Atropine in Inferior STEMI with Bradycardia and Wide Pulse Pressure Hypertension: a Case of Heart Rate-Mediated Systolic Decline and Diastolic Rise

Atropine in Inferior STEMI with Bradycardia and Wide Pulse Pressure Hypertension: a Case of Heart Rate-Mediated Systolic Decline and Diastolic Rise | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Atropine in Inferior STEMI with Bradycardia and Wide Pulse Pressure Hypertension: a Case of Heart Rate-Mediated Systolic Decline and Diastolic Rise Behaylu Tesfamaryam Hagos, Rediwan Gashaw Geto, Molalign Fenta Alemu, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8514813/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 5 You are reading this latest preprint version Abstract Background Atropine sulfate is first-line therapy for symptomatic bradycardia in acute coronary syndromes. Its primary vagolytic effect aims to increase heart rate and cardiac output. We present a case that demonstrates the drug's distinct and sequential effects, where an initial rise in diastolic pressure is followed by a fall in systolic pressure .This underscores a potential hemodynamic risk in preload-dependent states. Case Presentation: A 69-year-old male with hypertension and chronic coronary syndrome presented with an inferior ST-elevation myocardial infarction (STEMI). Upon ICU admission, he had persistent chest pain with symptomatic bradycardia (52–56 bpm) and significant hypertension with a widened pulse pressure (187/75 mmHg). Intravenous atropine (0.5 mg) was administered. The hemodynamic response followed a definitive sequence: first, heart rate increased to 68–70 bpm. Subsequently, diastolic blood pressure rose to 91 mmHg, while systolic pressure fell to 148 mmHg, thereby narrowing the pulse pressure. Conclusion This response demonstrates atropine's dual hemodynamic actions. The increase in heart rate likely shortened diastolic filling time, reducing left ventricular preload and stroke volume, which consequently decreased systolic pressure. This case highlights that in patients with inferior STEMI and hypertension, atropine's efficacy for bradycardia may be accompanied by a reduction in systolic pressure, a consequence of reduced preload rather than vasodilation. Clinicians should be aware of this mechanism, especially in patients who may be preload-dependent. Atropine ST Elevation Myocardial Infarction STEMI Hemodynamics Bradycardia Preload Stroke Volume hypertension wide pulse pressure Figures Figure 1 Figure 2 Background Symptomatic bradycardia in acute inferior ST-elevation myocardial infarction (STEMI) presents a common therapeutic challenge. Atropine sulfate, a muscarinic antagonist, is the first-line agent for increasing heart rate and, evidently, cardiac output in this setting. Its primary vagolytic action is well-established in guidelines for managing bradycardia with hypotension or poor perfusion[ 1 ]. A more complex hemodynamic dilemma arises when inferior STEMI, on rare occasion, is accompanied by bradycardia and significant hypertension. In this scenario, traditional antihypertensives are problematic: beta-blockers can worsen bradycardia, and vasodilators may induce dangerous hypotension in preload-dependent states like right ventricular involvement[ 2 ]. This creates a paradoxical situation where both the bradycardia and the hypertension require treatment, but standard approaches are contraindicated. A critical, yet less emphasized, physiological concept is that bradycardia itself can be the direct cause of systolic hypertension. A prolonged diastolic filling time increases left ventricular preload and stroke volume. Ejection of this larger volume into a stiff arterial system can generate exaggerated systolic pressure, while prolonged diastolic runoff lowers diastolic pressure, resulting in a widened pulse pressure[ 3 – 5 ]. This dynamic may precipitate a supply-demand mismatch, worsening ischemia. While atropine is routinely used for bradycardia, its comprehensive hemodynamic effects in the specific context of bradycardia-induced hypertension during STEMI are not commonly detailed. This case report elucidates the sequential dual hemodynamic response to atropine—a rise in diastolic pressure followed by a fall in systolic pressure—and explains the underlying mechanisms. It highlights how correcting heart rate can simultaneously address the hypertensive crisis and myocardial ischemia, while also noting the potential risks of this preload-modifying effect in vulnerable patients. Case Presentation A 69-year-old male with a history of hypertension and stable ischemic heart disease (chronic coronary syndrome), maintained on enalapril (5 mg twice daily), atenolol (25 mg daily), aspirin (81 mg daily), and atorvastatin (40 mg daily), presented with squeezing left-sided chest pain radiating to the left arm and peri-umbilical area of 3 hours duration. Symptoms were associated with nausea, vomiting, and diaphoresis. Initial vital signs in the emergency department included bradycardia (heart rate 58-62 bpm), elevated blood pressure (137/76 mmHg), tachypnea (24 breaths/min), and normothermia (36.8 °C). Physical examination was otherwise unremarkable. Electrocardiography (Figure 1) demonstrated sinus bradycardia with ST-segment elevation, pathological Q waves, and T-wave inversion in the inferior leads (II, III, aVF), consistent with an acute ST-elevation myocardial infarction (STEMI). The patient was admitted to the intensive care unit, loaded with aspirin (325 mg) and clopidogrel (300 mg), and anticoagulated with subcutaneous unfractionated heparin. One-hour post-admission, he reported persistent chest pain. His heart rate declined further to 48-56 bpm, and he developed significant hypertension with a widened pulse pressure (blood pressure peaking at 187/75 mmHg, mean arterial pressure 158 mmHg), as shown in Figure 2A. For this symptomatic bradycardia with hypertensive emergency, intravenous atropine (0.5 mg) was administered. The hemodynamic response to atropine followed a distinct temporal sequence: the heart rate improved first (increasing to 68-70 bpm), followed by a rise in diastolic pressure, and finally a decline in systolic pressure. Consequently, 15 minutes post-administration, the blood pressure was 148/91 mmHg with a normalized pulse pressure and a mean arterial pressure of 117 mmHg (Figure 2). On hospital day two, following confirmation of normal renal function (creatinine 0.8 mg/dL), his home dose of enalapril was increased to 10 mg PO twice daily. He was monitored for 10 days, during which his heart rate remained within the low-normal range (62-70 bpm) and blood pressure was controlled below 160/90 mmHg. Definitive reperfusion therapies, including PCI and thrombolysis, were unavailable at our institution; furthermore, the patient was unable to afford referral to a facility where these treatments were offered. Discussion The simultaneous presentation of hypertension and bradycardia typically suggests a limited differential, such as the Cushing reflex[ 4 ]. However, this case illustrates a more nuanced hemodynamic relationship: bradycardia-induced hypertension. Pathological bradycardia allows for a prolonged diastolic filling period and diastolic runoff—an effect significantly pronounced in patients with underlying arterial stiffening. According to the Frank-Starling principle, this increased preload leads to an oversized stroke volume. When this volume is ejected into a non-compliant arterial system, it generates a disproportionately high systolic pressure (e.g., 187 mmHg). Conversely, the rapid arterial "run-off" during the long pauses between beats causes the diastolic pressure to drop (e.g., 75 mmHg), resulting in a wide pulse pressure. This creates a severe supply-demand mismatch: while myocardial oxygen demand rises due to increased wall tension (Laplace's Law), the coronary perfusion pressure—the gradient between aortic diastolic pressure and left ventricular end-diastolic pressure (LVEDP)—is critically diminished[ 6 – 8 ]. The left ventricle is uniquely susceptible to this mismatch because it is perfused almost exclusively during diastole. Its own powerful systolic contraction restricts coronary flow, making it exquisitely dependent on both the duration and the driving pressure of the diastolic phase. Furthermore, since resting myocardial oxygen extraction is near-maximal, increased demand must be met almost solely by raising coronary blood flow. This flow is regulated by the effective perfusion gradient, defined as the difference between the diastolic pressure and the coronary zero-flow pressure (Pzf). In this case, Pzf is elevated by high extravascular compression and increased wall tension. Despite a longer diastolic interval, the actual perfusion pressure may remain below the elevated Pzf for extended periods, leading to the "bradycardic angina" observed in this patient[ 8 – 10 ]. The management of hypertensive emergency in the setting of acute inferior wall ST-elevation myocardial infarction (STEMI) presents a profound pharmacological paradox when accompanied by symptomatic bradycardia. In this case, the patient’s wide pulse pressure hypertension (187/75mmHg) was not an independent primary pathology, but rather a compensatory physiological response to a severely reduced heart rate. This clinical triad (ischemia, bradycardia, and hypertension) demands, in our view, a strategy that prioritizes the restoration of heart rate over traditional blood pressure reduction. Traditional antihypertensives in this context are fraught with risk. Beta-blockers were strictly contraindicated[ 11 ], as they would have exacerbated the bradycardia and increased diastolic filling time, further increasing stroke volume and myocardial wall tension, thereby worsening the oxygen supply-demand mismatch. Similarly, vasodilators such as Nitroglycerin were avoided due to the high probability of right ventricular involvement common in inferior MIs. In such patients, the heart is "preload-dependent"; a sudden reduction in venous return, coupled with an inability to increase heart rate, can lead to a catastrophic collapse in cardiac output and mean arterial pressure[ 12 , 13 ]. Given the persistence of chest pain and the diagnostic suspicion that bradycardia was the primary driver, Atropine was utilized as a definitive therapeutic challenge. The clinical response to Atropine provided a real-time validation of this physiological model. As the heart rate gradually increased, a specific sequence of hemodynamic shifts was observed: Initial Rise in Diastolic Pressure : By shortening the diastolic run-off time, Atropine allowed the aortic pressure to remain higher at the end of the cardiac cycle, immediately improving the coronary perfusion gradient (increasing effective afterload). Subsequent Fall in the Systolic and Mean Arterial Pressure : As the increased heart rate reduced end-diastolic volume (preload), the subsequent stroke volume decreased. Ejecting a smaller volume into the stiff arterial tree prevented the exaggerated systolic "spikes.", and the mean arterial pressures dropped from 158 mmHg to 117 mmHg. Resolution of chest pain : Following the above hemodynamic changes, the chest pain subsided, suggesting improved blood flow. While Atropine was therapeutic here and is the first line for patients with symptomatic bradycardia with hypotension[ 14 , 15 ], the significant reduction in preload make this intervention potentially dangerous in specific patient populations. For patients with conditions that are heavily preload-dependent, such as right ventricular Infarction, severe aortic stenosis, or hypertrophic obstructive cardiomyopathy (HOCM), the sudden decrease in filling time and volume could lead to a catastrophic drop in cardiac output and obstructive shock. However, unlike pure vasodilators, the increase in heart rate that accompanies atropine administration may partially compensate for the reduced stroke volume, thereby mitigating the potential fall in cardiac output. This case highlights that in the setting of bradycardia-dependent hypertension, the most effective "antihypertensive" may actually be a chronotropic agent, provided that long-term afterload control is simultaneously optimized with agents such as Enalapril. Conclusion This case clarifies a significant clinical paradox. For patients with comorbid ischemic disease and arterial stiffness, the theoretical 'benefit' of increased diastolic filling time during bradycardia is offset by a maladaptive surge in myocardial oxygen demand and concurrent impairment of diastolic perfusion. The resolution of both the hypertension and the angina following Atropine administration confirms that the bradycardia was not a secondary symptom, but the primary etiology of the hypertensive crisis. Abbreviations aVF Augmented Vector Foot (Lead) bpm beats per minute HOCM Hypertrophic Obstructive Cardiomyopathy ICU Intensive Care Unit IV Intravenous LVEDP Left Ventricular End-Diastolic Pressure MAP Mean Arterial Pressure MI Myocardial Infarction PO Per Os (by mouth) Pzf Zero-Flow Pressure STEMI ST-Elevation Myocardial Infarction Declarations Ethical Approval: Not applicable. Consent for publication: Written informed consent was obtained from the patient. A copy of the written consent is available for review by the editors of this journal. Availability of Data and Materials: The data that support the findings of this study are available from the corresponding author upon reasonable request. Competing Interests: The authors declare that there are no competing interests related to this review. Funding: All authors have declared that no financial support was received from any organization for the submitted work Author's contribution: B.T.H: contributed to patient care, conceptualization, data curation, analysis and interpret patient's data, literature review and drafting the manuscript. R.G.G: contributed to patient care, data curation, analysis and interpret patient's data, critically reviewed and approved the final version. M.F.A: contributed to patient care, data curation, analysis and interpret patient's data, critically reviewed and approved the final version. Y.T.M: contributed to patient care, data curation, critical review, and approved the final version. Acknowledgement We would like to express our profound appreciation to the stuff at Enat General Hospital, especially those within the Emergency Department and Intensive Care Unit, for their unwavering commitment and valuable contribution in the management of this challenging case. References Kusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ et al. ACC / AHA / HRS GUIDELINE 2018 ACC / AHA / HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay. 2019. Guidelines CP, ACC / AHA / ACEP / NAEMSP / SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. 2025 : A Report of the American College of Cardiology / American Heart Association Joint Committee on Clinical Practice Guidelines. 2025. Ellims AH, Mariani JA, Schlaich MP. Restoration of blood pressure control with pacemaker implantation in a patient with bradycardia and resistant hypertension: A case report. Int J Cardiol [Internet] Elsevier. 2013;167(2):e38–40. https://doi.org/10.1016/j.ijcard.2013.03.080 . Kulesza B. Bradycardia Concomitant with Hypertension. Med Discov [Internet]. 2023;2(11). https://meddiscoveries.org/articles/1092.html Myrmel GMS, Ali A, Lunde T, Mancia G, Saeed S. An Unexpected Cause of Severe Hypertension and Bradycardia: The Role of Hemodynamic Assessment by Echocardiography. Pulse [Internet]. 2022;10(1–4):46–51. 10.1159/000525078 . https://karger.com/article/doi/ . Mangoni AA. Diastolic and Pulse Pressure: The Old and the New? Hypertension. 2004;43:531–2. Hoffman JIE, Buckberg GD. The Myocardial Oxygen Supply:Demand Index Revisited. J Am Heart Assoc [Internet]. 2014;3(1):1–10. 10.1161/JAHA.113.000285 . https://www.ahajournals.org/doi/ . Goodwill AG, Dick GM, Kiel AM, Tune JD. Regulation of Coronary Blood Flow. Comprehensive Physiology [Internet]. Wiley; 2017. pp. 321–82. https://onlinelibrary.wiley.com/doi/ . 10.1002/cphy.c160016 . Pathania V, Clark S. The coronary circulation in healthy and diseased states. BJA Educ [Internet]. Br J Anaesth. 2024;24(6):210–6. https://doi.org/10.1016/j.bjae.2024.03.003 . Fowler PBS, Ikram H, Maini RN, Makey AR, Kirkham JS. Bradycardiac Angina: Haemodynamic Aspects and Treatment. BMJ [Internet]. 1969;1(5636):92–4. 10.1136/bmj.1.5636.92 . https://www.bmj.com/lookup/doi/ . Farzam K, Jan A. Beta blockers. In: StatPearls [Internet]. Drexel University: StatPearls Publishing; 2025. https://www.ncbi.nlm.nih.gov/books/NBK532906/ Ventetuolo CE, Klinger JR. Management of Acute Right Ventricular Failure in the Intensive Care Unit. (1). Arrigo M, Huber LC, Winnik S, Mikulicic F, Guidetti F, Frank M, Flammer AJ, Ruschitzka F. Right Ventricular Failure: Pathophysiology, Diagnosis and Treatment. Card Fail Rev. 2019;5(3)140–6 [Internet]. Radcliffe Cardiology; 2019; https://doi.org/10.15420/cfr.2019.15.2 Scheinman BMM, Thorburn D, Abbott JA. Use of Atropine in Patients with Acute Myocardial Infarction and Sinus Bradyeardia. Circulation. 1975;52:627–33. Klein MD, Barret J, Ryan TJ, Flessas AP. Atropine dose in acute myocardial infarction in man. Cardiol Switz. 1975;60(4):193–205. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Reviewers invited by journal 29 Jan, 2026 Editor invited by journal 07 Jan, 2026 Editor assigned by journal 05 Jan, 2026 Submission checks completed at journal 05 Jan, 2026 First submitted to journal 04 Jan, 2026 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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05:34:10","extension":"xml","order_by":7,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":42400,"visible":true,"origin":"","legend":"","description":"","filename":"8bcb2c3773d740f597dac8128ae25fa71structuring.xml","url":"https://assets-eu.researchsquare.com/files/rs-8514813/v1/a7548e3cde3c20596a1f5280.xml"},{"id":100753144,"identity":"089dc771-8ec9-4b96-a06a-b8cb1dcfb000","added_by":"auto","created_at":"2026-01-21 05:34:10","extension":"html","order_by":8,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":49064,"visible":true,"origin":"","legend":"","description":"","filename":"earlyproof.html","url":"https://assets-eu.researchsquare.com/files/rs-8514813/v1/574be584b2450ac1432506ca.html"},{"id":100753135,"identity":"dfc40157-3b38-4023-b9fb-0f89c424f9d9","added_by":"auto","created_at":"2026-01-21 05:34:08","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":641858,"visible":true,"origin":"","legend":"\u003cp\u003eElectrocardiogram on admission showing sinus bradycardia with ST-segment elevation, pathological Q waves, and T-wave inversion in leads II, III, and aVF.\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-8514813/v1/b108a4e5ddf512f86fbebcc6.png"},{"id":100753149,"identity":"b7f51236-a23a-4858-a433-62898270982d","added_by":"auto","created_at":"2026-01-21 05:34:14","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":660625,"visible":true,"origin":"","legend":"\u003cp\u003eSerial hemodynamic tracings before and after 0.5 mg IV atropine. Initial tracing (A) demonstrates bradycardia (56 bpm) with a widened pulse pressure. Following administration, tracings at 10 minutes (B) and 15 minutes (C) illustrate a progressive increase in heart rate (62 to 68 bpm), an initial rise in diastolic pressure (91 mmHg), and a subsequent reduction in systolic pressure (148 mmHg).\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-8514813/v1/2211c450354b792350610b91.png"},{"id":100804129,"identity":"af911f52-b190-4597-ae1f-664878cb4d24","added_by":"auto","created_at":"2026-01-21 14:37:52","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1962174,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8514813/v1/68eb7916-e5ef-4449-be2f-1b75ed6f6e9b.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Atropine in Inferior STEMI with Bradycardia and Wide Pulse Pressure Hypertension: a Case of Heart Rate-Mediated Systolic Decline and Diastolic Rise","fulltext":[{"header":"Background","content":"\u003cp\u003eSymptomatic bradycardia in acute inferior ST-elevation myocardial infarction (STEMI) presents a common therapeutic challenge. Atropine sulfate, a muscarinic antagonist, is the first-line agent for increasing heart rate and, evidently, cardiac output in this setting. Its primary vagolytic action is well-established in guidelines for managing bradycardia with hypotension or poor perfusion[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eA more complex hemodynamic dilemma arises when inferior STEMI, on rare occasion, is accompanied by bradycardia and significant hypertension. In this scenario, traditional antihypertensives are problematic: beta-blockers can worsen bradycardia, and vasodilators may induce dangerous hypotension in preload-dependent states like right ventricular involvement[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. This creates a paradoxical situation where both the bradycardia and the hypertension require treatment, but standard approaches are contraindicated.\u003c/p\u003e \u003cp\u003eA critical, yet less emphasized, physiological concept is that bradycardia itself can be the direct cause of systolic hypertension. A prolonged diastolic filling time increases left ventricular preload and stroke volume. Ejection of this larger volume into a stiff arterial system can generate exaggerated systolic pressure, while prolonged diastolic runoff lowers diastolic pressure, resulting in a widened pulse pressure[\u003cspan additionalcitationids=\"CR4\" citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. This dynamic may precipitate a supply-demand mismatch, worsening ischemia.\u003c/p\u003e \u003cp\u003eWhile atropine is routinely used for bradycardia, its comprehensive hemodynamic effects in the specific context of bradycardia-induced hypertension during STEMI are not commonly detailed. This case report elucidates the sequential dual hemodynamic response to atropine\u0026mdash;a rise in diastolic pressure followed by a fall in systolic pressure\u0026mdash;and explains the underlying mechanisms. It highlights how correcting heart rate can simultaneously address the hypertensive crisis and myocardial ischemia, while also noting the potential risks of this preload-modifying effect in vulnerable patients.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eA 69-year-old male with a history of hypertension and stable ischemic heart disease (chronic coronary syndrome), maintained on enalapril (5 mg twice daily), atenolol (25 mg daily), aspirin (81 mg daily), and atorvastatin (40 mg daily), presented with squeezing left-sided chest pain radiating to the left arm and peri-umbilical area of 3 hours duration. Symptoms were associated with nausea, vomiting, and diaphoresis. Initial vital signs in the emergency department included bradycardia (heart rate 58-62 bpm), elevated blood pressure (137/76 mmHg), tachypnea (24 breaths/min), and normothermia (36.8 \u0026deg;C). Physical examination was otherwise unremarkable. Electrocardiography (Figure 1) demonstrated sinus bradycardia with ST-segment elevation, pathological Q waves, and T-wave inversion in the inferior leads (II, III, aVF), consistent with an acute ST-elevation myocardial infarction (STEMI). The patient was admitted to the intensive care unit, loaded with aspirin (325 mg) and clopidogrel (300 mg), and anticoagulated with subcutaneous unfractionated heparin.\u003c/p\u003e\n\u003cp\u003eOne-hour post-admission, he reported persistent chest pain. His heart rate declined further to 48-56 bpm, and he developed significant hypertension with a widened pulse pressure (blood pressure peaking at 187/75 mmHg, mean arterial pressure 158 mmHg), as shown in Figure 2A. For this symptomatic bradycardia with hypertensive emergency, intravenous atropine (0.5 mg) was administered. The hemodynamic response to atropine followed a distinct temporal sequence: the heart rate improved first (increasing to 68-70 bpm), followed by a rise in diastolic pressure, and finally a decline in systolic pressure. Consequently, 15 minutes post-administration, the blood pressure was 148/91 mmHg with a normalized pulse pressure and a mean arterial pressure of 117 mmHg (Figure 2).\u003c/p\u003e\n\u003cp\u003eOn hospital day two, following confirmation of normal renal function (creatinine 0.8 mg/dL), his home dose of enalapril was increased to 10 mg PO twice daily. He was monitored for 10 days, during which his heart rate remained within the low-normal range (62-70 bpm) and blood pressure was controlled below 160/90 mmHg. Definitive reperfusion therapies, including PCI and thrombolysis, were unavailable at our institution; furthermore, the patient was unable to afford referral to a facility where these treatments were offered.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThe simultaneous presentation of hypertension and bradycardia typically suggests a limited differential, such as the Cushing reflex[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. However, this case illustrates a more nuanced hemodynamic relationship: bradycardia-induced hypertension. Pathological bradycardia allows for a prolonged diastolic filling period and diastolic runoff\u0026mdash;an effect significantly pronounced in patients with underlying arterial stiffening. According to the Frank-Starling principle, this increased preload leads to an oversized stroke volume. When this volume is ejected into a non-compliant arterial system, it generates a disproportionately high systolic pressure (e.g., 187 mmHg). Conversely, the rapid arterial \"run-off\" during the long pauses between beats causes the diastolic pressure to drop (e.g., 75 mmHg), resulting in a wide pulse pressure. This creates a severe supply-demand mismatch: while myocardial oxygen demand rises due to increased wall tension (Laplace's Law), the coronary perfusion pressure\u0026mdash;the gradient between aortic diastolic pressure and left ventricular end-diastolic pressure (LVEDP)\u0026mdash;is critically diminished[\u003cspan additionalcitationids=\"CR7\" citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThe left ventricle is uniquely susceptible to this mismatch because it is perfused almost exclusively during diastole. Its own powerful systolic contraction restricts coronary flow, making it exquisitely dependent on both the duration and the driving pressure of the diastolic phase. Furthermore, since resting myocardial oxygen extraction is near-maximal, increased demand must be met almost solely by raising coronary blood flow. This flow is regulated by the effective perfusion gradient, defined as the difference between the diastolic pressure and the coronary zero-flow pressure (Pzf). In this case, Pzf is elevated by high extravascular compression and increased wall tension. Despite a longer diastolic interval, the actual perfusion pressure may remain below the elevated Pzf for extended periods, leading to the \"bradycardic angina\" observed in this patient[\u003cspan additionalcitationids=\"CR9\" citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThe management of hypertensive emergency in the setting of acute inferior wall ST-elevation myocardial infarction (STEMI) presents a profound pharmacological paradox when accompanied by symptomatic bradycardia. In this case, the patient\u0026rsquo;s wide pulse pressure hypertension (187/75mmHg) was not an independent primary pathology, but rather a compensatory physiological response to a severely reduced heart rate. This clinical triad (ischemia, bradycardia, and hypertension) demands, in our view, a strategy that prioritizes the restoration of heart rate over traditional blood pressure reduction.\u003c/p\u003e \u003cp\u003eTraditional antihypertensives in this context are fraught with risk. Beta-blockers were strictly contraindicated[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e], as they would have exacerbated the bradycardia and increased diastolic filling time, further increasing stroke volume and myocardial wall tension, thereby worsening the oxygen supply-demand mismatch. Similarly, vasodilators such as Nitroglycerin were avoided due to the high probability of right ventricular involvement common in inferior MIs. In such patients, the heart is \u003cem\u003e\"preload-dependent\";\u003c/em\u003e a sudden reduction in venous return, coupled with an inability to increase heart rate, can lead to a catastrophic collapse in cardiac output and mean arterial pressure[\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eGiven the persistence of chest pain and the diagnostic suspicion that bradycardia was the primary driver, Atropine was utilized as a definitive therapeutic challenge. The clinical response to Atropine provided a real-time validation of this physiological model. As the heart rate gradually increased, a specific sequence of hemodynamic shifts was observed:\u003c/p\u003e \u003cp\u003e \u003col\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eInitial Rise in Diastolic Pressure\u003c/b\u003e: By shortening the diastolic run-off time, Atropine allowed the aortic pressure to remain higher at the end of the cardiac cycle, immediately improving the coronary perfusion gradient (increasing effective afterload).\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eSubsequent Fall in the Systolic and Mean Arterial Pressure\u003c/b\u003e: As the increased heart rate reduced end-diastolic volume (preload), the subsequent stroke volume decreased. Ejecting a smaller volume into the stiff arterial tree prevented the exaggerated systolic \"spikes.\", and the mean arterial pressures dropped from 158 mmHg to 117 mmHg.\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003e \u003cb\u003eResolution of chest pain\u003c/b\u003e: Following the above hemodynamic changes, the chest pain subsided, suggesting improved blood flow.\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003c/ol\u003e \u003c/p\u003e \u003cp\u003eWhile Atropine was therapeutic here and is the first line for patients with symptomatic bradycardia with hypotension[\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e, \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e], the significant reduction in preload make this intervention potentially dangerous in specific patient populations. For patients with conditions that are heavily preload-dependent, such as right ventricular Infarction, severe aortic stenosis, or hypertrophic obstructive cardiomyopathy (HOCM), the sudden decrease in filling time and volume could lead to a catastrophic drop in cardiac output and obstructive shock. However, unlike pure vasodilators, the increase in heart rate that accompanies atropine administration may partially compensate for the reduced stroke volume, thereby mitigating the potential fall in cardiac output.\u003c/p\u003e \u003cp\u003eThis case highlights that in the setting of bradycardia-dependent hypertension, the most effective \"antihypertensive\" may actually be a chronotropic agent, provided that long-term afterload control is simultaneously optimized with agents such as Enalapril.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThis case clarifies a significant clinical paradox. For patients with comorbid ischemic disease and arterial stiffness, the theoretical 'benefit' of increased diastolic filling time during bradycardia is offset by a maladaptive surge in myocardial oxygen demand and concurrent impairment of diastolic perfusion. The resolution of both the hypertension and the angina following Atropine administration confirms that the bradycardia was not a secondary symptom, but the primary etiology of the hypertensive crisis.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cdiv class=\"DefinitionList\"\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eaVF\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eAugmented Vector Foot (Lead)\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003ebpm\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003ebeats per minute\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eHOCM\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eHypertrophic Obstructive Cardiomyopathy\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eICU\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eIntensive Care Unit\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eIV\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eIntravenous\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eLVEDP\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eLeft Ventricular End-Diastolic Pressure\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eMAP\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eMean Arterial Pressure\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eMI\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eMyocardial Infarction\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003ePO\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003ePer Os (by mouth)\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003ePzf\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eZero-Flow Pressure\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eSTEMI\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eST-Elevation Myocardial Infarction\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthical Approval: Not applicable.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication:\u0026nbsp;\u003c/strong\u003eWritten informed consent was obtained from the patient. A copy of the written consent is available for review by the editors of this journal.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of Data and Materials:\u0026nbsp;\u003c/strong\u003eThe data that support the findings of this study are available from the corresponding author upon reasonable request.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting Interests:\u0026nbsp;\u003c/strong\u003eThe authors declare that there are no competing interests related to this review.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding:\u0026nbsp;\u003c/strong\u003eAll authors have declared that no financial support was received from any organization for the submitted work\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor\u0026apos;s contribution: \u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eB.T.H:\u0026nbsp;\u003c/strong\u003econtributed to patient care, conceptualization, data curation, analysis and interpret patient\u0026apos;s data, literature review and drafting the manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eR.G.G:\u0026nbsp;\u003c/strong\u003econtributed to patient care, data curation, analysis and interpret patient\u0026apos;s data, critically reviewed and approved the final version.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eM.F.A:\u0026nbsp;\u003c/strong\u003econtributed to patient care, data curation, analysis and interpret patient\u0026apos;s data, critically reviewed and approved the final version.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eY.T.M:\u0026nbsp;\u003c/strong\u003econtributed to patient care, data curation, critical review, and approved the final version.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgement\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe would like to express our profound appreciation to the stuff at Enat General Hospital, especially those within the Emergency Department and Intensive Care Unit, for their unwavering commitment and valuable contribution in the management of this challenging case.\u0026nbsp;\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eKusumoto FM, Schoenfeld MH, Barrett C, Edgerton JR, Ellenbogen KA, Gold MR, Goldschlager NF, Hamilton RM, Joglar JA, Kim RJ et al. ACC / AHA / HRS GUIDELINE 2018 ACC / AHA / HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay. 2019.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGuidelines CP, ACC / AHA / ACEP / NAEMSP / SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. 2025 : A Report of the American College of Cardiology / American Heart Association Joint Committee on Clinical Practice Guidelines. 2025.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eEllims AH, Mariani JA, Schlaich MP. Restoration of blood pressure control with pacemaker implantation in a patient with bradycardia and resistant hypertension: A case report. 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BMJ [Internet]. 1969;1(5636):92\u0026ndash;4. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1136/bmj.1.5636.92\u003c/span\u003e\u003cspan address=\"10.1136/bmj.1.5636.92\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.bmj.com/lookup/doi/\u003c/span\u003e\u003cspan address=\"https://www.bmj.com/lookup/doi/\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFarzam K, Jan A. Beta blockers. In: StatPearls [Internet]. 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Radcliffe Cardiology; 2019; \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.15420/cfr.2019.15.2\u003c/span\u003e\u003cspan address=\"10.15420/cfr.2019.15.2\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eScheinman BMM, Thorburn D, Abbott JA. Use of Atropine in Patients with Acute Myocardial Infarction and Sinus Bradyeardia. Circulation. 1975;52:627\u0026ndash;33.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKlein MD, Barret J, Ryan TJ, Flessas AP. Atropine dose in acute myocardial infarction in man. Cardiol Switz. 1975;60(4):193\u0026ndash;205.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-cardiovascular-disorders","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bcar","sideBox":"Learn more about [BMC Cardiovascular Disorders](http://bmccardiovascdisord.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bcar/default.aspx","title":"BMC Cardiovascular Disorders","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Atropine, ST Elevation Myocardial Infarction, STEMI, Hemodynamics, Bradycardia, Preload, Stroke Volume, hypertension, wide pulse pressure","lastPublishedDoi":"10.21203/rs.3.rs-8514813/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8514813/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eAtropine sulfate is first-line therapy for symptomatic bradycardia in acute coronary syndromes. Its primary vagolytic effect aims to increase heart rate and cardiac output. We present a case that demonstrates the drug's distinct and sequential effects, where an initial rise in diastolic pressure is followed by a fall in systolic pressure .This underscores a potential hemodynamic risk in preload-dependent states.\u003c/p\u003e\u003ch2\u003eCase Presentation:\u003c/h2\u003e \u003cp\u003eA 69-year-old male with hypertension and chronic coronary syndrome presented with an inferior ST-elevation myocardial infarction (STEMI). Upon ICU admission, he had persistent chest pain with symptomatic bradycardia (52\u0026ndash;56 bpm) and significant hypertension with a widened pulse pressure (187/75 mmHg). Intravenous atropine (0.5 mg) was administered. The hemodynamic response followed a definitive sequence: first, heart rate increased to 68\u0026ndash;70 bpm. Subsequently, diastolic blood pressure rose to 91 mmHg, while systolic pressure fell to 148 mmHg, thereby narrowing the pulse pressure.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eThis response demonstrates atropine's dual hemodynamic actions. The increase in heart rate likely shortened diastolic filling time, reducing left ventricular preload and stroke volume, which consequently decreased systolic pressure. This case highlights that in patients with inferior STEMI and hypertension, atropine's efficacy for bradycardia may be accompanied by a reduction in systolic pressure, a consequence of reduced preload rather than vasodilation. Clinicians should be aware of this mechanism, especially in patients who may be preload-dependent.\u003c/p\u003e","manuscriptTitle":"Atropine in Inferior STEMI with Bradycardia and Wide Pulse Pressure Hypertension: a Case of Heart Rate-Mediated Systolic Decline and Diastolic Rise","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-01-21 05:33:35","doi":"10.21203/rs.3.rs-8514813/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"reviewersInvited","content":"","date":"2026-01-29T11:02:48+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-01-07T07:43:10+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-01-05T14:31:04+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-01-05T14:30:34+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Cardiovascular Disorders","date":"2026-01-04T17:47:51+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-cardiovascular-disorders","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bcar","sideBox":"Learn more about [BMC Cardiovascular Disorders](http://bmccardiovascdisord.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bcar/default.aspx","title":"BMC Cardiovascular Disorders","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"65b5a1c9-db84-4697-a05d-7258af0803f6","owner":[],"postedDate":"January 21st, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-01-29T11:09:07+00:00","versionOfRecord":[],"versionCreatedAt":"2026-01-21 05:33:35","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8514813","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8514813","identity":"rs-8514813","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}