Transcript Document

Disorders of potassium
Dr Muhammad Rizwan ul Haque
Assisstant Professor of Nephrology
Shaikh Zayed Postgraduate Medical institute
Lahore
Potassium Functions
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Most abundant intracellular cation
Regulates heart function
Essential for protein and nucleic acid
synthesis
Important for neuromuscular excitability
Maintains resting membrane potential
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).
Serum Potassium Regulation
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Well-developed systems for sensing
potassium by the pancreas and adrenal
glands
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High serum potassium - h insulin –
stimulation of sodium potassium pump in
muscles - h muscle uptake of potassium
h aldosterone- enhancement of distal renal
expression of secretory potassium channels
(ROMK) – h potassium excretion
Serum Potassium Regulation
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Low potassium states
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result in insulin resistance, impairing
potassium uptake into muscle cells
cause decreased aldosterone release
leading to decrease renal potassium
excretion
Potassium Metabolism
K+
K+
K+ +
K +
+
K + K +
K+ + K K+ K K+
K +
+
K + K K+
K +
K +
K +
K
K+
In Renal Failure
2-3 %
K+
88-90 %
9-10%
SA Node Action Potential
-35
-60
Normal Cardiac Tissue
Excitability +20
0
- 60
Threshold Potential
Excitability Potential
- 90
Resting Membrane
Potential
Nernst Equation
Resting membrane potential is the
combination of equilibrium potential
and conductance of various ions
Equilibrium Potential
61
Xi
Ex = x log
Z
Xo
Equilibrium Potential
Nernst Equation
96-(134+52)=-90 mv
Disorders of Potassium
• Hyperkalemia
• Intake > Excretion (loss)
• Transcellular shift
• Hypokalemia
• Excretion (loss) > Intake
• Transcellular shift
Renal Excretion of Potassium
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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.
Increased Renal Excretion
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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)
Decreased Renal Excretion
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Aldosterone deficiency or resistance to
aldosterone
Low distal delivery of sodium
Low urine flow rate
Low serum potassium
Renal failure
Trans-cellulr shift
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Glucoregulatory hormones
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Adrenergic stimuli:
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Insulin enhances potassium entry into cells,
Glucagon impairs potassium entry into cells
Beta-adrenergic stimuli enhance potassium entry
into cells
Alpha-adrenergic stimuli impair potassium entry
into cells
pH:
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Alkalosis enhances potassium entry into cells
Acidosis impairs potassium entry into cells
Transcellular Potassium Shift
HYPERKALEMIA
HYPOKALEMIA
K+
K+
K+
• 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+
• Insulin
• Beta-adrenergic
stimuli
• Alkalemia
• Blood at higher temp
K+
K+
Hyperkalemia
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5 % in general population
10 % of hospitalized patients
Classification of Hyperkalemia
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5.5-6.0 mEq/L – Mild Hyperkalemia
6.1-7.0 mEq/L - Moderate
7.0 mEq/L and greater - Severe
Mortality
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Overall mortality rate 14.3%. The risk
increasing as the potassium level
increases.
Serum Potassium
7 meq/l
<6.5 meq/l
Mortality rate
28 %
9%
Causes of Hyperkalemia
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For excessive potassium intake,
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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 highpotassium diets
Use of potassium supplements in over-the-counter
herbal supplements, salt substitutes, or prescribed
pharmacologic agents
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
Causes of Hyperkalemia
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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
Pseudohyperkalemia
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Prolonged use of tourniquet
Hemolysis (in vitro)
Delay in processing of blood
Severe leukocytosis
Severe thrombocytosis
Symptoms
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Nonspecific, related to muscular or
cardiac function.
Weakness and fatigue.
Occasionally, frank muscle paralysis or
shortness of breath.
May be palpitations or chest pain.
Hyperkalemia- Signs
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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.
ECG in Hyperkalemia
Normal Cardiac Tissue
Excitability +20
0
- 60
Threshold Potential
Excitability Potential
- 90
Resting Membrane
Potential
Increased Excitability
- 60
- 70
- 90
Threshold Potential
Excitability Potential
Resting Membrane
Potential
Persistent Depolarization in
Hyperkalemia
Threshold Potential
Excitability Potential
Resting Membrane
Potential
Work-up
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Urinary potassium, serum sodium, urine
osmolality
Transtubular potassium gradient =
(urine K x serum osmolarity)/(serum K x urine
osmolarity)
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TTKG of < 3 - lack of aldosterone effect on
collecting tubules – decreased excretion
TTKG greater > 7 - an aldosterone effect, normal excretion
24 hour urinary potassium.
Transtubular Potassium Gradient
(TTKG)
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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
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Aldosterone deficiency/resistance
or
Nonrenal causes.
Clinical correlation and potassium intake should be
assessed.
TTKG = (Ku/Ks) × (Sosm/Uosm)
Transtubular Potassium Gradient
Evaluation of Hyperkalemisa
Are ECG changes
are present
Emergently treat K+
Are K sparing
medications are being
administered
Treatment
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Evaluation for potential toxicities
Decreasing potassium intake
Increasing potassium uptake into cells
Increasing potassium excretion
Determining the cause to prevent future
episodes
Treatment of Hyperkalemia
Drug
Onset
Duration
1-3 min
30 min
InsulinIV
Glucose
Beta adrenergic 20 mg in 4 ml
nebulize in 10 m
20-30
minutes
15-30 min
2 hours
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
Immediate
Until dialysis
completed
Calcium
Hemodialysis
Route of
Admin.
IV 10 cc 10%
30 min- 3
hrs
Normal Cardiac Tissue
Excitability – Effect of Calcium
High Serum Calcium
- 60
Threshold Potential
Excitability Potential
- 90
Resting Membrane
Potential
Increased Excitability
- 60
- 30
- 90
Threshold Potential
Excitability Potential
Resting Membrane
Potential
Increased Excitability- Effect
of Calcium
-40
30
30
-60
10
- 70
-90
Threshold Potential
Excitability Potential
Resting Membrane
Potential
Hypokalemia
Hypokalemia
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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.
Symptoms
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Palpitations
Skeletal muscle weakness or cramping
Paralysis, paresthesias
Constipation
Nausea or vomiting
Abdominal cramping
Polyuria, nocturia, or polydipsia
Psychosis, delirium, or hallucinations
Depression
Signs
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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
ECG in Hypokalemia
Hyperpolarization in Hypokalemia
Threshold Potential
Excitability Potential
Resting Membrane
Potential
-120
Causes of Hypokalemia
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Medications:
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Thiazide and loop diuretics,
aminoglycosides, amphotericin B, β2agonists, and adrenal steroids, Chronic
laxative abuse
GI
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Vomiting, diarrhea, NG suction
Causes of Hypokalemia
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Renal:
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Renal tubular acidosis, (type 1 , 2)
Magnesium deficiency
Primary hyperaldosteronism
Cushing Syndrome
Salt-losing nephropathies
Bartter and Gitelman syndromes
Therapeutic alkalinization of the urine
Causes of Hypokalemia
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Treatment of megaloblastic anemia with
vitamin B12 and folate
Miscellaneous toxic conditions:
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Barium intoxication; chloroquine toxicity;
glue sniffing due to hippurate
accumulation,
Tocolytic therapy in pregnant women to
treat premature labor
Amphotericin B therapy
Causes of Hypokalemia
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Genetics disorders
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Familial (hypokalemic) periodic paralysis
Congenital adrenogenital syndromes
Liddle syndrome
Bartter and Gitelman syndromes
Familial interstitial nephritis
Glucocorticoid-remediable aldosteronism
Diagnostic Workup of Hypokalemia
Treatment of Hypokalemia
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Potassium replacement
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How much?
What route?
How fast ?
What salt ?
Treatment
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Asymptomatic mild hypokalemia
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Oral replacement
Moderate to severe (no emergency)
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Intravenous
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40 meq/l
160 meq per day
Hypokalemia with cardiac dysarrythmias
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20 meq/100 cc /hr under ECG monitoring
Treatment of Hypokalemia
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Metabolic alkalosis
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Metabolic acidosis
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Potassium chloride
Potassium citrate/acetate
Diabetic ketoacidosis (+hyphosphatemia)
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Potassium phophate
Hyperpolarization in Hypokalemia
Threshold Potential
Excitability Potential
Resting Membrane
Potential
-120
Hyperpolarization in Hypokalemia
Ca++ administration
Threshold Potential
Excitability Potential
Resting Membrane
Potential
-120
Low Serum Potassium & Calcium
S. Potassium correction
in hypocalcemia
Hypocalcemia
Threshold Potential
-120
Excitability Potential
Resting Membrane
Potential
Low Serum Potassium & Calcium
S. Calcium correction
in hypokalemia
Hypocalcemia
Threshold Potential
-120
Excitability Potential
Resting Membrane
Potential