Cardiac Injury After Traumatic Brain Injury: Clinical Consequences and Management

被引:15
作者
Coppalini, Giacomo [1 ,2 ,3 ]
Salvagno, Michele [1 ]
Peluso, Lorenzo [1 ,2 ,4 ]
Bogossian, Elisa Gouvea [1 ]
Cornejo, Armin Quispe [1 ]
Labbe, Vincent [1 ]
Annoni, Filippo [1 ]
Taccone, Fabio Silvio [1 ]
机构
[1] Univ Libre Bruxelles ULB, Hop Univ Bruxelles HUB, Dept Intens Care, Route Lennik 808, B-1070 Brussels, Belgium
[2] Humanitas Univ, Dept Biomed Sci, I-20072 Milan, Italy
[3] IRCCS Humanitas Res Hosp, Dept Anesthesiol & Intens Care, I-20089 Milan, Italy
[4] Humanitas Gavazzeni, Dept Anesthesia & Intens Care, Via M Gavazzeni 21, I-24125 Bergamo, Italy
关键词
Traumatic brain injury; Heart; Cardiac injury; Hemodynamic impairment; Therapy; Beta-blocker; SUBARACHNOID HEMORRHAGE; HEART-FAILURE; BETA-BLOCKERS; DYSFUNCTION; PULMONARY; ABNORMALITIES; COMPLICATIONS; ASSOCIATION; DOBUTAMINE; PREVALENCE;
D O I
10.1007/s12028-023-01777-3
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Traumatic brain injury (TBI) is a significant public health issue because of its increasing incidence and the substantial short-term and long-term burden it imposes. This burden includes high mortality rates, morbidity, and a significant impact on productivity and quality of life for survivors. During the management of TBI, extracranial complications commonly arise during the patient's stay in the intensive care unit. These complications can have an impact on both mortality and the neurological outcome of patients with TBI. Among these extracranial complications, cardiac injury is a relatively frequent occurrence, affecting approximately 25-35% of patients with TBI. The pathophysiology underlying cardiac injury in TBI involves the intricate interplay between the brain and the heart. Acute brain injury triggers a systemic inflammatory response and a surge of catecholamines, leading to the release of neurotransmitters and cytokines. These substances have detrimental effects on the brain and peripheral organs, creating a vicious cycle that exacerbates brain damage and cellular dysfunction. The most common manifestation of cardiac injury in TBI is corrected QT (QTc) prolongation and supraventricular arrhythmias, with a prevalence up to 5 to 10 times higher than in the general adult population. Other forms of cardiac injury, such as regional wall motion alteration, troponin elevation, myocardial stunning, or Takotsubo cardiomyopathy, have also been described. In this context, the use of & beta;-blockers has shown potential benefits by intervening in this maladaptive process. & beta;-blockers can limit the pathological effects on cardiac rhythm, blood circulation, and cerebral metabolism. They may also mitigate metabolic acidosis and potentially contribute to improved cerebral perfusion. However, further clinical studies are needed to elucidate the role of new therapeutic strategies in limiting cardiac dysfunction in patients with severe TBI.
引用
收藏
页码:477 / 485
页数:9
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