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PCI in Hyperkalemia
Case Report
Primary PCI in a Patient of Inferior ST-segment Elevation Myocardial
Infarction in the Time of Severe Hyperkalemia: A Case Report.
Deepak Natarajan, Chiranjib Deb, Vijeta Maheshwari,Mafooza Rashid,
Betsheba Dinaker, Nirmalya Mukherjee.
Department of Interventional Cardiology, Moolchand MedCity, New Delhi. Abstract
This case report describes the management of a middle-aged hypertensive male patient who presented with acute
inferior ST-segment elevation myocardial infarction accompanied with severe hyperkalemia. His coronary
angiography revealed a thread like right coronary artery along its entire course and normal left coronary artery
system with patent coronary stents in the left anterior descending and left circumflex arteries. Subsequent to
correction of hyperkalemia with intravenous calcium gluconate and regular insulin the patient underwent primary
percutaneous coronary intervention (PPCI)of the right coronary artery with the deployment of a sirolimus eluting
stent. The patient received overnight an infusion of tirofiban at half the usual dose between the diagnostic coronary
angiogram and PPCI.
Key Words : Hyperkalemia, ST-segment elevation myocardial infarction, calcium gluconate, primary percutaneous
coronary intervention, regular insulin.
INTRODUCTION
Severe hyperkalemia defined as serum potassium level greaterthan 6.5 mEq/L albeit not uncommon is a life threatening conditionthat if not treated immediately can be catastrophic. We describethe management of a middle aged male patient who presentedwith acute inferior ST-segment elevation myocardial infarctionaccompanied by severe hyperkalemia.
CASE REPORT
A 63 year old hypertensive male was admitted for severe Figure 1: Peaking of T waves from V2 to V5 and absence of P waves.
intermittent retrosternal chest pain for the previous 10 hours. Hehad underwent percutaneous coronary intervention (PCI) 4 A diagnosis of acute inferior ST elevation myocardial infarction years ago when 2 bare metal stents had been deployed in mid left (STEMI) with right ventricle infarction was made. Two litres of anterior descending (LAD) and left circumflex (LCX) arteries. He normal saline were rapidly infused intravenously and after an had been on 75 mgm of aspirin, 5 mgm of ramipril, sustained informed consent the patient was shifted to the catheterization release 25 mgm metoprolol and 10 mgm of atorvostatin. He had laboratory for primary PCI. His coronary angiogram done from however resumed smoking more than 15 cigarettes a day. He had the right femoral route showed patent stents in the LAD and LCX on this occasion consumed more than a couple of diclofenac arteries with no significant lesions in the left coronary system tablets at his chest pain onset. On admission to the ER he ( figure 2). The right coronary artery ( RCA) however was thread appeared disoriented and agitated, had a heart rate of 35 to 40 like in appearance . There was no change in the caliber of the RCA per minute, systolic blood pressure of 70 mm Hg and had 86% following 2 (50 mcg) boluses of intracoronary nitroglycerin ( oxygen saturation breathing room air. There were basal crepitations while his respiration was 28 to 30 per minute. His 12 His laboratory investigations showed hemoglobin 12 gm %, total lead ECG revealed a sinus rate of 38 per minute, significant ST leukocytes 11,000 per cc, and platelets of 160,000 per cc. He had segment elevation in L2,L3 and AVF with ST segment depression random sugar of 110 mgm % , blood urea 60 mgm %, serum in the precordial leads. There was also suggestion of peaking of creatinine 2.2 mgm %, serum potassium of 7.8 mEq/L, sodium 142 T waves from V2 to V5 and absence of P waves ( figure 1). The mEq/L and severe metabolic acidosos ( pH 7.20, CO2 46 mmHg, 2D echocardiogram demonstrated a normal sized left venticle O2 82 mmHg, HCO3 -18 mEq/L, lactic acid 2.50 mEq/L). The CPK with akinesia of the inferior wall and an ejection fraction of 50%.
was 1715 units and CPK-MB was 102 units.
Correspondence: Dr. Deepak Natarajan, Department of Interventional Cardiology, Moolchand MedCity, New Delhi.
E-mail: deepaknatarajan19@gmail.com
Natarajan et al.
Figure 2: Patent stents in the
Figure 3: The right coronary
Figures 5-6: Brisk antegrade TIMI 3 flow was achieved with no residual
The hyperkalemia was immediately treated with intravenous 10ml of 10% calcium gluconate, 10 units of regular insulin in 100 mlof 50% dextrose intravenously and 50 mmol of intravenoussodium bicarbonate. This regimen was repeated twice more at 6hour intervals.
In view of the severe hypekalemia it was decided to correct theelectrolyte imbalance first and then proceed to PCI. The patientwas given a bolus of 15 mcg/Kg of tirofiban followed by aninfusion of (0.075 mcg/Kg/ minute) for 10 hours.
The next morning subsequent to positioning a temporary pacinglead in the right ventricle apex his RCA injection revealed a criticaltight 90% proximal ulcerated stenosis (figure 4). His potassium Figure 7: ECG on discharge exhibited sinus rhythm with fully resolved
ST segment resolution and small Q waves in the inferior leads, without
had normalized to 4.1 mEq/L while his creatinine was 2.1 mgm%.The RCA was engaged by a 6 Fr JR guiding catheter and DISCUSSION
a 0.014 inch floppy wire was negotiated across the block. A 2.25X 16 mm sirolimus stent was deployed at 16 atm subsequent to This report describes the management of a patient with an acute predilatation with a 1.5 X 10 mm balloon. Brisk antegrade TIMI inferior STEMI accompanied by severe hyperkalemia. Severe 3 flow was achieved with no residual stenosis ( Figures 5-6).
hyperkalemia ( potassium more than 7.5 mEq/L) if left untreated The patient was kept on ion exchange resins till discharge along carries a high mortality of more than 65%. It is imperative that with dual antiplatelet and statin thereapy.At discharge the hyperkalemia presenting with electrocadiographic changes or potassium was 4.3 mEq/L, sodium 135 mEq/L, blood urea 61 more than 6.5 mEq/L is rapidly corrected 1-4.
mgm% and serum creatinine 1.8 mgm%. The ECG on discharge However in almost 50% of patients with serum potassium more exhibited sinus rhythm with fully resolved ST segment resolution than 6.5 mEq/L there may be no electrocardiographic changes5.The and small Q waves in the inferior leads, without evidence of other point to bear in mind for the clinician is that more than 60% hyperkalemia. Segment resolution and small Q waves in the patients presenting with severe hyperkalemia have an underlying inferior leads, without evidence of hyperkalemia ( Figure 7).
renal impairment or have been on a single or a cocktail ofpotassium retaining medication.
The earliest ECG change observed with hyperkalemia are anabsence of P wave, peaking and narrowing of T wave andshortening of the corrected QT interval. In cases of severehyperkalemia other ECG manifestations seen are left and rightbundle branch like widening of QRS complexes that can bedistinguished from genuine bundle bundle branch block by thefact that in the latter the conduction delay is in the middle or thefinal stage whereas in hyperkalemia the widening is diffuse. Inthe final stages there is merging of the QRS complex and T waveproducing a sinusoidal wave with QT interval prolongation . Insome patients ST -segment elevation and depression can also Figure 4: RCA revealed a critical tight 90% proximal ulcerated stenosis.
PCI in Hyperkalemia
be seen mimicking an acute myocardial infarction. This is known and eptifibatide can both be given as usual boluses but the as a “ dialyzable injury current” 6-8.
infusion rate will need to be halved. Eptifibatide is contraindicated Emergency treatment for severe hyperkalemia should be initiated immediately with intravenous infusion of calcium gluconate that A tight almost ulcerated subtotal occlusion of the RCA was seen begins to stabilizes the myocardial cell within 2-3 minutes but the following morning subsequent to 10 hours tirofiban ( half acts for only 30 to 60 minutes. Calcium chloride can also be used dose) infusion and this was easily treated by percutaneous but as it is three times potent than calcium gluconate the dose intervention deploying a sirolimus stent. The patient was has to be reduced. Calcium stabilizes the cell by maintaining the subsequently managed on aspirin, clopidogrel, and atorvastatin.
15 mV gap between the resting membrane and threshold potentials. The normal resting membrane potential is made less negative CONCLUSION
from -90 mV to -80 mV. This is closer to the threshold potential This report underscores the fact that a patient presenting with of -75 mV and thereby makes it more vulnerable to lethal tachy- acute STEMI accompanied with severe hyperkalemia requires arrhythmias. Calcium may also speed up impulse formation in the immediate treatment of the raised potassium levels with calcium sinoatrial and atrioventricular nodal cells reversing myocardial (because of its rapid stabilization of the myocardial cell) followed depression seen with hyperkalemia 9-10.
by insulin with or without glucose. Ion exchange resins are Serum potassium is next reduced with 10 units of regular insulin employed next to continue reducing serum potassium.
given intravenously.Insulin drives the excess potassium into Percutaneous coronary intervention is safe and effective the intracellular space by stimulating the Na-K ATPase pump in subsequent to normalization of potassium serum levels.
exchange with sodium in a 2:3 ratio. This effect is independent Adjunctive GPI’s can be used with careful monitoring of dosage of glucose Therefore if a patient is already hyperglycemic extra dextrose need not be administered. Insulin begins to act in 30 to60 minutes and reduces potassium by 0.5 to 1.0 mEq/L 11.
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