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1.
Ann Intensive Care ; 11(1): 36, 2021 Feb 18.
Artigo em Inglês | MEDLINE | ID: mdl-33604873

RESUMO

SARS-CoV-2, the causative agent of coronavirus disease 2019 (COVID-19), is responsible for the largest pandemic facing humanity since the Spanish flu pandemic in the early twentieth century. Since there is no specific antiviral treatment, optimized support is the most relevant factor in the patient's prognosis. In the hospital setting, the identification of high-risk patients for clinical deterioration is essential to ensure access to intensive treatment of severe conditions in a timely manner. The initial management of hypoxemia includes conventional oxygen therapy, high-flow nasal canula oxygen, and non-invasive ventilation. For patients requiring invasive mechanical ventilation, lung-protective ventilation with low tidal volumes and plateau pressure is recommended. Cardiovascular complications are frequent and include myocardial injury, thrombotic events, myocarditis, and cardiogenic shock. Acute renal failure is a common complication and is a marker of poor prognosis, with significant impact in costs and resources allocation. Regarding promising therapies for COVID-19, the most promising drugs until now are remdesivir and corticosteroids although further studies may be needed to confirm their effectiveness. Other therapies such as, tocilizumab, anakinra, other anti-cytokine drugs, and heparin are being tested in clinical trials. Thousands of physicians are living a scenario that none of us have ever seen: demand for hospital exceed capacity in most countries. Until now, the certainty we have is that we should try to decrease the number of infected patients and that an optimized critical care support is the best strategy to improve patient's survival.

2.
ESC Heart Fail ; 8(2): 943-952, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33498096

RESUMO

AIMS: Patients with advanced heart failure (HF) with reduced left ventricular ejection fraction (HFrEF) and concurrent coronavirus disease 2019 (COVID-19) might have a higher risk of severe events. METHODS AND RESULTS: We retrospectively studied 16 patients with advanced HFrEF who developed COVID-19 between 1 March and 29 May 2020. Follow-up lasted until 30 September. Ten patients previously hospitalized with decompensated HFrEF were infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) during hospitalization. Six patients undergoing ambulatory care at initiation of COVID-19 symptoms were hospitalized because of advanced HFrEF. All patients who experienced worsening of HFrEF due to COVID-19 required higher doses or introduction of additional inotropic drugs or intra-aortic balloon pump in the intensive care unit. The mean intravenous dobutamine dose before SARS-CoV-2 infection in previously hospitalized patients (n = 10) and the median (inter-quartile range) peak intravenous dobutamine dose during SARS-CoV-2 infection in all patients (n = 16) were 2 (0-7) µg/kg/min and 20 (14-20) (P < 0.001), respectively. During follow-up, 56% underwent heart transplantation (n = 2) or died (n = 7). Four patients died during hospitalization from mixed shock consequent to severe acute respiratory syndrome with inflammatory storm syndrome associated with septic and cardiogenic shock during COVID-19. After COVID-19 recovery, two patients died from mixed septic and cardiogenic shock and one from sustained ventricular tachycardia and cardiogenic shock. Five patients were discharged from hospital to ambulatory care. Four were awaiting heart transplantation. CONCLUSION: Worsening of advanced HF by COVID-19 is associated with high mortality. This report highlights the importance of preventing COVID-19 in patients with advanced HF.


Assuntos
COVID-19/complicações , Insuficiência Cardíaca/mortalidade , Insuficiência Cardíaca/terapia , Adulto , Idoso , COVID-19/mortalidade , COVID-19/terapia , Fármacos Cardiovasculares/uso terapêutico , Cuidados Críticos , Feminino , Insuficiência Cardíaca/virologia , Transplante de Coração , Hospitalização , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Volume Sistólico , Taxa de Sobrevida , Resultado do Tratamento
8.
Arq. bras. cardiol ; 111(3 supl.1): 167-167, set., 2018. ilus.
Artigo em Português | Sec. Est. Saúde SP, SESSP-IDPCPROD, Sec. Est. Saúde SP | ID: biblio-1045966

RESUMO

O lítio causa alterações eletrocardiográficas (ECGs) benignas (achatamento da onda "T", ondas "U" e elevação de ST), a potencialmente fatais (bloqueios avançados, QT longo, TV e FV). Relatamos o caso de paciente hígida, jovem, sem fatores de risco para intoxicação, que apresentou grave intoxicação por lítio com múltiplas manifestações ECGs. Paciente feminina, 54, procurou o PS por tremores, pré-síncope e confusão. Antecedente de depressão psicótica em uso de sertralina, lamotrigina e carbonato de lítio 1200mg/d (há 1 ano). Ao exame estava desorientada, PA 150x70 mmHg, FC 30 bpm, SaO2 97%, glicemia 107 mg/dL. Restante normal. Em ECG observada bradicardia com pausas sinusais, dissociação isorrítmica com ritmo atrial ectópico variável e escape juncional, além de padrão de QT longo (Figs. 1 e 2). Aventada hipótese de intoxicação por Lítio. Litemia de 3,3 mmol/L. ECO transtorácico e TC de crânio sem alterações significativas, assim como exames demais exames laboratoriais. Foi suspensa a medicação e iniciada dopamina com aumento da FC e melhora parcial. Paciente seguiu sob monitorização. Apresentou redução do nível sérico de lítio para 1,3mmol/L em 96h, com remissão dos sintomas e das alterações ECGs (Fig. 3). Alta no 7o dia de internação. Em consulta de 6 meses, segue sem uso de Lítio e sem novas intercorrências. Realizado Holter de 24 horas e ECG basal, dentro da normalidade. (AU)


Assuntos
Humanos , Eletrocardiografia , Lítio/efeitos adversos
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