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Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;41(8): 648-656, Aug. 2008. graf, tab
Article de Anglais | LILACS | ID: lil-491920

RÉSUMÉ

We evaluated the recovery of cardiovascular function after transient cardiogenic shock. Cardiac tamponade was performed for 1 h and post-shock data were collected in 5 domestic large white female pigs (43 ± 5 kg) for 6 h. The control group (N = 5) was observed for 6 h after 1 h of resting. During 1 h of cardiac tamponade, experimental animals evolved a low perfusion status with a higher lactate level (8.0 ± 2.2 vs 1.9 ± 0.9 mEq/L), lower standard base excess (-7.3 ± 3.3 vs 2.0 ± 0.9 mEq/L), lower urinary output (0.9 ± 0.9 vs 3.0 ± 1.4 mL·kg-1·h-1), lower mixed venous saturation, higher ileum partial pressure of CO2-end tidal CO2 (EtCO2) gap and a lower cardiac index than the control group. Throughout the 6-h recovery phase after cardiac tamponade, tamponade animals developed significant tachycardia with preserved cardiac index, resulting in a lower left ventricular stroke work, suggesting possible myocardial dysfunction. Vascular dysfunction was present with persistent systemic hypotension as well as persistent pulmonary hypertension. In contrast, oliguria, hyperlactatemia and metabolic acidosis were corrected by the 6th hour. The inflammatory characteristics were an elevated core temperature and increased plasma levels of interleukin-6 in the tamponade group compared to the control group. We conclude that cardiovascular recovery after a transient and severe low flow systemic state was incomplete. Vascular dysfunction persisted up to 6 h after release of tamponade. These inflammatory characteristics may also indicate that inflammatory activation is a possible pathway involved in the pathogenesis of cardiogenic shock.


Sujet(s)
Animaux , Femelle , Tamponnade cardiaque/physiopathologie , Hypotension artérielle/physiopathologie , Choc cardiogénique/physiopathologie , Syndrome de réponse inflammatoire généralisée/physiopathologie , Tamponnade cardiaque/sang , Hypotension artérielle/étiologie , Récupération fonctionnelle , Suidae , Choc cardiogénique/sang , Syndrome de réponse inflammatoire généralisée/étiologie , Facteurs temps
2.
Article de Anglais | WPRIM | ID: wpr-228090

RÉSUMÉ

Eosinophilic myocarditis usually results from myocardial damage as a result of drugs or parasites, and is generally associated with increased peripheral eosinophil count. This form of myocarditis is difficult to diagnose clinically. A 25 year-old previously healthy woman was transferred from a local clinic because of hypotension and dyspnea with sudden cardiogenic shock after a three day history of gastrointestinal illness. Echocardiography revealed concentric left ventricular wall thickening with moderate pericardial effusion. Biopsy of endomyocardial tissue from the right ventricle showed diffuse infiltration of inflammatory cells, mostly eosinophils, even though the patient had a peripheral eosinophil count that was normal at the time of biopsy. The patient was treated with corticosteroids for the symptoms of pericarditis, and she recovered without cardiac sequelae, clinically and echocardiographically. We here report a case of acute eosinophilic myopericarditis, with cardiogenic shock, diagnosed by endomyocardial biopsy with normal peripheral eosinophil count at the time of biopsy, and complete recovery without sequelae.


Sujet(s)
Humains , Femelle , Adulte , Choc cardiogénique/sang , Péricardite/sang , Myocardite/sang , Numération des leucocytes , Granulocytes éosinophiles , Éosinophilie/sang , Maladie aigüe
3.
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