Potassium disturbances

Hyperkalemia
JOHN PACY
14/6/17
 BASIC

 Total body K+: 50mEq/Kg:

- K+ in Intracellular fluid: 98%.
- K+ in Extracellular fluid: 2%. Plasma accounts for 20% of extracellular fluid  K+ in
plasma = 0,4% total body K+.

Ex: a 50 kg person: 2500mEq total body K+ K+ plasma: 10mEq

 This emphasizes the limited size of the K+ plasma that is available for evaluating total body
potassium
 BASIC

 K+ is lost in stool (5-10 mEq/d), swear(0-10 mEq/d), and the major lost is in urine (40-
120 mEq/d), depending on K+ intake
 K+ is:
- Filtered at the glomerulus
- Passively absorbed in the proximal tubules
- Secreted in the distal tubules and collecting ducts
- Potassium excretion in urine is controlled by plasma K+ and aldosteron
 HYPERKALEMIA

 > 5,5 mEq/l

 Life-threating condition!!!
 Pseudohyperkalemia:
- Potassium release from traumatic hemolysis during venipuncture (20%)
- K+ release from muscle during fist clenching
- Severe leukocytosis (>50000/mm3)
- Severe thrombocytosis (>1million/mm3)
 ETIOLOGY

 Excessive intake K+: foods, drinks, IV fluid.

 Transcellular shift
 Impaired renal excretion
 ETIOLOGY

Transcellular shift
 Acidosis: BUT
- Organic acidosis ( lactic acidosis and ketoacidosis) is not associated with
hyperkalemia (MARINO THE ICU BOOK 4th)
- Respiratory acidosis has an inconsistent relationship with hyperkalemia
 Drugs: digitalis( only when acute toxicity, not chronic), beta blockers,……….
 Blood transfusions (massive transfusion, at least 7 units of RBC!!!)
 Rhabdomyolysis
 Tumor lysis syndrome: within 7 days after the initial chemical therapy

Rhabdomyolysis (tiêu cơ vân)

 ETIOLOGY

Impaired renal excretion

 Decreased GFR:
- Oliguric or anuric AKI
- End-stage CKD
 Normal GFR but decreased renal excretion of K+
- Cirrhosis, CHF: Decreased EABV (K+ excretion limited by distal Na delivery & urine flow )
- NSAIDS, HIV, diabetic nephropathy: Decreased renin
- ACEI, ARB, heparin, primary adrenal insufficient: Decreased aldosterol
- K+-sparing diuretic, bactrim, SLE, diabetes: Decreased response to aldosterol
EABV: effective arterial blood volume
SLE: systemic lupus ethrymatous
Clinical manifestations

Twitch: co giật
Paresthesia: mất ngủ
Irritability: kích thích, kích
động
ECG abnormalities
(from mild to severe)
 T Waves in hyperkalemia

 very tall, symmetric, steep, peaked T waves with narrow base ("Eiffel

Tower" effect) in several precordial leads
 T Waves in others

 Normal (repolarization) variant: suspect when T wave peaking has a more rounded summit with assymetric
ascent and descent and a broader base-especially if the patient is totally healthy and without any apparent reason
to have hyperkalemia

 Ischemia: the less common cause of T wave peaking than hyperkalemia and normal repolarization variants – it
should be appreciated that MI ( in the area of the left ventricular posterior wall) may sometimes present with the
ECG findings of tall peaked T waves in the anterior leads
 Beware of ischemia as a possible cause of T wave peaking in leads V1,2,3 when a patient with known (or
suspected) coronary artery disease presents with chest pain – especially if there is other evidence on the tracing to
suggest ischemia or infarction ( Ex: inferior T wave inversion or ST depression)
SINE WAVE!!!
 ECG ABNORMALITIES

 ECG is not sensitive.

 VF, asystole, cardiac arrest can be the first manifestation.
 Otherwise, a rare case reported that a patient who has 14 mEq/l serum potassium BUT ECG is
totally normal.

Don’t depends totally on ECG to diagnose

 TREATMENTS

 3 goals:
- Antagonism of the cardiac effects of hyperkalemia
- Transcellular shift of K+ into cells
- Removal of excess K+ from the body
 MEMBRANE ANTAGONISM

- Mechanism: Calcium increases the electrical charge difference across myocardial cell membranes, oppose the
depolarization produced by hyperkalemia  Stabilizes cell membrane
- Calcium gluconate 10% 10ml = 1 ampule contains 1g elemental calcium
 Use: 1 ampule IV over 3 min, repeat after 5 min if necessary
 Caution
 With the patients on digitalis, hypercalcemia can aggravates digitalis toxicity. Calcium gluconate can be added in
100 ml of NaCl 0,9% IV over 20-30 min.
 If hyperkalemia is a manifestation of digitalis toxicity, calcium is contraindicated the administration of
digoxin-specific antibody fragments is the preferred therapy
 Hyperkalemia + shock, cardiac arrest: CaCl2 is preferred.
 Should be the initial treatment, especially if ECG abnormalities because it helps prevent cardiac complications,
early onset in < 3 min. it should be combined with other therapies.
 Transcellular shift

Insulin + dextrose
Regular insulin: 10 UI IV bolus 10% dextrose at 50 – 75 ml/h
50% dextrose: 50 ml IV bolus Monitoring blood glucose every 4-6h

Regular insulin: 10 – 20 UI
IV in 60 min
10% dextrose: 500 ml

If the patient has been already hyperglycemic ≥250 mg/dL (13.9 mmol/L) ,only insulin and no
dextrose.
 Transcellular shift

SALBUTAMOL
 Use: Salbutamol 0,5 mg IV ( 1 ampule salbutamol 0,5mg/1 ml)
OR
10 – 20 mg ( 4 ampule ventolin 2,5 mg in 4 ml saline) nebulized over 10 min
 Caution: Salbutamol dose is needed to significantly drop K+ is at 4 – 8 times the bronchodilation dose
 unwanted side effects  not advised
 Side effects: Mild Tachycardia, angina  should probably be avoided in patients with active coronary
disease.
 Transcellular shift

BICARBONATE
 Short-term have no effect on serum K+
 Bicarbonate can form complexes with calcium
 It should be avoided unless there is acidemia. In that case, we recommended isotonic
bicarbonate 1,4%
 Potassium removal

 Via the bowel: cation-exchange resin (Kayexalate)

 Via the blood stream: hemodialysis is the most effect method
 Via the urinary tract: Furosemide ( in patients without severe renal impairment) 40 mg
every 12 hours.
 Mainstay therapy

 Calcium gluconate 10% 10ml : 1 ampule IV over 3 min, repeat after 5 min if necessary
 10 – 20 UI regular insulin AND 10% dextrose 500 ml: IV in 60 minutes
 Furosemide ( in patients without severe renal impairment) 40 mg every 12 hours.
 Some conclusions

 Serum Potassium is just only the tip of the iceberg. And the iceberg here is total body
potassium !!!. Remember a number 0,4%
 Hypokalemia is often well tolerated BUT hyperkalemia is life-threatening condition
 Remember to rule out pseudohyperkalemia before management of hyperkalemia
 ECG is not sensitive. Don’t depends totally on ECG to diagnose.
 Before administering calcium, you must check if the patient is using digitalis or not,
check for the manifestations of digitalis toxicity.
 You need to make sure that 3 goals is done concomitantly: Calcium gluconate , insulin +
dextrose and Furosemide.
 Some questions for you!!

 How much does the serum potassium accounts for of total body potassium?
 List some causes that induce hyperkalemia?
 What is 3 goals in management of severe hyperkalemia?
 Can you list some ECG abnormalities in hyperkalemia (from mild to severe)?
 Give me some manifestations of hyperkalemia?
 How do we use calcium in the Patients who are using digitalis (heart failure maybe)?
 How do we use calcium in management of hyperkalemia that is a manifestation of digitalis toxicity?
 How can we push K+ into cells to decrease seum K+?
 How do we use insulin in management of hyperkalemia? In case of patients with hyperglycemia
 How do we use loop diuretics in management of hyperkalemia?