Effects of Hypo/Hyperkalemia on ECG

The role of Ca-gluconate in reversing hyperkalemia

effects

&

Ayoub Moh. Elqahwaji

Saher Mah. Abed

Cardiac conduction system . Cardiac cell action potential . Normal ECG . Hypo/Hyperkalemia & their effect on ECG

. Using Ca-gluconate to reverse

hyperkalemia effect .Treatment of hyperkalemia . Conclusion .

References .

Outline

Cardiac conduction systemSinoatrial node

AV node

A-V bundle

Bundle Branches

Purkinje fibers

Animation of normal cardiac conduction system

Ventricular action potential

Na+

Ca2+Extracellular K+

3Na+

2K+

K+

K+

Voltage gated Na channel Voltage gated

K channel

L-Ca channe

l

Normal ECG

Definition . Study of waveform . We can identify by ECG ….

Modern ECG Instrument

ECG or EKG : is a representation of the electrical events of

the cardiac cycle .

The study of waveform can lead to greater insight into a patient’s cardiac patho-physiology.

Def.

The “ PQRST ”

• QRS – Ventriculardepolarization

• P-wave – Atrialdepolarization

• T-wave – Ventricular repolarization

The PR IntervalAtrial depolarization

+delay in AV junction

The QT IntervalDepolarization & repolarization of

ventricleThe ST segment

Period when ventricular depolarized

We can identify by ECG ….

Arrhythmias . Myocardial ischemia and infarction . Pericarditis . Chamber hypertrophy . Electrolyte disturbances

( K+,Na+,Ca2+ ..etc ) Drug toxicity (Ex. Digoxin )

Hypo/Hyperkalemia &

their effects on ECG

In many metabolic processes e.g. ( Regulation of protein and glycogen synthesis ) .

Maintain osmotic and acid-base balance between intra and extra cell .

Maintain resting membrane potential of cellular membrane .

Potassium Function

What is kalemia ?

• The presence of potassium in the blood .

• Normal range : 3.5 – 5 mEq/L

Hypokalemia

Hypokalemia serum potassium level < 3.5 mEq/L

Severe hypokalemiaserum potassium < 2.5 mEq/L

Causes of hypokalemia1- Transcellular movement into cells

a. Alkalosis ( increase pH )2- Reduce intake K+

3- loss from GITa. Laxativesb. Chronic diarrheac. Persistent vomiting

4- Loss in urine a. Diureticsb. Cushing syn.c. Conn’s syn.

Clinical featuresA small drop in potassium level often does not

cause symptoms, which may be mild, and may include : Muscle weakness Hypotonia Constipation Depression & Confusion Increase toxicity of digoxin

ECG changes :1. Slightly prolonged PR interval 2. Flattened T wave3. Presence of U waves (in most of

leads)4. ST depression ( in severe cases )

U-Wave

T-Wave

ST-segment

Hyperkalemia Hyperkalemia

serum potassium level < 5 mEq/L Severe hyperkalemia

serum potassium < 7 mEq/LPseudo-Hyperkalemia

Occur due to destruction of RBCs in delayed investigated blood sample .

1- Increase intake K+

all meats, some types of fish (such as salmon, cod ), and many fruits, vegetables, and legumes..

2-Impaired excretion of K+

a. Acute & chronic renal failureb. Addison diseasec. ACEI + K sparing diuretics

3- Transcellular movement out cellsa. Hemolysisb. DKA

Causes of hyperkalemia

Clinical features Abnormal heart rhythms

(arrhythmias) .

Hyperkalemia may lead cardiac arrest

if the level exceed 7 mEq/L

ECG changes :1) Tall peaked T wave with narrow base .2) QT shortened .

3) Prolong PR interval ( bundle branch block )

4) Widening QRS complex ( more than 3 small boxes )

5)Sometimes loss of P wave

Using of Ca-gluconate to reverse hyperkalemia

effect .

Why Calcium ?? Calcium antagonizes the effects of hyperkalemia at

the cellular level and actually increases the threshold potential (i.e.- from -75 mV to -65 mV)

Calcium allows for an action potential to occur at a more physiologic level and actually re-establishes the normal gradient .

Calcium salts• Calcium chloride ??!!!! • Calcium gluconate

Why Ca-gluconate use ?! Calcium chloride Has greater bioavailability & three times more potent than the

other formulation, (calcium gluconate) The onset of action with both agents CaCl2 & Ca-

gluconate is less than three minutesHowevercalcium chloride is also more irritating & if given too

rapidly ,It can lead to infiltration and possible loss of

the intravenous site.

Calcium Salts :Reduces the risk of ventricular fibrillation caused by

hyperkalemia . Insulin administered with glucose :

50g glucose with 20 unit insulin ( lower serum K level within 30 min.) increasing shift of K into cell .

Beta 2-adrenergic agonists : Promote cellular reuptake of potassium .

Diuretics : ( loop , thiazide )Cause potassium loss through the kidney .

Drugs used in the treatment of hyperkalemia

Binding exchange resins : ( polystyrene cation )

Promote the remove of potassium form the body . Alkalinizing agents : ( bicarbonate )

Increases the pH, which results in a temporary potassium shift from the extracellular to the intracellular environment; these agents enhance the effectiveness of insulin in patients with acidemia .

Cont..

Potassium is very important mineral for the

proper function of all cells, tissues in the human body .

crucial to heart function and plays a key role in skeletal and smooth muscle contraction.

Conclusion

The hyperkalemia is common, silent, and potentially lethal clinical condition, it is difficult to avoid patients with hyperkalemia .◦ This electrolyte imbalance is seen in both

inpatient and outpatient settings in alarming numbers.

However, is the ability to appropriately treat hyperkalemia and avoid fatal arrhythmias.

Potassium

https://med.uth.edu/internalmedicine/files/2013/10/11-Hyperkalemia-A-Potential-Silent-Killer.pdf

http://www.mayoclinic.org/symptoms/hyperkalemia/basics/causes/sym-20050776

http://www.livestrong.com/article/458069-calcium-gluconate-in-hyperkalemia/

http://lifeinthefastlane.com/ecg-library/basics/hypokalaemia/

References

http://lifeinthefastlane.com/hyperkalemia/ http://umm.edu/health/medical/ency/articls/

high-potassium-levels http://emedicine.medscape.com/article/766

479-overview http://lifeinthefastlane.com/ccc/calcium-digo

xin-toxicity-and-stone-heart-theory/

FinishSupervised by :Dr-Hala Zakaria

Alagha