Hans-Ulrich Strohmenger

Vasopressin administration in refractory cardiac arrest

In studies done in pigs, the administration of exogenous vasopressin during closed- and open-chest cardiopulmonary resuscitation has been shown to be more effective than optimal doses of epinephrine in improving vital organ blood flow and increasing perfusion pressure [1, 2]. Interest in the potential value of vasopressin administration during cardiopulmonary resuscitation also stems from human studies showing high levels of circulating vasopressin in patients in cardiac arrest [3, 4]. Higher levels of endogenous vasopressin are associated with greater chances for survival, and higher endogenous levels of epinephrine and norepinephrine are associated with decreased chances for survival [4]. To date, no case reports or controlled studies have addressed the potential value of exogenous vasopressin for the treatment of patients having cardiac arrest. In light of the data from the animal studies, eight patients having refractory in-hospital cardiac arrest were treated with vasopressin after standard therapies, including intravenous administration of epinephrine, had failed. Methods In a final effort to resuscitate patients in whom standard American Heart Association Advanced Cardiac Life Support therapies after in-hospital cardiac arrest had failed, arginine vasopressin was administered centrally as an initial 40-U bolus. Each patient had received standard manual cardiopulmonary resuscitation with at least 1 mg of epinephrine and an attempt at direct-current shock before receiving vasopressin through either a femoral or jugular vein. Table 1 lists patient demographic characteristics, and Table 2 provides some details of therapy and outcome after cardiac arrest. One of eight patients (patient 2) had an unwitnessed arrest. Cardiopulmonary resuscitation was initiated less than 1 minute after arrest in the remaining patients; cardiopulmonary resuscitation and advanced cardiac life support were done on all patients for at least 12 minutes (mean SD, 21.6 11.8 minutes) before vasopressin was administered. Three patients were discharged from the hospital with good neurologic recovery. Table 1. Demographic Characteristics of Patients Having In-Hospital Cardiac Arrest Refractory to Epinephrine*. Table 2. Time Intervals and Outcome in Patients Having In-Hospital Cardiac Arrest Refractory to Epinephrine*. Case Highlights Patient 4 Four days after having a hemicolectomy, a 78-year-old woman developed pulmonary emboli and ventricular fibrillation. Defibrillation (200 J) led to asystole. The patient received cardiopulmonary resuscitation and epinephrine (1-mg, 3-mg, and 5-mg doses administered 3 minutes apart). After the 5-mg bolus, ventricular fibrillation evolved but was resistant to repeated direct-current shocks and to lidocaine (100 mg). Central administration of vasopressin (40 U) followed by direct-current shock (360 J) resulted in a supraventricular rhythm with a palpable carotid pulse. A systolic blood pressure of approximately 100 mm Hg was maintained with a norepinephrine infusion of 0.15 g/kg of body weight per minute. After uncomplicated embolectomy, the patient was transferred to the intensive care unit for 3 days and was discharged without neurologic deficit 4 weeks later. Patient 5 A 71-year-old woman developed ventricular fibrillation while her chest was being scrubbed before implantation of a permanent pacemaker. Closed-chest cardiac massage was initiated within seconds. After three successive direct-current shocks (200 J, 300 J, and 300 J) followed by epinephrine (1 mg) and another direct-current shock (300 J), the patient remained in ventricular fibrillation. Examination of arterial blood gases showed a pH of 7.33 and a Po 2 of 60 mm Hg before endotracheal intubation. Additional epinephrine (1 mg) and defibrillation efforts were unsuccessful. Vasopressin (40 U) was administered 50 minutes after the arrest, and spontaneous circulation returned immediately after a 300-J direct-current shock. Immediately before vasopressin administration, the patients arterial blood had a pH of 7.18 and a Po 2 of 543 mm Hg. The patient was treated with dopamine (10 g/kg per minute) intravenously. Forty-five minutes later, she again developed hypotension followed by ventricular fibrillation. Cardiopulmonary resuscitation was reinitiated, but direct-current shock (300 J), epinephrine (1 mg), and another direct-current shock (300 J) failed to revive her. Vasopressin (20 U) followed 30 seconds later by direct-current shock (300 J) was unsuccessful; more vasopressin (20 U) was administered 2 minutes after the first 20-U dose. Thirty seconds later, a direct-current shock (300 J) led to an immediate return of spontaneous circulation. The patients pulmonary capillary wedge pressure at this time was 25 mm Hg, and her pulmonary systolic pressure was 35 mm Hg. Twenty minutes after her second and final resuscitation effort, she became hypotensive and bradycardic and died secondary to pulseless electrical activity. Patient 6 Immediately after induction with a standard cardiac general anesthetic for placement of an implantable cardioverter-defibrillator, a 45-year-old man developed pulseless electrical activity. Standard closed-chest manual cardiopulmonary resuscitation was started immediately. The patient received fluids (500 mL of normal saline), atropine (1 mg intravenously), and epinephrine (1 mg intravenously). After 10 minutes and another 1-mg epinephrine dose, he developed ventricular fibrillation. Several efforts to defibrillate failed. Twenty minutes after cardiac arrest, the patient received vasopressin (40 U); after a single 360-J transthoracic direct-current shock, spontaneous circulation promptly returned. The patient remained hemodynamically stable for 30 minutes. Despite intravenous fluids, dopamine (10 g/kg per minute), and placement of an intra-aortic balloon pump, he again developed hypotension, followed by ventricular fibrillation. After an effort to resuscitate the patient with standard cardiopulmonary resuscitation, epinephrine (1 mg), and direct-current shock was unsuccessful, the patient was given vasopressin (40 U) and was successfully resuscitated with direct-current shock. An angiogram showed a large thrombus at the site of an angioplasty done 2 weeks earlier; the vessel was again dilated. Within 30 minutes, the patient developed polymorphous ventricular tachycardia and had another cardiac arrest. Standard manual cardiopulmonary resuscitation, intravenous vasopressin (40 U), and direct-current shock were not effective. The patient received active compression-decompression cardiopulmonary resuscitation and vasopressin (40 U). Systolic arterial pressure increased to more than 100 mm Hg; when active compression-decompression cardiopulmonary resuscitation was stopped, the patient spontaneously convertedwithout direct-current shockto sinus tachycardia. One hour later, ventricular fibrillation again developed. Resuscitation efforts were terminated. Patient 8 A 31-year-old man had several internal injuries after a car accident. He developed ventricular fibrillation on the way to the operating room for emergent repair of a ruptured aorta. Fibrillation persisted despite many direct-current shocks and the administration of epinephrine (2 1 mg repeated after 3 minutes). After 4 minutes of closed-chest cardiopulmonary resuscitation, examination of the arterial blood showed a pH of 7.16, a Pco 2 of 54 mm Hg, a Po 2 of 49 mm Hg (fraction of inspired oxygen, 1.0), a potassium level of 2.8 mmol/L, and a hemoglobin level of 9.1 g/L. Despite treatment with epinephrine, diastolic arterial pressures remained less than 15 mm Hg. Administration of vasopressin (40 U) increased the diastolic arterial pressure to 30 mm Hg, and a subsequent direct-current shock (360 J) restored a stable heart and blood pressure. After the operation, the patient was transferred to the intensive care unit. Discussion These cases show that in patients in cardiac arrest who are receiving closed-chest cardiopulmonary resuscitation and have not responded to the standard doses of epinephrine recommended by the American Heart Association, spontaneous circulation can be restored by intravenous administration (through the femoral or jugular vein) of 40 U of vasopressin. These results are consistent with recent data from animals showing that vasopressin has greater efficacy than epinephrine during cardiopulmonary resuscitation [1, 2]. Although the prognosis was poor in all cases and all conventional measures had failed, spontaneous circulation was restored in all eight patients after vasopressin administration. Three patients survived to hospital discharge with minimal or no neurologic deficit. In addition, when active compression-decompression cardiopulmonary resuscitation was combined with the use of vasopressin, one patient had spontaneous conversion to sinus rhythm without the use of direct-current shock. Although the optimal dose of vasopressin in humans is not known, 40 U was effective in all of our patients. In one patient, a dose of 20 U was not effective. In the eight patients studied, an initial dose of 1 mg of epinephrine was administered. In four of these eight patients, an escalating dose of epinephrine (from 1 mg to 3 mg to 5 mg) was used but was similarly ineffective. In humans having cardiac arrest, epinephrine therapy is used on the basis of case reports and animal studies [5, 6]. Recent clinical trials comparing low-dose with high-dose epinephrine show that the latter has no significant advantage [7, 8]. A more recent placebo-controlled trial showed that neither high- nor low-dose epinephrine had benefit compared with placebo [9]. In our patients, vasopressin may have been more effective because of several factors. Vasopressin exerts a greater vasoconstrictive effect under conditions of hypoxia and acidosis than does epinephrine, and the effects of vasopressin last longer [1, 2]. Vasopressin causes a greater increase in arterial tone than does epine

A Comparison of the Combination of Epinephrine and Vasopressin with Lipid Emulsion in a Porcine Model of Asphyxial Cardiac Arrest After Intravenous Injection of Bupivacaine

BACKGROUND:In a porcine model, we compared the effect of the combination of vasopressin/epinephrine with that of a lipid emulsion on survival after bupivacaine- induced cardiac arrest. METHODS:After administration of 5 mg/kg of a 0.5% bupivacaine solution IV, ventilation was interrupted for 2 ± 0.5 (mean ± sd) min until asystole occurred. Cardiopulmonary resuscitation (CPR) was initiated after 1 min of untreated cardiac arrest. After 2 min of CPR, 10 animals received, every 5 min, either vasopressin combined with epinephrine or 4 mL/kg of a 20% lipid emulsion. Three minutes after each drug administration, up to three countershocks (4, 4, and 6 J/kg) were administered; all subsequent shocks with 6 J/kg. Blood for determination of the plasma bupivacaine concentration was drawn throughout the experiment. RESULTS:In the vasopressor group, all five pigs survived, whereas none of five pigs in the lipid group had restoration of spontaneous circulation (P < 0.01). There was no significant difference between groups in the plasma concentration of total bupivacaine. CONCLUSION:In this model of a bupivacaine-induced cardiac arrest, the vasopressor combination of vasopressin and epinephrine compared with lipid emulsion resulted in higher coronary perfusion pressure during CPR and survival rates.

The predictive value of ventricular fibrillation electrocardiogram signal frequency and amplitude variables in patients with out-of-hospital cardiac arrest.

We evaluated ventricular fibrillation frequency and amplitude variables to predict successful countershock, defined as pulse-generating electrical activity. We also elucidated whether bystander cardiopulmonary resuscitation (CPR) influences these electrocardiogram (ECG) variables. In 89 patients with out-of-hospital cardiac arrest, ECG recordings of 594 countershock attempts were collected and analyzed retrospectively. By using fast Fourier transformation analysis of the ventricular fibrillation ECG signal in the frequency range 0.333–15 Hz (median [range]), median frequency, dominant frequency, spectral edge frequency, and amplitude were as follows: 4.4 (2.4–7.5) Hz, 4.0 (0.7–7.0) Hz, 7.7 (3.7–13.7) Hz, and 0.94 (0.24–1.95) mV, respectively, before successful countershock (n = 59). These values were 3.8 (0.8–7.7) Hz (P = 0.0002), 3.0 (0.3–9.7) Hz (P < 0.0001), 7.3 (2.0–14.0) Hz (P < 0.05), and 0.53 (0.03–3.03) mV (P < 0.0001), respectively, before unsuccessful countershock (n = 535). In patients in whom bystander CPR was performed (n = 51), ventricular fibrillation frequency and amplitude before the first defibrillation attempt were higher than in patients without bystander CPR (n = 38) (median frequency, 4.4 [2.4–7.5] vs 3.7 [1.8–5.3] Hz, P < 0.0001; dominant frequency, 3.8 [0.9–7.7] vs 2.6 [0.8–5.9] Hz, P < 0.0001; spectral edge frequency, 8.4 [4.8–12.9] vs 7.2 [3.9–12.1] Hz, P < 0.05; amplitude, 0.79 [0.06–4.72] vs 0.67 [0.16–2.29] mV, P = 0.0647). Receiver operating characteristic curves demonstrate that successful countershocks will be best discriminated from unsuccessful countershocks by ventricular fibrillation amplitude (3000-ms epoch). At 73% sensitivity, a specificity of 67% was obtained with this variable.

The effects of repeated doses of vasopressin or epinephrine on ventricular fibrillation in a porcine model of prolonged cardiopulmonary resuscitation.

This study evaluated ventricular fibrillation mean frequency and amplitude to predict defibrillation success in a porcine cardiopulmonary resuscitation (CPR) model using repeated administration of vasopressin or epinephrine. After 4 min of cardiac arrest and 3 min of CPR, 10 pigs were randomly assigned to receive either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 units/kg, respectively, n = 5) or epinephrine (early epinephrine: 45, 45, and 200 &mgr;g/kg, respectively, n = 5). Another 11 animals were randomly allocated after 4 min of cardiac arrest and 8 min of CPR to receive every 5 min either vasopressin (late vasopressin: 0.4 and 0.8 units/kg, respectively, n = 5) or epinephrine (late epinephrine: 45 and 200 &mgr;g/kg, n = 6). Ventricular fibrillation mean frequency and amplitude on defibrillation were significantly higher in the vasopressin groups than in the epinephrine groups, respectively. In vasopressin versus epinephrine animals, mean frequency immediately before defibrillation was 9.6 ± 1.5 Hz vs 7.0 ± 0.7 Hz (P < 0.001), mean amplitude was 0.65 ± 0.26 mV vs 0.21 ± 0.14 mV (P < 0.001, and coronary perfusion pressure was 27 ± 9 mm Hg vs 8 ± 4 mm Hg (P < 0.00001), respectively. In contrast to no epinephrine animals, all vasopressin animals were successfully defibrillated and survived 1 h (P < 0.05). Mean fibrillation frequency and amplitude predicted successful defibrillation and may serve as noninvasive markers to monitor continuing CPR efforts. Furthermore, vasopressin was superior to epinephrine in maintaining these variables above a threshold necessary for successful defibrillation. Implications Mean frequency and amplitude of ventricular fibrillation predicted successful defibrillation in pigs. Vasopressin was superior to epinephrine in maintaining these variables above a success defibrillation threshold.

Frequency of ventricular fibrillation as a predictor of defibrillation success during cardiac surgery

The purpose of this study was to record median frequency of ventricular fibrillation (VF) in patients undergoing cardiopulmonary bypass for cardiac surgery, and to assess whether defibrillation success depends upon median VF frequency. Data were collected from 20 patients undergoing aortocoronary bypass grafting. Using computerized fast Fourier transformation of the signal from the electrogram, median VF frequency was assessed from onset of VF until aortic cross-clamping and during the 4-s period immediately before each defibrillation during the reperfusion phase. During VF, when an adequate coronary perfusion was maintained by cardiopulmonary bypass prior to aortic cross-clamping, median VF frequency (5.8 +/- 0.1 Hz to 6.2 +/- 0.1 Hz) remained constant for the entire observation interval (96 +/- 25 s; mean +/- SEM). A total of 42 defibrillations were performed: 22 resulted in supraventricular rhythm, 10 in VF, 6 in asystole, and 4 in electromechanical dissociation (EMD). Median VF frequency before defibrillation resulting in supraventricular rhythm was 4.7 +/- 0.17 Hz. In contrast, median VF frequencies before unsuccessful defibrillation resulting in persistent VF (3.5 +/- 0.28 Hz; P < 0.05), EMD (2.9 +/- 0.15 Hz; P < 0.01), or asystole (2.8 +/- 0.28 Hz; P < 0.01) were significantly lower. Above a threshold of 3.0 Hz, the probability of successful defibrillation increased as median VF frequency increased. The probability of success was 100% at a frequency of > or = 5.5 Hz. We conclude that median VF frequency is a reliable noninvasive variable which can be used to predict defibrillation success during the reperfusion phase after cardiac surgery.

Analysing ventricular fibrillation ECG-signals and predicting defibrillation success during cardiopulmonary resuscitation employing N(α)-histograms

Mean fibrillation frequency may predict defibrillation success during cardiopulmonary resuscitation (CPR). N(alpha)-histogram analysis should be investigated as an alternative. After 4 min of cardiac arrest, and 3 versus 8 min of CPR, 25 pigs received either vasopressin or epinephrine (0.4, 0.4, and 0.8 U/kg vasopressin versus 45, 45, and 200 microg/kg epinephrine) every 5 min with defibrillation at 22 min. Before defibrillation, the N(alpha)-parameter histogramstart/histogramwidth and the mean fibrillation frequency in resuscitated versus non-resuscitated pigs were 2.9+/-0.4 versus 1.7+/-0.5 (P=0.0000005); and 9.5+/-1.7 versus 6.9+/-0.7 (P=0.0003). During the last minute prior to defibrillation, histogramstart/histogramwidth of > or =2.3 versus mean fibrillation frequency > or =8 Hz predicted successful defibrillation with subsequent return of a spontaneous circulation for more than 60 min with sensitivity, specificity, positive predictive value and negative predictive value of 94 versus 82%, 96 versus 89%, 98 versus 93% and 90 versus 74%, respectively. We conclude, that N(alpha)-analysis was superior to mean fibrillation frequency analysis during CPR in predicting defibrillation success, and distinction between vasopressin versus epinephrine effects.

Effects of graded doses of vasopressin on median fibrillation frequency in a porcine model of cardiopulmonary resuscitation: results of a prospective, randomized, controlled trial.

OBJECTIVE To assess the effects of graded doses of vasopressin vs. saline on median fibrillation frequency and defibrillation success in a porcine model of cardiopulmonary resuscitation. DESIGN Prospective, randomized, controlled trial. SETTING Animal laboratory in a university medical center. SUBJECTS Twenty-eight domestic pigs (body weight between 26 and 31 kg), aged 12 to 14 wks. INTERVENTIONS AND MAIN RESULTS After 4 mins of ventricular fibrillation and 3 mins of closed-chest cardiopulmonary resuscitation, the animals were allocated to receive either 0.2 U/kg of vasopressin (n = 7), 0.4 U/kg of vasopressin (n = 7), 0.8 U/kg of vasopressin (n = 7), or 10 mL of saline (n = 7, control group). Using radiolabeled microspheres, myocardial blood flow rates during cardiopulmonary resuscitation-before drug administration and 90 secs and 5 mins after drug administration-were as follows in the four groups (mean +/- SEM): 18.8 +/- 0.9, 17.2 +/- 1.1, and 14.6 +/- 1.4 mL/min/100 g in the control group; 17.8 +/- 2.2, 49.6 +/- 6.3 (p < .01 vs. control group), and 29.4 +/- 3.1 mL/min/100 g (p < .05 vs. control group) in the group receiving 0.2 U/kg of vasopressin; 17.1 +/- 1.0, 52.4 +/- 7.5 (p < .01 vs. control group), and 52.2 +/- 5.8 mL/min/100 g (p < .001 vs. control group) in the group receiving 0.4 U/kg of vasopressin; and 18.1 +/- 1.6, 94.9 +/- 9.2 (p < .001 vs. control group), and 57.2 +/- 6.3 mL/min/100 g (p < .001 vs. control group) in the group receiving 0.8 U/kg of vasopressin. Using spectral analysis, median frequencies of ventricular fibrillation-before drug administration and 90 secs and 5 mins after drug administration-were as follows in the four groups: 9.6 +/- 0.4, 8.5 +/- 0.8, and 7.2 +/- 1.0 Hz in the control group; 9.7 +/- 0.5, 12.9 +/- 0.8 (p < .01 vs. control group), and 12.7 +/- 0.8 Hz (p < .001 vs. control group) in the group receiving 0.2 U/kg of vasopressin; 10.3 +/- 0.2, 12.7 +/- 0.9 (p < .01 vs. control group), and 12.8 +/- 0.7 Hz (p < .001 vs. control group) in the group receiving 0.4 U/kg of vasopressin; and 10.0 +/- 0.9, 14.1 +/- 0.9 (p < .001 vs. control group), and 12.5 +/- 0.9 Hz (p < .001 vs. control group) in the group receiving 0.8 U/kg of vasopressin at the same points in time. Median frequency before the first defibrillation attempt was 12.3 +/- 0.4 Hz in the resuscitated animals (n = 19) and 8.2 +/- 1.2 Hz in the nonresuscitated animals (n = 9) (p < .001). CONCLUSIONS This study contributes to the characterization of the effect of increasing global myocardial blood flow on median fibrillation frequency after administration of graded doses of vasopressin in a porcine model of ventricular fibrillation. Interventions such as vasopressor treatment that increase fibrillation frequency improve the chance of successful defibrillation.

The beneficial effect of basic life support on ventricular fibrillation mean frequency and coronary perfusion pressure

BACKGROUND AND OBJECTIVE Chest compressions before initial defibrillation attempts have been shown to increase successful defibrillation. This animal study was designed to assess whether ventricular fibrillation mean frequency after 90 s of basic life support cardiopulmonary resuscitation (CPR) may be used as an indicator of coronary perfusion and mean arterial pressure during CPR. METHODS AND RESULTS After 4 min of ventricular fibrillation cardiac arrest in a porcine model, CPR was performed manually for 3 min. Mean ventricular fibrillation frequency and amplitude, together with coronary perfusion and mean arterial pressure were measured before initiation of chest compressions, and after 90 s and 3 min of basic life support CPR. Increases in fibrillation mean frequency correlated with increases in coronary perfusion and mean arterial pressure after both 90 s (R=0.77, P<0.0001, n=30; R=0.75, P<0.0001, n=30, respectively) and 3 min (R=0.61, P<0.001, n=30; R=0.78, P<0.0001, n=30, respectively) of basic life support CPR. Increases in fibrillation mean amplitude correlated with increases in mean arterial pressure after both 90 s (R=0.46, P<0.01; n=30) and 3 min (R=0.42, P<0.05, n=30) of CPR. Correlation between fibrillation mean amplitude and coronary perfusion pressure was not significant both at 90 s and 3 min of CPR. CONCLUSIONS In this porcine laboratory model, 90 s and 3 min of CPR improved ventricular fibrillation mean frequency, which correlated positively with coronary perfusion pressure, and mean arterial pressure.

Arginine vasopressin during cardiopulmonary resuscitation and vasodilatory shock: current experience and future perspectives.

Epinephrine use during cardiopulmonary resuscitation (CPR) is controversial because of its receptor-mediated adverse effects such as increased myocardial oxygen consumption, ventricular arrhythmias, ventilation-perfusion defect, postresuscitation myocardial dysfunction, ventricular arrhythmias, and cardiac failure. In the CPR laboratory, vasopressin improved vital organ blood flow, cerebral oxygen delivery, resuscitability, and neurologic recovery more than did epinephrine. In patients with out-of-hospital ventricular fibrillation, a larger proportion of patients treated with vasopressin survived 24 hours than did patients treated with epinephrine. Currently, a large trial of out-of-hospital cardiac arrest patients being treated with vasopressin versus epinephrine is ongoing in Germany, Austria, and Switzerland. The new international CPR guidelines recommend 40 U vasopressin intravenously, and 1 mg epinephrine intravenously, as equally effective for the treatment of adult patients in ventricular fibrillation; however, no recommendation for vasopressin has been made to date for adult patients with asystole and pulseless electrical activity, or in children, because of lack of clinical data. When adrenergic vasopressors were unable to maintain arterial blood pressure in patients with vasodilatory shock, continuous infusions of vasopressin (0.04-0.10 U/min) stabilized cardiocirculatory parameters and even ensured weaning from catecholamines.

Comparison of mechanical characteristics of the human and porcine chest during cardiopulmonary resuscitation

BACKGROUND Most studies investigating cardiopulmonary resuscitation (CPR) interventions or functionality of mechanical CPR devices have been performed using porcine models. The purpose of this study was to identify differences between mechanical characteristics of the human and porcine chest during CPR. MATERIAL AND METHODS CPR data of 90 cardiac arrest patients was compared to data of 14 porcine from two animal studies. Chest stiffness k and viscosity mu were calculated from acceleration and pressure data recorded using a Laerdal Heartstart 4000SP defibrillator during CPR. K and mu were calculated at chest compression depths of 15, 30 and 50mm for three different time periods. RESULTS At a depth of 15mm porcine chest stiffness was comparable to human chest stiffness at the beginning of resuscitation (4.8 vs. 4.5N/mm) and clearly lower after 200 chest compressions (2.9 vs. 4.5N/mm) (p<0.05). At 30 and 50mm porcine chest stiffness was higher at the beginning and comparable to human chest stiffness after 200 chest compressions. After 200 chest compressions porcine chest viscosity was similar to human chest viscosity at 15mm (108 vs. 110Ns/m), higher for 30mm (240 vs. 188Ns/m) and clearly higher for 50mm chest compression depth (672 vs. 339Ns/m) (p<0.05). CONCLUSION In conclusion, human and porcine chest behave relatively similarly during CPR with respect to chest stiffness, but differences in chest viscosity at medium and deep chest compression depth should at least be kept in mind when extrapolating porcine results to humans.