Successful Resuscitation of Cardiac Arrest with Concurrent Intravenous Thrombolysis during Cardiopulmonary Resuscitation

Summary

This case report describes the successful management of a patient with acute myocardial infarction complicated by cardiac arrest, who underwent cardiopulmonary resuscitation and received intravenous thrombolysis during resuscitation. The case highlights the potential feasibility and clinical relevance of thrombolysis administered concurrently with resuscitation efforts.

Abstract

Thrombolytic therapy has long been considered a relative contraindication during cardiopulmonary resuscitation (CPR), mainly due to concerns about fatal bleeding complications. However, in patients with acute myocardial infarction (AMI), untreated coronary thrombosis remains a major cause of unsuccessful resuscitation. We report the case of a 66-year-old man with a history of hypertension and cerebral infarction who presented with chest pain, subsequently developed cardiac arrest, and was successfully resuscitated after concurrent intravenous thrombolysis during CPR. The patient collapsed after 1 h of persistent chest pain. Emergency medical services initiated advanced life support, including chest compressions, airway management, and adrenaline administration. On hospital arrival, the patient experienced recurrent cardiac arrest. Despite prolonged resuscitation attempts, spontaneous circulation could not be sustained. Following family consent, intravenous thrombolytic therapy with heparin and alteplase was administered during ongoing CPR. Following thrombolytic therapy, sustained return of spontaneous circulation was achieved. Coronary angiography confirmed right coronary artery thrombosis, and percutaneous coronary intervention with stent implantation was performed. The patient was stabilized with temporary pacing, transferred to the intensive care unit, and later discharged with full neurological recovery. This case suggests that intravenous thrombolysis administered during CPR for AMI-related cardiac arrest may be a feasible rescue strategy when conventional measures are insufficient. Early thrombolytic decision-making, high-quality CPR, and multidisciplinary collaboration contributed to the favorable outcome. This report adds to the growing body of evidence regarding the potential role of thrombolysis in selected resuscitation scenarios.

Introduction

Acute myocardial infarction (AMI) is among the most common etiologies of sudden cardiac arrest (CA) and accounts for a substantial proportion of cardiovascular mortality worldwide^1,2. Despite continuous improvements in prehospital emergency care, defibrillation techniques, and coronary interventions, survival after out-of-hospital CA remains low, with neurologically intact discharge rates reported to be less than 10%^3,4. Cardiopulmonary resuscitation (CPR) constitutes the cornerstone of emergency management, providing temporary perfusion to vital organs. However, CPR does not address the underlying pathology in AMI, namely, acute coronary thrombosis. Without definitive reperfusion, return of spontaneous circulation (ROSC) is often transient, and long-term outcomes remain poor^5,6,7.

In patients with AMI-related CA, prompt restoration of coronary blood flow is essential for survival. Percutaneous coronary intervention (PCI) represents the gold standard reperfusion strategy, yet timely access to the catheterization laboratory is not always feasible in emergency scenarios. Delays may result from the need for patient stabilization, transport logistics, or limited availability of interventional facilities, particularly in resource-constrained settings⁸. Thrombolysis, as a pharmacologic reperfusion strategy, has been extensively validated in AMI and remains recommended when PCI cannot be performed within guideline-recommended timelines⁹. However, its application during ongoing CPR has traditionally been considered a relative contraindication. Current guidelines from the American Heart Association and European Society of Cardiology caution against routine use of thrombolysis during CPR due to concerns regarding severe bleeding complications, especially intracranial hemorrhage⁹. Similarly, national consensus statements classify prolonged CPR as a relative contraindication, largely based on theoretical risks rather than high-level clinical evidence¹⁰. Nevertheless, the evidence base underlying this contraindication remains limited. These recommendations are largely based on expert consensus and extrapolation rather than robust randomized trial evidence. Emerging observational data and case reports suggest that systemic thrombolysis during CPR may be feasible in selected patients, particularly when acute myocardial infarction or pulmonary embolism is strongly suspected^7,10. Retrospective analyses have further indicated that fibrinolytic therapy administered during cardiopulmonary resuscitation may increase the likelihood of return of spontaneous circulation in selected patients, especially in the presence of a thrombotic etiology^11,12. In addition, registry-based studies have reported that selective prehospital thrombolysis may improve short-term resuscitation outcomes, although its effect on long-term survival remains inconsistent^13,14,15,16. Case series and literature reviews focusing on cardiac arrest secondary to pulmonary embolism have similarly demonstrated improved short-term outcomes with thrombolytic therapy, further supporting its potential role in thrombus-driven arrest scenarios^17,18. Mechanistically, thrombolysis directly targets coronary thrombotic occlusion and may improve both macrovascular and microvascular perfusion. Experimental studies indicate that myocardial microcirculatory flow during CPR is closely linked to coronary perfusion pressure, and pharmacologic clot dissolution may enhance myocardial blood flow and increase the likelihood of return of spontaneous circulation(ROSC)^9,11,12. A meta-analysis including more than 4,000 patients reported improved ROSC rates with thrombolysis during CPR, although long-term neurological benefits remain uncertain⁹. However, it is important to acknowledge that evidence in this field remains conflicting. The thrombolysis in cardiac arrest (TROICA) trial, the largest randomized controlled trial evaluating thrombolysis during out-of-hospital cardiac arrest, was terminated early after enrolling approximately 1,000 patients due to the lack of demonstrated survival benefit¹¹. This negative finding contrasts with observational studies and meta-analyses reporting improved ROSC rates, highlighting the complexity of interpreting outcomes in this setting⁹. One possible explanation is that randomized trials such as TROICA included heterogeneous patient populations, many of whom did not have a confirmed thrombotic etiology, thereby diluting the potential benefit of thrombolysis. In contrast, observational studies and case reports often involve selected patients with a high likelihood of thrombotic causes, such as acute myocardial infarction or pulmonary embolism. Similarly, systematic reviews and registry-based analyses have reported heterogeneous findings regarding survival and neurological outcomes following thrombolysis during cardiac arrest^9,12. These discrepancies underscore that, although thrombolysis may improve short-term endpoints such as ROSC, its impact on long-term survival and neurological recovery remains uncertain. Therefore, thrombolysis during CPR should not be considered routine therapy, but rather a potential rescue strategy in carefully selected patients in whom a thrombotic cause is strongly suspected and alternative reperfusion strategies are not immediately available.

In patients who remain pulseless or hemodynamically unstable, deferral of reperfusion until after transfer to the catheterization laboratory may prove futile. In such cases, thrombolysis during ongoing CPR provides a potential “bridge therapy” to definitive revascularization, as in the present case. Moreover, compared with post-ROSC thrombolysis, administration during CPR maximizes the time-dependent benefit of reperfusion, potentially limiting infarct size and preventing recurrent arrest¹³. The global literature reflects heterogeneity in practice. Case reports and small series have described successful outcomes with systemic thrombolysis administered during CPR in both AMI and pulmonary embolism (PE)^14,15. Some observational registries indicate improved ROSC and survival-to-admission rates, whereas others report no survival benefit, underscoring the importance of case selection and CPR quality^9,16. Importantly, most reports emphasize that thrombolysis should not replace high-quality CPR but rather complement it, with guidelines recommending that chest compressions be maintained for at least 60–90 min after thrombolytic administration to allow sufficient therapeutic effect^17,18. Despite ongoing debate, thrombolysis remains the only widely available pharmacologic reperfusion option in settings where PCI cannot be performed immediately. As such, clinical decision-making must balance the risks of bleeding against the potential futility of continued CPR without reperfusion. This case provides additional clinical context for this scenario for several reasons. First, the patient’s clinical scenario exemplifies a typical indication: acute inferior ST-segment elevation myocardial infarction complicated by recurrent CA and refractory hemodynamic instability. Second, despite prolonged and high-quality CPR, ROSC was unsustainable until thrombolysis was administered, suggesting a temporal association between thrombolysis and the achievement of sustained ROSC, rather than a definitive causal relationship. Third, subsequent coronary angiography confirmed right coronary artery thrombosis, validating the underlying pathophysiology and justifying thrombolysis as a temporizing measure until PCI could be performed. Finally, the favorable neurological recovery highlights that thrombolysis during CPR can yield meaningful survival, even after prolonged resuscitation, when integrated with multidisciplinary decision-making and rapid transition to interventional therapy.

The overall goal of this report is to illustrate the potential role of intravenous thrombolysis during CPR in AMI-related CA, an area where robust randomized evidence is lacking and clinical practice remains variable. By presenting the decision-making rationale, therapeutic process, and outcome in this patient, we aim to provide clinicians with practical insights into an uncommon but potentially life-saving strategy. We also seek to stimulate further discussion and systematic evaluation of thrombolysis during CPR, particularly in settings where PCI is delayed or unavailable.

Case Presentation:
A 66-year-old man with a history of hypertension and prior cerebral infarction presented with persistent chest pain lasting approximately one hour prior to collapse. Emergency medical services found the patient diaphoretic and intermittently responsive, with electrocardiographic evidence of an inferior ST-segment elevation myocardial infarction. Initial vital signs showed relative bradycardia and preserved blood pressure; however, the patient rapidly deteriorated and developed cardiac arrest with asystole. Advanced life support was initiated immediately, including chest compressions, airway management, and intravenous administration of epinephrine. After approximately 25 min of resuscitation, ROSC was achieved, but hemodynamic instability persisted. Upon arrival at the emergency department, the patient experienced recurrent cardiac arrest requiring repeated resuscitation efforts.

Diagnosis, Assessment, and Plan:
Based on electrocardiographic findings and clinical presentation, an acute inferior ST-segment elevation myocardial infarction was diagnosed as the primary cause of cardiac arrest. The persistence of hemodynamic instability and recurrent arrest despite advanced life support suggested ongoing coronary occlusion as the underlying mechanism. Differential diagnoses included pulmonary embolism and primary arrhythmic causes; however, the presence of ST-segment elevation and subsequent angiographic findings supported coronary thrombosis as the principal etiology.

Given the inability to achieve sustained ROSC and the anticipated delay in immediate PCI, a multidisciplinary decision was made to initiate systemic thrombolysis during ongoing CPR as a time-critical reperfusion strategy. The risks of bleeding were carefully weighed against the high likelihood of mortality without reperfusion. After obtaining informed consent from the patient’s family, intravenous thrombolytic therapy with alteplase and adjunctive anticoagulation was administered. Following successful ROSC, the patient was stabilized and transferred for urgent coronary angiography and PCI, which confirmed right coronary artery occlusion and enabled definitive revascularization.

Protocol

This study was conducted in accordance with the Declaration of Helsinki and was approved by the Ethics Committee of Yantaishan Hospital. Written informed consent for publication was obtained from the patient’s family. This protocol narrates the real-world clinical course of a 66-year-old man with inferior ST-segment elevation myocardial infarction (STEMI) who suffered recurrent cardiac arrest (CA). Intravenous thrombolysis with alteplase was administered during ongoing cardiopulmonary resuscitation (CPR), followed by definitive revascularization with PCI. Timings, doses, monitoring, and decision points reflect the actual care pathway in this case.

1. Prehospital scene assessment and initial management

1. The patient had developed epigastric chest pain and chest tightness after stair climbing, persisting without relief for 1 h, and subsequently lost consciousness for 30 min before arrival. On assessment, the patient was diaphoretic and somnolent but intermittently responsive to verbal stimulus, indicating epigastric discomfort.
   NOTE: Scene safety was confirmed, and the patient was positioned on a flat surface with continuous monitoring applied. The time of symptom onset was documented to guide subsequent reperfusion decision-making.
2. Continuous electrocardiogram (ECG) monitoring showed inferior ST-segment elevation, consistent with acute inferior STEMI. Initial vital signs recorded a heart rate of approximately 50 bpm, blood pressure 130/70 mmHg, and oxygen saturation 90–95% with supplemental oxygen.
   NOTE: A 12-lead ECG was obtained and archived. ST-segment elevation in the inferior leads was confirmed to guide triage and early reperfusion planning.
3. Intravenous access was secured and isotonic fluids initiated (250 mL of normal saline). During IV placement, the patient experienced sudden unresponsiveness with asystole on the monitor and loss of carotid pulse.
   NOTE: A rhythm strip documenting the transition to asystole was obtained and archived. The time of arrest initiation was recorded to support accurate resuscitation timeline documentation.
4. High-priority resuscitation commenced with manual chest compressions performed at a rate of 100–120 compressions/min and a depth of approximately 5–6 cm, allowing full chest recoil and minimizing interruptions to less than 10 s during rhythm and pulse checks^4,5.
   ​NOTE: High-quality CPR in this protocol followed guideline-recommended parameters and was continuously monitored using end-tidal CO₂ as a surrogate marker of perfusion. CPR quality was maintained through structured team role allocation and compressor rotation approximately every 2 min to reduce fatigue and ensure consistency.
   1. A supraglottic airway was used initially, followed by endotracheal intubation with tube depth confirmed by bilateral chest auscultation and waveform capnography.
   2. Mechanical ventilation was then provided with an FiO₂ of 100%, tidal volume of approximately 6–8 mL/kg predicted body weight, and a respiratory rate of 10 breaths/min. Intravenous epinephrine (1 mg) was administered at approximately 3-min intervals⁴.
      ​NOTE: Tube position was verified by waveform capnography and auscultation. Compressor and airway roles were assigned, and medication administration times were recorded on a code sheet.
5. After 25 min of continuous CPR, ROSC was achieved with sinus bradycardia (40–50 bpm) and hypotension (BP approximately 70/40 mmHg).
   1. Atropine (1 mg IV) was given as a slow bolus. Dopamine 100 mg was diluted in 100 mL of normal saline and started via infusion pump, with the rate titrated based on blood pressure and heart rate responses during transport preparation.
      NOTE: A palpable carotid pulse was restored, and end-tidal CO₂ increased from low values to a stable plateau. A transport checklist was completed, confirming that the airway was secured, monitors were attached, vasopressor infusion was ongoing, and intravenous lines were patent. End-tidal CO₂ was continuously monitored and used as a surrogate marker of CPR quality and perfusion^5,11.

2. Emergency department reassessment and recurrent arrest

1. On arrival, the patient was comatose with HR 50 bpm, RR 12, BP 60/40 mmHg, SpO₂ 90%. Pupils measured 4.0 mm with sluggish light reflexes; lungs had coarse breath sounds; heart rhythm was regular but bradycardic.
   NOTE: Continuous monitoring displayed sinus bradycardia with poor perfusion indices. A nursing flowsheet was initiated for ongoing clinical documentation.
2. Shortly after arrival in the emergency department, recurrent cardiac arrest occurred with asystole on the monitor and absent arterial pulsation. CPR was resumed immediately. Epinephrine 1 mg IV was administered at 3–5-min intervals. Atropine (1 mg IV) was repeated for bradyasystolic tendencies; Shenfu injection (100 mL) and crystalloids were continued to support perfusion.
   NOTE: Rhythm and pulse checks were performed approximately every 2 min. Compressor changes were made at similar intervals, when personnel were available, to reduce fatigue and maintain compression quality⁴.
3. Several minutes after resuscitation was resumed, pulseless electrical activity (PEA) appeared with a rate of 30–40 bpm, but no palpable carotid pulse. High-quality compressions continued; atropine (1 mg IV) was administered again at the treating team’s judgment; vasopressor/inotrope infusions were maintained.
   NOTE: PEA was confirmed on multi-lead monitoring. An arterial line was not yet available; therefore, pulse checks and ultrasound-assisted assessments were used for correlation.

3. Decision to initiate systemic thrombolysis during CPR

1. Given inferior STEMI, refractory arrests, and unstable hemodynamics despite advanced life support, the emergency physician, cardiologist, and family members conducted an urgent bedside discussion regarding the indication, expected benefit, and major bleeding risk of thrombolysis during ongoing CPR^9,10. After verbal agreement was obtained from the patient’s family, the decision and time of consent were documented in the medical record by the physician in charge.
   NOTE: Consent was documented in the medical record. A team briefing was conducted to outline the expected benefits, risks, and workflow during thrombolytic infusion.
2. Heparin (5,000 U IV) was administered as a bolus through a dedicated venous line immediately before thrombolysis⁹.
   NOTE: Anticoagulation was administered and independently double-checked by two clinicians using dose-patient-drug verification. The infusion pump was primed for thrombolytic delivery.
3. Alteplase was administered through a separate intravenous line as a 15 mg IV bolus, followed by 50 mg diluted in 100 mL of normal saline for infusion over 30 min and then 35 mg over 60 min using an infusion pump^9,17. Before infusion, the drug name, dose, line patency, and pump settings were verified independently by two clinicians.
4. CPR was continued throughout thrombolysis, with interruptions limited to brief rhythm and pulse checks every 2 min.
   NOTE: Infusion pump parameters, including rate, volume, and time, were cross-checked. Tubing was secured to prevent dislodgment during chest compressions, and the cumulative dose was displayed and recorded.
5. During thrombolytic infusion, recurrent asystole episodes were managed with uninterrupted CPR. Shortly thereafter, PEA reappeared (30–40 bpm) without a palpable pulse. Arterial blood gas analysis was obtained immediately at the bedside, and sodium bicarbonate (125 mL IV) was administered after metabolic acidosis was identified.
6. Additional normal saline 250 mL was infused, and dopamine support was continued with bedside reassessment of blood pressure, pulse status, and oxygen saturation^17,18.
   NOTE: The arterial blood gas panel was printed, and the bicarbonate dose and administration time were documented. Vasopressor dose adjustments were recorded alongside MAP/SpO₂ trends.
7. After approximately 50 min of combined CPR and thrombolysis, sustained ROSC was achieved with sinus bradycardia 38 bpm; BP 85/51 mmHg, SpO₂ 90% on mechanical ventilation. The patient exhibited agitation and involuntary struggling, for which diazepam (10 mg IV) was administered; dopamine infusion was continued.
   NOTE: A palpable pulse was documented by two providers. Perfusion parameters improved, and the sedation level was reassessed after diazepam administration, with ventilator synchrony restored.

4. Post-ROSC bedside assessment and stabilization

1. Bedside transthoracic echocardiography was performed using standard parasternal and apical views immediately after ROSC to assess ventricular function, wall motion abnormalities, and right-sided chamber size¹⁰. Segmental wall motion abnormalities involving the septum and inferior wall, right ventricular dilatation, mild-to-moderate tricuspid regurgitation, and reduced LV systolic function with an EF of 35% were documented and archived⁴.
   NOTE: Echocardiographic images were saved with measurements, and cine loops were archived. Hemodynamic implications, including RV strain and LV dysfunction, were discussed with the team.
2. Repeat 12-lead ECG showed persistent inferior ST-segment elevation, suggesting incomplete reperfusion. Point-of-care tests returned troponin-T 0.079 ng/mL and pro-BNP 451.3 pg/mL.
   NOTE: ECG strips were labeled with time, and biochemical results were appended to the medical chart. The reperfusion criteria checklist was updated, indicating incomplete ST-segment resolution.
3. Cardiology and intensive care teams were consulted; definitive coronary angiography and PCI were recommended. During continued stabilization, the patient remained intermittently agitated; a second dose of diazepam (10 mg IV) was given to facilitate ventilator synchrony and safe transport.
   NOTE: Airway security was reconfirmed, including cuff pressure and ETT depth. Vasopressor infusion rates and IV line patency were rechecked, and transport documentation was completed.

5. Preparation and transfer to the catheterization laboratory

1.  Prior to transfer, a transport checklist that included confirmation of endotracheal tube depth and fixation, ventilator function, battery status, oxygen supply, infusion pump settings, drug availability, and continuous ECG, blood pressure, and pulse oximetry monitoring was completed⁵. A physician, nurse, and porter accompanied the patient during transfer, with emergency drugs and a manual resuscitation bag available at the bedside.
   NOTE: The transport safety checklist was completed and signed, confirming airway, breathing, circulation, medications, and equipment readiness. The destination team was informed, and the estimated time of arrival was communicated.
2. Upon arrival in the cath lab, the patient experienced a brief arrest with idioventricular rhythm and no carotid pulse. Chest compressions were resumed promptly; epinephrine (1 mg IV) was given. ROSC returned within 1 min.
   NOTE: Real-time rhythm documentation was captured, and the time to ROSC was recorded. The procedure proceeded after a team huddle confirmed clinical stability.

6. Coronary angiography, PCI, and rhythm management

1. Coronary angiography was performed immediately upon arrival in the catheterization laboratory using standard femoral arterial access under sterile conditions^6,7. Diagnostic angiographic projections were obtained to systematically evaluate the left and right coronary arteries. Angiography demonstrated three-vessel coronary artery disease with acute thrombotic occlusion of the right coronary artery (RCA), confirming the culprit lesion. The thrombolysis in myocardial infarction (TIMI) flow grade was assessed before intervention.
   NOTE: Angiographic images were archived with lesion labeling. TIMI flow grading was documented before and after the intervention.
2. Culprit-lesion PCI was performed on the RCA. After guidewire passage across the occlusion, balloon predilation was conducted, followed by stent implantation to restore antegrade coronary blood flow^6,13. Final angiography confirmed successful revascularization with improved TIMI flow.
3. Due to persistent bradycardia and hemodynamic instability, a temporary transvenous pacemaker was inserted via venous access under fluoroscopic guidance. Proper positioning was confirmed, and pacing capture and threshold were verified before completion of the procedure.
   NOTE: The final angiogram confirmed revascularization of the RCA. Pacing thresholds and capture were verified, and device parameters were documented.
4. Throughout the procedure, the patient remained intubated and mechanically ventilated with continuous ECG, blood pressure, and oxygen saturation monitoring. Sedation was maintained with intermittent intravenous diazepam as needed to ensure ventilator synchrony. Intravenous fluids and vasoactive support (dopamine infusion) were titrated according to hemodynamic parameters.
5. At the end of the procedure, the vascular access site was carefully inspected and compressed to achieve hemostasis, and no immediate bleeding complications were observed.
   NOTE: The post-PCI hemodynamic panel was saved. Sedation scale scores and ventilator parameters were trended, and access site hemostasis was checked before transfer.

7. Immediate post-procedural care, ICU course, and outcome

1. The patient was transferred to the ICU with ongoing vasopressor support and mechanical ventilation⁵. Over the ensuing hours to days, hemodynamics improved, sedation was tapered, and ventilator weaning was initiated as gas exchange and neurological examination allowed.
   NOTE: Daily laboratory values and ABGs were trended. Vasopressor dose down-titrations were correlated with MAP, and delirium and sedation scale scores were recorded.
2. Neurological status and respiratory function were evaluated daily. Readiness for extubation was determined based on improvement in consciousness, stable spontaneous breathing, adequate oxygenation, and intact airway protective reflexes. After meeting these criteria, the endotracheal tube was successfully removed.
3. Follow-up electrocardiography performed within the first 24 h after PCI, once hemodynamic stabilization was achieved in the intensive care unit, demonstrated normalization of ST segments. The patient regained clear consciousness without neurological deficits, allowing transfer to the general ward.
   NOTE: ECG comparison, including index and post-reperfusion recordings, was attached. The extubation criteria checklist was satisfied, and swallow and cough reflexes were documented.
4. The patient was discharged in good clinical condition with plans for regular outpatient follow-up. The case timeline, including arrest durations, drug doses, thrombolysis schedule, angiographic findings, and complications, was summarized in the discharge documentation to support continuity of care and future quality review.
   NOTE: The discharge summary included a succinct event timeline and medication log. The outpatient plan and warning signs were communicated to the patient and family.

8. Quality and safety notes

1. Team roles (code leader, compressor, airway, medication nurse, recorder) were explicitly assigned at each resuscitation phase to reduce task overlap and maintain closed-loop communication during drug administration and infusion pump adjustments.
2. A two-clinician check was employed for drug verification for heparin and alteplase dosing and pump programming, recorded with time stamps that aligned with rhythm checks, to ensure synchronized assessments and minimize compression pauses.
3. Transport safety emphasized redundancy (backup oxygen/batteries) and pre-transfer huddles to anticipate re-arrest, which did occur briefly on cath-lab arrival and was rapidly reversed with compressions and epinephrine, minimizing delays to angiography.
4. Documentation fidelity (arrest onset/offset times, ROSC times, rhythm transitions, ABG results, sedation, and vasopressor titrations) was maintained, facilitating retrospective case review and informed subsequent protocol refinement for similar scenarios.

Results

Application of the above management strategy resulted in successful resuscitation and full clinical recovery. On initial prehospital assessment, continuous electrocardiographic monitoring demonstrated acute inferior ST-segment elevation myocardial infarction, confirming the diagnosis of STEMI (Figure 1). Despite fluid resuscitation and vasopressor therapy, the patient experienced cardiac arrest with asystole. After approximately 25 min of advanced life support, ROSC was achieved, although profound bradycardia and hypotension persisted. At that time, heart rate was approximately 40–50 beats per minute, and blood pressure was approximately 70/40 mmHg. Upon arrival at the emergency department, the patient suffered recurrent cardiac arrest. Prolonged resuscitation with concurrent intravenous thrombolysis eventually resulted in sustained ROSC. Sustained ROSC was achieved after approximately 50 min of combined CPR and thrombolytic therapy. At the time of ROSC, heart rate was approximately 38 beats per minute, blood pressure was 85/51 mmHg, and oxygen saturation was approximately 90% under mechanical ventilation. Bedside echocardiography performed after resuscitation revealed segmental wall motion abnormalities involving the septum and inferior wall, right ventricular dilatation, tricuspid regurgitation, and reduced left ventricular systolic function with an ejection fraction of approximately 35%. Cardiac biomarker testing showed a troponin-T level of 0.079 ng/mL and a pro-BNP level of 451.3 pg/mL.

A repeat electrocardiogram obtained shortly after ROSC showed persistent inferior ST-segment elevation, indicating incomplete reperfusion (Figure 2). The patient was stabilized with vasopressor infusion and mechanical ventilation, and was transferred urgently for coronary angiography. Coronary angiography confirmed triple-vessel coronary artery disease with acute thrombotic occlusion of the RCA. Successful balloon angioplasty and stent implantation were performed, and a temporary pacemaker was inserted to stabilize cardiac rhythm (Figure 3, Figure 4, and Figure 5). Post-procedural monitoring demonstrated stabilization of the heart rate at 65–75 beats per minute and blood pressure at 75–85/45–50 mmHg with ongoing vasopressor support. Serial electrocardiographic changes and biomarker trends further supported objective assessment of reperfusion and recovery. Importantly, no clinically significant bleeding complications were observed during or after thrombolytic therapy and PCI. The vascular access site was regularly inspected, and no hematoma or active bleeding was identified. Serial laboratory monitoring demonstrated stable hemoglobin levels without evidence of significant decline. Coagulation parameters, including prothrombin time and activated partial thromboplastin time, remained within acceptable ranges, and platelet counts were stable throughout hospitalization. No signs of intracranial hemorrhage or other major bleeding events were detected.

Following the intervention, the patient was admitted to the intensive care unit. Hemodynamic stability improved gradually, sedation was weaned, and neurological function returned without evidence of hypoxic brain injury. The patient was successfully weaned from mechanical ventilation after stabilization and regained full consciousness. A follow-up electrocardiogram demonstrated normalization of ST-segments prior to discharge (Figure 6). The patient was discharged in good condition and remained stable on outpatient follow-up, underscoring the potential role of thrombolysis administered during CPR as a bridge to definitive revascularization.

Figure 1: Initial prehospital electrocardiogram. Twelve-lead ECG recorded by emergency medical services showing marked ST-segment elevation in the inferior leads, consistent with acute inferior STEMI. Please click here to view a larger version of this figure.

Figure 2: Electrocardiogram following return of spontaneous circulation. Repeat ECG obtained shortly after resuscitation showing persistent inferior ST-segment elevation, indicating incomplete coronary reperfusion. Please click here to view a larger version of this figure.

Figure 3: Coronary angiography: initial findings. Coronary angiography confirming triple-vessel disease with acute thrombotic occlusion of the right coronary artery (RCA). Please click here to view a larger version of this figure.

Figure 4: Coronary angioplasty of the RCA. Balloon angioplasty performed on the occluded RCA as part of primary percutaneous coronary intervention. Please click here to view a larger version of this figure.

Figure 5: Coronary stent implantation. Final angiographic image showing successful stent deployment and restored blood flow in the RCA. Please click here to view a larger version of this figure.

Figure 6: Electrocardiogram before hospital discharge. Follow-up ECG demonstrating normalization of ST-segments, indicating successful reperfusion and recovery. Please click here to view a larger version of this figure.

Discussion

This case demonstrates the successful use of systemic thrombolysis administered during ongoing cardiopulmonary resuscitation (CPR) in a patient with an acute inferior ST-segment elevation myocardial infarction complicated by recurrent cardiac arrest. Despite prolonged resuscitation efforts, sustained ROSC was achieved after thrombolysis, suggesting a temporal association between reperfusion and restoration of effective circulation, rather than a definitive causal relationship. Subsequent coronary angiography confirmed right coronary artery thrombosis, and stent implantation consolidated reperfusion, supporting the potential role of thrombolysis as a bridge to definitive intervention.

Several methodological elements may have contributed to this outcome. High-quality CPR, delivered with minimal interruptions, sustained coronary perfusion pressures, and may have facilitated the effectiveness of thrombolysis. In this case, high-quality CPR was defined and maintained according to established guideline-recommended parameters, including a compression rate of 100–120/min, depth of 5–6 cm, full chest recoil, and minimal interruptions (<10 s). CPR quality was continuously monitored using end-tidal CO₂ as a surrogate marker of perfusion, along with structured team role allocation and regular compressor rotation to minimize fatigue. The decision to initiate thrombolysis during CPR, rather than after repeated unsuccessful attempts at ROSC, maximized the therapeutic window for reperfusion. Careful dosing of alteplase, synchronized with vasopressor support and secured airway management, ensured effective drug delivery under conditions of maintained circulation. These steps illustrate the interdependence of CPR quality, early therapeutic decision-making, and coordinated team execution in determining success.

In this case, the informed consent process was conducted under extreme time-critical conditions. Given the patient’s refractory cardiac arrest and the high likelihood of mortality without immediate reperfusion, a rapid bedside discussion was undertaken with the patient’s family. The indication, potential benefits, and major risks, particularly the risk of severe bleeding associated with thrombolysis during ongoing CPR, were clearly explained to the patient’s family. Given the critical condition and limited treatment options, verbal consent was obtained and documented in the medical record in accordance with institutional emergency protocols. This process reflects real-world decision-making in life-threatening scenarios where immediate intervention is required. Bleeding risk was carefully considered prior to thrombolysis. The patient had no known history of recent major bleeding, intracranial hemorrhage, or contraindications to thrombolytic therapy. Following thrombolysis, close monitoring for bleeding complications was implemented, including repeated assessment of puncture sites, hemodynamic stability, neurological status, and serial laboratory testing, including serial assessment of hemoglobin levels, coagulation parameters (prothrombin time, activated partial thromboplastin time), and platelet counts. No clinically significant bleeding events were observed during hospitalization, supporting the safety of the intervention in this selected case.

Nevertheless, important limitations must be acknowledged. Systemic thrombolysis carries inherent bleeding risks, which may be amplified by trauma from prolonged chest compressions¹⁹. As a single-patient observation, this report cannot establish causality or generalize efficacy. Objective CPR quality metrics, such as compression depth or perfusion pressures, were not quantified and may confound interpretation. Furthermore, outcomes in this patient may not be replicable in different clinical settings, particularly in patients with advanced age, multiple comorbidities, or non-thrombotic causes of cardiac arrest¹⁴. Importantly, causality cannot be established from a single-case observation. Although sustained ROSC occurred after initiation of thrombolysis, alternative explanations must be considered. Prolonged high-quality CPR alone can occasionally result in delayed ROSC, even after extended resuscitation efforts. In addition, multiple concurrent interventions were administered in this case, including vasopressor support, sodium bicarbonate correction of metabolic acidosis, and ongoing advanced life support measures, all of which may have contributed to hemodynamic recovery. Therefore, the observed outcome likely reflects the combined effect of multiple resuscitative interventions rather than thrombolysis alone.

Comparison with alternative strategies provides an important clinical perspective. Conventional CPR with pharmacologic support rarely produces durable outcomes in AMI-related arrest, as coronary occlusion persists⁵. Post-ROSC thrombolysis delays reperfusion beyond the critical therapeutic window, while PCI remains the standard of care but is often delayed by logistics or instability⁶. In this scenario, thrombolysis during CPR offered immediate pharmacological reperfusion, enabling ROSC and safe transition to PCI. This case suggests that early pharmacological reperfusion and subsequent mechanical intervention may act synergistically, rather than competitively, in selected patients⁷.

Future directions extend beyond single cases. Registry-based studies and multicenter cohorts are needed to define patient selection, timing, and dosing strategies for thrombolysis during CPR. The use of real-time monitoring, such as end-tidal CO₂, echocardiography, or cerebral oximetry, may improve clinical decision-making and help predict patient outcomes. Beyond myocardial infarction, thrombolysis during CPR warrants evaluation in cardiac arrest secondary to pulmonary embolism, where thrombotic obstruction is likewise the critical reversible cause.

Finally, reproducibility and clinical usability are central considerations. These approaches, including standardized CPR, structured drug administration, and multidisciplinary coordination, can be applied in other advanced resuscitation settings. Nonetheless, their successful replication requires trained personnel, infrastructure for rapid post-ROSC PCI, and adherence to rigorous protocols. By detailing the procedural sequence, decision-making checkpoints, and integration of thrombolysis with ongoing resuscitation, this case contributes to the existing clinical literature and may help inform clinical decision-making in carefully selected scenarios.

In summary, systemic thrombolysis during CPR may represent a potential adjunctive strategy in selected cases of AMI-related cardiac arrest when conventional measures fail, and immediate PCI is not possible. While promising, this approach must be applied judiciously, with careful attention to bleeding risks and clinical limitations. Expanding systematic data collection will be essential to establish its role within contemporary resuscitation practice.

Materials

List of materials used in this article

Name	Company	Catalog Number	Comments
Alteplase (rt-PA)	Boehringer Ingelheim	NDC 00597-0050-54	15 mg IV bolus + 85 mg infusion protocol; systemic thrombolysis
Arterial blood gas analyzer	Radiometer	ABL800 FLEX	Point-of-care ABG test
Atropine injection	Fresenius Kabi	NDC 63323-039-01	1 mg/amp; used for bradycardia/asystole
Capnography monitor	Medtronic	CS20	Verification of intubation and CPR quality
Coronary angiography system	Siemens Healthineers	Artis zee 2 ceiling	Cath lab PCI and angiography system
Coronary balloon catheter	Medtronic	NC Trek 1012560	Balloon dilatation prior to stent implantation
Coronary stent	Abbott	Xience Sierra RX4180	Drug-eluting stent; deployed in RCA
Defibrillator/monitor	Philips	M3535A	Multiparameter monitor with ECG/defibrillation
Diazepam injection	Roche	NDC 50419-460-05	10 mg/2 mL; sedation for ventilator synchrony
Dopamine hydrochloride injection	Fresenius Kabi	NDC 63323-082-10	200 mg/20 mL; vasopressor infusion
ECG machine (12-lead)	Nihon Kohden	CardioFax GEM 9022	Standard 12-lead ECG monitoring
Echocardiography system	GE Healthcare	H45052AA	Bedside echo; EF and wall motion assessment
Endotracheal tube	Teleflex	REF 100/185	ID 7.0–8.0 mm; airway intubation
Epinephrine injection	Hospira	NDC 00409-4927-10	1 mg/amp; administered every 3–5 min during CPR
Heparin sodium injection	Pfizer	NDC 00409-2721-01	5000 U/amp; IV bolus before thrombolysis
Infusion pump	B. Braun	8713050U	Continuous infusion of rt-PA and vasopressors
Shenfu injection	Livzon	NDC 69281-123-10	100 mL; adjunctive circulatory support
Sodium bicarbonate injection	Baxter	NDC 0338-0517-10	5% 125 mL; correction of metabolic acidosis
Supraglottic airway (LMA)	Ambu	322100000	Size 4/5; initial airway management
Temporary pacing lead	Medtronic	6416	Transvenous pacing catheter post-PCI