ACID –BASE IMBALANCES IN ADULTS MANAGEMENT.pptx

IMBALANCE

1. ACID –BASE BALANCE

2. ACIDS AND BASES ARE FORMED DURING NORMAl METABOLIC PROCESSESS. ACIDS- END PRODUCT OF GLUCOSE, FATS PROTEINS H + IONS DETERMINE ACIDITY BASE BINDS OH- COMMON BASE IS HCO3 SERUM p H = 7.35-7.45

3. ACID BASE CONTROL

4. Control of Acid-Base Balance The body's balance between acidity and alkalinity is referred to as acid-base balance. The body uses different mechanisms to control the blood's acid-base balance. These mechanisms involve the Lungs Kidneys Buffer systems Role of the lungs One mechanism the body uses to control blood pH involves the release of carbon dioxide from the lungs. Carbon dioxide, which is mildly acidic , is a waste product of the processing (metabolism) of oxygen and nutrients (which all cells need) and, as such, is constantly produced by cells. It then passes from the cells into the blood. The blood carries carbon dioxide to the lungs, where it is exhaled. As carbon dioxide accumulates in the blood, the pH of the blood decreases (acidity increases).

5. Brain regulates -by controlling the speed and depth of breathing (ventilation). The amount of carbon dioxide, increases as breathing becomes faster and deeper. By adjusting the speed and depth of breathing, the brain and lungs are able to regulate the blood pH minute by minute

6. Role of the kidneys The kidneys affect blood pH by excreting excess acids or bases. The kidneys have some ability to alter the amount of acid or base that is excreted, but because the kidneys make these adjustments more slowly than the lungs do, this compensation generally takes several days .

7. Types of Acid-Base Disorders There are two abnormalities of acid-base balance: Acidosis : The blood has too much acid (or too little base), resulting in a  decrease  in blood pH. Alkalosis : The blood has too much base (or too little acid), resulting in an  increase  in blood pH.

8. Types of acidosis and alkalosis Acidosis and alkalosis are categorized depending on their primary cause as Metabolic Respiratory Metabolic acidosis  and  metabolic alkalosis  are caused by an imbalance in the production of acids or bases and their excretion by the kidneys. Respiratory acidosis  and  respiratory alkalosis  are caused by changes in carbon dioxide exhalation due to lung or breathing disorders.

9. Primary Disturbance Example Initial Blood pH Compensatory Mechanism Compensatory Change in Blood pH Metabolic acidosis Increased acid production in people with diabetes due to  diabetic ketoacidosis Too low Increased breathing rate to expel carbon dioxide Increases back toward normal Respiratory acidosis Decreased ability to breathe due to severe  chronic lung disease Too low Increased excretion of acid in the urine Increases back toward normal Metabolic alkalosis Loss of stomach acid due to vomiting Too high Decreased breathing rate to retain carbon dioxide Decreases back toward normal Respiratory alkalosis Hyperventilation due to anxiety Too high Increased excretion of alkali in the urine Decreases back toward normal Acid-Base Disturbances and the Body's Response

10. RESPIRATORY ACIDOSIS Respiratory acidosis is a state in which there is usually a failure of ventilation and an accumulation of carbon dioxide . The primary disturbance of elevated arterial PCO2 is the decreased ratio of arterial bicarbonate to arterial PCO2, which leads to a lowering of the pH.

11.  In the presence of alveolar hypoventilation , 2 features commonly are seen are respiratory acidosis and hypercapnia .  To compensate  for the disturbance in the balance between carbon dioxide and bicarbonate (HCO3-), the kidneys begin to excrete more acid in the forms of hydrogen and ammonium and reabsorb more base in the form of bicarbonate . This compensation helps to normalize the pH

12. Etiology The respiratory centers in the pons and medulla control alveolar ventilation . Chemoreceptors for PCO2, PO2, and pH regulate ventilation . Central chemoreceptors in the medulla are sensitive to changes in the pH level. A decreased pH level influences the mechanics of ventilation and maintains proper levels of carbon dioxide and oxygen. When ventilation is disrupted , arterial PCO2 increases and an acid-base disorder develop .

13. This may be due to cerebrovascular accidents , use of central nervous system (CNS) depressants such as opioids , narcotics, sedatives or inability to use muscles of respiration because of disorders like myasthenia gravis, muscular dystrophy or Guillain-Barre Syndrome . chest wall disorders- kyphoscoliosis , pectus conditions COPD, asthma, chronic bronchitis

14. Because of its acute nature, there is a slight compensation occurring minutes after the incidence. On the contrary, chronic respiratory acidosis may be caused by COPD where there is a decreased responsiveness of the reflexes to states of hypoxia and hypercapnia .

15. Chronic respiratory acidosis can also be seen in obesity hypoventilation syndrome, also known as Pickwickian syndrome , amyotrophic lateral sclerosis, and in patients with severe thoracic skeletal defects.

16. Respiratory acidosis may cause slight elevations in ionized calcium and an extracellular shift of potassium . However , hyperkalemia is usually mild. In chronic respiratory acidosis, renal compensation occurs gradually over the course of days

17. The increased CO2 is what leads to an increase in hydrogen ions and a slight increase in bicarbonate, as seen by a right shift in the following equilibrium reaction of carbon dioxide: CO2 + H2O -> H2CO3- -> HCO3- + H+

18. Patients can present with dyspnea , anxiety , wheezing, and sleep disturbances . In some cases, patients may present with cyanosis due to hypoxemia. If severe and accompanied by prolonged hypoventilation, the patient may have additional symptoms such as altered mental status, myoclonus, and possibly even seizures. Respiratory acidosis leads to hypercapnia , which induces cerebral vasodilation.

19. Cases of chronic respiratory acidosis may cause memory loss, impaired coordination, polycythemia , pulmonary hypertension, and heart failure.

20. Evaluation In respiratory acidosis, the ABG will show an elevated PCO2 (>45 mmHg), elevated HCO3- (>30 mmHg), and decreased pH (<7.35 ). secondary polycythemia serum electrolyte Xray,MRI ECG.

21. Treatment / Management The hypercapnia should be corrected gradually because rapid alkalization of the cerebrospinal fluid (CSF) may lead to seizures. Pharmacologic therapy can also be used to help improve ventilation. Bronchodilators like beta-agonists( that relax your airways) , anticholinergic drugs( Ipratropium), and methylxanthines can be used in treating patients with obstructive airway diseases. Naloxone can be used in patients who overdose on opioid use

22. LOW ALVEOLAR VENTILATION- CONSIDER ENDOTRACHEAL INTUBATION, SIMV/CMV PEEP- PREVENTS ALVELOAR COLLAPSE O2 THERAPY SMOKING CESSATION TREAT INFECTIONS- ANTITBIOTICS iv NaHco3

23. Respiratory Alkalosis Respiratory alkalosis is the most common acid-base abnormality with no discrimination between genders . The exact frequency and distribution of disease are dependent upon the etiology . Likewise, the morbidity and mortality rates are dependent on the etiology of the disease   Respiratory alkalosis is by definition a disease state where the body’s pH is elevated to greater than 7.45 secondary to some respiratory or pulmonary process . D ecrease PaCO2(less than 35mmHg)

24. Pathophysiology Respiratory alkalosis is induced by a process involving hyperventilation.   These include central causes, hypoxemic causes, pulmonary causes, and iatrogenic causes.  Central sources - head injury, stroke, hyperthyroidism, anxiety-hyperventilation, pain, fear, stress, drugs, medications such as salicylates, and various toxins.

25. Pulmonary causes - pulmonary embolisms, pneumothorax, pneumonia, and acute asthma or COPD exacerbations . Iatrogenic causes -due to hyperventilation in intubated patients on mechanical ventilation.

26. Respiratory alkalosis may be an acute process or a chronic process - based on the level of metabolic compensation for the respiratory disease.

27. Excess HCO3 levels are buffered to reduce levels and maintain a physiological pH through the renal decrease of H secretion and increasing HCO3 secretion; however, this metabolic process occurs over the course of days whereas respiratory disease can adjust CO2 levels in minutes to hours.

28. Therefore, acute respiratory alkalosis is associated with high bicarbonate levels since there has not been sufficient time to lower the HCO3 levels and chronic respiratory alkalosis is associated with low to normal HCO3 levels

29. History and Physical Since the primary cause of all respiratory alkalosis etiologies is hyperventilation, many patients present with complain to shortness of breath . a cute onset dyspnea , fever, chills, peripheral edema , orthopnea , weakness, confusion, light-headedness, dizziness, anxiety, chest pain, wheezing, hemoptysis , trauma, history of central line catheter, recent surgery, history of thromboembolic disease, history of asthma, history of COPD , acute focal neurological signs, numbness, paresthesia , abdominal pain, nausea, vomiting, tinnitus, or weight loss.

30. Physical exam – fever , tachycardia, tachypnea , diaphoresis, hyper or hypotension, altered mental status, productive or non-productive cough, wheezing, rales , crackles , cardiac murmur or arrhythmia, jugular venous distension, meningeal signs, focal neurological loss, Trousseau sign, Chvostek sign, jaundice

31. Evaluation should always begin with a thorough history and physical exam. Magnesium and phosphate are also essential. chest x-ray ABG analysis CT or MRI 

32. Treatment / Management Treating the underlying pathology. In anxious patients, anxiolytics may be necessary. In infectious disease, antibiotics targeting sputum or blood cultures are appropriate. In embolic disease, anticoagulation is necessary. Ventilator support may be necessary for patients with acute respiratory failure, acute asthma, or acute, chronic obstructive pulmonary disease (COPD) exacerbation if they show signs of respiratory fatigue. In ventilator controlled patients, it may be necessary to reevaluate their ventilator settings to reduce respiratory rate.

33. beta adrenergic blockers