Presentation on theme: "Zoya Minasyan, RN, MSN-Edu. Purpose Maintain a balance between acids and bases to achieve homeostasis: State of equilibrium Health problems lead to imbalance."— Presentation transcript:
Zoya Minasyan, RN, MSN-Edu
Purpose Maintain a balance between acids and bases to achieve homeostasis: State of equilibrium Health problems lead to imbalance Diabetes mellitus Vomiting and diarrhea Respiratory conditions Chemotherapy- N/V
pH Measure of H + ion concentration Blood is slightly alkaline at pH 7.35 to <7.35 is acidosis. >7.45 is alkalosis.
Range of pH Fig The normal range of plasma pH is 7.35 to A normal pH is maintained by a ratio of 1 part carbonic acid to 20 parts bicarbonate.
Regulators of Acid/Base Metabolic processes produce acids that must be neutralized and excreted. Regulatory mechanisms Buffers Respiratory system Renal system
Regulators of Acid/Base Buffers: Act chemically to neutralize acids or change strong acids to weak acids Primary regulators React immediately Cannot maintain pH without adequate respiratory and renal function The buffers in the body include carbonic acid–bicarbonate monohydrogen- dihydrogen phosphate intracellular and plasma protein hemoglobin
Regulators of Acid/Base Respiratory system: Eliminates CO 2 Respiratory center in medulla controls breathing. Responds within minutes/hours to changes in acid/base. Increased respirations lead to increased CO 2 elimination decreased CO 2 in blood.
Regulators of Acid/Base When released into circulation, CO 2 enters RBCs and combines with H 2 O to form H 2 CO 3. This carbonic acid dissociates into hydrogen ions and bicarbonate. The free hydrogen is buffered by hemoglobin molecules, and the bicarbonate diffuses into the plasma. In the pulmonary capillaries, this process is reversed, and CO 2 is formed and excreted by the lungs. As a compensatory mechanism, the respiratory system acts on the CO 2 + H 2 O side of the reaction by altering the rate and depth of breathing to “blow off” (through hyperventilation) or “retain” (through hypoventilation) CO 2. If a respiratory problem is the cause of an acid-base imbalance (e.g., respiratory failure), the respiratory system loses its ability to correct a pH alteration.
Regulators of Acid/Base Renal system: Eliminates H + and reabsorbs HCO 3 Reabsorption and secretion of electrolytes (e.g., Na +, Cl ) Responds within hours to days
Regulators of Acid/Base The three mechanisms of acid elimination are secretion of small amounts of free hydrogen into the renal tubule, combination of H + with ammonia (NH 3 ) to form ammonium (NH 4 + ), and excretion of weak acids. The body depends on the 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.
Alterations in Acid-Base Balance Imbalances occur when compensatory mechanisms fail. Classification of imbalances Respiratory: Affect carbonic acid concentration Metabolic: Affect bicarbonate
Respiratory Acidosis Carbonic acid excess caused by Hypoventilation Respiratory failure Compensation Kidneys conserve HCO 3 and secrete H + into urine.
Respiratory Acidosis Hypoventilation results in a buildup of CO 2 carbonic acid accumulates in the blood Carbonic acid dissociates, liberating H +, and a decrease in pH occurs. If CO 2 is not eliminated from the blood, acidosis results from the accumulation of carbonic acid. In acute respiratory acidosis, the renal compensatory mechanisms begin to operate within 24 hours.
Respiratory Alkalosis Carbonic acid deficit caused by Hyperventilation Hypoxemia from acute pulmonary disorders
Metabolic Acidosis Base bicarbonate deficit caused by Ketoacidosis Lactic acid accumulation (shock) Severe diarrhea Kidney disease Metabolic acidosis (base bicarbonate deficit) occurs when an acid other than carbonic acid accumulates in the body, or when bicarbonate is lost from body fluids. Compensatory mechanisms Compensatory mechanisms Increased CO 2 excretion by lungs Increased CO 2 excretion by lungs Kussmaul respirations (deep and rapid) Kussmaul respirations (deep and rapid) Kidneys excrete acid Kidneys excrete acid
Metabolic Alkalosis Base bicarbonate excess caused by Prolonged vomiting or gastric suction Gain of HCO 3 Compensatory mechanisms Decreased respiratory rate to increase plasma CO 2 Renal excretion of HCO 3
Blood Gas Values Arterial blood gas (ABG) values provide information about Acid-base status Underlying cause of imbalance Body’s ability to regulate pH Overall oxygen status
Interpretation of ABGs Diagnosis in six steps: Evaluate pH. Analyze PaCO 2. Analyze HCO 3 Determine if CO 2 or HCO 3 matches the alteration. Decide if the body is attempting to compensate.
Normal Blood Gas Values Table Normal Arterial Blood Gas Values *.
Sample ABG Interpretation Table Arterial Blood Gas (ABG) Analysis.
Acid-Base Mnemonic—ROME R espiratory O pposite Alkalosis ↑ pH ↓ PaCO 2 Acidosis ↓ pH ↑ PaCO 2 M etabolic E qual Acidosis ↓ pH ↓ HCO3 Alkalosis ↑ pH ↑ HCO3
Interpretation of ABGs pH 7.18 PaCO 2 38 mm Hg PaO 2 70 mm Hg HCO 3 15 mEq/L What is this? Metabolic acidosis
Interpretation of ABGs pH 7.58 PaCO 2 35 mm Hg PaO 2 75 mm Hg HCO 3 50 mEq/L What is this? Metabolic alkalosis
A patient with an acid-base imbalance has an altered potassium level. The nurse recognizes that the potassium level is altered because: 1. Potassium is returned to extracellular fluid when metabolic acidosis is corrected. 2. Hyperkalemia causes an alkalosis that results in potassium being shifted into the cells. 3. Acidosis causes hydrogen ions in the blood to be exchanged for potassium from the cells. 4. In alkalosis, potassium is shifted into extracellular fluid to bind excessive bicarbonate. Question 24
Answer Answer: 3 Rationale: Changes in pH (hydrogen ion concentration) will affect potassium balance. In acidosis, hydrogen ions accumulate in the intracellular fluid (ICF), and potassium shifts out of the cell to the extracellular fluid to maintain a balance of cations across the cell membrane. In alkalosis, ICF levels of hydrogen diminish, and potassium shifts into the cell. If a deficit of H + occurs in the extracellular fluid, potassium will shift into the cell. Acidosis is associated with hyperkalemia Alkalosis is associated with hypokalemia.
Case Study 1: Jeri Jeri’s been on a 3-day party binge. Friends are unable to awaken her. Assessment reveals level of consciousness difficult to arouse. Respiratory rate 8 Shallow breathing pattern Diminished breath sounds 1. What ABGs do you expect? 2. What is your treatment? 26
Case Study 1: Jeri What ABGs do you expect? Respiratory acidosis reflected by pH 45 mm Hg. The HCO 3 will be normal (20-30 mEq/L) if her respiratory depression has lasted less than 24 hours; if longer than 24 hours, the HCO 3 may be elevated as the result of compensation. The PaO 2 may be <80 mm Hg because of respiratory depression leading to hypoxemia. 2. What is your treatment? Determine the cause of the respiratory depression. If induced by opioids or benzodiazepines, treat with appropriate antagonists. If induced by alcohol or other CNS depressants, breathing must be stimulated until the effects of drugs have worn off. Mechanical ventilation may be necessary to increase respiratory rate and depth, increasing oxygenation and promoting excretion of carbon dioxide.
Case Study 2: Mayna 1. What ABGs do you expect? Respiratory alkalosis indicated by pH >7.45 and PCO 2 <35 mm Hg. The HCO 3 will be normal (20-30 mEq/L) because compensation will not occur in this acute event. 2. What is your treatment? Relieve her anxiety and coax her to take slow breaths. Carbon dioxide may be administered by mask, or she may be asked to breathe into a paper bag placed over her nose and mouth.
Case Study 3: Allen 17 years old History of Feeling bad Fatigue Constant thirst Frequent urination Blood sugar is 484 mg/dL. Respirations are 28 and deep. Breath has a fruity odor. Lungs are clear. 1. What ABGs do you expect? 2. What is your treatment?
Case Study 3: Allen What ABGs do you expect? A diabetic ketoacidosis is a metabolic acidosis indicated by a pH <7.35 and a HCO 3 <20 mEq/L. The PCO 2 will be within the normal range if the acidosis is uncompensated, but will be <35 mm Hg if compensation has occurred. The PaO 2 will not be affected. 2. What is your treatment? Administration of insulin to promote normal glucose metabolism and administration of fluids and electrolytes to replace those lost because of the hyperglycemia.
Fluid volume deficit Can occur with Abnormal loss of body fluids- Diarrhea, hemorrhage, polyuria Inadequate fluid intake Shift of fluid from plasma into interstitial space Treatment Correct the underlining cause Replace the fluid and electrolyte (LR or NS isotonic solutions)
Fluid volume excess May result from excessive intake of fluid Abnormal retention of fluids(heart failure, renal failure) Shift of fluid from interstitial fluid into plasma fluid o Collaborative care o ID primary cause o Diuretics and fluid restriction o Restriction of Na intake Fluid excess may result to ascites or pleural effusion, and paracentesisi or thoracentsis may be necessary.
Commonly prescribed crystalloid solutions Dextrose in water 5% isotonic 10% hypertonic Saline 0.45% hypotonic 0.9% isotonic 3.0% hypertonic Dextrose in Saline 5% in 0.225% isotonic 5% in 0.45% hypertonic 5% in 0.9% hypertonic Multiple Electrolyte Solutions Ringer’s solution- isotonic, includes CL, Na, K, Ca Lactated Ringer’s solution- isotonic-Na, K, Cl, Ca, and lactate(the precursor of bicarbonate)
CVADs Catheters placed in large blood vessels of people who require frequent access to the vascular system Subclavian vein, jugular vein Three different methods Centrally inserted catheter(by MD) Peripherally inserted central catheter Implanted ports( by MD)
CVADs Permit frequent, continuous, rapid, or intermittent administration or monitoring Indicated for patients with limited peripheral vascular access or need for long-term vascular access
Centrally Inserted Catheter Inserted into a vein in the neck, chest, or groin with tip resting in the distal end of the superior vena cava Single, double, triple, or quad lumen Nontunneled or tunneled
Implanted Infusion Ports Central venous catheter connected to an implanted, single or double subcutaneous injection port Port is metal sheath with self-sealing silicone septum.
Implanted Infusion Port
Port accessed with special Huber-point needle Advantages Good for long-term therapy Low risk of infection Cosmetic discretion Care requires regular flushing. Complication: (table page 330) Cath occlusion(kinked, precipitate build up) Embolism( dislodgment of thrombus, air entry, cath breaking) Cath related infection Cath Migration
Nursing Management Inspect catheter and insertion site. Assess pain. Change dressing and clean according to institution policies. Change injection caps. Flushing is important. Catheter and insertion site assessments include inspection of the site for redness, edema, warmth, drainage, and tenderness or pain. Observation of the catheter for misplacement or slippage is important. Transparent dressing or gauze may be used. Discuss cleaning techniques with chlorhexidine-based preparations, povidone-iodine, and isopropyl alcohol Teach the patient to turn the head to the opposite side of the CVAD insertion site during cap change. Flushing: Use a normal saline solution in a syringe that has a barrel capacity of 10 mL or more to avoid excess pressure on the catheter. If resistance is felt, force should not be applied.
Removing CVADs Should be done according to policy and procedures. Gently withdraw. Apply pressure. Ensure that catheter tip is intact.