Hyperkalemia electrocardiogram: Difference between revisions
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==Electrocardiogram== | ==Electrocardiogram== | ||
* Elevated [[potassium]] level increases the activity of some [[potassium channels]] and speeds membrane [[repolarization]]. Hyperkalemia causes an overall membrane repolarization that inactivates many sodium channels. Changes in extracellular potassium disrupts the normal electrophysiology of the [[heart]] through the following mechanisms: | * Elevated [[potassium]] level increases the activity of some [[potassium channels]] and speeds membrane [[repolarization]]. Hyperkalemia causes an overall membrane repolarization that inactivates many sodium channels. Changes in extracellular potassium disrupts the normal electrophysiology of the [[heart]] through the following mechanisms: | ||
** Prolongation of membrane [[depolarization]] | ** Prolongation of membrane [[depolarization]] that will cause peaked T waves | ||
** Slower myocardial conduction | ** Slower myocardial conduction that will prolong QRS interval and bradycardia | ||
** Shortening of the [[repolarization]] time<ref name="pmid16572868">{{cite journal| author=Parham WA, Mehdirad AA, Biermann KM, Fredman CS| title=Hyperkalemia revisited. | journal=Tex Heart Inst J | year= 2006 | volume= 33 | issue= 1 | pages= 40-7 | pmid=16572868 | doi= | pmc=PMC1413606 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16572868 }} </ref> | ** Shortening of the [[repolarization]] time resulting in absence of p waves <ref name="pmid16572868">{{cite journal| author=Parham WA, Mehdirad AA, Biermann KM, Fredman CS| title=Hyperkalemia revisited. | journal=Tex Heart Inst J | year= 2006 | volume= 33 | issue= 1 | pages= 40-7 | pmid=16572868 | doi= | pmc=PMC1413606 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16572868 }} </ref> | ||
===EKG Changes in Chronological Order=== | ===EKG Changes in Chronological Order=== | ||
| Line 22: | Line 22: | ||
* [[Peaked T waves]] are the earliest sign of hyperkalemia. | * [[Peaked T waves]] are the earliest sign of hyperkalemia. | ||
* They occur when K > 5.5 meq/L. | * They occur when K > 5.5 meq/L. | ||
* The differential diagnosis of this [[EKG]] change are [[bradycardia]] or [[stroke]] | * The differential diagnosis of this [[EKG]] change are [[bradycardia]] or [[stroke]] | ||
====Interventricular Conduction Delay==== | ====Interventricular Conduction Delay==== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]
Overview
Extreme degrees of hyperkalemia are considered a medical emergency due to the risk of potentially fatal arrhythmias. The EKG is an important tool in evaluating a patient who has hyperkalemia as well as in diagnosing hyperkalemia. However, EKG changes do not always correlate with the degree of hyperkalemia. Some of the EKG changes that can be seen associated with hyperkalemia include peaked T waves, PR interval prolongation, QRS complex widening, absence of P waves, sine wave pattern and sinus arrest.
Electrocardiogram
- Elevated potassium level increases the activity of some potassium channels and speeds membrane repolarization. Hyperkalemia causes an overall membrane repolarization that inactivates many sodium channels. Changes in extracellular potassium disrupts the normal electrophysiology of the heart through the following mechanisms:
- Prolongation of membrane depolarization that will cause peaked T waves
- Slower myocardial conduction that will prolong QRS interval and bradycardia
- Shortening of the repolarization time resulting in absence of p waves [1]
EKG Changes in Chronological Order
Peaked T Waves
- Peaked T waves are the earliest sign of hyperkalemia.
- They occur when K > 5.5 meq/L.
- The differential diagnosis of this EKG change are bradycardia or stroke
Interventricular Conduction Delay
- It is observed when K > 6.5 meq/L
- Interventricular conduction delay is reflected by QRS widening that are inconsistent with LBBB or RBBB.
- Another manifestation of interventricular conduction delay is PR segment prolongation.
- There is a modest correlation of the QRS duration with serum potassium level.
- As the serum potassium level rises, the QRS complexes may resemble sine waves.
Loss of P Waves
- Decreased P wave amplitude occurs when K is > 7.0 meq/L with subsequent absence of P waves when K is > 8.8 meq/L.
- The SA node, being less susceptible to hyperkalemia than the atrial cells, continues to fire and stimulate the ventricles without any atrial activity. This is called sinoventricular conduction. The absence of atrial activity is depicted by the absence of P waves, which should not confused with sinus arrest.
- The absence of P wave along with wide QRS can be confused with ventricular tachycardia.[1][2]
Sinus Arrest with Accelerated Junctional Rhythm
- It is observed when K>10meq/L.
- Moderate or severe hyperkalemia can cause sinus arrest[3] leading to an accelerated junctional rhythm. This condition should be differentiated from sinoventricular conduction during which the SA node is still firing electrical impulses.[4]
- Accelerated junctional rhythm occurs when junctional pacemaker begin firing electrical impulses as a result of complete disruption of the sinoatrial conduction.[1][2]
Sine Wave Pattern
- As potassium level continues to rise, the QRS interval will continue to widen until it fuses with the T wave.
- The result of the fusion of the QRS interval and T wave is reflected by a sine wave pattern.[1][2]
Ventricular Fibrillation
- Hyperkalemia can lead to ventricular fibrillation, and subsequent asystole, if the cardiac myocardium was not stabilized.[1][2]
EKG Examples
Shown below is an EKG demonstrating peaked T waves, loss of P wave and wide QRS complex depicting hyperkalemia.
Shown below is an EKG demonstrating wide QRS complexes, tall peaked T waves an fusion of the QRS complex and the T wave.
Shown below is an EKG demonstrating tall, narrow and peaked T waves.
Shown below is an EKG demonstrating tall, narrow and peaked T waves.
Shown below is an EKG demonstrating sine wave pattern depicting severe hyperkalemia.
Shown below are a series of EKG images demonstrating interventricular conduction defect before, during and after treatment of hyperkalemia.
- Before treatment
- During treatment
- After treatment
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Parham WA, Mehdirad AA, Biermann KM, Fredman CS (2006). "Hyperkalemia revisited". Tex Heart Inst J. 33 (1): 40–7. PMC 1413606. PMID 16572868.
- ↑ 2.0 2.1 2.2 2.3 Petrov DB (2012). "Images in clinical medicine. An electrocardiographic sine wave in hyperkalemia". N Engl J Med. 366 (19): 1824. doi:10.1056/NEJMicm1113009. PMID 22571204.
- ↑ Bonvini RF, Hendiri T, Anwar A (2006). "Sinus arrest and moderate hyperkalemia". Annales De Cardiologie Et D'angéiologie. 55 (3): 161–3. PMID 16792034. Unknown parameter
|month=ignored (help) - ↑ Mehta NJ, Chhabra VK, Khan IA (2001). "Sinus arrest or sinoventricular conduction in mild hyperkalemia". J Emerg Med. 20 (2): 163–4. PMID 11207412.