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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