ACID - BASE BALANCE BY KRUTIKA BHANDARI - PRESENTATION

krutikanitinbhandari 608 views 24 slides Jul 19, 2024
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About This Presentation

Human blood has a hydrogen ion concentration [H+ ] of 35 to 45 nmol/L and it is essential that its concentration is maintained within this narrow range.
Hydrogen ions are nothing but protons which can bind to proteins and alter their characteristics.
All the enzymes present in the body are proteins ...


Slide Content

ACID - BASE BALANCE Presented by – Krutika Bhandari BHMS-III Roll no : 13 Guided by – Department of Surgery & Homoeopathic Therapeutics, M(N)MHC, Nashik

INTRODUCTION Human blood has a hydrogen ion concentration [H+ ] of 35 to 45 nmol/L and it is essential that its concentration is maintained within this narrow range. Hydrogen ions are nothing but protons which can bind to proteins and alter their characteristics. All the enzymes present in the body are proteins and an alteration in these enzyme systems can change the homeostatic mechanisms of the body. Hence, a disturbance in acid-base balance can result in malfunction of the various organ systems.

BASIC DEFINITIONS What is pH? pH notation is a more common method of expressing the hydrogen ion concentration . It is defined as the negative logarithm to base IO of the [H+ ] expressed in mol/L. pH of blood= 7.4 What is an acid? • An acid is a substance that dissociates in water to produce H + What is a base? A base is a substance that accepts H + .

What is a buffer? A buffer is a combination of a weak acid and its conjugate base. By combining with a strong acid or a strong base , they produce the corresponding salt and a weak acid or a weak base respectively. The hydrogen ion concentration of blood is maintained within narrow limits because of the presence of buffers in the body. These natural buffers are of two types : Intracellular Extracellular Hb Other proteins Bicarbonate/carbonic acid buffer system Phosphate buffer system Plasma proteins

The hydrogen ion concentration, carbonic acid levels and the bicarbonate levels of blood are related according to the following equation: H ENDERSON & HENDERSON – HASSELBALCH EQUATION

REGULATION OF ACID BASE BALANCE The normal pH of blood is 7.35-7.45. Acidosis is defined as a pH Less than 7.35. Conversely, when the pH is more than 7.45 , alkalosis is said to exist. Acidosis and alkalosis are of two types each: respiratory and metabolic .

An increase in carbon dioxide (CO2 ) levels increases the plasma [H+ ] and decreases the pH (respiratory acidosis). Similarly, a decrease in plasma carbon dioxide levels reduces the [H+ ] and increases the pH (respiratory alkalosis). A decrease in [HC03 -] reduces the pH and is called metabolic acidosis. Similarly, an increase in [HC03 -] increases the pH and produces metabolic alkalosis . The pH is regulated in the human body mainly by two organs: the respiratory system and the renal system .

The arterial carbon dioxide levels are regulated by the respiratory system . Any increase in carbon dioxide levels stimulates the respiratory centre in the medulla thus augmenting respiration, alveolar ventilation and elimination of extra CO2 levels. A decrease in CO2 levels may reduce the stimulus to breathe and cause hypoventilation . This response is limited by hypoxia as the hypoxic drive stimulates the patient to maintain respiration. Respiratory response to changes in CO2 level occurs very fast .

The plasma bicarbonate levels are regulated by the kidneys. Any decrease in [HC03 -] stimulates the kidney to retain and synthesise bicarbonate. High [HC03 -] results in elimination of more bicarbonate in urine. In general, the pulmonary response to a change in acid-base status is faster and occurs immediately. However, renal regulation takes time , a few hours to days. Kidneys filter and reabsorb all the bicarbonate in the urine . When necessary, kidneys can also produce extra bicarbonate through the glutamine pathway.

ACID – BASE DISORDERS When an acid-base disorder occurs, the initial disturbance that occurs is termed the primary disorder . The body attempts to normaliZe the pH by certain compensatory mechanisms resulting in a secondary disorder , e.g. primary metabolic acidosis results in an increase in hydrogen ions and a consequent decrease in bicarbonate ions. To compensate for this, the patient hyperventilates and reduces the arterial carbon dioxide levels, thus moving the pH back to normal ( compensatory respiratory alkalosis ).

Primary & secondary disorders Primary Disorder Secondary Disorder Respiratory acidosis Metabolic alkalosis Respiratory alkalosis Metabolic acidosis Metabolic acidosis Respiratory alkalosis Metabolic alkalosis Respiratory acidosis

Causes This disorder occurs when the patient's ability to maintain minute ventilation is compromised . This may be acute or chronic in origin. The causes may be classified as follows: Central nervous system: Central nervous system depression due to trauma, tumour , infections, ischaemia or drug overdose. Spinal cord injuries, especially cervical or high thoracic can cause respiratory muscle paralysis. Peripheral nervous and muscular system: Guillain-Barre syndrome, tetanus, organophosphorus poisoning, poliomyelitis, myasthenia gravis. Primary pulmonary disease: Asthma, chronic obstructive pulmonary disease, acute respiratory distress syndrome, pneumonia. Loss of mechanical integrity: Flail chest Clinical Features The features of the underlying problem predominate the clinical picture. If acute , hypoxia and hypercarbia result in tachycardia, hypertension, arrhythmias, confusion, drowsiness and coma . The hypoxia, if untreated, can be fatal. If gradual in onset , as in chronic obstructive pulmonary disease (COPD), the patient's kidneys may compensate by retaining bicarbonate resulting in compensatory metabolic alkalosis . Arterial blood gas analysis in these patients typically shows low Pa02 , high PaC02, high bicarbonate levels and a near-normal pH. Treatment Treat the cause Maintenance of oxygenation and ventilation using mechanical ventilatory support till recovery of the primary problem occurs . RESPIRATORY ACIDOSIS

Causes Clinical Features Usually features of the underlying disease predominate the picture. Acute severe hypocarbia (PaC02 < 20 mmHg) may cause cerebral vasoconstriction, reduced cerebral blood flow, confusion, seizures and tetany. The alkalosis and consequent hypokalaemia can also cause cardiac arrhythmias . RESPIRATORY ALKALOSIS This occurs due to an increase in minute ventilation. This increase can be sustained only in abnormal conditions. This may be acute or chronic in origin • Supratentorial lesions: Head injury • Cirrhosis of liver • Pain • Anxiety, hysterical hyperventilation • High altitudes • It may also occur secondarily as a compensation to primary metabolic acidosis

Causes Clinical Features Treatment METABOLIC ACIDOSIS This is associated with a decrease in bicarbonate ions due to one of two reasons: 1. Overproduction or retention of nonvolatile acids in the body , as in • Diabetic ketoacidosis • Lactic acidosis • Salicylate poisoning, methanol poisoning • Renal failure 2. Loss of bicarbonate ions from the body as in • Diarrhoea • Intestinal fistulae • Usually features of the underlying disease predominate the picture. • Hypotension, reduced cardiac output • Hyperventilation -rapid, deep respirations Deep, gasping type of respiration seen in diabetic ketoacidosis is called Kussmaul's respiration. • Hyperkalaemia, arrhythmias • Lethargy, coma • Identify the cause and treat • Adequate ventilation must always be ensured in all these critically ill patients. • If pH < 7.1 and the patient is unstable , may administer sodium bicarbonate . The chances of life-threatening arrhythmias are reduced when pH is> 7.2. Bicarbonate requirement (mmol) = Body weight (kg) x base deficit (mmol/L) x 0.3

ANION GAP The law of electroneutrality states that the total number of positive charges must be equal to the total number of negative charges in the body fluids. Thus, cations (positively charged ions such as sodium and potassium) must produce a charge exactly balanced by anions. However, the concentrations of only sodium, potassium, chloride and bicarbonate ions are routinely measured in clinical practice. The sum of the measured cations (Na+ , K + ) exceeds the sum of measured anions (Cl- and HCO3- ) producing a 'deficit' called the "anion gap". The nornal anion gap is 9-14 mmol/L. This gap is due to the presence of unmeasured anions in the body. Since the extracellular concentrations of potassium is small, it is often ignored in the calculation of anion gap. The equation may be written as follows:

Anion gap may be used to distinguish the cause of metabolic acidosis . • Anion gap is increased (> 14 mmol/L) in metabolic acidosis due to an increase in fixed acid load . These acids react with the bicarbonate ions in the plasma lowering its concentration. The anion portion of the fixed acid is not measured in the laboratory and contributes to the 'unmeasured anion' concentration, thus increasing the anion gap. • Anion gap remains unchanged in metabolic acidosis due to loss of bicarbonate ions as the lost bicarbonate ions are replaced by chloride ions. This type of metabolic acidosis is also called " hyperchloraemic acidosis".

Causes Clinical Features Treatment METABOLIC ALKALOSIS This may be either due to loss of acid from the body or retention of bicarbonate. It may be due to: Loss of gastric hydrochloric acid as in vomiting, prolonged nasogastric drainage Excessive loss of H+ from kidneys in exchange for K+ in severe hypokalaemia Primary or secondary hyperaldosteronism Excessive exogenous administration of alkali , e.g. indiscriminate use of NaHCO3 antacid abuse Retention of bicarbonate in exchange for loss of chloride ions as in diarrhoea . It is one of the common acid-base disorders in the intensive care unit. The underlying problem gives a clue to the cause of metabolic alkalosis. When severe, can cause hypoventilation and seizures . Associated hypokalaemia can cause arrhythmias and contribute to difficulty in weaning patients off a ventilator. Treat the primary problem Most of the metabolic alkalosis are “chloride-responsive ’’. Administration of saline and correction of potassium deficits reduce the alkalosis. Rarely, as in life-threatening metabolic alkalosis (pH > 7.7), rapid correction may be necessary and may be achieved by administration of H+ in the form of dilute hydrochloric acid or ammonium chloride.

1. Oxygenation Status 2. Ventilatory Status 3. Acid – Base Status RAPID INTERPRETATION OF AN ABG REPORT Analysis and conclusion of arterial blood gas (ABG ) report must always be done in conjunction with history and clinical examination. ABG analysis is done to assess: The partial pressure of oxygen in arterial blood (PaO2) of a normal, healthy, young adult is usually 90-100 mmHg. An increase in inspired oxygen concentration (FIO2) is expected to increase the PaO2. The expected PaO2 of a normal person may be estimated rapidly using the following formula: For example: A person breathing 40% oxygen is expected to have a PaO2 of 40 x 5 = 200 mmHg. The normal PaCO2, is 35-45 mmHg. The PaCO2, must always be related to the alveolar ventilation of the patient . The minute volume of a normal healthy adult at rest would be 100 ml/kg/ min. Sixty to sixty-five per cent of this actually ventilates the alveoli, the rest is dead space ventilation. The assessment of acid—base status must be done in three steps and in the following order. Assess the pH first: Normal pH—7.35 to 7.45. Assess the PaCO2, next: The normal PaCO2, is 35-45 mmHg. Assess the bicarbonate level last: The normal plasma bicarbonate level is 22—26 mmol/L.

THANK YOU ‘BALANCE IS THE ESSENCE OF LEADING A HAPPY, HEALTHY AND PROSPEROUS LIFE’