DOI: 10.1097/CCM.0b013e31828fd73d
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PMID: 23979375
Issn Print: 0090-3493
Publication Date: 2013/09/01
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Excerpt
Cardiac dysfunction is the detrimental complication of patients with sepsis (2), increasing the mortality rate up to 70% (3). During sepsis and septic shock, the imbalance between oxygen supply and demand causes the microcirculatory disturbance and tissue hypoxia. Unfortunately, the clinically important question of how to keep the balance remains unanswered despite the large numbers of previous clinical and basic science studies performed.
To adequately perfuse organs/tissue and maintain the microcirculation, heart performance has to be intensified, hence mobilizing the adrenergic responses, especially at the early phase of sepsis that results in increased cardiac contractility and heart rate. However, this compensatory work increases the cardiac energy demands. As sepsis progresses, adenosine-5′-triphosphate formation and energy supply are rapidly reduced at the cellular level (4). When energy demand exceeds the actual supply, the myocytes are at high risk of death, leading to heart failure that further augments microcirculatory disturbance and tissue hypoxia. This paradox raises the next question of whether the adrenergic agonist or antagonist should be used in septic patients, and if either one is chosen, when and how to use it?
Morelli et al propose an unconventional approach for the management of septic shock patients with titrated β1 blocker, esmolol. Although this is not a randomized and controlled study, the results favor for use of β1 blocker for the management of patients with sepsis and septic shock. In their study, slowing the heart rate below 95 bpm reduced cardiac output as expected, but this improved the microvascular blood flow and reduced the norepinephrine requirement without affecting the stroke volume, mean arterial pressure, and lactate levels. The results are exciting. However, the questions how low we can go with cardiac output without an extra harm to the patients and how esmolol protects the compromised heart remain unanswered. Is reduction of the heart rate sufficient to produce these beneficial effects?
In this regard, it is worth to note that Herndon and colleagues (5, 6) successfully use titrated propranolol to reduce heart rate by 20% in burned septic patients. Their published studies on propranolol revolutionized our way of thinking about shock resuscitation. Later on Suzuki et al (7) and Aboab et al (8) used same strategy reducing the heart rate by 20% esmolol in their rat and swine models of sepsis, respectively, and demonstrated favorable outcomes.
Thus, it makes sense to “calm down” the heart in the circumstance when its need outstrips the capacity. However, we must not forget the other side of the story that decreasing the cardiac output (by excessive β blockade with negative inotropic effects) below the borderline needed to maintain organ and tissue perfusion can be deleterious. This drives to the next question of how to find this magical borderline, and unfortunately, the answer remains still mysterious. Perhaps, carefully designed, prospective, randomized, controlled, and larger clinical trials may help answer these questions. Hence, titrated selective and ultra-short acting β blockers could be precociously used for management of patients with sepsis with close hemodynamic monitoring for the timely detection of any adverse effects.
