Is It Possible to Maintain Consciousness and Spontaneous Ventilation with Chest Compression in the Early Phase of Cardiac Arrest?

Hindawi Publishing Corporation Case Reports in Anesthesiology Volume 2016, Article ID 3158015, 4 pages http://dx.doi.org/10.1155/2016/3158015 Case Report Is It Possible to Maintain Consciousness and Spontaneous Ventilation with Chest Compression in the Early Phase of Cardiac Arrest? Menekse Oksar and Selim Turhanoglu Department of Anesthesiology and Reanimation, Mustafa Kemal University Faculty of Medicine, 31100 Hatay, Turkey Correspondence should be addressed to Menekse Oksar; Received 29 October 2015; Revised 5 January 2016; Accepted 17 January 2016 Academic Editor: Pavel Michalek Copyright © 2016 M. Oksar and S. Turhanoglu. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Chest compression is important in cardiopulmonary resuscitation. However, life support algorithms do not specify when chest compression should be initiated in patients with persistent spontaneous normal breathing in the early phase after cardiac arrest. Here we describe the case of a 69-year-old man who underwent femoral bypass surgery and was extubated at the end of the procedure. After extubation, the patient’s breathing pattern and respiratory rate were normal. The patient subsequently developed ventricular fibrillation, evident on two monitors. Because defibrillation was ineffective, chest compression was initiated even though the patient had spontaneous normal breathing and defensive motor reflexes, which were continued throughout resuscitation. He regained consciousness and underwent tracheal extubation without neurological sequelae on postoperative day 1. This case highlights the necessity of chest compression in the early phase of cardiac arrest. 1. Introduction 2. Case Report The 2010 American Heart Association recommendations and European Resuscitation Council guidelines for cardiopulmonary resuscitation (CPR) focus on the requirement of immediately initiating chest compression and ventilation to maintain cerebral blood flow and adequate gas exchange, respectively [1]. Maintaining cerebral perfusion prevents neurological damage. Some studies have shown that conscious, spontaneous breathing may continue for a short time after cerebral perfusion stops; for example, repeated rhythmic coughs every 1–3 s maintained consciousness for up to 39 s in three patients who developed ventricular fibrillation during coronary arteriography [2]. Cardiac arrest survivors recall memories of awareness, fear, and persecution after CPR [3]. Early diagnosis of cardiac arrest may prolong spontaneous breathing and consciousness by maintaining cerebral perfusion through effective chest compression. We present a 69-year-old man with uninterrupted spontaneous normal breathing during CPR. A 69-year-old man (American Society of Anesthesiologists class 2; weight 70 kg; height 1.72 m) with peripheral arterial disease and diabetes mellitus underwent femoral bypass surgery. Anesthesia was induced using 2 mg midazolam, 100 𝜇g fentanyl, and 2 mg/kg propofol. Endotracheal intubation was achieved with 40 mg rocuronium, anesthesia was maintained by 2% sevoflurane with N2 O and 50% O2 , and diuretic and insulin infusions were administered as required. The patient showed normal blood gas levels (pH, 7.36; PaCO2 , 43 mmHg; PaO2 , 92 mmHg; lactate, 3.5 mmol/L; and base excess, 1.2 mmol/L). His blood glucose level was 220 mg/dL, O2 saturation level was 99% on 50% O2 , heart rate (HR) was 88 beats/min, and mean arterial pressure (MAP) was 70 mmHg. Neuromuscular blockade was reversed using 200 mg sugammadex, and the patient was extubated. Thereafter, his breathing pattern was regular, with a respiratory rate of 17 breaths/min and a tidal volume of 600 mL. Oxyhemoglobin saturation determined using pulse oximetry 2 was 99%, invasive arterial blood pressure was 140/90 mmHg (MAP, 106 mmHg), and HR was 100 beats/min. Further, a transport monitor was connected. The patient subsequently developed ventricular fibrillation (VF), evident on 2 monitors. A biphasic 150-J shock was administered immediately, and ventilation was initiated with a facemask supplying O2 at 6 L/min before his trachea was reintubated without a neuromuscular blocking agent. Ventilatory support was manually administered because he was breathing spontaneously. After the first shock, external cardiac massage was applied for 2 min. However, the patient remained in VF; therefore, a second shock was administered, followed by further chest compression. The patient became asystolic and received 1 mg intravenous epinephrine. Although spontaneous breathing persisted, CPR was continued. Shocks and chest compression continued for 1 h, with epinephrine administered every 3–5 min with short breaks to assess cardiac rhythm. The chest compression evoked defensive motor reflexes, such as flexion of the neck, trunk, and arms, and arterial traces were determined to originate from external cardiac massage during resuscitation. During resuscitation, arterial blood gas recordings showed acidosis with an abnormally low pH, high lactate, and low base excess. PaCO2 was normal during VF and resuscitation, but it increased by the end of resuscitation. Although assisted breathing was provided throughout resuscitation, the rate of spontaneous breathing was 16-17 breaths/min with a tidal volume of 600 mL/min. During resuscitation, endtidal CO2 was 19–22 mmHg. The potassium level was normal intraoperatively (3.6 mmol/L), reduced during resuscitation (2.0 mmol/L), and increased with potassium replacement therapy by the end of resuscitation (3.2 mmol/L). The patient remained asystolic until circulation resumed spontaneously. After resuscitation, the HR was recorded at 51 beats/min with ST depression observed on electrocardiography (ECG) (Table 1). Measurements recorded at baseline, preoperatively, during CPR, and after CPR are shown in Table 1. Spontaneous breathing continued without interruption throughout the entire CPR period. Following tracheal intubation, ventilation was manually assisted with the balloon of a breathing circuit throughout the entire CPR period and an Ambu bag during patient transfer following resuscitation. The actual measured duration of asystole was 50 min. VF lasted for approximately 10 minutes. During cardiac arrest, defibrillation attempts were made and chest compression was initiated in order to maintain adequate blood pressure. CPR was continued until potential underlying correctable causes of VF (such as the hypokalemia and low arterial pH levels in the present case) were determined and corrective interventions could be performed. Approximately 1 hour after correction of the metabolic causes of VF, during which spontaneous breathing and continued motor responses to chest compression without QRS complexes on electrocardiography were observed, the patient was reviewed by a cardiologist and was subsequen (...truncated)