TABLE 1.
Dosing and timing of βB in critical illness.
| Sepsis | Population | β-Blockade | Initiation | Outcome |
|---|---|---|---|---|
| Study | ||||
| Schmittinger et al. (2008) Retrospective | 40 patients with septic shock and cardiac depression | Metoprolol 25–47.5 mg PO Increased gradually to achieve target HR (65–95 bpm) (n = 40) | Initiated only after stabilization of cardiovascular function (17.7 ± 15.5 h after shock onset or ICU admission) | HR control was achieved in 97.5% of patients (n = 39) within 12.2 ± 12.4 h HR, CVP, and norepinephrine, vasopressin, and milrinone dosages decreased (all p < 0.001) CI remained unchanged whereas SVI increased (p = 0.002) |
| Gutierrez et al. (2009) Retrospective | 83 septic patients | Any βB exposure (n = 54) vs. no exposure (n = 29) Dosing not reported | Not reported | βB not significantly associated with mortality in the univariate (OR = 1.83; 95% CI = 0.59–5.69) nor multivariate model (OR = 1.843; 95% CI = 0.56–6.10) |
| Berk et al. (1972) Case series | 26 patients with refractory septic shock and SBP <70 mm Hg and UOP <12 ml/h | Propranolol 5 mg given over 2–3 h period followed by another 5 mg during the next 6–12 h (n = 11) | Approximately 24–48 h from start of shock. Considered refractory to all conventional interventions (fluids, antibiotics, steroids) | Increased BP, PaO2, urinary output, and total peripheral resistance in before and after propranolol use case series Decreased CVP, CO, and HR Survival resulted in the 8 who had a normal or increased CO prior to βB. The 3 who did not survive had very low CO |
| Gore and Wolfe (2006) Prospective | 6 moderately septic, mechanically ventilated patients with pneumonia | Esmolol infusion to target 20% HR reduction (range: 6–22 mg/min) (n = 6) | Infusion started immediately following 5 h basal measurements | Significant decrease in CI (p < 0.05) proportional to decrease in HR (p < 0.05) No significant difference in SVR, SVI, BP, extremity/hepatic blood flow, REE, oxygen consumption |
| Balik et al. (2012) Prospective | 10 septic patients | Esmolol bolus (0.2–0.5 mg/kg) followed by continuous 24 h infusion with titration to achieve 20% decrease of baseline HR (n = 10) | After correction of preload (2 h after sepsis) | HR decreased from mean 142 ± 11/min to 112 ± 9/min (p < 0.001) Insignificant reduction of CI (4.94 ± 0.76 to 4.35 ± 0.72 L/min/m2). SV insignificantly increased. No significant changes of norepinephrine infusion (0.13 ± 0.17 to 0.17 ± 0.19 μg/kg/min), DO2, VO2, OER or arterial lactate |
| Morelli et al. (2016) Pilot | 45 septic shock patients, with an HR ≥ 95 bpm and requiring norepinephrine to maintain MAP ≥65 mmHg | Titrated esmolol infusion to maintain HR between 80 and 94 bpm (n = 45) | ≥24 h after hemodynamic optimization | Decreased HR Decrease in Ea Decreased SV (all p < 0.05) CO, EF unchanged NE requirements were reduced (p < 0.05) |
| Shang et al. (2016) Prospective | 151 patients with severe sepsis | Esmolol infusion initial dose 0.05 mg/kg/min adjusted to target HR 70–100 bpm (n = 75) vs control (n = 76) | Not reported | HR reached target within 72 h for both treatment groups ScvO2 increased in the esmolol group and decreased in the control group (p < 0.01). Lactate reduction in control group at 48 h (p < 0.05) Shorter duration of mechanical ventilation in the esmolol group (p < 0.05) |
| Du et al. (2016) Prospective | 63 patients with septic shock within 48 h of diagnosis | Esmolol 20 mg loading dose following by 25 mg/h infusion to achieve HR reduction by 10–15% from baseline (n = 63) | Hemodynamically stable with HR ≥ 100 bpm <48 h after septic shock started | BP was unaltered SV was increased compared with before esmolol therapy (43.6 ± 22.7 vs. 49.9 ± 23.7 ml; p = 0.047) Decreased lactate levels (1.4 ± 0.8 vs. 1.1 ± 0.6 mmol/L; p = 0.015) |
| Morelli et al. (2013) RCT | 154 septic patients | Esmolol 25 mg/h (titrated every 20 min to reach target HR 80–94 bpm) (n = 77) vs control (n = 77) | Initiated after randomization that was performed after resuscitation with fluid and vasopressors for 24 h | Decreased HR—28 bpm [IQR −7−21; p < 0.001] Decreased NE requirement −0.01 [IQR −0.2–0.44; p = 0.003] Decreased 28-days mortality 49.4 vs. 80.5% (p < 0.001) |
| Yang et al. (2014) RCT | 41 septic patients | Esmolol 0.05 mg/kg/min (adjusted to achieve HR of <100 bpm in 2 h) (n = 21) vs. control (n = 20) | Initiated after randomization that was performed after 6-h resuscitation with fluid and vasopressors | Decreased HR 12 h (93 ± 4; p < 0.05); Decreased CI (3.3 ± 0.8; p < 0.05) No significant changes in MAP, CVP, or SVI ScVO2 was not decreased |
| Wang et al. (2015) RCT | 90 septic patients | Esmolol + milrinone (n = 30) vs. milrinone (n = 30) vs. control (n = 30) Dosing not reported | Not reported | 100% HR control (74–94 bpm) within 96 h of initiation (p < 0.001 vs. milrinone) Increased 28-days survival 60 vs. 33.3% (milrinone) vs. 26.7% (control) Decreased NE use 0.07 ± 0.04 |
| Xinqiang et al. (2015) RCT | 48 septic patients | Esmolol 0.05 mg/kg/min (adjusted to achieve HR of <100 bpm within 24 h) (n = 24) vs. control (n = 24) | Initiated after randomization that was performed after resuscitation with fluid and vasopressors for 6 h | Decreased LOS (13.75 ± 8.68 vs. 21.7 ± 6.06; p < 0.001) Decreased 28-days mortality (25.0 vs. 62.5%; p < 0.009) Decreased HR, arterial lactate levels Increased SVRI, SVI, ScVO2 (all p < 0.01) |
| Wang et al. (2017) RCT | 76 septic patients | Esmolol 0.05 mg/kg/hr (titrated every 5 min to reach the HR of <95/min within 4 h) (n = 30) vs. control (n = 30) | Initiated after randomization that was performed after resuscitation with fluid and vasopressors for 24 h | HR decreased significantly at each time point No significant difference in MAP CI significantly increased at > 24 h SVI significantly increased at > 4 h No difference in 28-days mortality (30 vs. 36.7%; p = 0.583) |
| Liu et al. (2019) RCT | 100 septic patients | Esmolol 25 mg/h (titrated every 20 min to reach the HR between 80 and 100/min within 12 h) (n = 50) vs control (n = 50) | Initiated after randomization that was performed after being resuscitated with fluid and vasopressors for 24 h | No difference in 28-days mortality (62 vs 68%; p = 0.529) Lower HR on day 1–7; but overall no statistically significant difference in HR (p > 0.05) No significant difference in total does of NE, lactate level, inflammatory markers, APACHEⅡ, SOFA, hospital LOS (all p > 0.05) |
| Kakihana et al. (2020) RCT | 151 septic patients with HR > 100 bpm and diagnosis of atrial fibrillation, atrial flutter, or sinus tachycardia | Landiolol 1 μg/kg/min (titrated every 15–20 min, until the HR decreased to less than 95 bpm) (n = 76) vs. control (n = 75) | Landiolol was initiated within 2 h after randomization that was conducted after being resuscitated with fluid and vasopressors (mean time from ICU admission to randomization: 15.8 h in landiolol vs. 13.5 h in control) | Larger proportion of patients had HR 60–94 bpm 24 h after randomization (55% [41 of 75] vs. 33% [25 of 75]), with a between-group difference of 23.1% (95% CI 7.1–37.5; p = 0.0031) Decreased incidence of new-onset arrhythmia by 168 h (9 vs. 25%; p = 0.015) No significant difference in 28-days mortality (p = 0.22), hospital free days (p = 0.91), ICU free days (p = 0.55), and ventilator free days (p = 0.47) |
| Walkey et al. (2016) Retrospective | 39,693 septic patients with atrial fibrillation | CCB (n = 14,202) vs. βB (IV metoprolol, esmolol, atenolol, labetalol, and propranolol; n = 11,290) vs. digoxin (n = 7,937) vs. amiodarone (n = 6,264) | On average, received first atrial fibrillation medication 1–2 days into hospital stay | βB were associated with lower hospital mortality when compared with CCBs (n = 18,720; relative risk [RR] = 0.92; 95% CI = 0.86–0.97), digoxin (n = 13,994; RR = 0.79; 95% CI = 0.75–0.85), and amiodarone (n = 5,378; RR = 0.64; 95% CI = 0.61–0.69) Results were similar among subgroups with new-onset or preexisting AF, heart failure, vasopressor-dependent shock, or hypertension |
| Bosch et al. (2020) Retrospective | 666 septic patients with atrial fibrillation with rapid ventricular response | CCB (n = 225) vs. βB (IV metoprolol or esmolol; n = 67) vs. amiodarone (n = 337) vs. digoxin (n = 37) | Amiodarone and CCB added within 1–2 h of start of atrial fibrillation vs 4.9 h for digoxin vs. 10.2 h for βB | The adjusted hazard ratio for HR of <110 beats/min by 1 h was 0.50 (95% CI = 0.34–0.74) for amiodarone vs. βB, 0.37 (95% CI = 0.18–0.77) for digoxin vs. βB, and 0.75 (95% CI = 0.51–1.11) for CCB vs. βB |
| Macchia et al. (2012) Retrospective | 9,465 septic patients | Chronic outpatient βB (n = 1,061) vs. no previous βB treatment (n = 8,404) | N/A Pre-morbid βB | Lower mortality at 28 days (188/1,061 [17.7%]) than those previously untreated (1857/8,404 [22.1%]) (OR = 0.78; 95% CI = 0.66–0.93; p = 0.005) |
| Fuchs et al. (2017) Prospective (secondary analysis) | 296 septic patients with chronic βB treatment | Continuation of βB during acute phase of sepsis (n = 167) vs. discontinuation during sepsis (n = 129) | Acute phase of sepsis defined as 2 days before to 3 days after disease onset | Continuation of βB therapy was significantly associated with decreased hospital (p = 0.03), 28-days (p = 0.04) and 90-days mortality rates (40.7 vs. 52.7%; p = 0.046) |
| Singer et al. (2017) Retrospective | 6,839 septic patients | Chronic outpatient βB (n = 2,838) vs. no previous βB treatment (n = 4,001) | N/A Pre-morbid βB | Decreased mortality during hospitalization (24 vs 31%; p < 0.0001) Multivariable logistic regression models 31% decrease in in-hospital mortality (adjusted OR = 0.69; CI = 0.62–0.77) Decreased 30-days mortality (13 vs. 18%; p < 0.0001) |
| Guz et al. (2021) Prospective | 1,186 septic patients | Chronic outpatient βB (n = 320) vs no previous βB treatment (n = 866) | N/A Pre-morbid βB | No significant difference in crude 30-days and 90-days mortality rates (30 days, 15 vs 19% [p = 0.25]; 90 days, 22 vs 24% [p = 0.51]) Reduction in 30-days mortality rates for patients with absolute tachycardia (OR = 0.406; 95% CI = 0.177–0.932) 30-days survival benefit in the subgroup of patients with relative tachycardia in both univariate and multivariate analysis (OR = 0.496; 95% CI = 0.258–0.955; p = 0.04) |
| Burns | ||||
| Study | Population | Beta-blockade | Initiation | Outcome |
| Baron et al. (1997) Prospective | 22 pediatric burn patients (>40% of TBSA) | Propranolol 0.5–1 mg/kg PO or IV Q 8 h for 10 days (n = 22) | During the catecholamine-induced hypermetabolic phase | Propranolol use significantly decreased daily average HR (10–13%) and RPP (10–16%) compared to 24-h mean pre-treatment |
| Herndon et al. (2001) RCT | 25 pediatric burn patients (>40% of TBSA) | Propranolol 0.33 mg/kg/4 h through NGT (n = 13) vs. control (n = 12) (dose later adjusted for HR 20% less than basal) | Propranolol was initiated immediately following the second staged grafting procedure (approximately 8–12 days after initial admission) | Propranolol decreased HR (p = 0.001) decreased REE (p = 0.001), oxygen consumption (p = 0.002), and prevented lean mass loss (p = 0.01) |
| Jeschke et al. (2007) RCT | 245 pediatric burn patients (>40% of TBSA) | Propranolol 0.5–1.5 mg/kg/6 h PO (n = 102) vs. control (n = 143) | Started after 7 days | No significant difference between groups in terms of mortality (5 vs. 6%), incidence of infections (21 vs. 30%), or sepsis (7 vs. 10%) Decreased REE (p < 0.05) |
| Herndon et al. (2012) RCT | 179 pediatric burn patients (>30% of TBSA) | Propranolol dose required to reduce HR 15% (mean dose 4 mg/kg/day PO) (n = 90) vs control (n = 89) | Propranolol started 3 ± 2 days after admission | Propranolol reduces HR (p = 0.01), cardiac work, central body mass and trunk fat, and improves lean body mass and bone mineral density (p = 0.02) Decreased likelihood of total body mass loss at 6 months (OR = 0.5; 95% CI = 0.25–0.75) No difference in mortality (p = 0.72) |
| Williams et al. (2011) RCT | 406 pediatric burn patients (>30% of TBSA) | Propranolol 1 mg/kg/day PO (divided Q 6 h; adjusted for HR 15–20% less than basal) (n = 171) vs. control (n = 235) | From 24 to 72 h until end of admission (once patients were fluid stabilized) | Propranolol at dose of 1 mg/kg/day reduces HR 15% with respect to basal The dose must increase to 4 mg/kg/day the first 10 days in order to maintain the effect (p < 0.05) |
| Arbabi et al. (2004) Retrospective | 129 adult burn patients (mean TBSA 14 ± 12%); 21 pre-hospital βB vs 22 hospital βB vs. 86 control | Metoprolol, atenolol, esmolol, labetalol, or propranolol (at therapeutic doses) | All pre-hospital βB patients remained on treatment once admitted Hospital βB patients were initiated on βB a mean 8.8 days postinjury | In multivariate analyses, pre-hospital βB use was associated with significant decrease in fatal outcome and healing time (5 vs 13% control; p < 0.05) |
| Mohammadi et al. (2009) RCT | 79 adult burn patients (20–50% of TBSA) | Propranolol 1 mg/kg/d and max dose of 1.98 mg/kg/d given in six divided doses (adjusted to achieve 20% HR reduction from baseline) (n = 37) vs. control (n = 42) | Started on 4th day of admission after hemodynamic stabilization | Decreased healing time (16.13 ± 7.40 days vs. 21.52 ± 7.94 days; p = 0.004) Less time required before skin grafting procedure (28.23 ± 8.43 days vs. 33.46 ± 9.17 days; p = 0.007) Decreased size of burn wound that needed grafting (p = 0.006) Shorter hospital LOS (30.95 ± 8.44 days vs. 24.41 ± 8.11 days; p = 0.05) |
| Ali et al. (2015) RCT | 69 adult burn patients (>30% of TBSA) | Propranolol at a dose that reduces HR by 20% (average dose 3.3 ± 3.0 mg/kg/day) (n = 35) vs. control (n = 34) | Administered within 48 h of burn and given throughout hospital stay | Lower daily average HR over 30 days (p < 0.05) Decreased blood loss during grafting procedures (5–7% improvement in perioperative hematocrit; p = 0.002) Decreased time between grafting procedures (10 ± 5 days vs. 17 ± 12 days; p = 0.02) |
| Cheema et al. (2020) RCT | 70 adult burn patients (20–40% of TBSA) | Propranolol at dose of 0.5–3 mg/kg/day (adjusted to achieve a 20% max HR reduction) (n = 35) vs. control (n = 35) | Started on 3rd postburn day after hemodynamic stabilization | Less muscle wasting (mean mid-arm circumference 27.57 ± 1.62 cm vs. 24.46 ± 1.77 cm; p < 0.0001) Faster wound healing (13.20 ± 1.90 days vs 20.34 ± 2.32 days; p < 0.001) Less time required before skin grafting procedure (23.87 ± 2.36 vs. 33.64 ± 3.15 days; p < 0.001) Shorter hospital LOS (26.69 ± 3.58 days vs 37.71 ± 3.68 days; p < 0.001) |
| Traumatic Brain Injury (TBI) | ||||
| Study | Population | Beta-blockade | Initiation | Outcome |
| Cruickshank et al. (1987) RCT | 114 patients with acute head injury | Atenolol 10 mg IV Q 6 h for 3 days followed by atenolol 100 mg PO once daily for 4 days (n = 56) vs control (n = 58) | Immediately after hemodynamic stabilization (mean 20.2 h after trauma) | Significantly inhibited the rise in arterial CKMB (p < 0.01) Abolished focal myocardial necrotic lesions Reduced likelihood of SVT and ST-segment and T-wave changes |
| Arbabi et al. (2007) Retrospective | 4,117 trauma patients with and without head injury | βB therapy (n = 303) vs. control (n = 3,814) | Administration of scheduled βB during the hospital stay | Significantly decreased risk of mortality in all patients (OR = 0.3; p < 0.001) and patients with severe head injury (OR = 0.2; p < 0.001) No significant difference in late deaths after 48 h of hospitalization (OR = 0.7; p = 0.2) |
| Cotton et al. (2007) Retrospective | 420 patients with a head Abbreviated Injury Scale ≥3 | Metoprolol, propranolol, labetalol, atenolol, esmolol, or sotalol use (n = 174) vs. control (n = 246) | Administration of βB for at least 2 consecutive days during hospitalization | Significantly decreased mortality rate (p = 0.036) |
| Inaba et al. (2008) Retrospective | 1,156 patients with blunt head injuries requiring ICU admission | βB therapy (n = 203) vs control (n = 953) | Administration of βB during hospitalization in the ICU | Significantly decreased overall mortality rate (adjusted OR = 0.54; 95% CI = 0.33–0.91; p = 0.01) Significantly decreased mortality rate in patients ≥55 years old with severe head injuries (28 vs. 60%; OR = 0.3; 96% CI = 0.1–0.6; p = 0.001) |
| Schroeppel et al. (2010) Retrospective | 2,601 patients with blunt TBIs | Atenolol, carvedilol, esmolol, labetalol, metoprolol, nadolol, propranolol, or sotalol use (n = 506) vs. control (n = 2,095) | Administration of more than one dose of a βB during hospitalization | Decreased mortality rate (OR = 0.347; CI = 0.246–0.490; p < 0.0001) |
| Schroeppel et al. (2014) Retrospective | 1,755 patients with TBIs | Atenolol, carvedilol, esmolol, labetalol, metoprolol, propranolol, or sotalol (n = 427) vs. control (n = 1,328) Propranolol (n = 78) vs. other βB (n = 349) | Administration of more than one dose of a βB during hospitalization | No difference in mortality rate between βB and control with the adjusted analysis (adjusted OR = 0.850; 95% CI = 0.536–1.348) Decreased mortality rate with propranolol compared to other βB (3 vs 15%; p = 0.002) |
| Zangbar et al. (2016) Retrospective | 356 patients with blunt TBIs requiring ICU admission | Metoprolol (n = 178) vs. no βB (n = 178) | Administration of at least one dose of a metoprolol during hospitalization in the ICU | Significantly decreased mortality rate (78 vs 68%; p = 0.04) No difference in the mean heart rate (p = 0.99) |
| Mohseni et al. (2015) Retrospective | 874 patients with an isolated severe TBI and an intracranial injury with Abbreviated Injury Scale ≥3 | Labetalol, metoprolol, or other βB (n = 287) vs. control (n = 587) | Administration of a βB during hospitalization with median time to first admission of 1 day and 75% of patients receiving the first dose by day 3 | Significantly decreased mortality rate (11 vs 17%; p = 0.007) Significantly increased mortality rate in patients not on pre-hospitalization βB (adjusted OR = 3.0; 95% CI = 1.2–7.1; p = 0.015) |
| Ko et al. (2016) Retrospective | 440 patients with a moderate to severe TBI (head Abbreviated Injury Scale 3–5) requiring ICU admission | Propranolol 1 mg IV Q 6 H within 24 h of admission while in the ICU, then 40 mg PO BID after patient transferred to the floor (n = 109) vs. control (n = 331) | Administration of propranolol within 24 h of admission | Significantly decreased mortality rate after predictors of mortality were adjusted (adjusted OR = 0.25; p = 0.012) |
| Murry et al. (2016) Retrospective | 38 patients with moderate to severe TBI requiring ICU admission | Early low dose propranolol 1 mg IV Q 6 H (n = 28) vs. standard of care, which could include βB (labetalol, metoprolol) at any point during hospitalization (n = 10) | Administration of propranolol within 12 h of ICU admission and for a minimum of 48 h | Decreased rates of bradycardia events (1.6 vs. 5.8; p = 0.05) Decreased rates of hypotensive events (0.8 vs. 0.5; p = 0.6) Decreased ICU LOS (15.4 vs. 30.4 days; p = 0.02) and hospital LOS (10 vs. 19.1 days; p = 0.05) Similar mortality rates (10 vs. 10.7%; p = 0.9) |
| Ley et al. (2018) Prospective | 2,252 patients with TBI requiring ICU admission | Atenolol, esmolol, propranolol, metoprolol, labetalol, or another βB (n = 1,120) vs. control (n = 1,132) | Administration of βB during hospitalization | Decreased 30-days mortality rate (13.8 vs 17.7%; p = 0.013) Decreased 30-days mortality rates with propranolol vs. other βB (9.3 vs. 15.9%; p = 0.003) Increased hospital LOS (21 ± 25 days vs 10 ± 37 days; p < 0.01) Increased hospital LOS with propranolol vs. other βB (21 ± 25 days vs. 13 ± 14 days; p < 0.01) |
| Cardiac Arrest | ||||
| Study | Population | Beta-blockade | Initiation | Outcome |
| Lee et al. (2016) Retrospective | 41 patients with RVF in out-of-hospital cardiac arrest | Esmolol (loading dose: 500 μg/kg, infu- sion: 0–100 μg/kg/min) (n = 16) vs control (n = 25) | Given after obtaining verbal informed consent from patient’s proxies, written consent afterwards | Significantly more sustained ROSC (56 vs 16%; p = 0.007) Increased survival and good neurological outcomes at 30 days, 2 months, and 6 months (18.8 vs. 8%; p = 0.36) |
| Driver et al. (2014) Retrospective | 25 patients with RVF in out-of-hospital cardiac arrest | Esmolol (loading dose: 500 μg/kg, infu- sion: 0–100 μg/kg/min) (n = 6) vs control (n = 19) | Approximately 46 min into cardiac arrest (range 34–59 min) | Higher rates of temporary (67 vs. 42%) and sustained ROSC (67 vs. 32%) Increased survival to ICU admission (66 vs. 32%) and discharge (50 vs. 16%) Increased discharge with favorable neurologic outcome (50 vs. 11%) No stats are significant given small sample size |
| Nademanee et al. (2000) Prospective | 49 patients with frequent VF/VT episodes with recent MI | Propranolol IV 0.15-mg/kg dose over 10 min and then as a 3–5-mg dose Q 6 h (n = 14) vs Esmolol IV 300–500-mg/kg loading dose for 1 min followed by maintenance dose of 25–50 mg/kg/min (n = 7) vs LSGB (n = 6) vs. antiarrhythmic (n = 22) | Received sympathetic blockade treatment within 1 h after all of the antiarrhythmic medications initiated during the code were discontinued | Decreased mortality significantly at 1-week (22 vs. 82%; p < 0.0001) and 1 year (67 vs. 5%; p < 0.0001) compared to antiarrhythmic medication |
| Chatzidou et al. (2018) Prospective | 60 ICD patients with recurrent VF/VT within a 24-h period | Propranolol 40 mg PO Q 6 h (cumulative dose 160 mg/24 h) (n = 30) vs Metoprolol 50 mg PO Q 6 h (cumulative dose 200 mg/24 h) (n = 30) | Not documented | Propranolol patients had decreased incidence of VT/VF (p = 0.001) and decreased ICD discharges (p = 0.004) More propranolol patients were free of arrhythmic events within 24 h (90 vs 53.3%; p = 0.03) Arrhythmic events were more likely to be terminated with propranolol (hazard ratio = 0.225; 95% CI = 0.112–0.453; p < 0.001) Time to arrhythmia termination and hospital LOS were significantly shorter with propranolol compared to metoprolol (p < 0.05 for both) |
| Skrifvars et al. (2003) Retrospective | 98 patients receiving post-resuscitation care within 72 h of out-of-hospital VF arrest (79 βB vs 19 control) | Metoprolol (at least 50 mg PO BID or 5 mg IV BID) or bisoprolol (at least 2.5 mg two times a day orally) n breakdown not reported | Initiated within 72 h post-resuscitation | Increased survival in multiple regression model (44 vs 79%; p = 0.005) |
| KEY | ||||
| APACHE II = acute physiology and chronic health evaluation | βB = beta-blockers | BID = twice daily | BP = blood pressure | |
| CCB = calcium channel blocker | CI = cardiac index, confidence interval | CKMB = myocardial isoenzyme of creatine kinase | CO = cardiac output | |
| CVP = central venous pressure | DO2/VO2 = systemic oxygen delivery/consumption | Ea = static arterial elastance | EF = ejection fraction | |
| HR = heart rate | ICD = implantable cardioverter defibrillator | ICU = Intensive Care Unit | IV = intravenous | |
| LOS = length of stay | LSGB = left stellate ganglionic blockade | MAP = mean arterial pressure | MI = myocardial infarction | |
| N/A = not applicable | NGT = nasogastric tube | NE = norepinephrine | OER = oxygen extraction ratio | |
| OR = odds ratio | PaO2 = arterial oxygen pressure | PO = oral | REE = resting energy expenditure | |
| ROSC = return of spontaneous circulation | RPP = rate pressure product | R/VF = refractory ventricular fibrillation | SBP = systolic blood pressure | |
| ScVO2 = central venous oxygen saturation | SOFA = sequential organ failure assessment | SV = stroke volume | SVI = stroke volume index | |
| SVR = systemic vascular resistance | SVRI = systemic vascular resistance index | SVT = supraventricular tachycardia | TBSA = total body surface area | |
| VT = ventricular tachycardia |