disorders of potassium dr muhammad rizwan ul haque assisstant professor of nephrology shaikh zayed...
TRANSCRIPT
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Disorders of potassium
Dr Muhammad Rizwan ul Haque
Assisstant Professor of NephrologyShaikh Zayed Postgraduate Medical
instituteLahore
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Potassium Functions
Most abundant intracellular cation Regulates heart function Essential for protein and nucleic
acid synthesis Important for neuromuscular
excitability Maintains resting membrane
potential
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Potassium Metabolism
• Normal potassium level is 3.5-5.0 mEq/L
• Poor indicator of total body stores• Total body potassium stores are
approximately 50 mEq/kg (3500 mEq in a 70-kg person).
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Serum Potassium Regulation
Well-developed systems for sensing potassium by the pancreas and adrenal glands High serum potassium - insulin –
stimulation of sodium potassium pump in muscles - muscle uptake of potassium
aldosterone- enhancement of distal renal expression of secretory potassium channels (ROMK) – potassium excretion
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Serum Potassium Regulation
Low potassium states result in insulin resistance, impairing
potassium uptake into muscle cells cause decreased aldosterone release
leading to decrease renal potassium excretion
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Potassium Metabolism
88-90 %
2-3 %
9-10%
In Renal Failure
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
K+K+
K+
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-35
-60
SA Node Action Potential
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Threshold Potential
Resting MembranePotential
Excitability Potential
Normal Cardiac Tissue Excitability
- 90
- 60
+20
0
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Nernst Equation
Ex = - x log 61Z
Xi
Xo
Resting membrane potential is the combination of equilibrium potential and conductance of various ions
Equilibrium Potential
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Equilibrium PotentialNernst Equation
96-(134+52)=-90 mv
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Disorders of Potassium
• Hyperkalemia• Intake > Excretion (loss)
• Transcellular shift
• Hypokalemia• Excretion (loss) > Intake
• Transcellular shift
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Renal Excretion of Potassium
Renal adaptive mechanisms allow the kidneys to maintain potassium homeostasis until the GFR drops to less than 15-20 mL/min
Obligatory renal losses are 10-15 mEq/day.
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Increased Renal Excretion
Aldosterone High distal delivery of sodium
(diuretics) High urine flow rate (osmotic
diuresis) High serum potassium Delivery of non-absorbable anions to
collecting duct. (bicarbonate)
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Decreased Renal Excretion
Aldosterone deficiency or resistance to aldosterone
Low distal delivery of sodium Low urine flow rate Low serum potassium Renal failure
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Trans-cellulr shift Glucoregulatory hormones
Insulin enhances potassium entry into cells, Glucagon impairs potassium entry into cells
Adrenergic stimuli: Beta-adrenergic stimuli enhance potassium entry
into cells Alpha-adrenergic stimuli impair potassium entry into
cells pH:
Alkalosis enhances potassium entry into cells Acidosis impairs potassium entry into cells
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Transcellular Potassium Shift
• Insulin• Beta-adrenergic stimuli• Alkalemia• Blood at higher temp
• Glucagon• Beta blockers• Alpha adrnerigic stimulation
• Tissue destruction• Acidemia• Acute increase in serum osmolility• Blood stored at <4 Co
K+
K+
K+
K+
K+
K+K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
HYPOKALEMIAHYPERKALEMIA
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Hyperkalemia
5 % in general population 10 % of hospitalized patients
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Classification of Hyperkalemia
5.5-6.0 mEq/L – Mild Hyperkalemia 6.1-7.0 mEq/L - Moderate 7.0 mEq/L and greater - Severe
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Mortality
Overall mortality rate 14.3%. The risk increasing as the potassium level increases.
Serum Potassium Mortality rate
7 meq/l 28 %<6.5 meq/l 9 %
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Causes of Hyperkalemia
For excessive potassium intake, Eating disorders - exclusively high-potassium
foods, such as fruits, dried fruits, juices, and vegetables with little to no sodium
Heart healthy diets - Very low–sodium and high-potassium diets
Use of potassium supplements in over-the-counter herbal supplements, salt substitutes, or prescribed pharmacologic agents
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Causes of Hyperkalemia
• Renal failure• Ingestion of drugs that interfere with
potassium excretion • Potassium-sparing diuretics,• Angiotensin-converting enzyme inhibitors,• Nonsteroidal anti-inflammatory drugs,
• Impaired responsiveness of the distal tubule to aldosterone• Type IV renal tubular acidosis observed
with diabetes mellitus, sickle cell disease.• Chronic partial urinary tract obstruction
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Causes of Hyperkalemia Hyperosmolality Rhabdomyolysis Tumor lysis syndrome Succinylcholine administration, which
depolarizes the cell membrane EACA (Epsilon aminocapric acd), arginine and
lysine administration Hyperkalemic periodic paralysis Insulin deficiency or insulin resistance (ie, type
I or type II diabetes mellitus) Use of beta-adrenergic antagonist therapy (eg,
for hypertension or angina
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Pseudohyperkalemia
Prolonged use of tourniquet Hemolysis (in vitro) Delay in processing of blood Severe leukocytosis Severe thrombocytosis
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Symptoms
Nonspecific, related to muscular or cardiac function.
Weakness and fatigue. Occasionally, frank muscle
paralysis or shortness of breath. May be palpitations or chest pain.
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Hyperkalemia- Signs
Bradycardia due to heart block or tachypnea due to respiratory muscle weakness.
Muscle weakness and flaccid paralysis
Depressed or absent deep tendon reflexes
Muscle tenderness, weakness, suggesting rhabdomyolysis.
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ECG in Hyperkalemia
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Threshold Potential
Resting MembranePotential
Excitability Potential
Normal Cardiac Tissue Excitability
- 90
- 60
+20
0
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Threshold Potential
Resting MembranePotential
Excitability Potential
Increased Excitability
- 60
- 70
- 90
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Threshold Potential
Resting MembranePotential
Excitability Potential
Persistent Depolarization in Hyperkalemia
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Work-up Urinary potassium, serum sodium, urine
osmolality Transtubular potassium gradient = (urine K x serum osmolarity)/(serum K x urine
osmolarity) TTKG of < 3 - lack of aldosterone effect
on collecting tubules – decreased excretion
TTKG greater > 7 - an aldosterone effect, - normal excretion
24 hour urinary potassium.
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Transtubular Potassium Gradient (TTKG)
It is a measurement of net K+ secretion by the distal nephron after correcting for changes in urinary osmolality
Determine whether hyperkalemia is caused by Aldosterone deficiency/resistance
or Nonrenal causes.
Clinical correlation and potassium intake should be assessed.
TTKG = (Ku/Ks) × (Sosm/Uosm)
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Transtubular Potassium Gradient
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Evaluation of Hyperkalemisa
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Emergently treat K+
Are K sparing medications are being administered
Are ECG changes are present
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Treatment
Evaluation for potential toxicities Decreasing potassium intake Increasing potassium uptake into
cells Increasing potassium excretion Determining the cause to prevent
future episodes
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Treatment of HyperkalemiaDrug Route of
Admin.Onset Duration
Calcium IV 10 cc 10% 1-3 min 30 min
Insulin- Glucose
IV 20-30 minutes
2 hours
Beta adrenergic
20 mg in 4 ml nebulize in 10 m
15-30 min 30 min- 3 hrs
Ion exchange resins
15 G in 15-30 ml 70% sorbitol
2-6 hrs 6-12 hrs
Diuretics IV 40-80 mg Furosemide
15 min 2-3 hours
Hemodialysis Immediate
Until dialysis completed
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Threshold Potential
Resting MembranePotential
Excitability Potential
Normal Cardiac Tissue Excitability – Effect of Calcium
- 90
- 60
High Serum Calcium
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Threshold Potential
Resting MembranePotential
Excitability Potential
Increased Excitability
- 60
- 90
- 30
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Threshold Potential
Resting MembranePotential
Excitability Potential
Increased Excitability- Effect of Calcium
-60
- 70
-90
-40
30
1030
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Hypokalemia
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Hypokalemia
Defined as a potassium level less than 3.5 mEq/L.
Mild hypokalemia - serum level of 3-3.5 mEq/L.
Moderate hypokalemia - serum level of 2.5-3 mEq/L.
Severe hypokalemia - level less than 2.5 mEq/L.
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Symptoms Palpitations Skeletal muscle weakness or cramping Paralysis, paresthesias Constipation Nausea or vomiting Abdominal cramping Polyuria, nocturia, or polydipsia Psychosis, delirium, or hallucinations Depression
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Signs Signs of ileus Hypotension Ventricular arrhythmias Cardiac arrest Bradycardia or tachycardia Premature atrial or ventricular beats Hypoventilation, respiratory distress Respiratory failure Lethargy or other mental status changes Decreased muscle strength, fasciculations, or
tetany Decreased tendon reflexes
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ECG in Hypokalemia
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Threshold Potential
Resting MembranePotential
Excitability Potential
Hyperpolarization in Hypokalemia
-120
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Causes of Hypokalemia
Medications: Thiazide and loop diuretics,
aminoglycosides, amphotericin B, β2-agonists, and adrenal steroids, Chronic laxative abuse
GI Vomiting, diarrhea, NG suction
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Causes of Hypokalemia
Renal: Renal tubular acidosis, (type 1 , 2) Magnesium deficiency Primary hyperaldosteronism Cushing Syndrome Salt-losing nephropathies Bartter and Gitelman syndromes Therapeutic alkalinization of the urine
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Causes of Hypokalemia
Treatment of megaloblastic anemia with vitamin B12 and folate
Miscellaneous toxic conditions: Barium intoxication; chloroquine toxicity;
glue sniffing due to hippurate accumulation,
Tocolytic therapy in pregnant women to treat premature labor
Amphotericin B therapy
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Causes of Hypokalemia Genetics disorders
Familial (hypokalemic) periodic paralysis Congenital adrenogenital syndromes Liddle syndrome Bartter and Gitelman syndromes Familial interstitial nephritis Glucocorticoid-remediable aldosteronism
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Diagnostic Workup of Hypokalemia
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Treatment of Hypokalemia
Potassium replacement How much? What route? How fast ? What salt ?
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Treatment
Asymptomatic mild hypokalemia Oral replacement
Moderate to severe (no emergency) Intravenous
40 meq/l 160 meq per day
Hypokalemia with cardiac dysarrythmias 20 meq/100 cc /hr under ECG monitoring
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Treatment of Hypokalemia
Metabolic alkalosis Potassium chloride
Metabolic acidosis Potassium citrate/acetate
Diabetic ketoacidosis (+hyphosphatemia) Potassium phophate
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Threshold Potential
Resting MembranePotential
Excitability Potential
Hyperpolarization in Hypokalemia
-120
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Threshold Potential
Resting MembranePotential
Excitability Potential
Hyperpolarization in Hypokalemia
-120
Ca++ administration
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Threshold Potential
Resting MembranePotential
Excitability Potential
Low Serum Potassium & Calcium
-120
S. Potassium correction in hypocalcemia
Hypocalcemia
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Threshold Potential
Resting MembranePotential
Excitability Potential
Low Serum Potassium & Calcium
-120
S. Calcium correction in hypokalemia
Hypocalcemia
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