fluidandelectrolytes 090911071435 phpapp01
TRANSCRIPT
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