Kyoung Chul Cha

Optimal position for external chest compression during cardiopulmonary resuscitation: an analysis based on chest CT in patients resuscitated from cardiac arrest

Objectives This study was conducted to determine the proper hand position on the sternum for external chest compression to generate a maximal haemodynamic effect during cardiopulmonary resuscitation (CPR). Methods 114 patients with cardiac arrest who underwent chest CT after successful resuscitation from January 2006 to August 2009 were included in the study. To evaluate the area of the cardiac chambers subjected to external chest compression, the area of each cardiac chamber under the sternum was measured using cross-sectional CT at three different locations: the internipple line on the sternum (point A), halfway between point A and the sternoxiphoid junction (point B) and at the sternoxiphoid junction (point C). Results The widest total heart area, total ventricular area and left ventricular area (LVA) were observed most frequently at point C (58%, 85% and 78% of all cases, respectively). Few cases (six in total heart area, one in total ventricular area and one in LVA) were observed as the widest at point A. Predicted compressed areas of the right and left ventricle were wider at point C than at points A or B (right ventricular area: 366±536 mm2 at point A, 961±653 mm2 at point B and 1383±689 mm2 at point C, p<0.001; LVA: 65±236 mm2 at point A, 365±506 mm2 at point B and 1099±817 mm2 at point C, p<0.001). Conclusions Only a small proportion of the ventricle is subjected to external chest compression when CPR is performed according to the current guidelines. Compression of the sternum at the sternoxiphoid junction might be more effective to compress the ventricles.

HEMODYNAMIC EFFECT OF EXTERNAL CHEST COMPRESSIONS AT THE LOWER END OF THE STERNUM IN CARDIAC ARREST PATIENTS

BACKGROUND Little is known about the hemodynamic effects of chest compression at different positions on the sternum during cardiopulmonary resuscitation (CPR). OBJECTIVES This study aimed to test whether external chest compression at the lower end of the sternum as an alternative position (alternative compression) results in superior hemodynamic effects compared to standard external chest compression (standard compression). METHODS We enrolled 17 patients with non-traumatic cardiac arrest who failed to regain spontaneous circulation within 30 min after CPR initiation. Standard compression was begun when cardiac arrest was confirmed. Alternative compression was performed for 2 min if spontaneous circulation was not attained after 30 min of standard CPR. We compared hemodynamics and end-tidal CO2 pressure during the last 2 min of standard compression and during alternative compression. RESULTS Peak arterial pressure during compression systole (114 ± 51 vs. 95 ± 42 mm Hg, p < 0.001) and end-tidal CO2 pressure (11.0 ± 6.7 vs. 9.6 ± 6.9 mm Hg, p < 0.05) were higher with alternative than standard compression, whereas arterial pressure during compression diastole, peak right atrial pressure, and coronary perfusion pressure did not differ between standard and alternative compression. CONCLUSIONS Compared to standard compression, alternative compression results in a higher peak arterial pressure and end-tidal CO2 pressure, but no change in coronary perfusion pressure.

Outcome and current status of therapeutic hypothermia after out-of-hospital cardiac arrest in Korea using data from the Korea Hypothermia Network registry

Objective Therapeutic hypothermia (TH) has become the standard strategy for reducing brain damage in the postresuscitation period. The aim of this study was to investigate current TH performance and outcomes in out-of-hospital cardiac arrest (OHCA) survivors using data from the Korean Hypothermia Network (KORHN) registry. Methods We used the KORHN registry, a web-based multicenter registry that includes 24 participating hospitals throughout the Republic of Korea. Adult comatose OHCA survivors treated with TH between 2007 and 2012 were included. The primary outcomes were neurological outcome at hospital discharge and in-hospital mortality. The secondary outcomes were TH performance and adverse events during TH. Results A total of 930 patients were included, of whom 556 (59.8%) survived to discharge and 249 (26.8%) were discharged with good neurologic outcomes. The median time from return of spontaneous circulation (ROSC) to the start of TH was 101 minutes (interquartile range [IQR], 46 to 200 minutes). The induction, maintenance, and rewarming durations were 150 minutes (IQR, 80 to 267 minutes), 1,440 minutes (IQR, 1,290 to 1,440 minutes), and 708 minutes (IQR, 420 to 900 minutes), respectively. The time from the ROSC to coronary angiography was 1,045 hours (IQR, 121 to 12,051 hours). Hyperglycemia (46.3%) was the most frequent adverse event. Conclusion More than one-quarter of the OHCA survivors (26.8%) were discharged with good neurologic outcomes. TH performance was appropriately managed in terms of the factors related to its timing, including cooling start time and rewarming duration.

Features and predictors of myocardial injury in carbon monoxide poisoned patients

Background and purpose By contrast with neurologic injury, myocardial injury associated with carbon monoxide (CO) poisoning has not been well investigated. Therefore, this study assessed features and predictors of myocardial injury in CO poisoned patients. Subjects and methods 250 CO poisoning cases that were diagnosed and treated by the emergency department of Wonju Christian Hospital from January 2006 to February 2012 were retrospectively reviewed. Results Fifty (20%) out of 250 patients with CO poisoning developed myocardial injury. Among those with elevated troponin I (Tn I), peak levels occurred at 11.0 (IQR, 4.5–18.5) h normalising by 65.0 (IQR 44.0–96.0) h. CO exposure time, and total and ICU admission length was longer (7.5 (IQR 3.7–10.0) h vs 3.0 (IQR 1.0–7.5) h, p<0.001; 3.5 (IQR 0.0–7.0) days and 0.0 (IQR 0.0–1.25) days vs 0.0 (IQR 0.0–2.0) days and 0.0 (IQR 0.0–0.0) days, p<0.001, respectively) in the myocardial vs non-myocardial injury group. The predictors of myocardial injury were male gender, Glasgow Coma Scale (GCS) ≤14, and CO exposure time ≥2 h (OR (95% CI) of 3.341 (1.171 to 9.531), 9.920 (3.763 to 26.150), and 7.743 (1.610 to 37.238), respectively). Conclusions Myocardial injury developed in 20% of CO poisoned patients. Time to normalisation and of peak Tn I level in elevated Tn I group was 65.0 (IQR 44.0–96.0) h and 11.0 (IQR 4.5–18.5) h. Presence of myocardial injury was associated with poorer prognosis. Predictors of myocardial injury included male gender, GCS of 14 or less, or CO exposure times greater than 2 h.

Effect of cardiopulmonary resuscitation on restoration of myocardial ATP in prolonged ventricular fibrillation

BACKGROUND There has been controversy over whether a short period of cardiopulmonary resuscitation (CPR) prior to defibrillation improves survival in patients who experienced a sudden cardiac arrest. However, there have been no reports about whether CPR restores the myocardial energy source during prolonged ventricular fibrillation (VF). The aim of this study is to investigate the effect of CPR in restoring myocardial high energy phosphates during prolonged VF. METHODS AND RESULTS Seventy-two adult male Sprague-Dawley rats were used in this study. Baseline adenosine triphosphate (ATP) and adenosine diphosphate (ADP) prior to induction of VF were measured in nine rats, the No-VF group. Sixty-three rats were subjected to 4 min of untreated VF. Animals were then randomized into two groups: No-CPR (n=37) and CPR (n=26). In the No-CPR group, ATPs and ADPs were measured at 4 min (No-CPR4), 6 min (No-CPR6), 8 min (No-CPR8) or 10 min (No-CPR10) after the induction of VF. The CPR group received 2 min (CPR2), 4 min (CPR4) or 6 min (CPR6) of mechanical chest compressions before ATP was measured. Myocardial ATP (nmol/mg protein) was decreased as VF duration was prolonged (No-VF: 5.49±1.71, No-CPR4: 4.27±1.58, No-CPR6: 4.13±1.31, No-CPR8: 3.77±1.42, No-CPR10: 3.52±0.90, p<0.05 between each of No-CPRs vs. No-VF). Two minutes of CPR restored myocardial ATP to the level of No-VF group (5.27±1.67 nmol/mg protein in CPR2, p>0.05 vs. No-VF group). However, myocardial ATP (nmol/mg protein) decreased if the duration of CPR was longer than 2 min (CPR4: 3.77±1.05, CPR6: 3.49±1.08, p<0.05 between CPR4 and CPR6 vs. No-VF). CONCLUSIONS CPR for 2 min helps to maintain myocardial ATP after prolonged VF.

Incidence and patterns of cardiomyopathy in carbon monoxide-poisoned patients with myocardial injury

Abstract Objectives: Sustained myocardial injury is a significant predictor of mortality in carbon monoxide (CO) poisoning. There are few reports in the literature regarding the presence of CO-induced cardiomyopathy from early stages in the emergency department (ED). We prospectively investigated the early incidence of CO-induced cardiomyopathy and its patterns in patients with cardiomyopathy. Materials and methods: During a 10-month period, transthoracic echocardiography (TTE) was performed in 43 consecutive patients with CO poisoning and myocardial injury, which was defined as elevated high-sensitive troponin I within 24 h after ED arrival. Measurements of left ventricular ejection fraction and wall motion abnormalities were performed to evaluate cardiac function. If a patient had CO-induced cardiomyopathy, we measured cardiac function at the time of patient admission, day 1, day 2, and once within seven days of hospitalization. Results: The incidence of cardiomyopathy was as high as 74.4% (32 of 43 patients) in CO-poisoned patients with myocardial injury based on initial ED results. Echocardiographic patterns included non-cardiomyopathy (25.6%), global dysfunction (51.2%), and Takotsubo-like cardiomyopathy (23.2%). Patients in the global dysfunction group had significantly more normalized cardiac dysfunction within 72 h than did those in the Takotsubo-like cardiomyopathy group (81.8% vs. 22.2%, p = 0.001). Discussion and conclusion: Patients with CO poisoning and myocardial injury experienced cardiomyopathy, including reversible global dysfunction and a Takotsubo-like pattern. Investigation of cardiomyopathy needs to be considered in patients with CO poisoning and myocardial injury.

Prognostic value of gray matter to white matter ratio in hypoxic and non-hypoxic cardiac arrest with non-cardiac etiology

PURPOSE This study evaluated the prognostic performance of the gray to white matter ratio (GWR) on brain computed tomography (CT) in out-of-hospital cardiac arrest (OHCA) survivors with a noncardiac etiology and compared the prognostic performance of GWR between hypoxic and nonhypoxic etiologies. METHODS Using a multicenter retrospective registry of adult OHCA patients treated with targeted temperature management, we identified those with a noncardiac etiology who underwent brain CT within 24 hours after restoration of spontaneous circulation. Attenuation of the gray matter and white matter (at the level of the basal ganglia, centrum semiovale, and high convexity) were measured and GWRs were calculated. The primary outcome was neurologic outcome. RESULTS Of 164 patients, 145 (88.4%) were discharged with a poor neurologic outcome. Lower GWR was associated with a poor neurologic outcome. The sensitivities of this marker were markedly low (9.7%-43.5%) at cutoff values, with 100% sensitivity. The cutoff values of the GWR for hypoxic arrest showed higher sensitivities than those for nonhypoxic arrest. The area under the curve (AUC) values of the GWR for the caudate nucleus/posterior limb of the internal capsule, putamen/corpus callosum, and basal ganglia were significant in the hypoxic group, whereas the AUC of the putamen/corpus callosum was the only significant GWR in the nonhypoxic group. CONCLUSION A low GWR is associated with poor neurologic outcome in noncardiac etiology OHCA patients treated with targeted temperature management. Gray to white matter ratio can help to predict the neurologic outcome in a cardiac arrest with hypoxic etiology rather than a nonhypoxic etiology.

Pyrethroid poisoning: features and predictors of atypical presentations

Background Although pyrethroids are known for low toxicity to humans, clinical systemic characteristics of pyrethroid poisoning remain undefined. We investigated atypical presentations of pyrethroid poisoning and the predictors, among those readily assessed in the emergency department. Methods 59 pyrethroid poisoning cases that were diagnosed and treated at the emergency department of Wonju Severance Christian Hospital from September 2004 to December 2012 were retrospectively reviewed. Results Atypical presentations were seen in 22 patients (39.3%). Atypical presentations after pyrethroid poisoning included respiratory failure requiring ventilator care (10 patients, 17.9%), hypotension (systolic blood pressure <90 mm Hg) (6 patients, 10.7%), pneumonia (4 patients, 7.1%), acute kidney injury (6 patients, 10.7%), Glasgow Coma Scale (GCS) <15 (19 patients, 33.9%), seizure (2 patients, 3.6%) and death (2 patients, 3.6%). There were differences between atypical versus typical groups in terms of age (62.1±3.7 vs 51.0±2.9, p=0.020), ingested amounts (300 (IQR 100–338) cc vs 100 (IQR 50–300) cc, p=0.002), and bicarbonate and serum lactate (17.4±1.1 vs 20.5±0.4, p=0.011; and 4.42 (IQR 3.60–7.91) mmol/L vs 3.01 (IQR 2.16–4.73) mmol/L, p=0.010, respectively) in initial arterial blood gas analysis. Predictors of the atypical presentations were ingested amount and serum lactate ((OR 1.004, 95% CI 1.001 to 1.008, p=0.013) and (OR 1.387, CI 1.074 to 1.791, p=0.012), respectively). The optimal points were 250 cc and 3.5 mmol/dL. Conclusions 39.3% of pyrethroid poisoned patients had atypical presentations with the most common being respiratory failure requiring ventilator care. Predictors of atypical presentation were ingested amount >250 cc and serum lactate >3.5 mmol/L.

Clinical outcomes of adverse cardiovascular events in patients with acute dapsone poisoning

Objective Adverse cardiovascular events (ACVEs) account for a large proportion of the morbidities and mortalities associated with drug overdose emergencies. However, there are no published reports regarding outcomes of ACVEs associated with acute dapsone poisoning. Here, the authors retrospectively analyzed ACVEs reported within 48 hours of treatment in patients with acute dapsone poisoning and assessed the significance of ACVEs as early predictors of mortality. Methods Sixty-one consecutive cases of acute dapsone poisoning that were diagnosed and treated at a regional emergency center between 2006 and 2014 were included in the study. An ACVE was defined as myocardial injury, shock, ventricular dysrhythmia, cardiac arrest, or any combination of these occurring within the first 48 hours of treatment for acute dapsone poisoning. Results Nineteen patients (31.1%) had evidence of myocardial injury (elevation of serum troponin-I level or electrocardiography signs of ischemia) after dapsone overdose, and there were a total of 19 ACVEs (31.1%), including one case of shock (1.6%). Fourteen patients (23.0%) died from pneumonia or multiple organ failure, and the incidence of ACVEs was significantly higher among non-survivors than among survivors (64.3% vs. 21.3%, P=0.006). ACVE was a significant predictor of mortality (odds ratio, 5.690; 95% confidence interval, 1.428 to 22.675; P=0.014). Conclusion The incidence of ACVE was significantly higher among patients who died after acute dapsone poisoning. ACVE is a significant predictor of mortality after dapsone overdose, and evidence of ACVE should be carefully sought in these patients.

Shock Duration after Resuscitation Is Associated with Occurrence of Post-Cardiac Arrest Acute Kidney Injury

This retrospective observational study investigated the clinical course and predisposing factors of acute kidney injury (AKI) developed after cardiac arrest and resuscitation. Eighty-two patients aged over 18 yr who survived more than 24 hr after cardiac arrest were divided into AKI and non-AKI groups according to the diagnostic criteria of the Kidney Disease/Improving Global Outcomes (KDIGO) Clinical Practice Guidelines for AKI. Among 82 patients resuscitated from cardiac arrest, AKI was developed in 66 (80.5%) patients (AKI group) leaving 16 (19.5%) patients in the non-AKI group. Nineteen (28.8%) patients of the AKI group had stage 3 AKI and 7 (10.6%) patients received renal replacement therapy during admission. The duration of shock developed within 24 hr after resuscitation was shorter in the non-AKI group than in the AKI group (OR 1.02, 95% CI 1.01-1.04, P < 0.05). On Multiple logistic regression analysis, the only predisposing factor of post-cardiac arrest AKI was the duration of shock. In conclusion, occurrence and severity of post-cardiac arrest AKI is associated with the duration of shock after resuscitation. Renal replacement therapy is required for patients with severe degree (stage 3) post-cardiac arrest AKI.