We describe a case of cardiac arrest in a 47-year-old male, 80kg, with history of moderate hypertension. Cardiac arrest happened in the patient’s house, in the presence of his wife. She immediately called for aid. 1 minute after the event cardiopulmonary resuscitation (CPR) was started by a policeman (BLS performer) called by the patient’s wife. 20 minutes later the Emergency Medical Service (EMS) arrived. The cardiac rhythm of presentation was a ventricular fibrillation (VF).
An Advanced Cardiac Life Support (ACLS) and Mechanical Chest Compressions (MCC) with the mechanical chest compression device LUCAS 3 (Stryker USA) were performed. An orotracheal tube was placed (the end tidal CO2 was > 15mmhg during the whole CPR time.
A total of 6 DC shock (200J-biphasic wave), Epinephrine 4mg and amiodarone 300mg were administered.
40 minutes after the event, the EMS arrived with a declared ongoing-cpr protocol in the cath-lab at Angel’s Hospital in Mestre (Venice). A total of 50 minutes of low flow ongoing-cpr were performed.
50 min after the event a veno-arterial ECMO support was started (Fig. 1).
We used a 21 Fr Maquet Arterial cannula and a 23Fr Maquet venous cannula (femoro-femoral cannulation) and a Cardiohelp system (Maquet, Getinge, Germany).
ECMO predicted BF was 4.2 l/min. A perfusion cannula (6-F introducer sheath (Avanti®+; Cordis Corp., Miami, FL, USA) for the superficial femoral artery was placed. Coronarography showed an occlusion of the descending anterior artery immediately treated with a PTCA (percutaneous transluminal coronary angioplasty) + drug coated stent (onyx 3.5 x 22) with a good result. The ECG rhythm was a Pulseless Electrical Activity (PEA) before the procedure. The ECG rhythm after the procedure was a sinus bradycardia. A total of 1 minute of no-flow and 49 minutes of low flow were recorded. The initial arterial gas analysis showed a pH < 7.00, lactates 13 mmol/L. The ECMO setting was BF 3,2 lpm, 2500rpm, FiO2 75%. The MAP (mean arterial pressure) was 65mmHg.The patient was then admitted to the Cardiac Intensive Care Unit.
Figure 1
Timeline from the cardiac arrest to discharged of the patient.
CPR (cardiopulmonary resuscitation), MCC (Mechanical Chest Compressions), EMS (Emergency Medical Service), CRRT (Continuous Renal Replacement Therapy), ECMO VA (Extracorporeal Membrane Oxygenation), BF (Blood flow), MVA (Mechanical Ventilation)
In the Cardiac Intensive Care Unit an echocardiography was performed, showing a systo-diastolic movement of the aortic valve.
Swan Ganz pulmonary catheter (Edwards Nyon, Switzerland), SJO2 (PediaSat catheter 15 cm Edwards Nyon, Switzerland), SedLine and NIRS were placed (Masimo Root, Irvine,CA, USA) (Table 1).
Table 1
Time (hours) | 0 | 3 | 4 | 6 | 72 | 96 | 120 |
PAPm | 18 | 20 | 25 | 22 | 16 | 18 | 18 |
SJO2 | 75 | 68 | 65 | 77 | 78 | 76 | 77 |
PAM | 65 | 45 | 38 | 65 | 70 | 72 | 70 |
NIRS dx | 60 | 55 | 52 | 58 | 61 | 59 | 61 |
NIRS sx | 59 | 54 | 51 | 57 | 60 | 59 | 62 |
SEDLine | 25 | 28 | 24 | 28 | 31 | 97 | 98 |
Hemodynamic and Oxygenation profile from starting ECLS to discharge from ICU. |
PAPm = Mean Pulmonary Artery Pressure, SJO2 = Jugular Bulb Venous Oxygen Saturation, PAM = Mean arterial pressure, NIRS = Near Infrared Spectroscopy, SEDLine = Sedation Monitoring by EEG analysis (Masimo USA) |
Table 1.
Hemodynamic and Oxygenation profile from starting ECLS to discharge from ICU.
PAPm = Mean Pulmonary Artery Pressure, SJO2 = Jugular Bulb Venous Oxygen Saturation, PAM = Mean arterial pressure, NIRS = Near Infrared Spectroscopy, SEDLine = Sedation Monitoring by EEG analysis (Masimo USA)
Continuous Renal Replacement Therapy (CRRT) treatment with Cytosorb (CytoSorbents Inc Monmouth Junction USA) was started to obtain the clearance of Myoglobin released after prolonged mechanical chest compression.
A systemic inflammatory response syndrome (SIRS) like syndrome frequently appears in ECLS treated patient (an element of Post Resuscitation Syndrome), and it is essential to use every kind of cytokine removal device in the first 24–48 hours. (1)
3 hours after the admission in the ICU, we observed a sudden hemodynamic instability, characterized by hypotension, MAP < 60 mmHg, increase in lactates, drastic decrease in ECMO blood flow (1,5 − 1,8 lpm) despite > 3000rpm.
The Cardiac Index measured on Swan Ganz catheter was 0,6l/min/m2, Ejection Fraction measure by Simpson method was 18%, tricuspid annular plane excursion
(TAPSE) was 13 with a collapsed Inferior Vena Cava (IVC).
It resulted impossible to increase ECMO blood flow despite an appropriate volemic expansion. With Swan Ganz catheter measurements the CI was of 1.0 l/min/m2 after the volemic expansion but it was not sufficient for obtaining an adequate splanchnic perfusion.
The drop pressure (DP) values was in range, < 20mmHg, and also the value of inlet pressure and outlet pressure on CardioHelp (Maquet) monitoring was in range of normality. No active source of acute bleeding was observed.
The abdomen was expanded and stiff. The IAP (measured by Unometer Abdopressure Convatec USA) was 18 cmH2O.
A naso-gastric tube and a rectal tube (Rectal tube, Bicakcilar- Istanbul, Turkye) were placed. The drainage from the rectal tube was 2500ml of liquid stools in 2 hours. The IAP dropped to 9 cmH2O, and ECMO blood flow raised to 3.2 lpm.
MAP was 65–70 mmHg, the lactates decreased (the following day lactates were < 2mmol/ml), cardiac index increased (1.6 l/min/m2).
The ECMO was weaned after 72 hours after a Levosimendan infusion of 24 hours; and the ejection fraction increased from 18–42%; TAPSE was 16mm.
72 hours later the patient had spontaneous diuresis (with depuration) and CRRT (Continuous Renal Replacement Therapy) was weaned.
96 hours later the patient was extubated with a CPC (Cerebral Performance Category) score of 2 because of a lower limbs residual paresis (ischemic myelopathy).
We discharged the patient to Sub Intensive Cardiac Unit after 120 hours from the admission