Hypoxic cardiopulmonary arrest with full recovery after induced hypothermic therapy

Abstract

Case

The patient's chart was reviewed, summarized, and presented.

Outcome

A 41‐year‐old male collapsed after complaining of dyspnea just before the end of a hemodialysis session. He was just being introduced to hemodialysis. The patient's percutaneous oxygen saturation dropped to 50% even under inhalation of 10 L/minute of oxygen and he developed pulseless electrical activity. After tracheal intubation, a return of spontaneous circulation was noted. His truncal CT disclosed a bilateral diffuse ground glass appearance and pleural effusion were noted. Induced mild hypothermic therapy and mechanical ventilation resulted in the improvement of his respiratory function and consciousness. A coronary angiogram and left ventriculography showed no significant lesion, and his pulmonary edema was considered to have been induced by over‐hydration due to renal failure, diastolic heart failure or dialysis disequilibrium syndrome. He was discharged without any neurological deficit.

Conclusion

Tracheal intubation with ventilation for hypoxic cardiopulmonary arrest and induced hypothermic therapy after obtaining spontaneous circulation may be factors of favorable outcome of this case.

Introduction

The outcome of patients with pulseless electrical activity is unfavorable in comparison to that of patients with shockable rhythm, such as ventricular fibrillation, because patients with pulseless electrical activity tend to have severe underlying diseases.1 In addition, the efficacy of induced hypothermia for patients who obtain a return of spontaneous circulation in the in‐hospital setting is controversial. Nichol et al. reported that induced hypothermia was not associated with either an improved or worsened survival or a neurologically favorable survival by a retrospective analysis of a multicenter prospective cohort of patients with in‐hospital cardiac arrest (IHCA) enrolled in an ongoing quality improvement project.2 In contrast, Kim et al. reported that induced hypothermia was associated with reduced in‐hospital mortality for adult patients resuscitated from non‐shockable cardiac arrest based on a systematic review and meta‐analysis.3 We herein report a case of in‐hospital hypoxic pulseless electrical activity where the patient obtained a full recovery after induced hypothermic therapy.

Case Report

A 41‐year‐old male collapsed after complaining of dyspnea just before the end of a hemodialysis session in our hospital. The patient was being introduced to hemodialysis and was undergoing his fifth course. He weighed 112 kg at the time of the first hemodialysis, which was reduced to 106 kg by the fifth hemodialysis, so dehydration was not carried out on that day. His past history included acute pancreatitis, diabetes mellitus, and hypertension, which had developed when he was 24 years old. He had prescriptions for ezetimibe, amlodipine, candesartan, furosemide, doxazosin mesilate, rosuvastatin, and esomeprazole to control his type 2 diabetes mellitus, hypertension, and hyperlipidemia, however, his diabetic retinopathy and nephropathy deteriorated, and he underwent laser photocoagulation, and dialysis was initiated. He had experienced a cough and low‐grade fever 1 week before, and had been treated with 250 mg levofloxacin. His mother and a younger brother also had diabetes mellitus.

The patient's percutaneous oxygen saturation dropped to 50% even under inhalation of 10 L/min of oxygen and he became unconscious. When an emergency physician checked him after a code blue was called, his vital signs were as follows: Glasgow Coma Scale score, E1V1M1; blood pressure, 232/136 mmHg; pulse rate, regular at 140 beats per minute; saturation of peripheral oxygen on 12 L/min was 47%. However, immediately after evaluation, the patient's blood pressure and pulse rate dropped to 92/30 mmHg and 45 beats per minute. Infusion of 0.5 mg atropine was not effective. The results of his arterial blood gas analysis are shown in Table 1. He thereafter developed pulseless electrical activity and was treated using chest compressions, the infusion of 1 mg adrenaline, and tracheal intubation. When tracheal intubation was carried out, a large amount of foamy fluid was recognized in his oral cavity. Two minutes after tracheal intubation, a return of spontaneous circulation was noted. At that time, the patient's systolic blood pressure was 220 mmHg, his pulse rate was 130 beats/minute and his arterial blood gas levels under FiO₂ 1.0 immediately after the return of spontaneous circulation showed combined acidosis (Table 1), which was corrected by the infusion of 200 mL bicarbonate. The estimated collapse time was 4 min. His electrocardiogram showed sinus tachycardia, and cardiac sonography revealed diffuse hypokinesis (ejection fraction <30%). His head CT showed no significant changes, and enhanced truncal CT disclosed no embolus in the pulmonary arteries, but a bilateral diffuse ground glass appearance and pleural effusion were noted (Fig. 1).

Table 1.

Time‐course of results of arterial blood gas analysis in a 41‐year‐old male who collapsed after complaining of dyspnea during hemodialysis

Timing	Oxygen condition	pH	PaCO2 (mmHg)	PaO2 (mmHg)	HCO3‐ (mmol/L)	BE (mmol/L)	Lactate (mmol/L)
Before CPA	12 L/min	7.187	71.0	16.0	25.9	−2.9	3.6
After ROSC	FiO2 1.0	7.069	76.5	88.1	21.1	−9.6	6.8
In ICU	FiO2 1.0	7.332	58.8	383.1	30.4	3.7	—

—, not measured. BE, base excess; CPA, cardiopulmonary arrest; ICU, intensive care unit; ROSC, return of spontaneous circulation.

Figure 1.

Chest computed tomography scan after obtaining spontaneous circulation in a 41‐year‐old male who collapsed after complaining of dyspnea during hemodialysis. The scan shows diffuse lung edema with bilateral pleural effusion.

A complete blood cell count showed white blood cells at 8,900/mm³, hemoglobin at 10.2 g/dL and platelets at 21.8 × 10⁴/mm³. The serum biochemical analyses revealed a total bilirubin level of 0.8 mg/dL, aspartate aminotransferase of 20 IU/L, alanine aminotransferase of 13 IU/L, blood urea nitrogen of 23.7 mg/dL, creatinine of 5.2 mg/dL, creatine phosphokinase of 508 IU/L, sodium if 143 mEq/L, potassium of 3.6 mEq/L, chloride of 103 mEq/L, C‐reactive protein of 1.2 mg/dL, prothombin time of 12.7 (11.8) s, activated partial thromboplastin time of 30.6 (27.7) s, fibrinogen degradation products of 20.7 μg/mL, and a brain natriuretic peptide level of 1,521 pg/mL. The results of the arterial blood gas analysis after mechanical ventilation are shown in Table 1. As the patient remained in a coma state after resuscitation, he underwent 24 h of induced mild hypothermic therapy (target temperature: 34°C ± 0.5°C for 24 h and rewarming for 8 h using a water blanket, midazolam, and vecuronium). The high blood pressure was controlled by an infusion of heparin and nitrate for suspected acute coronary syndrome, and continuous hemodiafiltration was carried out for the negative water balance. He temporarily showed signs of hypoxemia due to obstruction of the bronchus due to infectious sputum, and an infusion of an antibiotic and high positive end‐expiratory pressure mechanical ventilation resulted in the improvement of his respiratory function. The sputum culture was later found to be negative. In addition, his consciousness level also improved so that he could obey orders, and he was extubated on the sixth day after the collapse in the hospital.

A coronary angiogram on the 23rd hospital day revealed no significant stenosis, left ventriculography showed normal cardiac wall motion, and his pulmonary edema was considered to have been induced by overhydration due to renal failure, diastolic heart failure, or dialysis disequilibrium syndrome.4 He was discharged on foot without any neurological deficit on the 32nd hospital day.

Discussion

There are two learning points that can be obtained from the present case. First, tracheal intubation or securing an airway with instruments is extremely important when cardiopulmonary arrest is induced by hypoxemia. In recent studies, it has been shown that for advanced cardiac life support, chest compression is more important that tracheal intubation with regard to cardiopulmonary arrest. However, the patient in this case collapsed due to acute onset pulmonary edema, and simple oxygen inhalation or bag valve mask ventilation was not sufficiently effective due to the intra‐oral secretion induced by lung edema and the severe diffuse lung edema itself. In such cases, tracheal intubation with instruments using high positive end‐expiratory pressure ventilation is necessary to obtain a favorable outcome.5, 6, 7 Bilevel positive airway pressure or simple bag valve mask ventilation with oxygen is not effective for treating hypoxemia associated with a large amount of sputum, as was supported by our present case. Avoiding the interruption of chest compressions may be recommended when tracheal intubation is carried out, at least during initial phases of resuscitation,8 because continuous chest compression has been shown to improve the neurological outcome following cardiac arrest. After carrying out tracheal intubation, hyperventilation should be prevented, because hyperventilation increases the intrathoracic pressure, diminishes the venous return, and decreases the coronary perfusion.8

The second point is that induced hypothermia might be effective for patients with in‐hospital pulseless electrical activity. The majority of previous IHCA studies have shown that patient age, pre‐arrest morbidity, first monitored rhythm, time to cardiopulmonary resuscitation, defibrillation or return of spontaneous circulation (ROSC) and location of IHCA are associated with survival.9 In this case, the patient's younger age, the short time to cardiopulmonary resuscitation, and the short time to ROSC might have been factors associated with the favorable outcome. Nevertheless, the outcome for patients with pulseless electrical activity is generally unfavorable in comparison with patients with shockable rhythm. In addition, there have been no reports that have indicated the efficacy of induced hypothermic therapy for pulseless electrical activity, because patients with pulseless electrical activity tend to have severe underlying diseases that may preclude such treatment.1, 10 However, small studies have indicated the efficacy of hypothermic therapy for pulseless electrical activity if the patients do not have severe underlying disease and when the duration of collapse is short, as it was in our case.11, 12 As most of the previous studies had substantial risks of bias, and as the quality of evidence was low concerning the impact of induced hypothermia for patients who obtained a return of spontaneous circulation, further high quality randomized clinical trials are needed to confirm the benefits of induced hypothermia in this population.

Conflict of interest

None.