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Acid base imbalance PPT for nurses.
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- 2. Acid –Base Balance •Plasma pH is an indicator of hydrogen ion (H+) concentration. • Homeostatic mechanisms keep pH within a normal range (7.35-7.45) • The pH range compatible with life is 6.8-7.8. • Normally, there are 20 parts of Bicarbonate(HCO3 - ) to one part of carbonic acid (H2CO3 - ) that is important in maintaining pH . • Normal acid Base ratio is 1:20 ( H2CO3 - : HCO3 - )
- 3. Regulation of acid-basebalance The body has three mechanisms to maintain acid-base balance: 1. Chemical Buffering (reacts very rapidly; less than second) 2. The respiratory Regulation. (reacts rapidly; seconds to minutes) 3. The Renal Regulation.(reacts slowly; minutes to hours)
- 4. • Important extracellularbuffer is bicarbonate buffer. • Important Intracellular buffer are phosphate buffer & protein buffer,
- 5. Respiratory regulation ofacid- base balance • Chemo receptors in the medulla of the brain sense the pH changes and vary the rate and depth of breathing to compensate. • When pH decrease: Breathing faster or deeper(Hyperventilation) Eliminate more CO2 leading to increase PH. • When pH Increase: Slow and shallow breathing(Hypoventilation) Lead to accumulation of co2 decrease PH.
- 6. Renal regulation ofacid-base balance Kidneys make long- term adjustment to PH. • They reabsorb acids and bases or excrete them into urine, and can also produce HCO3 - to replenish lost supply. • If the blood contains too much acids or not enough base, the PH drops and the kidneys in response reabsorb NaHCO3 and excrete (H+) leading to normalization of PH.
- 7. Normal Value ofArterial Blood Parameter Normal range pH 7.35-7.45 PaO2 70-100mm Hg PaCO2 35-45mm Hg HCO3 - 22-26 mEq/L
- 8. Disorder Hydrogen ion(H+) pH Acidosis Alkalosis
- 10. Acid-Base Disorders &Compensation Disorder Initial event Compensation Respiratory acidosis • ↓pH • ↑ PaCO2 •Normal or ↑ HCO3 - •↑Renal acid excretion •↑serum HCO3 - Respiratory alkalosis •↑pH • ↓PaCO2 •Normal or ↓HCO3 - •↓Renal acid excretion •↓serum HCO3 - Metabolic acidosis • ↓pH • ↓HCO3 - • Normal or ↓PaCO2 • Hyperventilation Metabolic alkalosis • ↑pH • ↑ HCO3 - • Normal or ↑ PaCO2 •Hypoventilation
- 11. Respiratory Acidosis It occurwith any mechanism that decreases the rate of alveolar ventilation. It is characterized by: • pH< 7.35 •PaCO2 >45 mmHg •Compensatory increase in HCO3 -
- 12. Causes of respiratoryacidosis • Depression of respiratory center: Narcotics / over sedation, Anesthesia • Respiratory arrest. • Acute pulmonary edema • Severe pneumonia • Chronic emphysema (COPD) • Impairment or Paralysis of respiratory muscles eg; Myasthenia gravis, GB Syndrome etc. • Impaired ventilation. • Airway obstruction: Foreign body.
- 13. Signs and Symptomsrespiratory acidosis Decrease excitability of CNS: • Restlessness • Headache • Drowsiness • Disorientation • Coma Cardiovascular: • Dysrhythmias, • Decreased cardiac contractility • Hypotension. Increase electrolytes : • Hyperkalemia • Hypercalcemia
- 15. Treatment of RespiratoryAcidosis • Restore ventilation • IV lactate solution (RL ) • IV Sodium bicarbonate (NaHCO3 ) • Treat underlying dysfunction or disease • Place the patient in semi-Flower’s position
- 16. Respiratory Alkalosis It isdefined as a decrease in PaCo2 caused by increase alveolar ventilation. It is characterized by: • PH > 7.45 • PaCO2 < 35 mmHg • Compensatory decrease in HCO3 -
- 17. Causes of RespiratoryAlkalosis: Always caused by Hyperventilation due to: • Hypoxemia • Anemia • Fever • Anxiety • Early phase of salicylate toxicity • Early in exercises Angry
- 18. Signs and Symptomsassociated with Alkalosis Increase excitability of CNS: • Light headedness • Numbness • Tingling • Confusion • Inability to concentrate • Blurred vision. Decrease electrolytes: Hypokalemia Hypertension
- 20. Treatment of RespiratoryAlkalosis • Treat underlying cause • Reduce ventilation • Breathe into a close system (such as a paper bag ) • IV Chloride containing solution (Sodium is absorb with chloride in kidney & allow the excretion of excess bicarbonate)
- 21. Metabolic acidosis It isdefined as a primary decrease in plasma bicarbonate concentration(HCO3). It is characterized by: • PH < 7.35 • HCO3 - < 22 mEq/ L • Compensatory decrease in PaCO2
- 22. Causes of metabolicacidosis Loss of HCO3 • Prolonged severe diarrhea • Fistula Decreased elimination of acids • Renal failure Excess production of Acids: • Starvation • Cardiac arrest • Tissue hypoxia • Sepsis • Diabetic Ketoacidosis • Shock • Late phase of salicylate poisoning
- 24. Treatment of MetabolicAcidosis • Treatment - IV lactate solution (RL) • IV Sodium bicarbonate (NaHCO3 ) • Dialysis • Treat underlying cause
- 25. Metabolic alkalosis It isdefined as a primary increase in plasma bicarbonate concentration(HCO3). It is characterized by: • PH > 7.45 • HCO3 - > 26 mEq/ L • Compensatory increase in PaCO2
- 26. Causes of metabolicalkalosis Excess of base /loss of acid. Acute H+ ion loss: • Vomiting • Gastric suctioning • Diuretics as: Frusemide, thiazide (Loss of potassium) • Cushing syndrome Excess intake of Alkali. IV NaHCO3 administration.
- 28. Treatment of Metabolicalkalosis • Electrolytes to replace those lost - Ascorbic acid, tranexamic acid • IV chloride containing solution (Sodium is absorb with chloride in kidney & allow the excretion of excess bicarbonate) • Inj KCl to replace both potassium & chloride • Treat underlying disorder
Editor's Notes
- #13 Myasthenia gravis (MG) is a long-term neuromuscular disease that leads to varying degrees of skeletal muscle weakness.[1] The most commonly affected muscles are those of the eyes, face, and swallowing.[1] It can result in double vision, drooping eyelids, trouble talking, and trouble walking.[1] Onset can be sudden.[1] Those affected often have a large thymus or develop a thymoma.[1] Myasthenia gravis is an autoimmune disease which results from antibodies that block or destroy nicotinic acetylcholine receptors (AChR) at the junction between the nerve and muscle.[1] This prevents nerve impulses from triggering muscle contractions.[1] Most cases are due to immunoglobulin G1 (IgG1) and IgG3 antibodies that attack AChR in the postsynaptic membrane, causing complement-mediated damage and muscle weakness. Guillain–Barré syndrome (GBS) is a rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system.[2] Typically, both sides of the body are involved, and the initial symptoms are changes in sensation or pain often in the back along with muscle weakness, beginning in the feet and hands, often spreading to the arms and upper body.[2] The symptoms may develop over hours to a few weeks.[2] During the acute phase, the disorder can be life-threatening, with about 15 percent of people developing weakness of the breathing muscles and, therefore, requiring mechanical ventilation.[1] Some are affected by changes in the function of the autonomic nervous system, which can lead to dangerous abnormalities in heart rate and blood pressure.[2] Although the cause is unknown, the underlying mechanism involves an autoimmune disorder in which the body's immune system mistakenly attacks the peripheral nerves and damages their myelin insulation.[2] Sometimes this immune dysfunction is triggered by an infection or, less commonly, by surgery, and rarely, by vaccination.[1][2] The diagnosis is usually based on the signs and symptoms through the exclusion of alternative causes and supported by tests such as nerve conduction studies and examination of the cerebrospinal fluid.[2] There are a number of subtypes based on the areas of weakness, results of nerve conduction studies, and the presence of certain antibodies.[4] It is classified as an acute polyneuropathy.[1] In those with severe weakness, prompt treatment with intravenous immunoglobulins or plasmapheresis, together with supportive care, will lead to good recovery in the majority of people.[2]
- #14 If the PaCO2 is chronically higher than 50 mm the respiratory center becomes relatively insensitive to CO2 as a respiratory stimulant, leaving hypoxemia as the major drive for respiration. Oxygen administration may remove the stimulus of hypoxemia, and the pa-tient develops "carbon dioxide narcosis" unless the situation is quickly reversed. Therefore, oxygen is ad-ministered only with extreme caution.
- #23 A fistula is an abnormal communication between two epithelial surfaces. An intestinal fistula is a fistula that connects the intestine to an adjacent organ or surface. Examples include enterocutaneous fistulas, which connect the intestine to the skin, and enterovesicular fistulas, which connect the intestine to the bladder. Common causes of intestinal fistulas include surgical procedures, diverticular disease, inflammatory bowel disease, malignancy, radiation, and injury due to trauma or foreign bodies. This activity describes the evaluation, diagnosis, and management of intestinal fistulas and stresses the role of team-based interprofessional care for affected patients.