The DOI matches its Crossref record; 18 of the 18 references it cites were found in a registry or an index.
Sympathetic Overstimulation During Critical Illness: Adverse Effects of Adrenergic Stress
Abstract
The term ‘‘adrenergic’’ originates from ‘‘adrenaline’’ and describes hormones or drugs whose effects are similar to those of epinephrine. Adrenergic stress is mediated by stimulation of adrenergic receptors and activation of post-receptor pathways. Critical illness is a potent stimulus of the sympathetic nervous system. It is undisputable that the adrenergic-driven ‘‘fight-flight response’’ is a physiologically meaningful reaction allowing humans to survive during evolution. However, in critical illness an overshooting stimulation of the sympathetic nervous system may well exceed in time and scope its beneficial effects. Comparable to the overwhelming immune response during sepsis, adrenergic stress in critical illness may get out of control and cause adverse effects. Several organ systems may be affected. The heart seems to be most susceptible to sympathetic overstimulation. Detrimental effects include impaired diastolic function, tachycardia and tachyarrhythmia, myocardial ischemia, stunning, apoptosis and necrosis. Adverse catecholamine effects have been observed in other organs such as the lungs (pulmonary edema, elevated pulmonary arterial pressures), the coagulation (hypercoagulability, thrombus formation), gastrointestinal (hypoperfusion, inhibition of peristalsis), endocrinologic (decreased prolactin, thyroid and growth hormone secretion) and immune systems (immunomodulation, stimulation of bacterial growth), and metabolism (increase in cell energy expenditure, hyperglycemia, catabolism, lipolysis, hyperlactatemia, electrolyte changes), bone marrow (anemia), and skeletal muscles (apoptosis). Potential therapeutic options to reduce excessive adrenergic stress comprise temperature and heart rate control, adequate use of sedative/analgesic drugs, and aiming for reasonable cardiovascular targets, adequate fluid therapy, use of levosimendan, hydrocortisone or supplementary arginine vasopressin.
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Cites
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Cited by
Morelli, A., Ertmer, C., Westphal, M., Rehberg, S., Kampmeier, T., Ligges, S., Orecchioni, A., D’Egidio, A., D’Ippoliti, F., Raffone, C., et al. (2013) · JAMA · doi:10.1001/jama.2013.278477 · Cited by 720
Johansson, P. I., Stensballe, J., Rasmussen, L. S., & Ostrowski, S. R. (2011) · Annals of Surgery · doi:10.1097/sla.0b013e318226113d · Cited by 554
IL-18 cleavage triggers cardiac inflammation and fibrosis upon β-adrenergic insult
Xiao, H., Li, H., Wang, J.-J., Zhang, J.-S., Shen, J., An, X.-B., Zhang, C.-C., Wu, J.-M., Song, Y., Wang, X.-Y., et al. (2018) · European Heart Journal · doi:10.1093/eurheartj/ehx261 · Cited by 305
J. Romero-Bermejo, F., Ruiz-Bailen, M., Gil-Cebrian, J., & J. Huertos-Ranchal, M. (2011) · Current Cardiology Reviews · doi:10.2174/157340311798220494 · Cited by 287
Traumatic brain injury: pathophysiology for neurocritical care
Kinoshita, K. (2016) · Journal of Intensive Care · doi:10.1186/s40560-016-0138-3 · Cited by 257
Metadata
- Authors
- Dünser, M. W., & Hasibeder, W. R.
- Venue
- Journal of Intensive Care Medicine
- Publisher
- SAGE Publications
- Published
- 2009-08-23
- Volume
- 24
- Issue
- 5
- Pages
- 293-316
- ISSN
- 0885-0666 (ISSN-L)
- 1525-1489
- OpenAlex
- W2142798193
- Cited by
- 488
- References
- 18
- FWCI
- 13.57
- Type
- journal article
- Language
- en
- Open access
- closed
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