Nota: Estes posicionamentos se prestam a informar e não a substituir o julgamento clínico do médico que, em última análise, deve determinar o tratamento apropriado para seus pacientes.
Introduction: The knowledge on high-output cardiac failure (HOCF) has greatly improved in the last two decades. One of the advances was the identification of a new phenotype of HOCF, characterized by absence of ventricular dilation, already associated with liver disease, arteriovenous fistulas (AVF), lung disease, myelodysplastic syndromes, and obesity. However, it has been noted that any aetiology can present with one of the two phenotypes, depending on the evolution. Objective: To describe, through an integrative review, the physiopathology and aetiologies of HOCF and to discuss phenotypes associated with this condition. Methods: Revisions, guidelines, case-controls, cohort studies and clinical studies were searched in MEDLINE and LILACS, using the connectives in the "cardiac output, high" database [MeSH Terms] OR "high cardiac output" [All Fields]. Discussion: Two distinct phenotypes are currently described in the HOCF, regardless of the aetiology: 1) one with enlarged cardiac chambers; and 2) with normal heart chambers. The mechanisms related to HOCF are vasodilation, arteriovenous shunts that cause increased microvascular density, reduced systemic vascular resistance (RSVR), and high metabolism. These mechanisms lead to activation of the renin-angiotensin-aldosterone system, sodium and water retention, activation of neprilysin, of the sodium-glucose-2 transporter, which promote interstitial fibrosis, ventricular remodeling and a consequent increase in cardiac output >8L/min. Conclusion: Many aetiologies of HOCF have been described and some of them are potentially curable. Prompt recognition of this condition and proper treatment may lead to better outcomes.
Background: Hepatic congestion is a frequent finding in patients with heart failure (HF). Physical examination has limitations in quantifying systemic congestion and requires correlation with echocardiographic and laboratory data (usually B-type natriuretic peptide, BNP, or N-terminal pro-B type natriuretic peptide, NT-proBNP). Hepatic elastography evaluates liver stiffness using a transducer that transmits low-frequency vibrations (50 Hz), and the speed of shear waves propagating through the tissues is measured by ultrasound. The faster the vibrations propagate in the hepatic parenchyma, the stiffer the liver, which, in case of HF, can be correlated with hepatic congestion.Objective: In this systematic review, case-controls, cohort studies, and randomized clinical trials were searched in MEDLINE, LILACS and Cochrane Database of Systematic Review, to evaluate the use of elastography in the detection of hepatic congestion in patients with HF.Methods: From the 49 articles retrieved, seven were selected for review, according to the inclusion and exclusion criteria. The most used methods for the diagnosis and evaluation of HF were echocardiography combined with BNP and NT-proBNP measurements.Results: Elastography performed at bedside was able to establish a significant correlation between increased liver stiffness and increased venous capillary pressure. In addition, liver elastography performed at hospital discharge was able to predict rehospitalization and mortality. Conclusion:Liver elastography is a non-invasive method that can be useful in predicting prognosis and mortality of individuals with HF, contributing to the clinical management of these patients.
Introduction Cardiopulmonary exercise testing (CPET) has become an important clinical tool to predict outcome in patients with chronic heart failure (CHF) and help to select candidates for heart transplantation (HTx) or left ventricular assist devices (LVAD). Purpose To evaluate CPET measurements in advanced CHF patients that are being considered for HTx or LVAD and its association to early mortality regardless of the performed procedure. Methods Maximum intensity CPET was performed on a treadmil and ramp protocol in 65 patients with patients with CHF and reduced ejection fraction, NYHA functional classes III and IV between 2012 and 2018. Measurements derived from CPET were the following: peak V'O2, VO2 at the anaerobic threshold (AT), percentage of the VO2 of the anaerobic threshold in relation to the peak, the VE/VCO2 slope, maximum heart rate (HR), respiratory quotient (R), oxygen kinetics, circulatory power (CP), the recovery HR in the first minute and the oxygen uptake efficiency slope (OUES) and the relation (VE/VCO2 slope)/VO2 peak. Results Seventy-four percent were male. Mean age of 67±12 years. Amost half (47%) had ischemic etiology. There were no complications related to CPET. Ten patients were transplanted, six had an intracorporeal LVAD implanted and the reminder (49 patients) were kept in supervised physical rehabilitation program. There were 11 deaths, 2 in HTx, 2 in LVAD, 7 in the rehabilitation group. Mean follow-up among the survivors was 43 months ± 40.6 and it was 12.1±10.3 months in those who died. CPET derived measurements between survivors and non-survivors were as follows: V'O2 peak (mL kg–1 min–1): 12.6±4.6 and 8.6±2.7 (p=0.002); the VO2 AT (mL kg–1 min–1): 9.9±3.3 and 6.1±3.0 (p=0.002); VE/VCO2 slope: 34.2±12.1 and 68.1±68.7 (p=0.0003); R peak: 1.1±0.2 and 1.0±0.1 (p=0.009); t1/2, in seconds: 135.8±47.9 and 170.1±82.0 (p=0.03); HR at the first minute 16.6±13 and 7±5 (p=0.009); OUES (L min–1): 1.1±0.4 and 0.9±0.3 (p=0.04) and CP [(ml O2 kg–1 min–1) mmHg] 1.516.2±689. 3 and 960.6±363.6 (p=0.005). and the relation (VE/VCO2 slope)/V'O2 peak were 3.2±2.0 and 11.4±19.5 (p=0.001), respectively. Conclusion The predisposition to early death could be stratified by V'O2 peak, VO2 of the ventilatory threshold, VE/VCO2 slope, t1/2, recovery HR, OUES, CP, and by the relation (VE/VCO2 slope)/V'O2 peak. Funding Acknowledgement Type of funding source: Private hospital(s). Main funding source(s): own financing
IntroduçãoO uso de Dispositivos Cardíacos Implantáveis (DCI), como Marca-Passos (MP), desfibriladores e ressincronizadores, aumentou nas últimas duas décadas e, proporcionalmente, houve incremento das infecções associadas. Os DCI tornaramse sítios frequentes de Endocardite Infecciosa (EI), constituindo problema diagnóstico e terapêutico ainda mais desafiador do que quando a EI ocorre em valvas nativas. 1 O diagnóstico de EI pode ser facilmente estabelecido em pacientes com características clássicas. No entanto, na prática clínica, as apresentações atípicas em pacientes com cardiopatias complexas e inúmeras comorbidades levam ao frequente atraso no diagnóstico. 2 Na EI em DCI há a limitação do tratamento antimicrobiano exclusivo, sendo necessárias a retirada do dispositivo e a decisão da melhor forma de fazê-lo. O tamanho da vegetação é o parâmetro que sugere a etiologia, a gravidade e a abordagem invasiva. O caso ora relatado surpreende pelo grande tamanho da vegetação encontrada. Relato do casoPaciente do sexo feminino, 63 anos, portadora de MP, admitida com queixas de febre de origem desconhecida, astenia, perda de peso, petéquias nos membros superiores e inferiores, dispneia progressiva, tosse com hemoptise e edema de membros inferiores, nos últimos 3 meses. Relato de tratamento de infecção urinária com clindamicina e metronidazol 15 dias antes da admissão.Ao exame físico: fácies hipocrática, hipo-hidratada, anêmica (2+/4+) e ictérica (2+/4+). Pressão arterial de 150 × 80 mmHg, frequência cardíaca de 50 bpm, frequência respiratória de 22 irpm, temperatura axilar de 35,9ºC; turgência jugular patológica a 45º; ausculta respiratória normal; ritmo cardíaco regular, quarta bulha e presença de sopro sistólico (3+/6+) no foco tricúspide. Apresentava edema simétrico nos membros inferiores e lesões de Janeway nos dedos dos pés. O Ecocardiograma Transtorácico (ETT) mostrou grande massa, estimada maior que 30 mm, aderida ao cabo do MP e à valva tricúspide, causando estenose valvar (Figura 1 e Vídeo 1). A tomografia de crânio e abdome foi normal. Hemoglobina de 8 g/dL; leucócitos 16.900 mm 3 ; plaquetas 42.000/mm 3 ; ureia 155 mg/dL; creatinina 3,1 mg/ dL; eGFR 18 mL/min/1,73m 2 ; sódio 133 mEq/L; potássio 6,3 mEq/L; bilirrubina direta 1,96 mg/dL; Porção N-terminal do Pró-Hormônio do Peptídeo Natriurético do Tipo B (NT-proBNP) 48.014 pg/mL. Gasometria arterial com acidose metabólica. A análise urinária mostrou piúria, cilindrúria e hematúria. Foi feito teste para o HIV e para colagenoses, que foram negativos. Evoluiu com necessidade de hemodiálise. A remoção cirúrgica do cabo do MP foi realizada e uma válvula biológica nº 29 (Saint Jude Medical, EUA) foi implantada na posição tricúspide (Vídeo 2). Candida parapsilosis foi identificada em duas amostras de hemocultura, e o tratamento inicial com micafungina foi realizado. Foi instituído esquema com fluconazol por 6 semanas após teste de sensibilidade. A paciente recebeu alta hospitalar assintomática, com melhora da função renal. O exame histopatológico por macroscopia mostr...
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