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Year : 2022  |  Volume : 11  |  Issue : 4  |  Page : 377-381

Transient cardiac rhythm aberrancy in acute pancreatitis: A case report

Department of General Medicine, Government Medical College and Hospital, Chandigarh, India

Date of Submission11-Oct-2021
Date of Acceptance18-Mar-2022
Date of Web Publication17-Mar-2023

Correspondence Address:
Dr. Gautam Jesrani
Department of General Medicine, Government Medical College and Hospital, Sector 32, Chandigarh - 160 030
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jdrntruhs.jdrntruhs_137_21

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The cardiovascular system is one of the commonly affected systems in various inflammatory and metabolic conditions, and rhythm abnormalities are most vulnerable in this context. Here, we are describing a rare presentation of acute pancreatitis, in which a young male appeared with cardiac rhythm irregularity. The patient presented with localized chest pain of recent onset and had a blood pressure of 88/54 mm Hg initially. On electrocardiogram (ECG), an accelerated idio-ventricular rhythm was identified with the absence of P wave and borderline QRS complex duration. However, his electrolytes were normal, qualitative troponin T was negative, echocardiography ruled out structural cardiac anomalies, and coronary arteries had no occlusion in angiogram. In the absence of any identifiable cause, the recent alcohol intake history made us to measure his serum amylase and lipase levels, and surprisingly, the levels were more than three times the upper value. Additionally, his ultrasound of the abdomen depicted bulky pancreatic head, and thus, the diagnosis of acute pancreatitis was made. Rhythm abnormality subsided with conservative management and the patient was discharged with a normal ECG. The case will shed some light on pancreatitis-associated acute cardiac rhythm abnormality, which is uncommon in emergency department.

Keywords: Accelerated idio-ventricular rhythm, acute pancreatitis, cardiac manifestations, ECG, rhythm abnormalities

How to cite this article:
Jesrani G, Chhabra A, Gupta S, Rajesh R, Gupta M. Transient cardiac rhythm aberrancy in acute pancreatitis: A case report. J NTR Univ Health Sci 2022;11:377-81

How to cite this URL:
Jesrani G, Chhabra A, Gupta S, Rajesh R, Gupta M. Transient cardiac rhythm aberrancy in acute pancreatitis: A case report. J NTR Univ Health Sci [serial online] 2022 [cited 2023 Mar 21];11:377-81. Available from: https://www.jdrntruhs.org/text.asp?2022/11/4/377/371749

  Introduction Top

Acute pancreatitis (AP) is the inflammation of the pancreatic tissue, causing abdominal pain, nausea, vomiting, dyspepsia, and loss of appetite in most of the patients. Gall bladder stones and alcohol intake are two major identified etiologies for this pancreatic injury.[1] The disease has various local and systemic complications, which are not always limited to the gastro-intestinal system. In a study assessing 268 patients of severe AP, respiratory failure was most frequently encountered complication (35.1%), followed by cardiovascular (CV) failure (22.3%).[2] In CV system, hypovolemic shock, different arrhythmias, pericardial effusion, and fibrinous constrictive pericarditis like involvement have been linked with this infirmity.[3] Specifically, electrocardiographic abnormalities have been observed in 50% of the cases and include bradyarrhythmias, supraventricular tachycardia, short PR interval, bundle branch blocks, ST segment changes, and QT prolongation.[3]

  Case Presentation Top

A 36-year-old gentleman came to the emergency department with the complaints of chest pain and diaphoresis from the past 2 hours. The pain was acute in onset, dull aching, and localized to the center and lower parts of the chest without periodic variability. Associated nausea of the same duration was present, but he denied for vomiting, palpitation, or syncope. The patient was suffering with alcohol use disorder from the past 8 years, and the last intake was about 250 ml of country-made liquor 4 days back. He had no chronic illnesses like diabetes, hypertension or coronary artery disease, and long-term drug intake history. On presentation, the patient was having low blood pressure (88/54 mmHg) with a pulse rate of approximately 52/min (regular but low volume). He had a normal respiratory rate, capillary oxygen saturation, blood glucose levels, and oral temperature.

Systemic examination, including cardiovascular and gastro-intestinal system, did not reveal any abnormality. His chest x-ray was having bilaterally clear lung fields with a normal cardio-thoracic ratio, but the electrocardiogram (ECG) of the patient demonstrated absent P wave and regular QRS complexes of borderline duration [Figure 1]. These findings were consistent with accelerated idio-ventricular rhythm (AIVR) as the heart rate was more than 40/min. Therefore, acute coronary syndrome and electrolyte imbalance were suspected, and the patient was subjected to qualitative Troponin-T test but had a negative result. The electrolyte measurement demonstrated serum sodium of 137 mEq/L (normal 135-145) and potassium of 3.9 mEq/L (normal 3.5-5.5), and renal function tests (RFTs) were stable. His total leukocyte count was mildly raised (13.1 × 109/L, normal 4-11), but hemoglobin levels and platelet counts were within the reference range. So initially, intravenous fluids along with opioid analgesics (tramadol 50 mg) and domperidone (10 mg) twice a day were started, which led to an improvement in his blood pressure and alleviation of the pain. The qualitative Troponin-T test was repeated after 12 hours but still had a negative outcome.
Figure 1: Initial electrocardiogram of the patient demonstrating absent P wave and regular QRS complexes (duration 120 milliseconds), suggestive of accelerated idio-ventricular rhythm

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Meanwhile, the patient was shifted to the cardiac care unit, where two-dimensional echocardiography was performed, but fortunately, the modality did not detect any abnormality. Furthermore, coronary angiogram had no thrombotic occlusion, spasm, or stenosis. So the conservative management was continued and with this, his ECG demonstrated a fully normal sinus rhythm by day two of the treatment [Figure 2].
Figure 2: Subsequent electrocardiogram of the same patient demonstrating normal sinus rhythm with regular P wave and narrow QRS complex

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Repeat serum electrolytes and RFTs measurement delineated normal values throughout his hospital stay. Also, his serum magnesium levels (1.8 mg/mL, normal 1.2-2.5), calcium levels (9.2 mg/mL, normal 8.0-10.4), and phosphorus levels (3.3 mg/mL, normal 2.5-4.5) revealed no abnormality. Thyroid and liver function tests were also inconclusive, and the lipid profile was not deranged. In the absence of any identifiable etiology and the presence of remote alcohol intake history, his serum amylase and lipase levels were measured, and surprisingly, the parameters were raised significantly (amylase 913 IU/L, normal 25-125 and lipase 1328 IU/L, normal 13-60). Eventually, the diagnosis of AP was made and ultrasound scan of the abdomen confirmed this by demonstrating bulky head of the pancreas [Figure 3]. The scan had no evidence of gall stone disease, dilated hepato-biliary system, or anatomic pancreatic abnormality. As the electrical abnormality subsided spontaneously and uncomplicated AP requires no specific measures, the same treatment was continued for next 7 more days. After a total of 10 days' in-patient management, the patient was discharged with a normal ECG and advice of quieting alcohol. Currently, the patient is on regular follow-up with psychiatry department for de-addiction and having no cardio-vascular or pancreatic complications at 3 months.
Figure 3: Ultrasound scan of the abdomen demonstrating bulky pancreatic head (maximum diameter 34 millimetre)

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  Discussion Top

AP is one common gastrointestinal pathology, leading to high hospital admission rate, and has an incidence of 15 to 45 per 100,000 individuals per year.[4] The infirmity has been associated vastly with different conduction and non-conduction cardiac disorders in the current literature. In this, a study by Kong L et al. had 22.3%, Yaylaci S et al. had 43.7%, and Rubio-Tapia et al. had 55% CV involvement in AP.[2],[5],[6] The pathogenesis of cardiac manifestations in AP includes interstitial and intracellular myocardial edema, myocyte hypoxia, over-contractility, hypertrophy, and collagenization of myocardium.[3] Metabolic changes like hypo or hyperkalemia, hypomagnesemia, hypophosphatemia, and hypocalcaemia also contribute in this and predominantly affect the cardiac conduction apparatus.[3],[6]

Different ECG patterns have been observed in AP and almost every possible change has been linked, but sole presentation with AIVR is rare. In a study including 64 cases of AP, none of the study individuals experienced AIVR.[6] Abdominal pathology presenting as cardiac rhythm alteration is very uncommon, but numerous other CV morbidities have been associated with different abdominal infirmities [Table 1].[3],[7],[8],[9]
Table 1: Different Gastro-Intestinal Organ System Pathologies and Associated Cardiovascular Manifestations

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The mechanism for AIVR generation is still unknown, but the origin is deemed from the abnormal Purkinje fiber or bundle of His foci. The rhythm disturbance has a relatively benign clinical course in most of the cases and is well tolerated.[10] So, the most appropriate management is the correction of the underlying pathology and supportive care, but amplification of sinus rhythm with injectable atropine and atrial pacing can be used in refractory cases.[10]

Fluid resuscitation forms the cornerstone in AP management. In this, ringer lactate is considered superior to normal saline in decreasing systemic inflammation and can be started at 5-10 ml/kg/hour for the first 24 hours.[11] The fluid therapy should be maintained to achieve a heart rate of <120/min, mean arterial pressure between 65 and 85 mm Hg, and urine output of >0.5-1.0 ml/kg/hour.[11] Furthermore, aggressive fluid resuscitation has been associated with better clinical outcomes than the standard fluid therapy for AP.[12] Antibiotic prophylaxis, even in severe or necrotizing pancreatitis, is not routinely recommended.[12]

The future therapeutic agents in the management of AP include CM4620 (inhibits calcium signaling pathway), GSK-7975A (inhibit calcium signaling pathway), TRO40303 (decreases mitochondrial dysfunction), disaccharide trehalose (decreases autophagy), HMG-CoA inhibitors (alleviate unfolded protein response), Lactated Ringer's solution (anti-inflammatory), Pentoxifylline (anti-inflammatory), Orlistat (inhibits lipotoxicity), and Tocilizumab (anti-inflammatory).[12] These drugs act on the cellular pathophysiology pathway of AP and majority of them are under trial.

In a recent literature, electrocardiographic abnormalities were associated with higher incidence of severe AP and prolonged hospital stay.[13] Elevated cardiac biomarker, i.e., creatine kinase-MB (CK-MB) levels were also related to more pancreatic necrosis, hospital stay, and mortality. Thus, cardiac involvement, including ECG changes, carries a poor prognosis in AP.

A careful follow-up of AP patients is important as long-term complications are well defined in this disease. In this, recurrent episodes of AP are common and can be observed in 18% of the cases, leading to impairment of quality of life.[12] The recurrence rate is high among cases of alcohol induced AP, which can cause chronic pancreatitis in later life. Furthermore, endocrine insufficiency producing dysglycemia or overt diabetes may be seen in one-third, and exocrine function limitation can occur in about 20-40% of AP cases.[12]

  Conclusion Top

The report narrates the importance of considering AP as a differential for cardiac rhythm abnormalities in individuals with risk factors, i.e., alcohol abuse or gallstone disease. AP should be contemplated as culprit pathology for electrical disturbance after ruling out the other common etiologies like acute coronary syndrome, electrolyte imbalance, and endocrine disorders. Fluid resuscitation and analgesics form the cornerstone of uncomplicated AP management, but rhythm aberrancies may require anti-arrhythmic drugs and cardiac resynchronizing therapy.

Author contributions

GJ and AC: Case presentation, management, data collection, investigation, and writing of original draft.

SG, RR, and MG: Clinical management, discussion, literature review, and writing of original draft including conclusion, references, and formatting.

Consent to participate

A written patient consent is present, duly signed by the patient. The authors obtained the consent after explaining that no identity will be revealed and the case information, including pictures, will be used for education purpose only. He was also explained that journal publication will not contain any material or picture, disclosing his identity. The patient gave positive consent for publication.

Ethical approval

A proper written consent is present, which was obtained from the patient for the use of the data related to this case.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Chatila AT, Bilal M, Guturu P. Evaluation and management of acute pancreatitis. World J Clin Cases 2019;7:1006-20.  Back to cited text no. 1
Luo Y, Li Z, Ge P, Guo H, Li L, Zhang G, et al. Comprehensive mechanism, novel markers and multidisciplinary treatment of severe acute pancreatitis-associated cardiac injury-A narrative review. J Inflamm Res 2021;14:3145-69.  Back to cited text no. 2
Yegneswaran B, Kostis JB, Pitchumoni CS. Cardiovascular manifestations of acute pancreatitis. J Crit Care 2011;26:225. e11-8.  Back to cited text no. 3
Machicado JD, Yadav D. Epidemiology of recurrent acute and chronic pancreatitis: Similarities and differences. Dig Dis Sci 2017;62:1683-91.  Back to cited text no. 4
Rubio-Tapia A, García-Leiva J, Asensio-Lafuente E, Robles-Díaz G, Vargas-Vorácková F. Electrocardiographic abnormalities in patients with acute pancreatitis. J Clin Gastroenterol 2005;39:815-8.  Back to cited text no. 5
Yaylaci S, Kocayigit I, Genc AB, Cakar MA, Tamer A, Uslan MI. Electrocardiographic changes in patients with acute pancreatitis. Med J DY Patil Univ 2015;8:196-8.  Back to cited text no. 6
  [Full text]  
Gesualdo M, Scicchitano P, Carbonara S, Ricci G, Principi M, Ierardi E, et al. The association between cardiac and gastrointestinal disorders: Causal or casual link? J Cardiovasc Med (Hagerstown) 2016;17:330-8.  Back to cited text no. 7
Nikolic S, Dugic A, Steiner C, Tsolakis AV, Haugen Löfman IM, Löhr JM, et al. Chronic pancreatitis and the heart disease: Still terra incognita? World J Gastroenterol 2019;25:6561-70.  Back to cited text no. 8
Fouad YM, Yehia R. Hepato-cardiac disorders. World J Hepatol 2014;6:41-54.  Back to cited text no. 9
Nakanishi M, Masumo K, Oota T, Kato T, Imanishi T. Accelerated idioventricular rhythm observed under total intravenous anesthesia using remifentanil, propofol, and rocuronium. JA Clin Rep 2015;1:12.  Back to cited text no. 10
Boxhoorn L, Voermans RP, Bouwense SA, Bruno MJ, Verdonk RC, Boermeester MA, et al. Acute pancreatitis. Lancet 2020;396:726-34.  Back to cited text no. 11
Lee PJ, Papachristou GI. New insights into acute pancreatitis. Nat Rev Gastroenterol Hepatol 2019;16:479-96.  Back to cited text no. 12
Prasada R, Dhaka N, Bahl A, Yadav TD, Kochhar R. Prevalence of cardiovascular dysfunction and its association with outcome in patients with acute pancreatitis. Indian J Gastroenterol 2018;37:113-9.  Back to cited text no. 13


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1]


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