Electrolytes and Acid Base Balance Flashcards
Definition of Electrolytes
Substance that ionize (dissociates) in blood stream and body fluids
Examples of Electrolytes
Acids (H+)
Bases (HCO3-, PO4-2)
Inorganic Salts (K+, Na+, Cl-)
Mineral Ions (Mg2+, Fe2+, Fe3+, Ca2+)
Electrolytes Function
Maintain osmotic pressure of body fluid compartments
Regulate osmotic movement of H2O
Acid-Base Regulation
Found in tissues
Co-enzymes
Neuromuscular reactions
Imbalances in Electrolytes Caused By
Vomiting
Diarrhea
Sweating
Kidney Loss
Hormonal Imbalance
Acid-Base Imbalance
Tissue Destruction
Electrolyte Panel Ordered
Called “lytes”
Na+
K+
Cl-
HCO3- (noted as TCO2 on Blood Gas Report)
Calculated by Anion Gap
Sodium Function
Create Osmotic Pressure
Most Abundant in ECF - Major Extracellular cation
Essential for electrical activity of neurons and muscle cells
Hormonal Regulation of Na and H2O
Aldosterone
- controls Na+ reabsorption by kidneys
Juxtaglomerular apparatus turns on renin-angiotensin system
Decrease Aldosterone Production
Addison’s Disease
Increase Aldosterone Production
Cushing’s Disease
Hyponatremia
Decreased Plasma Na+
Associated with regulation of blood volume
Skin turgor, Venous Pressure, and Urine Na+ concentration
Hypovolemic Depletion Hyponatremia
Result of excess Na loss and excess H20 loss
Renal Loss Hypovolemic
Diuretics
Primary or secondary Addison’s disease
Non-renal loss Hypovolemic
GI loss from vomiting or diarrhea
Skin loss from burns or trauma
Hypervolemic Dilutional Hyponatremia
Relative change in measured Na+ due to increased H2O volume
- Syndrome of inappropriate ADH secretion
- Generalized edema (congestive heart failure, cirrhosis, nephrotic syndrome)
- Uncontrolled diabetes (high blood glucose) mellitus
Hypernatremia
Increased Plasma Sodium
Result of excess water loss or Na+ gain (rare)
Fluid loss of Hypernatremia
Loss of fluid by: GI tract, excessive sweating, hromone disorder
Diabetes insipidus
Absolute Na+ Gain Hypernatremia
Ingestion or infusion of NaCl or NaHCO3
Hyperaldosteronism
Acute Renal Failure
Function of Potassium
Creates Osmotic pressure in ICF
Must abundant cation in ICF
- Major Intracellular Cation
Electrical activity of neurons and muscle cells
Hydrogen Ion buffering
Kidney-Aldosterone Regulation Potassium
Decreased Plasma concentration by increasing rate of K+ secretion in the proximal convoluted tubules and duct
Cellular breakdown increase K+ released
Tied to H+ during metabolic acidosis
Effect of K+ on Heart
Increased plasma slows heart rate by decreasing resting membrane potential of heart
Decreased extracellular, causes myocardial excitability
Critical high K+ levels
Cause Cardiac shutdown
Too much Potassium
Critical low K+ levels
Causes arrythmia
Hypokalemia
Decreased plasma K+
Causes of Hypokalemia
Excessive GI loss, N-G tube, diarrhea, and laxative abuse
Renal losses hyperaldosteronism, renal tubular acidosis
Decreased dietary intake
Increased cellular uptake in alkalosis
Insulin excess
Symptoms of Hypokalemia
Muscle weakness
Cardia arrhythmia
Paralysis
Hperkalemia
Increased plasma K+
Causes of Hyperkalemia
Increased dietary intake
Increased tissue destruction
Altered cellular uptake in acidosis
Insuling deficiency
Impaired renal excretion in renal problems & hypoaldosteronism
False Cause of Hyperkalemia
Hemolyzed blood sample
Symptoms of Hyperkalemia
Muscle weakness
Slow or irregular pulse
EKG changes
Tingling
Chloride Function
Most abundant anion in ECG
- Major extracellular anion
Moves in and out of cells passively in association with Na+
Helps regulate osmotic pressure and thus H2O balance
Helps regulate electric neutrality
Component of HCl in gastric juice
Chloride balance
Passively follows Na+
Acid base balance and electric neutrality within the body
- Cl- ion shift is secondary to Na+ and HCO3- movement
Ingested in diet and absorbed in intestines
Hypochloremia
Decreased plasma Cl- levels
Causes of Hypochloremia
GI losses in prolonged comiting & nasogastric suction
Loss from traumatized skin in burns
Renal losses with diuretics
Metabolic acidosis
Hyperchloremia
Increased Plasma Cl- levels
Causes of Hyperchloremia
Dehydration
Renal Tubular Acidosis
Metabolic acidosis from prolonged diarrhea
Loss of NaHCO3
Salicylate Intoxication (Aspirin)
Sweat Chloride Test
Screening for Cystic Fibrosis
Characterized by excessive mucus secretion causing lung and upper respiratory obstruction & blockage
Increase of Na+ and Cl- in sweat
Sweat Chloride Test Measured
Pilocarpine Iontophoresis
Bicarbonate Function
Major component of bicarbonate buffer system
- 2nd largest anion found in ECF
Acid base balance as component of bicarbonate
- Carbonic acid buffer system
Bicarbonate Balance
Kidney reabsorption
Lungs - control through respiration
Decreased HCO3-
Results in Metabolic Acidosis
HCO3- Primary metabolic acidosis
Buffered during diabetes
Renal disease
Lactic acidosis
Other acidic conditions
Increased HCO3-
Results in Metabolic Alkalosis
HCO3- Primary metabolic alkalosis
Due to medications
Anion Gap Formula
Na - (Cl + HCO3)
Anion Gap <7
Low anion gap
Instrument error
Patient Condition
- Multiple myeloma w/ pos charged abnormal proteins
- Very rare
Anion Gap >16
High anion gap
Instrument error
Patient Condition
- Diabetic ketoacidosis
- Lactic acidosis
- Renal azotemia and retention of acids
Acid-Base Balance
State of equlibrium
pH is maintained regardless of metabolic stressors on the body
Acid-Base Balance Maintained BY
Controlling hydrogen concentrations of body fluids
pH within a narrow range 7.35 - 7.45
Hydrogen Ion homeostasis
Dependent on
- Bod buffer systems
- Respiratory mechanisms
- Renal function
Acid Production Metabolism
Krebs Cycle - ATP +H2O +CO2
Acid Production Metabolic Pathways
H+ + Anions
Excess H+ can be excreted or retained by kidneys
Body’s Buffer Systems
Prevent rapid, drastic changes in pH
Maintains pH consistancy
Consists of a pair of chemicals
Carbonic Acid-Bicarbonate Buffer System
CO2 + H2O = H2CO3 = HCO3- + H+
Most abundant buffer system buffer system in the ECF
Chloride Shift
Occurs inside RBCs
Way of buffering H+
Carbonic Acid-Bicarbonate Buffer Kidneys Role
HCO3- is reabsorbed along with Na+ for H+ under normal circumstances
Acidosis - this exchange increases
Alkalosis - this exchange is retained and more HCO3- is excreted
Phosphate Buffer System
Important in intracellular fluid and in urine
Weak base is monohydrogen phosphate (HPO4)2-
Weak Acid is dihydrogen phosphate (H2PO4-)
Protein Buffer System
Proteins are most important in buffering inside cells
Hgb is especially good buffer
Weak Base is Amine Group (NH2)
Weak Acid of carboxyl group (-COOH)
Hendersohn Hasselbalch Equation
pH = pKa + log (HCO3-/H2CO3)
Respiratory Acidosis Signs
Increased pCO2 and decreased pH
Common Cause of Respiratory Acidosis
Hypoventilation - retention of CO2 in blood stream
- Emphysema
- Pulmonary edema
- Trauma to respiratory center
- Airway obstruction (choking or asthma)
- Dysfunctional respiratory muscles
- Pneumonia
- Barbiturate poisoning
Metabolic Acidosis Signs
Decreased Bicarbonate and decreased pH
Common Cause of Metabolic Acidosis
- Loss of body bicarbonate due to diarrhea
- Accumulation of acid from increased production
- Retention due to decreased renal function
- Diabetic ketosis
- Lactic Acidosis
- Renal failure
-Ethylene glycol poisoning - Methanol ingestion
Respiratory Alkalosis Signs
Decreased pCO2 and increased pH
Common Cause of Respiratory Alkalosis
Anything that makes patient breath faster
Hyperventilation
- Oxygen deficiency
- Pulomonary disease
- Cerebral Vascular accident (CVA)
- Anxiety
- Fever
- Aspirin Overdose
Metabolic Alkalosis Signs
Increased bicarbonate and increased pH
Common Cause of Metabolic Alkalosis
- Loss of acid (vomiting or Gastric suctioning)
- Diuretic therapy
- Hyperaldosteronism or Cushing’s Disease
- Excessive intake of alkaline drugs
- Citrate toxicity after massive transfusion
Respiratory Compensation
Occurs in response to altered pH caused by metabolic changes
Respiratory Mechanisms for Compensation
Hypoventilation
Hyperventilation
-Occurs within minutes and maximized within hours
Blood Hydrogen Ion Concentration
Increase activates chemoreceptors in the medulla oblongata
- stimulates respiratory center
- Nerve impulses to respiratory muscles which contract more forcefully
- increases exhalation of CO2
Metabolic Compensation
Occurs in response to altered pH caused by respiratory changes
Metabolic Mechanisms for Compensation
Kidney excretion
Compensation begins in minutes but takes days to maximize
Renal Compensation
Renal tubules raised blood pH by
- secretion and excretion of H+
- reabsorption of filtered HCO3-
- synthesis and absorption of newly formed HCO3-
- Formation of NH4+ (ammonium)
