What Is Lazarus Phenomenon?
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First, you receive a phone call from the hospital. The officials reveal to you that your loved one has been pronounced dead. What would your reaction be if 2 hours later, the doctor calls you again to tell you that your loved one back alive? Puzzled? Numb? Going to get a second doctor’s opinion whether your loved one is really alive or dead by checking the name once again? Simply overjoyed? Call the doctor again and ask him to use a different stethoscope? Or maybe, call all your friends and relatives to have a “Welcome back, party?”.....Well, a series of perplexed thoughts are sure to run wild in our thoughts if this happens to our families. Of course, the variations, your heart beat rate and the intensity differs from individuals. Imagine the joy, of having to call out your relatives and friends again to notify that your loved dead is back from the dead. As for their reaction, your guess is as good as mine. After all, some would still want to see him/her and pat on the back and may want to say, “Hey, your lifeline has just been renewed and extended for an indefinite period of time, don't screw up your life and health with your second chance.” ...It’s called the Lazarus Phenomenon (sometimes called Lazarus syndrome) , and goes to prove what a fantastic machine the human body really is. What is Lazarus Phenomenon? The Lazarus phenomenon is described as delayed “Return Of Spontaneous Circulation” (ROSC) after cessation of cardiopulmonary resuscitation (CPR). This was first reported in the medical literature in 1982, and the term Lazarus phenomenon was first used by Bray in 1993. The term was coined from the story of Lazarus, who was resurrected by Jesus Christ four days after his death. Even though Lazarus phenomenon is rare, it is probably under reported. There is no doubt that Lazarus phenomenon is a reality but so far the scientific explanations have been inadequate. So far the only plausible explanation at least in some cases is auto-positive end- expiratory pressure (PEEP) and impaired venous return. In patients with pulseless electrical activity (PEA) or asystole, dynamic hyperinflation should be considered as a cause and a short period of apnoea (30-60 seconds) should be tried before stopping resuscitation. Since ROSC occurred within 10 minutes in most cases, patients should be passively monitored for at least 10 minutes after the cessation of CPR before confirming death. Case Report A 66-yr-old man, weighing 80 kg, was emergently brought to the operating room (OR) with a suspected leaking abdominal aortic aneurysm. His past history included hypertension and a transient ischemic attack 4 yr earlier. He also had a 50-pack/yr smoking history and chronic renal insufficiency (creatinine 2.3 mg/dL). He had no history of metabolic disorder. He had received 2600 mL of lactated Ringer’s solution before arrival in the OR. Vital signs on arrival included a heart rate of 120 bpm and a systolic blood pressure of 60 mm Hg. The patient was pale, mottled, diaphoretic, and tachypneic. Rapid administration of warmed IV fluids via two rapid infusion systems increased his systolic blood pressure to 120 mm Hg. Induction of anaesthesia proceeded uneventfully with d-tubocurarine 3 mg, fentanyl 250 µg, etomidate 20 mg, and succinylcholine 160 mg IV before rapid sequence endotracheal intubation. Maintenance of anesthesia included inhalation of isoflurane (as tolerated by blood pressure) in 100% oxygen. Pancuronium 6 mg was given for continued neuromuscular blockade. With induction of anesthesia, the vital signs remained stable (systolic blood pressure 110–120 mm Hg by automated cuff pressure) and surgical incision promptly followed at 5.30 p.m. An arterial blood gas drawn at this time revealed hemoglobin 8.1 g/dL, + K 3.8 mEq/L, glucose 185 mg/dL, pHa 7.24, PaCO2 41 mm Hg, PaO2 479 mm Hg, HCO316 mEq/L, and base excess −10.6 mEq/L. At this time, the end-tidal CO2 was 29 mm Hg. Electrocardiogram (ECG) showed a cardiac rhythm of sinus tachycardia. At 5.48 p.m. the surgeon placed a cross-clamp across the suprarenal aorta. This led to an increase in systolic pressure to 160 mm Hg, but no apparent changes on the ECG. At 5.53 p.m. the clamp was shifted to an infrarenal position. At 5.59 p.m., the cardiac rhythm suddenly deteriorated into ventricular tachycardia, which rapidly progressed to ventricular fibrillation. Chest compressions were initiated, and the patient was ventilated with 100% oxygen. This resuscitation continued for the next 17 min during which time the patient received a total of nine countershocks of 360 J each. Additionally, a total of 5 mg of epinephrine, 4 mg of atropine, 2 g of CaCl2, 400 mg of lidocaine, 150 mEq of NaHCO3 and 2 g of MgSO4 were given IV. Chest compressions were initially thought to be effective as the end-tidal CO2was maintained at 25–32 mm Hg. No arterial line was yet available to observe a waveform or to draw blood gases, and no single-stick arterial blood gas was drawn during the resuscitation. Despite the resuscitation efforts, the underlying rhythm continued to be asystole. This was confirmed by the palpation of a flaccid and pulseless (in the absence of chest compressions) proximal aorta. End-tidal CO2 had diminished to 8–10 mm Hg, and the pupils were widely dilated. Because of the patient’s complete lack of response and the apparent deterioration by end-tidal CO2, the attending surgeon and anesthesiologist mutually agreed to discontinue the resuscitation. The patient was pronounced dead at 6.17p.m. With cessation of the resuscitation, the IV medications and infusions were discontinued. The monitors were turned off, and the ventilator was disconnected although the endotracheal tube was left in situ. The surgeon stayed at the operating table, using the opportunity to teach residents and students. At 6.27p.m., 10 min after the pronounced death of the patient, the surgeon announced that he had begun to feel a pulse in the proximal aorta above the level of the aortic cross-clamp. Ventilation with 100% oxygen was recommenced and revealed an end- tidal CO2 of 29 mm Hg. The ECG was reconnected and showed a sinus rhythm of 90 bpm. Systolic blood pressure was 90 mm Hg by automated cuff. A radial arterial line was now inserted successfully, and at 0630, arterial blood gases were: hemoglobin 9.5 mg/dL, K+ 3.5 mEq/L, glucose 323 mg/dL, pHa 7.17, PaCO2 54.4 mm Hg, PaO2 438 mm Hg, and base excess −8.0 mEq/L. An esophageal temperature probe was inserted and measured 33.4°C. It was decided to proceed with the operation although neurologic prognosis was anticipated to be bleak. The patient was hemodynamically stable throughout the remainder of the procedure, requiring no inotropic support. Total fluid administration for the operation was 16 U of packed red blood cells, 8 U of fresh frozen plasma, 20 U of platelets, and 12 L of crystalloid solutions. Despite warming of all IV fluids and blood products and the use of a forced air warming blanket, the patient’s temperature ranged between 33° and 34°C for the remainder of the operation. The leaking aneurysm was resected uneventfully and the patient was transported to the intensive care unit. Postoperatively, the patient was maintained on mechanical ventilation for several days in the intensive care unit. The postoperative course was complicated by mild renal insufficiency and two bouts of atrial arrhythmias (both of which were self-limiting). Remarkably, the patient improved dramatically and, after tracheal extubation, was found to be completely neurologically intact. He appeared to have no short- or long-term memory deficits. He also had no recall of any events of the day of operation except for being initially brought into the OR. He was discharged home on postoperative Day 13 in excellent condition with no apparent neurologic deficit. Follow-up at 5 wk revealed that the patient had fully recovered, and had resumed full physical activities and his lifestyle of prior to the surgery. PROPOSED MECHANISMS The exact mechanism of delayed ROSC is unclear and it is possible that more than one mechanism is involved.Dynamic hyperinflation of the lung causing increased positive end expiratory pressure (PPEP) is one of the proposed mechanisms, which has some supporting evidence in patients with obstructive airways disease. Rapid manual ventilation without adequate time for exhalation during CPR can lead to dynamic hyperinflation of lungs. Dynamic hyperinflation may lead to gas trapping and an increase in the end-expiratory pressure (called auto-PEEP) leading to delayed venous return, low cardiac output and even cardiac arrest in patients with obstructive airways disease. The link between mechanical ventilation of patients with obstructive ventilatory defects and circulatory failure was first demonstrated in 1982. One report describes a patient with respiratory failure due to asthma whose blood pressure was undetectable five minutes after initiating artificial ventilation with a tidal volume of 700 mL and respiratory rate of 25 breaths per minute. Even after inotropes the systolic blood pressure did not exceed 70 mm Hg. The ventilator was adjusted to a respiratory rate of six breaths per minute and a tidal volume of 400 mL and the blood pressure gradually rose to 126/84 mm Hg. The physiology of severe auto-PEEP is similar to pericardial tamponade, where circulation can only be restored after removing the obstacle to cardiac filling. Auto-PEEP is a possible cause of pulseless electrical activity (PEA), and rapid ventilation during CPR should be avoided.