ACID BASE BALANCE

DR.GOUTHAM

Homeostasis

A delicate balance of fluids, electrolytes, and acids and bases is required to maintain good health.

This balance is called Homeostasis.

Body FluidsIntracellular fluid (ICF)

found within the cells of the bodyconstitutes 2/3 of total body fluid in adultsmajor cation is potassium

Extracellular fluid (ECF)found outside the cellsaccounts of 1/3 of total body fluidmajor cation is sodium

TermsOsmosis

movement of water across cell membranes from less concentrated to more concentrated

Solutessubstances dissolved in a liquid

Osmolalitythe concentration within a fluid

More TermsDiffusionmovement of molecules in liquids from an area of higher concentration to lower concentration

Filtrationfluid and solutes move together across a membrane from area of higher pressure to one of lower pressure

Active Transportsubstance moves across cell membranes from less concentrated solution to more concentrated - requires a carrier

Routes of Fluid Loss

UrineInsensible fluid lossFeces

ElectrolytesSodiumPotassiumChloridePhosphate

MagnesiumCalciumBicarbonate

Electrolytes are important for:. Maintaining fluid balance. Contributing to acid-base

regulation. Facilitating enzyme reactions. Transmitting neuromuscular

reactions

Acid-Base Balance

Acid-Base balance is:

the regulation of HYDROGEN ions.

pHThe acidity or alkalinity of a solution is measured as pH.The more acidic a solution, the lower the pH.The more alkaline a solution , the higher the pH.Water has a pH of 7 and is neutral.The pH of arterial blood is normally between 7.35 and 7.45

Acids are H+ donors.Bases are H+ acceptors, or give up OH- in solution.Acids and bases can be:

Strong – dissociate completely in solution

HCl, NaOHWeak – dissociate only partially in solution

Lactic acid, carbonic acid

The control of arterial CO2 tension (Paco2) by the central nervous system (CNS) and respiratory systems and the control of the plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation:

ph = 6.10 + log ([HCO3] / [0.03 x PCO2])

Hydrogen ions

The more Hydrogen ions, the more acidic the solution and the LOWER the pH

• The lower Hydrogen concentration, the more alkaline the solution and the HIGHER the pH

Small changes in pH can produce major disturbances• Most enzymes function only with narrow

pH ranges• Acid-base balance can also affect

electrolytes (Na+, K+, Cl-)• Can also affect hormones

The body produces more acids than bases

•Acids produced by metabolism of lipids and proteins•Cellular metabolism produces CO2.

•CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3-

Control of Acids1. Buffer systems

Take up H+ or release H+ as conditions change

Buffer pairs – weak acid and a baseExchange a strong acid or base for

a weak oneResults in a much smaller pH

change

Bicarbonate buffer• Sodium Bicarbonate (NaHCO3) and carbonic

acid (H2CO3)

• Maintain a 20:1 ratio : HCO3- : H2CO3

HCl + NaHCO3 ↔ H2CO3 + NaCl

NaOH + H2CO3 ↔ NaHCO3 + H2O

Phosphate buffer• Major intracellular buffer• H+ + HPO4

2- ↔ H2PO4-

Protein Buffers• Includes hemoglobin, work in blood• Carboxyl group gives up H+ • Amino Group accepts H+

• Side chains that can buffer H+ are present on 27 amino acids.

2. Respiratory mechanisms

• Exhalation of carbon dioxide• Powerful, but only works with volatile

acids• Doesn’t affect fixed acids like lactic acid• CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3

-

• Body pH can be adjusted by changing rate and depth of breathing

3. Kidney excretion• Can eliminate large amounts of acid• Can also excrete base• Can conserve and produce bicarb ions• Most effective regulator of pH• If kidneys fail, pH balance fails

Rates of correction• Buffers function almost instantaneously• Respiratory mechanisms take several

minutes to hours• Renal mechanisms may take several hours

to days

Factors Affecting Balance

• Age– especially infants and the elderly

• Gender and Body Size– amount of fat

• Environmental Temperature• Lifestyle

– stress

Acidosis• Principal effect of acidosis is depression of the CNS

through ↓ in synaptic transmission.• Generalized weakness• Deranged CNS function the greatest threat• Severe acidosis causes

– Disorientation– coma – death

Alkalosis• Alkalosis causes over excitability of the

central and peripheral nervous systems.• Numbness• Lightheadedness• It can cause :

– Nervousness– muscle spasms or tetany – Convulsions – Loss of consciousness– Death

Acid-Base Imbalances• Respiratory Acidosis• Respiratory Alkalosis• Metabolic Acidosis• Metabolic Alkalosis

Respiratory Acidosis• Respiratory acidosis can be due to severe

pulmonary disease, respiratory muscle fatigue, or abnormalities in ventilatory control and is recognized by an increase in Paco2 and decrease in pH

• Carbonic acid excess caused by blood levels of CO2 above 45 mm Hg.

• Hypercapnia – high levels of CO2 in blood

Causes• A. Central•       1. Drugs (anaesthetics, morphine,

sedatives)•       2. Stroke•       3. Infection•    B. Airway•       1. Obstruction•       2. Asthma

•  C. Parenchyma•       1. Emphysema•       2. Pneumoconiosis•       3. Bronchitis•       4. Adult respiratory distress syndrome•       5. Barotrauma

•   D. Neuromuscular•       1. Poliomyelitis•       2. Kyphoscoliosis•       3. Myasthenia•       4. Muscular dystrophies

•  E. Miscellaneous•       1. Obesity•       2. Hypoventilation•       3. Permissive hypercapnia

Clinical Features• The clinical features vary according to the severity

and duration of the respiratory acidosis, the underlying disease, and whether there is accompanying hypoxemia.

• A rapid increase in Paco2 may cause anxiety, dyspnea, confusion, psychosis, and hallucinations and may progress to coma.

• Lesser degrees of dysfunction in chronic hypercapnia include sleep disturbances; loss of memory; daytime somnolence; personality changes; impairment of coordination; and motor disturbances such as tremor, myoclonic jerks, and asterixis.

• Headaches and other signs that mimic raised intracranial pressure, such as papilledema, abnormal reflexes, and focal muscle weakness, are due to vasoconstriction secondary to loss of the vasodilator effects of CO2.

Signs and Symptoms of Respiratory Acidosis

• Breathlessness• Restlessness• Lethargy and disorientation• Tremors, convulsions, coma• Respiratory rate rapid, then gradually depressed• Skin warm and flushed due to vasodilation

caused by excess CO2

Compensation for Respiratory Acidosis

• Kidneys eliminate hydrogen ion and retain bicarbonate ion

• In acute respiratory acidosis, there is an immediate compensatory elevation (due to cellular buffering mechanisms) in HCO3, which increases 1 mmol/L for every 10-mmHg increase in Paco2.

• In chronic respiratory acidosis (>24 h), renal adaptation increases the [HCO3] by 4 mmol/L for every 10-mmHg increase in Paco2. The serum HCO3 usually does not increase above 38 mmol/L.

Treatment of Respiratory Acidosis

• Acute respiratory acidosis can be life-threatening, and measures to reverse the underlying cause should be undertaken simultaneously with restoration of adequate alveolar ventilation

• This may necessitate tracheal intubation and assisted mechanical ventilation

• Treat underlying dysfunction or disease

• Alkali therapy avoid alkali therapy except in patients

with associated metaboloic acidosis, severe acidemia

RESPIRATORY ALKALOSIS

• Alveolar hyperventilation decreases Paco2 and increases the HCO3/Paco2 ratio, thus increasing pH

• It occurs when respiratory disturbances causes excessive pulmonary CO2 excretion(hyperventilation) that exceeds metabolic production of CO2 by the tissues.

Diagnosis• Low PaCO2 <35 mm hg• Alkaline pH >7.45• Compensatory low HCO3

• A. Central nervous system stimulation•       1. Pain•       2. Anxiety, psychosis•       3. Fever•       4. Cerebrovascular accident•       5. Meningitis, encephalitis•       6. Tumor•       7. Trauma

• B. Hypoxemia or tissue hypoxia•       1. High altitude•       2. Pneumonia, pulmonary edema•       3. Aspiration•       4. Severe anemia•    C. Drugs or hormones•       1. Pregnancy, progesterone•       2. Salicylates•       3. Cardiac failure

•  D. Stimulation of chest receptors•       1. Hemothorax•       2. Flail chest•       3. Cardiac failure•       4. Pulmonary embolism

•    E. Miscellaneous•       1. Septicemia•       2. Hepatic failure•       3. Mechanical hyperventilation•       4. Heat exposure•       5. Recovery from metabolic acidosis

Clinical features– Tachypnea or Hyperpnea– Complaints of SOB, chest pain– Light-headedness, syncope, coma, seizures– Numbness and tingling of extremities– Difficult concentrating, tremors, blurred

vision– Weakness, paresthesias, tetany

Treatment• Treatment of underlying cause• Mild alkalosis with few symptoms needs no

treatment• As hypoxemia is common cause of

hyperventilation, O2 supplementation is required• In absence of hypoxemia, hyperventilation needs

reassurance and rebreathing into a paper bag• Pretreatment with acetazolamide minimizes

symptoms due to hyperventilation at high altitude

Metabolic Alkalosis• Metabolic alkalosis is manifested by an

elevated arterial pH, an increase in the serum [HCO3], and an increase in Paco2 as a result of compensatory alveolar hypoventilation

• Often accompanied by hypochloremia and hypokalemia.

• The arterial pH establishes the diagnosis, because it is increased in metabolic alkalosis and decreased or normal in respiratory acidosis.

• Metabolic alkalosis occurs as a result of net gain of [HCO3] or loss of nonvolatile acid (usually HCl by vomiting) from the extracellular fluid.

• Alkalosis most commonly occurs with renal dysfunction

• Respiratory compensation difficult – hypoventilation limited by hypoxia

• There are two steps involved in development of metabolic alkalosis

• Generation of metabolic alkalosis—primary rise in plasma HCO3 due to

1. Loss of hydrogen ion from upper GI tract(vomiting) or urine (diuretics)

2. Administration of HCO3 or its precursors as citrate(blood transfusions)

• Maintenance of metabolic alkalosis—normally excess bicarbonate is rapidly excreted in urine.For Maintenance of metabolic alkalosis impairment of renal bicarbonate is required

Causes– Excess vomiting = loss of stomach acid– Excessive use of alkaline drugs– Certain diuretics– Endocrine disorders– Heavy ingestion of antacids– Severe dehydration

Symptoms of Metabolic Alkalosis

• Respiration slow and shallow• Hyperactive reflexes ; tetany• Often related to depletion of electrolytes• Atrial tachycardia• Dysrhythmias

Treatment• This is primarily directed at correcting the underlying

stimulus for HCO3 generation. • If primary aldosteronism, renal artery stenosis, or

Cushing's syndrome is present, correction of the underlying cause will reverse the alkalosis.

• [H+] loss by the stomach or kidneys can be mitigated by the use of proton pump inhibitors or the discontinuation of diuretics.

• The second aspect of treatment is to remove the factors that sustain the inappropriate increase in HCO3 reabsorption, such as ECFV contraction or K+ deficiency.

• K+ deficits should always be repaired. Isotonic saline is usually sufficient to reverse the alkalosis if ECFV contraction is present.

• If associated conditions preclude infusion of saline, renal HCO3 loss can be accelerated by administration of acetazolamide, a carbonic anhydrase inhibitor, which is usually effective in patients with adequate renal function but can worsen K+ losses.

• Hemodialysis against a dialysate low in [HCO3] and high in [Cl] can be effective when renal function is impaired.

Metabolic Acidosis• It is characterised by fall in plasma HCO3 and

fall in PH Bicarbonate deficit - blood concentrations of bicarb drop below 22mEq/L

• Causes:– Loss of bicarbonate through diarrhea or renal

dysfunction– Accumulation of acids (lactic acid or ketones)– Failure of kidneys to excrete H+

• Calculation of anion gap is useful for etiological diagnosis

• AG=Na--(Cl + HCO3)• Normal value=12+/-2

Causes of metabolic acidosis with normal

anoin gap• Gastrointestinal bicarbonate loss•    A. Diarrhea•    B. External pancreatic or small-bowel drainage•    C. Ureterosigmoidostomy, jejunal loop, ileal loop•    D. Drugs•       1. Calcium chloride (acidifying agent)•       2. Magnesium sulfate (diarrhea)•       3. Cholestyramine (bile acid diarrhea)

• II. Renal acidosis•       1. Proximal RTA (type 2)•       Drug-induced: acetazolamide, topiramate•       2. Distal RTA (type 1)•       Drug induced: amphotericin B, ifosfamide   

Causes of metabolic acidosis with increased

anion gap• Lactic acidosis• Ketoacidosis      Diabetic      Alcoholic       Starvation• Renal failure (acute and chronic)

Clinical features• Pulmonary changes—KUSSMAUL’s

breathing(deep,irregular,sighing respiration) suggests presence of metabolic acidosis

• Cardiovascular changes—Increases susceptibility to cardiac arrhythmias, decreased response to inotropes and secondary hypotension may occur

• Neurological changes--CNS function is depressed, with headache, lethargy, stupor, and, in some cases, even coma.

Compensation for Metabolic Acidosis

• Increased ventilation• Renal excretion of hydrogen ions if

possible• K+ exchanges with excess H+ in ECF• ( H+ into cells, K+ out of cells)

Treatment of Metabolic Acidosis

• Specific treatment for underlying cause• Alkali therapy—should be reserved for

selective patients with severe acidaemia amount of HCO3 required=(Desired HCO3 –

Actual HCO3) x 0.5 x body wt in kgs• Correct volume and electrolytes deficits

Why Order an ABG?• Aids in establishing a diagnosis • Helps guide treatment plan• Aids in ventilator management• Improvement in acid/base

management allows for optimal function of medications

• Acid/base status may alter electrolyte levels critical to patient status/care

Logistics• When to order an arterial line --

– Need for continuous BP monitoring– Need for multiple ABGs

• Where to place -- the options– Radial– Femoral – Brachial– Dorsalis Pedis– Axillary

Interpreting ABGs• 1. Look at the pH

• is the primary problem acidosis (low) or alkalosis (high)

• 2. Check the CO2 (respiratory indicator)• is it less than 35 (alkalosis) or more than 45 (acidosis)

• 3. Check the HCO3 (metabolic indicator)• is it less than 22 (acidosis) or more than 26 (alkalosis)

• 4. Which is primary disorder (Resp. or Metabolic)?

• If the pH is low (acidosis), then look to see if CO2 or HCO3 is acidosis (which ever is acidosis will be primary).

• If the pH is high (alkalosis), then look to see if CO2 or HCO3 is alkalosis (which ever is alkalosis is the primary).

• The one that matches the pH (acidosis or alkalosis), is the primary disorder.

Compensation• The Respiratory system and Renal systems compensate

for each other – attempt to return the pH to normal

• ABG’s show that compensation is present when– the pH returns to normal or near normal

• If the nonprimary system is in the normal range (CO2 35 to 45) (HCO3 22-26), then that system is not compensating for the primary.

• For example: – In respiratory acidosis (pH<7.35, CO2>45), if the

HCO3 is >26, then the kidneys are compensating by retaining bicarbonate.

– If HCO3 is normal, then not compensating.

Example• A patient is in intensive care because he

suffered a severe myocardial infarction 3 days ago. The lab reports the following values from an arterial blood sample:– pH 7.3– HCO3- = 20 mEq / L ( 22 - 26)– pCO2 = 32 mm Hg (35 - 45)

Special conditions• This condition is caused by increased fatty

acid metabolism and the accumulation of ketoacids (acetoacetate and -hydroxybutyrate).

• DKA usually occurs in insulin-dependent diabetes mellitus in association with cessation of insulin or an intercurrent illness such as an infection, gastroenteritis, pancreatitis, or myocardial infarction, which increases insulin requirements temporarily and acutely.

• bicarbonate therapy is rarely needed except with extreme acidemia (pH < 7.1), and then in only limited amounts.

• Patients with DKA are typically volume depleted and require fluid resuscitation with isotonic saline

• Gastrointestinal loss of H+ from vomiting or gastric aspiration results in retention of HCO3.

• The loss of fluid and NaCl in vomitus or nasogastric suction results in contraction of the ECFV and an increase in the secretion of renin and aldosterone.

• Correction of the contracted ECFV with NaCl and repair of K+ deficits corrects the acid-base disorder, and chloride deficiency.

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