SIGNS AND SYMPTOMS OF ELECTROLYTE DISORDERS

HYPONATREMIA HYPERNATREMIA1. Headache 1. Lethargy2. Lethargy 2. Irritability3. Confusion 3. Thirst4. Weakness 4. Hyperreflexia5. Seizure 5. Seizures6. Coma 6. Coma7. Death 7. Death

SIGNS AND SYMPTOMS OF POTASSIUM DISORDER

HYPOKALEMIA HYPERKALEMIA1. NAUSEA 1. CRAMPING2. VOMITING 2. PARALYSIS3. WEAKNESS 3. NAUSEA4. CONSTIPATION 4. VOMITING5. ILEUS 5.

TACHYDYSRHYTHMIAS

6. PARALYSIS 6. CARDIAC ARREST7. RESPIRATORY INSUFFICIENCY8. TACHYDYSRHYTHMIAS

ECG FINDINGS

HYPOMAGNESEMIA HYPERMAGNESEMIA

1. Hyperreflexia 1. Nausea2. Tetany 2. Vomiting3. Constipation/Ileus 3. Hyporeflexia4. Vertigo/Ataxia 4. Hypotension5. Nystagmus 5. Respiratory Paralysis6. Parasthesias 6. Diplopia7. Seizures 7. Heart Block8. Coma 8. Paralysis9. Death 9. Cardiac Arrest10. Cardiac Dysrhythmias

HYPOCALCEMIA HYPERCALCEMIA

1. Tetany 1. Lethargy2. Seizures 2. Confusion3. Weakness 3. Obtundation4. Cramps 4. Seizures5. Confusion 5. Constipation/Ileus6. Dementia 6. Abdominal Pain7. Heart Block 7.Polyuria8. Cardiac Arrest 8. Polydipsia9. Laryngospasm 9. Cardiac Disrhythmias

HYPOPHOSPHATEMIA HYPERPHOSPHATEMIA

1. Muscle Weakness 1. Metastatic Calcification2. Respiratory Insufficiency 2. Signs and symptoms of

hypocalcemia

3. Decreased Cardiac Contractility 3. Anorexia

4. Paralysis 4. Ileus

5. Parasthesias6. Irritability7. Ataxia8. Tremor9. Seizures

ECG CHANGES IN ELECTROLYTES IN BALANCEHYPERKALEMIA

Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

HYPOKALEMIA

U Waves

T Wave Flattening

ST – segment changes

Arrhythmias

HYPERKALEMIA

Shortened QT interval

Prolonged PR and QRS intervals

Increased QRS voltage

T-wave flattening and widening

AV block (can progress to complete heart block)

HYPOCALCEMIA

Prolonged QT interval

T-wave inversion

Heart blocks

Ventricular fibrillations

HYPERMAGNESEMIA

Increased PR interval

Widened QRS complex

Elevated T-waves

HYPOMAGNESEMIA

Prolonged QT and PR interval

ST segment depression

Flattening or inversion of P waves

Arrythmias

TREATMENT OF HYPERKALEMIAMECHANISM THERAPHY DOSE ONSET OF

ACTIONDURATION OF ACTION

Membrane stabilization

Calcium gluconate 1-2 grams IV over 5-10 min.

1-2 min. 30 min.

Intracellular potassium shift

Sodium bicarbonate 50-100 meq IV over 2-5 min.

30 min. 2-6 hours

Insulin and glucose 5-10 units RHI IV with 50ml of 50% dextrose (25g)

15-45 min. 2-6 hours

ᵦ₂ agonists Albuterol

Depends upon drug 10-20 mg nebulized

20-30 min. 1-2 hours

Potassium removal Furosemide 20-40 mg IV. 5-15 min. 4-6 hours

Sodium polystyrene sulfonate

15-60 g PO or PR 4-6 hours 4-6 hours

Hemodialysis 2-4 hours Immediate Duration of dialysis

COMPOSITION OF INTRAVENOUS FLUIDS(mEq/L)

FLUID SODIUM POTASSIUM CHLORIDE CALCIUM MAGNESSIUM BICARBONATE OSMOLALITY

Plasma 141 4-5 103 5 2 27 289LR 130 4 109 3 0 28 2733% Saline 513 0 513 0 0 0 1026

0.9% Saline 154 0 154 0 0 0 308

0.45% Saline 77 0 77 0 0 0 154

0.2% Saline 34 0 34 0 0 0 68

D5W 0 0 0 0 0 0 253

DISORDER PRIMARY DISTURBANCE

COMPENSATORY RESPONSE

COMPENSATION FORMULA*

Metabolic acidosis ↓HCO-₃ ↓PaCO₂ ∆ PaCO₂ = 1.2 X ∆ HCO-₃

Metabolic alkalosis

↑HCO-₃ ↑PaCO₂ ∆ PaCO₂ = 0.6 X ∆ HCO-₃

Acute respiratory acidosis

↑PaCO₂ ↑HCO-₃ ∆ HCO-₃ = 0.1 X ∆ PaCO₂

Chronic respiratory acidosis

↑PaCO₂ ↑↑HCO-₃ ∆ HCO-₃ = 0.35 X ∆ PaCO₂

Acute respiratory alkalosis

↓PaCO₂ ↓HCO-₃ ∆ HCO-₃ = 0.2 X ∆ PaCO₂

Chronic respiratory alkalosis

↓PaCO₂ ↓↓HCO-₃ ∆ HCO-₃ = 0.5 X ∆ PaCO₂

CAUSE MECHANISM TREATMENT

METEBOLIC ACIDOSIS: ANION GAPRenal failure Accumulation of fixed

acids ( proteins, sulfates, phosphates), impaired bicarbonate reabsorption /regeneration

Low-protein diet, administration of sodium bicarbonate, dialysis

Lactic acidosis Accumulation of lactic acid caused by anaerobic glycolysis

Restoration of cellular oxygen delivery

Diabetic ketoacidosis, fasting, chronic alcoholism

Increased glucagon-to-insulin ratio leads to enhanced lipolysis and metabolism through ketoacids, dehydration

Administration of insulin (for diabetic ketoacidosis): provision of carbohydrate; rehydration

Toxic ingestions: salicylates, methanol, ethylene glycol, paraldehyde, toluene

Addition of fixed acids Emhancement of excretion ( hydration, dialysis); urine alkalinization for salicylate poisoning; ethanol was used in the past for the ethylene glycol and methanol poisoning to block the conversion by alcohol dehydrogenase into toxic metabolites, but now fomepizole is used

CAUSE MECHANISM TREATMENT

METABOLIC ACIDOSIS:NONANION GAPDiarrhea, ileus, fistula, and ureterosigmoidostomy

Gastrointestinal HCO-₃ loss

Replacement of volume and electrolytes

Proximal renal tubular acidosis, acetazolamide

Renal HCO-₃ loss Discontinuation of acetazolamide

Saline administration (large volumes administered quickly)

Renal HCO-₃ loss Avoidance

Distal renal tubular acidosis

Failure renal HCO-₃ loss production

Alkali administration

METABOLIC ALKALOSISChloride ResponsiveCAUSE MECHANISM TREATMENT

Vomiting nasogastric suction

Loss of HCI, to relative excess of HCO-₃ increased renal absorption of CI- because of depletion

Provision of CI’ ( as NaCl or KCl); restoration of intravascular volume

Diuretic Therapy CI- loss in urine, volume depletion, increased renal HCO-₃, generation, hypokalemia

Provision of CI’ as NaCl or KCl; restoration of intravascular volume

Posthypercapnia Renal excretion of acid and generation of HCO-₃ during respiratory

Provision of CI’

METABOLIC ALKALOSISChloride ResistantCAUSE MECHANISM TREATMENT

Mineralocorticoid excess(Cushing’s syndrome, hyperaldosteronism

Direct stimulation of Na⁺-H⁺ and Na⁺-K⁺ exchange in distal tubule; increased renal generation and reabsortion of HCO-₃

Correction of underlying disorder; spironolactone; K⁺ replacement

Bartter’s syndrome (renal tubular salt wasting)

Increased distal tubular Na⁺ delivery increases distal tubular Na⁺ reabsorption and exchange with K⁺ and H⁺

K⁺ replacement nonsteroidal antiinflammatory agents volume expansion

Excessive alkali administration

Usually associated with renal insufficiency; citrate (from red cell transfusions); hyperalimentation solutions; milk-alkali syndrome

Cessation of alkali administration

Severe potassium depletion

Impaired renal Cl’ reabsortion leading to increased Na⁺-H⁺ exchange and generation of HCO-₃

K⁺ repletion

RESPIRATORY ACIDOSISCAUSE MECHANISM TREATMENTSedatives, hypnotics, narcotics, central, nervous system lesions

Suppression of respiratory drive

Discontinuation or reversal of pharmacologic suppression of respiration; mechanical ventilation

Restrictive lung disease Increased work of breathing

Treatment of underlying disease; mechanical ventilation as needed

Pulmonary fibrosisPleuralAnkylosing spondylitisSevere kyphosis

Obstructive lung disease

Increased work of breathing

Treatment of underlying disease; mechanical ventilation as needed

Upper airway obstructionAsthmaMyopathies/neurophaties

Relative increase in work of breathing

Mechanical ventilation if severe

ParalysisGuillain-Barre’ syndromeFever, seizures Increased CO₂

production in the presence of a fixed minute ventilation

Control of fever; mechanical ventilation rarely required in cases of excess CO₂ production

Large pulmonary embolus

Increased alveolar dead space in the presence of a fixed minute ventilation

Thrombolytic therapy; mechanical ventilation to further increase minute ventilation

RESPIRATORY ALKALOSISCAUSE MECHANISM THERAPY

Pain, fever, gram-negative sepsis, cirrhosis, central nervous system lesions, pregnancy (progesterone effect), salicylates theophylline

Increased respiratory drive

Treatment of underlying cause; discontinuation/ increased elimination of pharmacologic stimulation

Hypoxia, hypotension Peripheral chemoreceptorstimulation

Correction of hypoxia, hypotension

Pneumonia, pulmonary edema, pulmonary embolus

Pulmonary receptor stimulation

Treatment of underlying cause