Acid-Base Balance Janis Rusin APN, MSN, CPNP-AC

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Presentation transcript:

Acid-Base Balance Janis Rusin APN, MSN, CPNP-AC Pediatric Nurse Practitioner Lurie Children’s Transport Team

Objectives Discuss the mechanisms for maintaining normal acid-base balance Define respiratory and metabolic acidosis and alkalosis Identify the common causes of acid base imbalance Define and differentiate between respiratory distress and failure Discuss interventions on transport for a patient with acid-base imbalance

Acid-Base Balance The human body must be maintained in a very narrow range of acid-base balance We use pH as our measure of acidity or alkalinity pH stands for “power” of hydrogen Normal pH is 7.35-7.45-Not a whole lot of wiggle room! Normal cellular metabolism occurs within this range The 2 major organs responsible for maintaining acid base balance are: The lungs-Respiratory balance The kidneys-Metabolic balance

Chemistry Flashback! An acid is a substance that releases hydrogen ions (when it dissociates) A base is a substance that accepts the hydrogen ions A buffer is a substance that protects the pH from derangements by binding with hydrogen ions HA  H+ + A-

The Bicarbonate Buffer System The bicarbonate buffer system is what we monitor clinically to assess acid base balance This system works in the plasma Relationship of carbon dioxide (CO2) to bicarbonate (HCO3-) CO2 is the acid and HCO3- is the base

Balancing Act Lungs Kidneys CO2 is an end product of normal cellular metabolism The lungs regulate the CO2 level through respiration Rapid response-quick fix! The lungs cannot regulate bicarbonate levels Kidneys The renal tubules reabsorb bicarbonate Excess hydrogen ions are excreted in the urine Slower process The kidneys cannot regulate CO2 levels

Clinical Applications Acidosis (blood pH < 7.35) A pathologic condition that causes an increase in the hydrogen ion concentration Alkalosis (blood pH > 7.45) A pathologic condition that causes a decrease in the hydrogen ion concentration A simple acid base disorder has just one disturbance The respiratory and metabolic systems compensate for each others deficiencies If there is more than one disturbance, the patient is said to have a mixed acid base disorder

Types of Acid Base Disorders Metabolic Alkalosis Metabolic Acidosis Respiratory Alkalosis Respiratory Acidosis

Metabolic Alkalosis An elevation in the serum pH associated with a decrease in hydrogen ion concentration and increase in bicarbonate ion concentration Chloride plays a big role 2 main categories Chloride Responsive Chloride levels are < 10 mEq/L Chloride Resistant Chloride levels are > 20 mEq/L

Metabolic Alkalosis Chloride Responsive Diuretics Post hypercapnia Hydrogen ions are lost Vomiting Loss of HCL from stomach contents, as well as Na and K Excessive NG suctioning Loss of both Hydrogen and Chloride ions The kidneys retain Na and K instead of H in order to maintain the Na-K pump function Diuretics Pull H2O from the extracellular space which is low in bicarb Results in an increased concentration of bicarb More bicarb available to bind with Hydrogen Post hypercapnia Compensation by kidneys to retain bicarb in presence of hypercapnia Metabolic alkalosis occurs transiently once PaCO2 levels corrected

Metabolic Alkalosis Chloride Resistant Bicarbonate is retained Hypokalemia Low serum K causes K to shift out of the cells and H to shift into the cells Excessive base intake Antacids Hypertension Aldosterone levels are elevated Results in Na and H2O retention Hydrogen and excess K are dumped by kidney K shifts into cells

Metabolic Acidosis A decrease in pH associated with a low serum bicarbonate concentration Three primary mechanisms: Bicarbonate is lost form the body Kidney function is impaired and acid cannot be excreted properly Endogenous or exogenous addition of acid to the body Common Diagnoses leading to MA Diarrhea Insulin Dependent Diabetes Mellitus (IDDM) Lactic Acidosis Poor perfusion and shock Renal Failure

Metabolic Acidosis Diarrhea Most common cause of MA Bicarbonate is lost in excessive stool The kidneys are unable to keep up with the losses Potassium is also lost in the stool Volume depletion results in aldosterone release Sodium is retained leading to further loss of K Hypokalemia results

Metabolic Acidosis Diabetic Ketoacidosis Insulin deficiency occurs stimulating the release of excess glucagon Glucagon stimulates the release of fatty acids from triglycerides Fatty acids are oxidized in the liver to ketone bodies, beta- hydroxybutrate and aceto-acetic acid These acids result in MA In addition, the DKA patient become volume depleted due to excessive urination Shock develops and further exacerbates the acidosis

Metabolic Acidosis Lactic acidosis Renal Failure Hypoxia or poor tissue perfusion Cells are forced into anaerobic metabolism producing lactic acid Shock Excessive exercise Ethanol toxicity Ethanol interferes with gluconeogenesis Anaerobic metabolism Renal Failure Distal RTA Failure of the distal tubule to properly excrete hydrogen ions Fanconi syndrome Failure of the proximal renal tubule to reabsorb bicarbonate, phosphate and glucose Causes include: Genetics Medications such as tetracycline and antiretrovirals Lead poisoning

Anion Gap Calculation that determines the gap between concentrations of positive (cations) and negative (anions) ions Useful in determining the cause of metabolic acidosis Calculated by: (Na+ + K+) – (HCO3- + Cl-) = 10-12mEq/L

Anion Gap Normal Anion Gap The loss of bicarbonate is compensated for by the retention of chloride Also known as Hyperchloremic Metabolic Acidosis Diarrhea Renal Failure, Proximal RTA Elevated Anion Gap MA due to increased H+ load MUDPILES Methanol Uremia DKA Propylene Glycol Isoniazid Lactic Acid Ethylene Glycol (antifreeze) Salicylates

Respiratory Alkalosis A condition in which the carbon dioxide content is significantly reduced (hypocapnia) Caused by: Hyperventilation Occurs within minutes of onset of hyperventilation Pulmonary disease CHF Hypermetabolic states Fever Anema Hyperthyroid

Respiratory Acidosis Occurs when ventilation of CO2 is inadequate and CO2 is retained (hypercapnia) Causes include airway obstruction, respiratory depression, pneumonia, asthma, pulmonary edema, chest trauma The renal buffer system is not effective for acute RA Chronic respiratory acidosis can be well compensated for by the kidneys

So, how do we make the diagnosis? Arterial Blood Gas-Normal Values pH (7.35-7.45) PCO2 (35-45) PO2 (80-100) HCO3 (22-26) Base Excess/Deficit (-2 to +2) Venous Blood Gas-Normal Values pH (7.31-7.41) PCO2 (40-50) PO2 (35-40) HCO3 (22-26) Base Excess/Deficit (-2 to +2)

Blood Gas Analysis Step 1: Look at the pH Step 2: Look at the PCO2 < 7.35 is acidic > 7.45 is alkalotic Step 2: Look at the PCO2 <35 is alkalotic > 45 is acidic Step 3: Look at the HCO3 < 22 is acidic > 26 is alkalotic Step 4:Match the pH to either the PCO2 or HCO3 Whichever one goes in the same direction as pH determines the primary disorder Respiratory = CO2 Metabolic = HCO3 Step 5:Which one goes in the opposite direction of the pH? This is the compensatory system Step 6: Look at the PO2 Determines presence of hypoxia

Blood Gas Interpretation Blood Gas Analysis 26 HCO3 22 Blood Gas Interpretation 45 PaCO2 35 Normal Values Respiratory Acidosis Metabolic Alkalosis Metabolic Acidosis Respiratory Alkalosis pH 7.35-7.45 Acidemia Alkalemia

Mixed Acid Base Disorders When to suspect a mixed acid base disorder: The expected compensatory response does not occur Compensatory response occurs, but level of compensation is inadequate or too extreme Whenever the PCO2 and HCO3 become abnormal in the opposite direction. In simple acid base disorders, the direction of the compensatory response will always be in the same as the direction of the initial abnormal change. pH is normal but PCO2 or HCO3- is abnormal General rule: If the pCO2 is elevated and HCO3 is reduced, then both respiratory and metabolic acidosis are present If the pCO2 is reduced and the HCO3 is elevated, then both respiratory and metabolic alkalosis are present

Respiratory Distress A compensated state in which oxygenation and ventilation are maintained Define oxygenation and ventilation How will the blood gas look? Characterized by any increased work of breathing Flaring, retractions, grunting What is grunting?

Respiratory Failure Compensatory mechanisms are no longer effective Inadequate oxygenation and/or ventilation resulting in acidosis Abnormal blood gas with hypercapnia and/or hypoxia Will begin to see decreasing LOC due to hypercapnia Medical emergency! Must protect airway! Strongly consider intubation

Respiratory Failure-Causes Pulmonary Causes Diffusion impairment Atelectasis Pneumonia Bronchiolitis Acute lung injury Pulmonary edema Shunting and V/Q mismatch Non-Pulmonary Causes Respiratory muscle compromise or fatigue Impairment of the nervous systems control of breathing Guillain-Barre Muscular Dystrophy Central hypoventilation syndrome Sedatives Head injury Upper airway obstructions

Indications for intubation Inability to protect airway No cough or gag Decreasing LOC GCS < 8 Cardiac or respiratory arrest Acute respiratory acidosis Refractory hypoxemia despite 100% FiO2

Goals of ventilation Correct acidosis Rest the respiratory muscles Correct hypoxemia Allows for delivery of high FiO2 PEEP Improves cardiac function Decreases preload Decreases metabolic demand

Initial Ventilator settings Volume Control Pressure Control Rate Normal for age Tidal Volume 8-10 cc/kg PEEP Start at 5cm H2O and increase as clinically indicated i-Time 1:2 (Must increase E-time in obstructive processes to avoid air trapping) Set pressure to produce adequate chest rise and TV’s (8-10/kg)

Correction of hypoxia and hypercarbia To increase PaO2 To decrease PaCO2 Increase FiO2 Increase Rate Increase PEEP Increase Tidal Volume or Pressure control Increase I-Time

Match the Gas Which patient does this gas belong to? pH 7.09 PCO2 98 PO2 218 HCO3 30 A) 22 y/o with Muscular Dystrophy. Severe and worsening muscle weakness B) 9 y/o with new onset Diabetic Ketoacidosis C) A 30 y/o patient presenting with a panic attack D) A 25y/o in a skiing accident presenting in respiratory distress

Match the Gas pH 7.09 PCO2 98 Po2 218 HCO3 30 A) 22 y/o with Muscular Dystrophy. Severe and worsening muscle weakness Chronic Respiratory Failure Uncompensated Respiratory Acidosis

Match the Gas Which patient does this gas belong to? pH 7.55 PCO2 28 PO2 63 HCO3- 23 A) 22 y/o with Muscular Dystrophy. Severe and worsening muscle weakness B) 9 y/o with new onset Diabetic Ketoacidosis C) A 30 y/o patient presenting with a panic attack D) A 25y/o in a skiing accident presenting in respiratory distress

Match the Gas Which patient does this gas belong to? pH 7.55 PCO2 28 PO2 63 HCO3- 23 C) A 30 y/o patient presenting with a panic attack Hyperventilation Uncompensated Respiratory alkalosis

Match the Gas Which patient does this gas belong to? pH 6.94 PCO2 26.6 PO2 55.7 HCO3 5.7 BD -27 A) 22 y/o with Muscular Dystrophy. Severe and worsening muscle weakness B) 9 y/o with new onset Diabetic Ketoacidosis C) A 30 y/o patient presenting with a panic attack D) A 25y/o in a skiing accident presenting in respiratory distress

Match the Gas pH 6.94 PCO2 26.6 PO2 55.7 HCO3 5.7 BD -27 B) 9 y/o with new onset Diabetic Ketoacidosis DKA Uncompensated Metabolic Acidosis

Match the Gas Which patient does this gas belong to? pH 7.27 PCO2 54.8 PO2 70 HCO3 26 BD -1 A) 22 y/o with Muscular Dystrophy. Severe and worsening muscle weakness B) 9 y/o with new onset Diabetic Ketoacidosis C) A 30 y/o patient presenting with a panic attack D) A 25y/o in a skiing accident presenting in respiratory distress

Match the Gas pH 7.27 PCO2 54.8 PO2 70 HCO3 26 BD -1 D) A 25y/o in a skiing accident presenting in respiratory distress Acute Respiratory Distress Uncompensated Respiratory Acidosis

Questions?