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<ref name="pmid8435272">{{cite journal| author=Freeman SJ, Fale AD| title=Muscular paralysis and ventilatory failure caused by hyperkalaemia. | journal=Br J Anaesth | year= 1993 | volume= 70 | issue= 2 | pages= 226-7 | pmid=8435272 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8435272 }} </ref><ref name="pmid3717152">{{cite journal| author=Szerlip HM, Weiss J, Singer I| title=Profound hyperkalemia without electrocardiographic manifestations. | journal=Am J Kidney Dis | year= 1986 | volume= 7 | issue= 6 | pages= 461-5 | pmid=3717152 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3717152 }} </ref> | * 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:<ref name="pmid8435272">{{cite journal| author=Freeman SJ, Fale AD| title=Muscular paralysis and ventilatory failure caused by hyperkalaemia. | journal=Br J Anaesth | year= 1993 | volume= 70 | issue= 2 | pages= 226-7 | pmid=8435272 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8435272 }} </ref><ref name="pmid3717152">{{cite journal| author=Szerlip HM, Weiss J, Singer I| title=Profound hyperkalemia without electrocardiographic manifestations. | journal=Am J Kidney Dis | year= 1986 | volume= 7 | issue= 6 | pages= 461-5 | pmid=3717152 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3717152 }} </ref> | ||
** Prolongation of membrane [[depolarization]] that will cause peaked T waves | ** Prolongation of membrane [[depolarization]] that will cause peaked T waves | ||
** Slower myocardial conduction that will prolong QRS interval and bradycardia | ** Slower myocardial conduction that will prolong QRS interval and bradycardia | ||
Latest revision as of 19:40, 30 July 2018
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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:[1][2]
- 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
EKG Changes in Chronological Order
Peaked T Waves
- Peaked T waves are the earliest sign of hyperkalemia[3].
- 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, continues to fire despite hyperkalemia and this results in atriventricular delay and responsible for absent p waves.le tlemia thanhe atr nduction. Thabsence onfused with rest
- The absence of P wave along with wide QRS can be confused with ventricular tachycardia.[4][5]
Sinus Arrest with Accelerated Junctional Rhythm
- It is observed when K>10meq/L.
- Moderate or severe hyperkalemia can cause sinus arrest[6] causing accelerated junctional rhythm.dinn accelrated junctional rhythmconditithe S ndecal imp
- Accelerated junctional rhythm occurs when junctional pacemaker begin firing electrical impulses as a result of complete disruption of the sinoatrial conduction.[4][5]
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.[4][5]
Ventricular Fibrillation
- Hyperkalemia can lead to ventricular fibrillation, and subsequent asystole, if the cardiac myocardium was not stabilized.[4][5]
EKG Examples
Shown below is an EKG demonstrating peaked T waves, loss of P wave and wide QRS complex depicting hyperkalemia [7].
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.[8]
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
- ↑ Freeman SJ, Fale AD (1993). "Muscular paralysis and ventilatory failure caused by hyperkalaemia". Br J Anaesth. 70 (2): 226–7. PMID 8435272.
- ↑ Szerlip HM, Weiss J, Singer I (1986). "Profound hyperkalemia without electrocardiographic manifestations". Am J Kidney Dis. 7 (6): 461–5. PMID 3717152.
- ↑ Montague BT, Ouellette JR, Buller GK (2008). "Retrospective review of the frequency of ECG changes in hyperkalemia". Clin J Am Soc Nephrol. 3 (2): 324–30. doi:10.2215/CJN.04611007. PMC 2390954. PMID 18235147.
- ↑ 4.0 4.1 4.2 4.3 Parham WA, Mehdirad AA, Biermann KM, Fredman CS (2006). "Hyperkalemia revisited". Tex Heart Inst J. 33 (1): 40–7. PMC 1413606. PMID 16572868.
- ↑ 5.0 5.1 5.2 5.3 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) - ↑ Bashour T, Hsu I, Gorfinkel HJ, Wickramesekaran R, Rios JC (1975). "Atrioventricular and intraventricular conduction in hyperkalemia". Am J Cardiol. 35 (2): 199–203. PMID 1119378.
- ↑ Patton KK, Ellinor PT, Ezekowitz M, Kowey P, Lubitz SA, Perez M; et al. (2016). "Electrocardiographic Early Repolarization: A Scientific Statement From the American Heart Association". Circulation. 133 (15): 1520–9. doi:10.1161/CIR.0000000000000388. PMID 27067089.