A 73-Year-Old Woman With Pulseless Electrical Activity Arrest

Purpose: We hypothesized that advanced circulatory compromise, as manifested by acidosis and hyperkalemia should be associated with worsened clinical outcomes in cardiac arrest patients treated with therapeutic hypothermia. Methods: Results of initial admission laboratory studies, medical history, and echocardiogram in 203 consecutive cardiac arrest patients (59 females, 59+/- 15 years old) undergoing therapeutic hypothermia were reviewed. Mortality was ascertained through hospital records. ANOVA, chi-square, Kaplan-Meier, and logistic regression analyses were used. The study was approved by the institutional IRB. Results: Increased mortality was noted with older age, decreased admission pH, elevated admission lactate, lower admission hemoglobin, and pulseless electrical activity or asystole as presenting rhythms (Table). Admission hypokalemia and ventricular fibrillation/tachycardia were associated with improved hospital mortality (Table). Potassium was significantly lower in patients admitted with ventricular fibrillation/tachycardia (3.897+/-0.92) as compared to patients with asystole (4.674+/-1.377) or pulseless electrical activity (4.491+/-1.055 mEq/dL, p<0.0001). In multivariate logistic regression analysis, independent predictors of increased hospital mortality included increased admission potassium (OR 2.0, 95%CI 1.291-3.170, p=0.002)), older age (OR 1.04, 95%CI 1.007-1.071, p=0.017), admission PEA (OR 3.7, 95%CI 1.358-10.282, p=0.011 when compared to ventricular fibrillation/tachycardia) or asystole (OR 17.2, 95%CI 4.423-66.810, p<0.001 when compared to ventricular fibrillation/tachycardia); while decreased mortality was associated with higher hemoglobin (OR 0.8, 95%CI 0.665-0.997, p=0.047). Conclusions: Hyperkalemia, pulseless electrical activity, and asystole are predictive of increased hospital mortality in survivors of cardiac arrest. An association between low or low-normal potassium, observed VT-VF, and better outcomes is unexpected and may be used for prognostic purposes. More prospective investigations of mortality predictors in these critically ill patients are needed.

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Abstract 150: Impact of Epinephrine on ECG Changes During Resuscitation From Out-of-Hospital Cardiac Arrest With Initial Pulseless Electrical Activity

Circulation ◽

10.1161/circ.138.suppl_2.150 ◽

2018 ◽

Vol 138 (Suppl_2) ◽

Author(s):

Gunnar W Skjeflo ◽

Eirik Skogvoll ◽

Jan Pål Loennechen ◽

Theresa M Olasveengen ◽

Lars Wik ◽

...

Keyword(s):

Heart Rate ◽

Cardiac Arrest ◽

Electrical Activity ◽

Multivariate Regression ◽

Life Support ◽

Controlled Trial ◽

Pulseless Electrical Activity ◽

Qrs Complex ◽

Epinephrine Administration ◽

Hospital Cardiac Arrest

Introduction: Presence of electrocardiographic rhythm, documented by the electrocardiogram (ECG), in the absence of palpable pulses defines pulseless electrical activity (PEA). Our aims were to examine the development of ECG characteristics during advanced life support (ALS) from Out-of-Hospital-Cardiac-Arrest (OHCA) with initial PEA, and to explore the effects of epinephrine on these characteristics. Methods: Patients with OHCA and initial PEA in a randomized controlled trial of ALS with or without intravenous access and medications were included. QRS widths and heart-rates were measured in recorded ECG signals during pauses in compressions. Statistical analysis was carried out by multivariate regression (MANOVA). Results: Defibrillator recordings from 170 episodes of cardiac arrest were analyzed, 4840 combined measurements of QRS complex width and heart rate were made. By the multivariate regression model both whether epinephrine was administered and whether return of spontaneous circulation (ROSC) was obtained were significantly associated with changes in QRS width and heart rate. For both control and epinephrine groups, ROSC was preceded by decreasing QRS width and increasing rate, but in the epinephrine group an increase in rate without a decrease in QRS width was associated with poor outcome (fig). Conclusion: The QRS complex characteristics are affected by epinephrine administration during ALS, but still yields valuable prognostic information.

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Abstract 143: Electrocardiographic Changes Preceding In-Hospital Cardiac Arrests From Pulseless Electrical Activity / Asystole Provide Insights into Underlying Cause and Pathophysiology

Circulation ◽

10.1161/circ.138.suppl_2.143 ◽

2018 ◽

Vol 138 (Suppl_2) ◽

Author(s):

Jason J Yang ◽

Duc H Do ◽

Xiao Hu ◽

Noel G Boyle

Keyword(s):

Electrical Activity ◽

Real Time ◽

Tertiary Care ◽

Pulseless Electrical Activity ◽

Spontaneous Circulation ◽

Care Hospital ◽

Right Ventricular Strain ◽

Wave Morphology ◽

Electrocardiographic Changes ◽

Ecg Data

Introduction: Survival from in-hospital cardiac arrests (IHCA) due to pulseless electrical activity (PEA) or asystole remains extremely poor. Our understanding of the pathophysiology of PEA is limited, and management of IHCA largely follows a “one size fits all” approach due to the lack of reliable methods to determine underlying cause in real-time. Hypothesis: Changes on continuous electrocardiogram (ECG) preceding IHCA reflect the underlying cause and pathophysiology of IHCA. Methods: We evaluated adult patients with IHCA from PEA/asystole at a tertiary care hospital between 3/2010 - 8/2014 with at least 3 hours of continuous ECG data preceding IHCA. We determined the likely cause of IHCA by reviewing of clinical, lab, imaging, and autopsy data. We analyzed up to 24 hours of continuous ECG data evaluating for changes in rhythm, PR interval, QRS and ST/T wave morphology leading up to IHCA. Results: Eighty-nine patients were studied (mean age 62 ± 18 years, 54% male). Return of spontaneous circulation was obtained in 65 (73%) and 24 (27%) survived to discharge. We found 5 distinct patterns of ECG changes leading up to and including the arrest rhythm (Table). Causes of cardiac arrest were significantly different between the group (Fischer’s exact p<0.001). Notably, a severe right ventricular strain ECG pattern was found preceding PEA caused by pulmonary embolism, asphyxia from large mucus plugs or massive aspiration, acute respiratory distress syndrome, and cardiogenic shock with biventricular failure. Conclusion: Distinct patterns of changes in rhythm and ECG morphology which reflect different underlying causes and pathophysiology of IHCA were identified. Recognition of these patterns may provide an opportunity for better understanding of PEA mechanisms and outcomes, and allow for real-time prediction of IHCA cause to help direct management.

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