slide bệnh Hyperkalemia và cách điều trị

Peaked T-waves 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 t

THÁI BÌNH DƯƠNG – hump Updated on 20/9/18

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

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

 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

 > 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)

- 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)

 Normal GFR but decreased renal excretion of K+

- Cirrhosis, CHF: Decreased EABV.

- 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

Clinical manifestations

Twitch: co giật Paresthesia: mất ngủ Irritability: kích thích, kích động

ECG abnormalities

(from mild to severe)

Peaked T-waves

 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

 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)

Peaked T Wave

QRS prolongation

Simple RBBB?

QRS ~200 ms

QRS prolongation

 RBBB by definition has a long QRS (at least 120 ms).  But very few are greater than 190 ms. 

 In one study with RBBB and Acute MI, only 2% of patients with pre-existing RBBB had a QRS duration greater than 200 ms. 

 LBBB: In one study, 13% had a QRS duration greater than 170 ms, and only 1% had a duration greater than 190 ms. 

 The point of this is that if you see BBB with a very long QRS, you must suspect hyperkalemia.  Then of course the peaked T-waves should tip you off.   Unless a

patient has severe hypercalcemia (this should be evident by a short QT on the ECG as seen at the bottom of this post), or severe hyperphosphatemia (which is very unusual), treatment with calcium is harmless if you read an ECG falsely positive for hyperkalemia

 So don't wait for the laboratory K or you might be resuscitating a cardiac arrest

Link gốc: http://hqmeded-ecg.blogspot.com/2018/04/is-this-just-right-bundle-branch-block.html

SINE WAVE!!!

ECG ABNORMALITIES

BRINGS TO HOME:

 ECG abnormalities is defined as emergency hyperkalemia

 ECG is not sensitive.

- The appearance of these various abnormalities does not correlate well with specific serum potassium levels

 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

 Antagonism of the cardiac effects of hyperkalemia

 Transcellular shift of K+ into cells

 Removal of excess K+ from the body

1 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

 Calcium chloride contains three times the concentration of elemental calcium compared with calcium gluconate (13.6

versus 4.6 meq in 10 mL of a 10 percent solution)

 However, calcium gluconate is generally preferred because calcium chloride may cause local irritation at the injection site

 Use: 1 ampule IV over 3 min, repeat after 5 min if necessary

1 MEMBRANE ANTAGONISM

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.

 Hyperkalemia + shock, cardiac arrest: CaCl2 is preferred

BRINGS TO HOME:

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.

2 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

10% dextrose: 500 ml

If the patient has been already hyperglycemic ( the serum glucose is ≥250 mg/dL = 13.9 mmol/L) , only insulin and no dextrose IV in 60 min

2 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

2 Transcellular shift

Bicarbonate

 There have been no studies that actually demonstrate an immediate or significant benefit (acute change in the serum potassium level) with

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%

BRINGS TO HOME:

Administer bicarbonate to the patient with severe hyperkalemia who is

not responding to traditional therapies, such as insulin and glucose and

beta-2 agonists

https://docs.google.com/document/d/1VJaWkMFTt2JIIPVABqeV0y8R625vwCKledcQ9p-ASpE/edit

3 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

 Sodium polystyrene (Kayexalate) is a cation exchange resin administered

orally or rectally that exchanges sodium for K+ and eliminates K+ via thegastrointestinal tract

 The evidence advocating the use of Kayexalate to treat hyperkalemia originates from a single study published in the 1960s that demonstrated a reduction in serum K+ in patients with acute and chronic renal failure

 Recent literature, however, recommends against routine

administration of Kayexalate in the hyperkalemic patient due to anunpredictable reduction of serum K+ and an increased risk of colonicnecrosis

http://rebelem.com/kayexalate-useful-treatment-hyperkalemia-emergency-department/

So in almost cases, you just remember…

 Calcium gluconate 10% 10ml : 1 ampule IV over 3 min, repeat after 5 min if necessary (first treatment!!)

 10 – 20 UI regular insulin AND 10% dextrose 500 ml: IV in 60 minutes, check blood glucose 4 – 6 h

 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 management of hyperkalemia?

 How do we use calcium in the Patients who are using digitalis (but not digoxin toxicity)?

 How can we push K+ into cells to decrease serum 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?

SOME MORE INFORMATION FOR YOU

 A 3-PRONGED APPROACH TO THE TREATMENT OF HYPERKALEMIA

https://docs.google.com/document/d/1bXICT0WxH6yJiqN-ASdWOr1cAU2-MfwP1bAUZQoXEmI/edit