three mechanism of acid elimination are
Secretion of small amount of free hydrogen in to the renal tubule
Combination of H+ with ammonia to form ammoniumum
Excretion of weak acids The body depends on kidneys to excrete a portion of the acid produced by cellular metabolism . Thus the kidneys normally excrete acidic urine(average pH equals 6). As a compensatory mechanism,the pH of the urine can decrease to 4 and increase to 8. If the renal system is the cause of an acid base imbalance (renal failure) it loses its ability to correct a pH alteration. ALTERATIONS IN ACID BALANCE An acid base imbalance is produced when the ratio of 1:20 between acid and base content is altered.A primary disease process may alter one side of the ratio(eg;CO retension in pulmonary disease). The compensatory process attempts to maintain to the other side of the ratio (eg. Increased renal bicarbonate reabsorption). When the compensatory mechanisms fails ,an acid base imbalance results.
CLASSSIFICATION
Acid base imbalance are classified as respiratory or metabolic. Respiratory imbalance affects carbonic acid concentrations.metabolic imbalance affects the base carbonate. Therefore acidosis can be caused by an increase in bicarbonate(respiratory acidosis) or a decrease in bicarbonate
Alkalosis can be caused by an increase in bicarbonate(metabolic alkalosis) or a decrease in carbonic acid(respiratory acidosis). Imbalences may be further classified as acute or chronic. Chronic imbalance allow greater time for compensatory changes.

RESPIRATORY ALKALOSIS Respiratory alkalosis is a state of relative excess of base in body fluids resulting from increased respiratory elimination of CO2. Acute respiratory alkalosis lasts for 24 hours or less. Chronic respiratory alkalosis persists longer.
Etiology and Risk factors Respiratory alkalosis is caused by alveolar hyperventilation,in which excess CO2 is eliminated. The main causes are
Hyperventilation caused by hypoxia,pulmonary emboli,anxiety,fear,pain,exercise,fever
Stimulated respiratory centre caused by septicemia,encephalitis,brain injury,salilcylate poisoning
Mechanical hyperventilation
Risk factors
High altitude
Pregnancy

Pathophysiology A low partial pressure of oxygen in arterial blood (PaO2) is sensed by peripheral chemoreceptors in the carotid bodies and aortic arch . the rate at which these receptors fire then increases,stimulating respiratory centre in the medulla and increasing the rate and depth of the ventilation.peripheral chemoreceptors are also stimulated in states of low blood flow such as shock. The central chemoreceptors and respiratory centre may be stimulated excessively by chemical or toxins. The buffering responses in acute respiratory alkalosis resuits from
Shifting of acid from intracellular fluid into the blood
Movement of HCO3- cells into cells in exchange for Cl- Renal compensation in chronic respiratory alkalosis involves decrease H+ secretion aswell as excretion of excessfiltered HCO3-
Clinical manifestations
Neurologic
Lethargy
Light headedness
Confusion
Cardiovascular
Tachycardia
Dysrhythmias Gastrointestinal
Nausea
Vomiting
Epigastric pain Neuromuscular
Tetany
Numbness
Tingling of extremities
Hyperreflexia
seizures Respiratory hyperventilation(lungs are unable to compensate when there is respiratory problem) Management
Treatment of underlying disorder electrolytes imbalance should be treated hypoxemia should be corrected
Respiratory support
Oxygen therapy may be used
Rebreathing of CO2(as from breathing into a paper bag or other closed system)

RESPIRATORY ACIDOSIS Respiratory acidosis is a state of relative excess of acid in body fluids resulting from retension or excessive production of CO2. Acute respiratory acidosis develops and resolves within 3 days or less,chronic respiratory acidosis persists over long period.

Etiology and risk factors

Chronic obstructive pulmonary diseases
Pneumonia
Pulmonary embolism
Asthma
Acute respiratory syndrome
Barbiturate or sedative overdose
Guillen barrie syndrome
Chest wall abnormality(obesity)
Mechanical hypoventilation

Pathophysiology CO2 accumulates in the blood and diffuse readily in to aii body components. This hypercapnea drives the hydrolysis reaction forward,generating carbonic acid that dissociates in to H+ and HCO3-. Renal compensation proceeds over 3-5 days,with greater secretion of H+ and regeneration of HCO3-. As serum HCO3- levels increases with the compensation Cl- is excreted in greater amount,potentially inducing hypochloremia in chronic respiratory acidosis. Renal retention of K+ and cellular cation shifts may lead to hyperkalemia.Displacement of Ca2+ from albumin may result in hypercalcemia. In acute respiratory acidosis the rapid rise in PaCO2 results in hypoxemia in clients who are breathing room air because retained CO2 displaces O2 in alveoli . academia alters the ionization of structural and regulatory proteins(enzyme) resulting in widespread manifestation of organ dysfunction
Clinical manifestations Neurologic
Drowsiness
Disorientation
Dizziness
Headache coma cardiovascular blood pressure
Ventricular fibrillation
Warm flushed skin(due to peripheral vasodilation) neuromuscular
Seizures
respiratory
Hypoventilation with hypoxia
Outcome management
Treatment of the underlying disorder
Antibiotics
Opioid antagonist
Dialysis to clear toxins
Electrolyte balance
Respiratory support
Mechanical ventilation
Oxygen therapy
Administration of exogenous alkali like sodium bicarbonate

METABOLIC ALKALOSIS it is a state of relatively excess of base(or H+ deficit) in body fluids resulting froma gain of bicarbonate or a loss of fixed acids.
Etiology and risk factors
Severe vomiting
Lactic acidosis
Starvation
Severe diarrhea
Renal tubular acidosis
Renal failure
Gastro intestinal fistula

Clinical manifestations Neurologic
Dizziness
Inability
Nervousness
Confusion
Cardiovascular
Tachycardia
Dysrhythmia
Gastrointestinal
Nausea
Vomiting
Anorexia
Neuromuscular
Tetany
Tremours
Tingling of fingures and toes
Muscle cramps seizures Out Come Management
Treatment of the underlying disorder
Replacement of lost fluids and electrolytes(potassium and magnesium)
Dialysis(with high chloride and low bicarbonate dialysate
Administration of azetamolide-diamox is a diuretic that inhibits CA and promotes lossof bicarbonate in the urine
Administration of exogenous acid-I V administration of acid (HCl)

METABOLIC ACIDOSIS It is a state of acid excess (or base deficit) in body fluids resuiting from a gain of fixed acids or a loss of bicarbonate Etiology and risk factors
Diabetic ketoacidosis
Lactic acidosis
Starvation
Severe diarrhea
Renal tubular acidosis
Renal failure
Gastro intestinal fistula shock Clinical manifestations cardiovascular Blood pressure
Dysrhythmia
Warm flushed skin
Neurologic
Drowsiness
Confusion
Headache
Coma
Gastrointestinal
Nausea ,
Vomiting
Diarrhea
Abdominal pain
Respiratory
Deep rapid respirations
Management
Treatment of the underlying disorder
Respiratory support
Administration of exogenous alkali

MIXED ACID–BASE DISORDERS
At times patients can simultaneously experience two or more independent acid–base disorders. A normal pH in the presence of changes in the PaCO2 and plasma HCO3 − concentration Immediately suggests a mixed disorder. The only mixed disorder that cannot occur is a mixed respiratory acidosis and alkalosis, because it is impossible to have alveolar hypoventilation and hyperventilation at the same time. An example of a mixed disorder is the simultaneous occurrence of metabolic acidosis and respiratory acidosis during respiratory and cardiac arrest.
COMPENSATION
Generally, the pulmonary and renal systems compensate for each other to return the pH to normal. In a single acid–base disorder, the system not causing the problem will try to compensate by returning the ratio of bicarbonate to carbonic acid to the normal 20_1. The lungs compensate for metabolic disturbances by changing CO2 excretion. The kidneys compensate for respiratory disturbances by altering bicarbonate retention and H+ secretion. In respiratory acidosis, excess hydrogen is excreted in the urine in exchange for bicarbonate ions. In respiratory alkalosis, the renal excretion of bicarbonate increases, and hydrogen ions are retained. In metabolic acidosis, the compensatory mechanisms increase the ventilation rate and the renal retention of bicarbonate. In metabolic alkalosis, the respiratory system compensates by decreasing ventilation to conserve CO2 and raise the PaCO2. Because the lungs respond to acid–base disorders within minutes, compensation for metabolic imbalances occurs faster than compensation for respiratory imbalances.
Blood gas values

Blood gas analysis is often used to identify the specific acid–base disturbance and the degree of compensation that has occurred. The analysis is usually based on an arterial blood sample, but when an arterial sample cannot be obtained, a mixed venous sample may be used. Results of arterial blood gas analysis provide information about alveolar ventilation, oxygenation, and acid–base balance. It is necessary to evaluate the serum electrolytes (sodium, potassium, and chloride) and carbon dioxide along with arterial blood gas data as they are often the first sign of an acid–base disorder. The health history, physical examination, previous blood gas results, and serum electrolytes should always be part of the assessment used to determine the cause of the acid–base disorder . Treatment of the underlying condition usually corrects most acid–base disorders.ABG values provide valuable information about patients acid base status

ABG ANALYSIS

ABG VALUES

ANALYSIS
1. PH
2. PaCO2 25 mm Hg
3. HCO3- 16 meq/l

1.pH<7.4 indicates acidosis
2.PaCO2 is low-respiratory acidosis

3.HCO3- is low indicating metabolic acidosis
4.metabolic acidosis matches the pH
5.CO2 does not match but is moving in opposite direction indicates Lungs are attempting to compensate for metabolic acidosis

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