<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.1 20151215//EN" "https://jats.nlm.nih.gov/publishing/1.1/JATS-journalpublishing1.dtd">
<article article-type="review-article" dtd-version="1.1" specific-use="sps-1.9" xml:lang="en" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">
	<front>
		<journal-meta>
			<journal-id journal-id-type="nlm-ta">abchf</journal-id>
			<journal-id journal-id-type="publisher-id">abchf</journal-id>
			<journal-title-group>
				<journal-title>ABC Heart Fail Cardiomyop</journal-title>
				<abbrev-journal-title abbrev-type="publisher">ABC Heart Fail Cardiomyop</abbrev-journal-title>
			</journal-title-group>
			<issn pub-type="ppub">2764-3107</issn>
			<publisher>
				<publisher-name>Sociedade Brasileira de Cardiologia - SBC</publisher-name>
			</publisher>
		</journal-meta>
		<article-meta>
			<article-id pub-id-type="publisher-id">abchf.20230093</article-id>
			<article-id pub-id-type="doi">10.36660/abchf.20230093</article-id>
			<article-categories>
				<subj-group subj-group-type="heading">
					<subject>Review Article</subject>
				</subj-group>
			</article-categories>
			<title-group>
				<article-title>Peculiarities in the Treatment of Cardiomyopathy Associated with High-Output Conditions</article-title>
			</title-group>
			<contrib-group>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0002-8966-1977</contrib-id>
					<name>
						<surname>Santos</surname>
						<given-names>Carolina Casadei dos</given-names>
					</name>
					<role>Conception and design of the research</role>
					<role>Writing of the manuscript and Critical revision of the manuscript for content</role>
					<role>Acquisition of data</role>
					<role>Analysis and interpretation of the data</role>
					<xref ref-type="aff" rid="aff1"><sup>1</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0002-5959-9359</contrib-id>
					<name>
						<surname>Rossi</surname>
						<given-names>João Manoel</given-names>
						<suffix>Neto</suffix>
					</name>
					<role>Conception and design of the research</role>
					<role>Writing of the manuscript and Critical revision of the manuscript for content</role>
					<role>Analysis and interpretation of the data</role>
					<xref ref-type="aff" rid="aff1"><sup>1</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0001-5565-4085</contrib-id>
					<name>
						<surname>Finger</surname>
						<given-names>Marco Aurelio</given-names>
					</name>
					<role>Conception and design of the research</role>
					<role>Writing of the manuscript and Critical revision of the manuscript for content</role>
					<xref ref-type="aff" rid="aff1"><sup>1</sup></xref>
				</contrib>
			</contrib-group>
			<aff id="aff1">
				<label>1</label>
				<institution content-type="orgname">Instituto Dante Pazzanese de Cardiologia</institution>
				<addr-line>
					<named-content content-type="city">São Paulo</named-content>
					<named-content content-type="state">SP</named-content>
				</addr-line>
				<country country="BR">Brazil</country>
				<institution content-type="original">Instituto Dante Pazzanese de Cardiologia, São Paulo, SP – Brazil</institution>
			</aff>
			<author-notes>
				<corresp id="c01"> Mailing Address: Carolina Casadei dos Santos • Av. Dr. Dante Pazzanse, 500. Postal Code 9012-909, São Paulo, SP – Brazil E-mail: <email>carolcasadei33@hotmail.com</email>
				</corresp>
				<fn fn-type="conflict">
					<p>Potential conflict of interest</p>
					<p>No potential conflict of interest relevant to this article was reported.</p>
				</fn>
			</author-notes>
			<pub-date date-type="pub" publication-format="electronic">
				<day>31</day>
				<month>12</month>
				<year>2023</year>
			</pub-date>
			<pub-date date-type="collection" publication-format="electronic">
				<year>2023</year>
			</pub-date>
			<volume>3</volume>
			<issue>2</issue>
			<elocation-id>e20230093</elocation-id>
			<history>
				<date date-type="received">
					<day>07</day>
					<month>12</month>
					<year>2023</year>
				</date>
				<date date-type="rev-recd">
					<day>16</day>
					<month>12</month>
					<year>2023</year>
				</date>
				<date date-type="accepted">
					<day>16</day>
					<month>12</month>
					<year>2023</year>
				</date>
			</history>
			<permissions>
				<license license-type="open-access" xlink:href="https://creativecommons.org/licenses/by/4.0/" xml:lang="en">
					<license-p> This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. </license-p>
				</license>
			</permissions>
			<abstract>
				<title>Abstract</title>
				<p>High-output heart failure (HOHF) is a less common form of heart failure and presents as the inability of the heart to supply enough blood for the body’s needs. HOHF can be divided into two categories: 1. increased demand for increased metabolism or 2. arteriovenous shunts increasing venous circulation flow and decreasing resistance, leading to increased oxygen consumption and low systemic vascular resistance. The most common causes are obesity, liver disease, shunts, lung disease, myeloproliferative diseases, hyperthyroidism, and thiamine deficiency.</p>
			</abstract>
			<kwd-group xml:lang="en">
				<kwd>Heart Failure</kwd>
				<kwd>High-Output</kwd>
			</kwd-group>
			<counts>
				<fig-count count="4"/>
				<table-count count="0"/>
				<equation-count count="0"/>
				<ref-count count="7"/>
			</counts>
		</article-meta>
	</front>
	<body>
		<sec sec-type="intro">
			<title>Introduction</title>
			<p>This article aims to carry out a systematic review of high-output heart failure (HOHF) and its peculiarities.</p>
			<p>HOHF is a less common form of heart failure, and although it may seem contradictory at first glance, it presents itself as the inability of the heart to supply enough blood for the body’s needs.<sup><xref ref-type="bibr" rid="B1">1</xref></sup></p>
			<p>Patients with HOHF have normal cardiac function and decreased systemic vascular resistance, either secondary to diffuse arteriolar dilation or possible shunts of arterioles and capillary beds, leading to neurohormonal activation.<sup><xref ref-type="bibr" rid="B2">2</xref>,<xref ref-type="bibr" rid="B3">3</xref></sup></p>
			<p>High cardiac output is a state of elevated cardiac output at rest greater than 8 L/min or a cardiac index greater than 4.0 L/min/m<sup><xref ref-type="bibr" rid="B2">2</xref></sup>,<sup><xref ref-type="bibr" rid="B1">1</xref></sup> and heart failure occurs when this cardiac output is insufficient to meet the demand hemodynamics.</p>
		</sec>
		<sec sec-type="methods">
			<title>Methods</title>
			<p>Systematic review on high-impact publishing platforms.</p>
			<sec>
				<title>Development</title>
				<p>Regarding the causes of HOHF, they can be divided into two categories: 1. increased demand for greater metabolism or 2. arteriovenous shunts that increase the flow of venous circulation and decrease systemic vascular resistance, leading to increased oxygen consumption and low systemic vascular resistance, respectively.<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B4">4</xref></sup></p>
				<p>According to a study by Anand of over 16,000 patients, the main causes of high-output HF are obesity 31%, liver disease (cirrhosis) 23%, arteriovenous shunts (systemic arteriovenous fistulas (AVF), hemodialysis fistulas and hereditary hemorrhagic telangiectasia) 22%, lung disease (chronic obstructive pulmonary disease, bronchiectasis bronchiolitis obliterans, interstitial disease) 16% and myeloproliferative disease 8%. Other causes that can lead to high-output HF include thiamine deficiency, causing a disease known as Beriberi, and finally, thyrotoxicosis.<sup><xref ref-type="bibr" rid="B5">5</xref></sup></p>
				<p>The treatment can be divided into two parts. First, it starts with acute heart failure intervention. Depending on the severity, treatment should be aimed at acute respiratory failure due to volume overload and, if present, hypotension. Initial management may range from intermittent diuretic therapy and oxygen supplementation to continuous diuretic infusion, non-invasive positive pressure ventilation, or intubation. If hypotension and decreased organ perfusion are evident, inotropic medications are required. Once patients are stabilized and are no longer in a decompensated state, treatment can be directed to the underlying etiology.<sup><xref ref-type="bibr" rid="B6">6</xref>,<xref ref-type="bibr" rid="B7">7</xref></sup></p>
				<p>The treatment of hyperthyroidism is focused on symptomatic therapy with the aim of reducing circulating thyroid hormones, either through medication and/or the use of radiotherapy or surgery if necessary. Myeloproliferative diseases are treated according to the specific underlying disease and may involve hematopoietic cell transplantation, depending on the severity. Treatment is widely variable depending on the disease and severity of symptoms. The Surviving Sepsis Campaign guidelines guide the treatment of sepsis and involve early recognition, immediate and aggressive resuscitation with intravenous fluids, and antibiotic therapy with investigation to determine the source of infection. Thiamine deficiency that causes Beriberi is treated with thiamine replacement for at least two weeks. Chronic lung disease is a progressive disease with treatment targeting the underlying lung disease. In general, hypoxia and hypercapnia are addressed, and management is symptomatic therapy that slows the progression of the underlying disease. Acquired AVFs are treated by closing or reducing blood flow. It is more pertinent in patients on hemodialysis who require access; however, if it presents with HOHF, closure may be necessary, and alternative access sites must be obtained. Treatment of congenital AVFs may involve medical therapy, invasive embolization, or surgical excision, depending on the exact cause. Liver cirrhosis advanced enough to cause high-output heart failure is end-stage, and treatment involves liver transplantation. Medical therapy has a role in fluid management for hypervolemia, involving the combined use of loop diuretics and antimineralocorticoids, which can limit flow through shunts.</p>
				<p>
					<fig id="f01">
						<label>Figure 1</label>
						<caption>
							<title>– Etiologies of high-output HF.</title>
						</caption>
						<graphic xlink:href="2764-3107-abchf-003-02-e20230093-gf01.tif"/>
					</fig>
				</p>
				<p>
					<fig id="f02">
						<label>Figure 2</label>
						<caption>
							<title>– Pathophysiology of the disease. Adapted Reddy et al.<xref ref-type="bibr" rid="B1"><sup>1</sup></xref>
							</title>
						</caption>
						<graphic xlink:href="2764-3107-abchf-003-02-e20230093-gf02.tif"/>
					</fig>
				</p>
			</sec>
			<sec>
				<title>Differential diagnosis</title>
				<p>Clinical heart failure is a diagnosis based on the patient’s history and physical examination at initial evaluation. Although the type may not be clear, most patients experience very similar, if not the same, symptoms. Hypervolemia, dyspnea at rest or exertion, orthopnea, and fatigue are the general symptoms of heart failure. Different types of heart failure include heart failure with reduced ejection fraction and heart failure with preserved ejection fraction, which can be differentiated from HOHF by measuring cardiac output and/or cardiac index and low systemic vascular resistance.</p>
			</sec>
			<sec>
				<title>Prognosis</title>
				<p>The prognosis for HOHF depends on the cause of the disease. Reddy published a retrospective analysis of patients with HOHF, reporting an increased mortality rate of three patients compared to the control group (individuals free from heart failure). The study reported a hazard ratio of 3.4 (1.6 to 7.6). This study further stated that among patients with HOHF, obesity-related causes had the lowest 5-year mortality, 19%, compared to liver disease (58%) and heart failure associated with shunt formation (59%), which presented the highest mortality in 5 years.<sup><xref ref-type="bibr" rid="B1">1</xref></sup></p>
				<p>HOHF is a rarely reported cardiovascular complication associated with non-cardiovascular diseases and is found in 0.07% of all HF cases. Although comparable in-hospital mortality was observed among the cohorts studied, there is a need to increase awareness and timely recognition of this entity.</p>
			</sec>
		</sec>
	</body>
	<back>
		<ref-list>
			<title>References</title>
			<ref id="B1">
				<label>1</label>
				<mixed-citation>1. Reddy YNV, Melenovsky V, Redfield MM, Nishimura RA, Borlaug BA. High-Output Heart Failure: A 15-Year Experience. J Am Coll Cardiol. 2016;68(5):473-82. doi: 10.1016/j.jacc.2016.05.043.</mixed-citation>
				<element-citation publication-type="journal">
					<person-group person-group-type="author">
						<name>
							<surname>Reddy</surname>
							<given-names>YNV</given-names>
						</name>
						<name>
							<surname>Melenovsky</surname>
							<given-names>V</given-names>
						</name>
						<name>
							<surname>Redfield</surname>
							<given-names>MM</given-names>
						</name>
						<name>
							<surname>Nishimura</surname>
							<given-names>RA</given-names>
						</name>
						<name>
							<surname>Borlaug</surname>
							<given-names>BA</given-names>
						</name>
					</person-group>
					<article-title>High-Output Heart Failure: A 15-Year Experience</article-title>
					<source>J Am Coll Cardiol</source>
					<year>2016</year>
					<volume>68</volume>
					<issue>5</issue>
					<fpage>473</fpage>
					<lpage>482</lpage>
					<pub-id pub-id-type="doi">10.1016/j.jacc.2016.05.043</pub-id>
				</element-citation>
			</ref>
			<ref id="B2">
				<label>2</label>
				<mixed-citation>2. Mehta PA, Dubrey SW. High Output Heart Failure. QJM. 2009;102(4):235-41. doi: 10.1093/qjmed/hcn147.</mixed-citation>
				<element-citation publication-type="journal">
					<person-group person-group-type="author">
						<name>
							<surname>Mehta</surname>
							<given-names>PA</given-names>
						</name>
						<name>
							<surname>Dubrey</surname>
							<given-names>SW</given-names>
						</name>
					</person-group>
					<article-title>High Output Heart Failure</article-title>
					<source>QJM</source>
					<year>2009</year>
					<volume>102</volume>
					<issue>4</issue>
					<fpage>235</fpage>
					<lpage>241</lpage>
					<pub-id pub-id-type="doi">10.1093/qjmed/hcn147</pub-id>
				</element-citation>
			</ref>
			<ref id="B3">
				<label>3</label>
				<mixed-citation>3. Anand IS, Florea VG. High Output Cardiac Failure. Curr Treat Options Cardiovasc Med. 2001;3(2):151-9. doi: 10.1007/s11936-001-0070-1.</mixed-citation>
				<element-citation publication-type="journal">
					<person-group person-group-type="author">
						<name>
							<surname>Anand</surname>
							<given-names>IS</given-names>
						</name>
						<name>
							<surname>Florea</surname>
							<given-names>VG</given-names>
						</name>
					</person-group>
					<article-title>High Output Cardiac Failure</article-title>
					<source>Curr Treat Options Cardiovasc Med</source>
					<year>2001</year>
					<volume>3</volume>
					<issue>2</issue>
					<fpage>151</fpage>
					<lpage>159</lpage>
					<pub-id pub-id-type="doi">10.1007/s11936-001-0070-1</pub-id>
				</element-citation>
			</ref>
			<ref id="B4">
				<label>4</label>
				<mixed-citation>4. Vieillard-Baron A, Cecconi M. Understanding Cardiac Failure in Sepsis. Intensive Care Med. 2014;40(10):1560-3. doi: 10.1007/s00134-014-3367-8.</mixed-citation>
				<element-citation publication-type="journal">
					<person-group person-group-type="author">
						<name>
							<surname>Vieillard-Baron</surname>
							<given-names>A</given-names>
						</name>
						<name>
							<surname>Cecconi</surname>
							<given-names>M</given-names>
						</name>
					</person-group>
					<article-title>Understanding Cardiac Failure in Sepsis</article-title>
					<source>Intensive Care Med</source>
					<year>2014</year>
					<volume>40</volume>
					<issue>10</issue>
					<fpage>1560</fpage>
					<lpage>1563</lpage>
					<pub-id pub-id-type="doi">10.1007/s00134-014-3367-8</pub-id>
				</element-citation>
			</ref>
			<ref id="B5">
				<label>5</label>
				<mixed-citation>5. McCulloch B. High-Output Heart Failure Caused by Thyrotoxicosis and Beriberi. Crit Care Nurs Clin North Am. 2015;27(4):499-510. doi: 10.1016/j.cnc.2015.07.004.</mixed-citation>
				<element-citation publication-type="journal">
					<person-group person-group-type="author">
						<name>
							<surname>McCulloch</surname>
							<given-names>B</given-names>
						</name>
					</person-group>
					<article-title>High-Output Heart Failure Caused by Thyrotoxicosis and Beriberi</article-title>
					<source>Crit Care Nurs Clin North Am</source>
					<year>2015</year>
					<volume>27</volume>
					<issue>4</issue>
					<fpage>499</fpage>
					<lpage>510</lpage>
					<pub-id pub-id-type="doi">10.1016/j.cnc.2015.07.004</pub-id>
				</element-citation>
			</ref>
			<ref id="B6">
				<label>6</label>
				<mixed-citation>6. Singh S, Sharma S. High-Output Cardiac Failure. In: StatPearls. Treasure Island: StatPearls Publishing; 2023.</mixed-citation>
				<element-citation publication-type="book">
					<person-group person-group-type="author">
						<name>
							<surname>Singh</surname>
							<given-names>S</given-names>
						</name>
						<name>
							<surname>Sharma</surname>
							<given-names>S</given-names>
						</name>
					</person-group>
					<chapter-title>High-Output Cardiac Failure</chapter-title>
					<source>StatPearls</source>
					<publisher-loc>Treasure Island</publisher-loc>
					<publisher-name>StatPearls Publishing</publisher-name>
					<year>2023</year>
				</element-citation>
			</ref>
			<ref id="B7">
				<label>7</label>
				<mixed-citation>7. Ávila DX, Villacorta H, Martins WA, Mesquita ET. High-output Cardiac Failure: a Forgotten Phenotype in Clinical Practice. Curr Cardiol Rev. 2022;18(1):e050821195319. doi: 10.2174/1573403X17666210805142010.</mixed-citation>
				<element-citation publication-type="journal">
					<person-group person-group-type="author">
						<name>
							<surname>Ávila</surname>
							<given-names>DX</given-names>
						</name>
						<name>
							<surname>Villacorta</surname>
							<given-names>H</given-names>
						</name>
						<name>
							<surname>Martins</surname>
							<given-names>WA</given-names>
						</name>
						<name>
							<surname>Mesquita</surname>
							<given-names>ET</given-names>
						</name>
					</person-group>
					<article-title>High-output Cardiac Failure: a Forgotten Phenotype in Clinical Practice</article-title>
					<source>Curr Cardiol Rev</source>
					<year>2022</year>
					<volume>18</volume>
					<issue>1</issue>
					<elocation-id>e050821195319</elocation-id>
					<pub-id pub-id-type="doi">10.2174/1573403X17666210805142010</pub-id>
				</element-citation>
			</ref>
		</ref-list>
		<fn-group>
			<fn fn-type="other">
				<p>Study association</p>
				<p>This study is not associated with any thesis or dissertation work.</p>
			</fn>
			<fn fn-type="other">
				<p>Ethics approval and consent to participate</p>
				<p>This article does not contain any studies with human participants or animals performed by any of the authors.</p>
			</fn>
		</fn-group>
		<fn-group>
			<fn fn-type="financial-disclosure">
				<p>Sources of funding: There were no external funding sources for this study.</p>
			</fn>
		</fn-group>
	</back>
	<sub-article article-type="translation" id="TRpt" xml:lang="pt">
		<front-stub>
			<article-categories>
				<subj-group subj-group-type="heading">
					<subject>Artigo de Revisão</subject>
				</subj-group>
			</article-categories>
			<title-group>
				<article-title>Peculiaridades no Tratamento da Cardiomiopatia Associada a Quadros de Alto Débito</article-title>
			</title-group>
			<contrib-group>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0002-8966-1977</contrib-id>
					<name>
						<surname>Santos</surname>
						<given-names>Carolina Casadei dos</given-names>
					</name>
					<role>Concepção e desenho da pesquisa</role>
					<role>Redação do manuscrito e Revisão crítica do manuscrito quanto ao conteúdo</role>
					<role>Obtenção de dados</role>
					<role>Análise e interpretação dos dados</role>
					<xref ref-type="aff" rid="aff1002"><sup>1</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0002-5959-9359</contrib-id>
					<name>
						<surname>Rossi</surname>
						<given-names>João Manoel</given-names>
						<suffix>Neto</suffix>
					</name>
					<role>Concepção e desenho da pesquisa</role>
					<role>Redação do manuscrito e Revisão crítica do manuscrito quanto ao conteúdo</role>
					<role>Análise e interpretação dos dados</role>
					<xref ref-type="aff" rid="aff1002"><sup>1</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0001-5565-4085</contrib-id>
					<name>
						<surname>Finger</surname>
						<given-names>Marco Aurelio</given-names>
					</name>
					<role>Concepção e desenho da pesquisa</role>
					<role>Redação do manuscrito e Revisão crítica do manuscrito quanto ao conteúdo</role>
					<xref ref-type="aff" rid="aff1002"><sup>1</sup></xref>
				</contrib>
			</contrib-group>
			<aff id="aff1002">
				<label>1</label>
				<country country="BR">Brazil</country>
				<institution content-type="original">Instituto Dante Pazzanese de Cardiologia, São Paulo, SP – Brazil</institution>
			</aff>
			<author-notes>
				<corresp id="c01002"> Correspondência: Carolina Casadei dos Santos • Av. Dr. Dante Pazzanse, 500. CEP 9012-909, São Paulo, SP – Brasil E-mail: carolcasadei33@hotmail.com </corresp>
				<fn fn-type="conflict">
					<p>Potencial conflito de interesse</p>
					<p>Não há conflito com o presente artigo</p>
				</fn>
			</author-notes>
			<abstract>
				<title>Resumo</title>
				<p>A insuficiência cardíaca de alto débito (ICAD) é uma forma menos comum de insuficiência cardíaca e se apresenta como a incapacidade do coração de fornecer sangue suficiente para as necessidades do corpo. A ICAD pode ser dividida em duas categorias: 1. aumento na demanda por maior metabolismo ou 2. shunts arteriovenosos aumentando o fluxo da circulação venosa e diminuindo a resistência, levando ao aumento do consumo de oxigênio e baixa resistência vascular sistêmica. As causas mais frequentes são obesidade, doença hepática, shunts, doença pulmonar, doenças mieloproliferativas, hipertireoidismos e deficiência de tiamina.</p>
			</abstract>
			<kwd-group xml:lang="pt">
				<kwd>Insuficiência Cardíaca</kwd>
				<kwd>Alto Débito</kwd>
			</kwd-group>
		</front-stub>
		<body>
			<sec sec-type="intro">
				<title>Introdução</title>
				<p>Esse artigo tem por objetivo realizar uma revisão sistemática sobre insuficiência cardíaca de alto débito (ICAD) e suas peculiaridades.</p>
				<p>A ICAD é uma forma menos comum de insuficiência cardíaca, e embora possa parecer contraditória à primeira vista, se apresenta como a incapacidade do coração de fornecer sangue suficiente para as necessidades do corpo.<sup><xref ref-type="bibr" rid="B1">1</xref></sup></p>
				<p>Pacientes com ICAD apresentam função cardíaca normal e diminuição da resistência vascular sistêmica, seja secundária à dilatação arteriolar difusa ou a possíveis shunts das arteríolas e leitos capilares, levando à ativação neurohormonal.<sup><xref ref-type="bibr" rid="B2">2</xref>,<xref ref-type="bibr" rid="B3">3</xref></sup></p>
				<p>O alto débito cardíaco e um estado de débito cardíaco elevado em repouso superior a 8 L/min ou um índice cardíaco superior a 4,0 L/min/m<sup><xref ref-type="bibr" rid="B2">2</xref></sup>,<sup><xref ref-type="bibr" rid="B1">1</xref></sup> e ocorre a insuficiência cardíaca quando esse débito cardíaco é insuficiente para suprir a demanda hemodinâmica.</p>
			</sec>
			<sec sec-type="methods">
				<title>Métodos</title>
				<p>Revisão sistemática em plataformas de publicações de alto impacto.</p>
				<sec>
					<title>Desenvolvimento</title>
					<p>Com relação às causas de ICAD, elas podem ser divididas em duas categorias: 1. aumento na demanda por maior metabolismo ou 2. shunts arteriovenosos que aumentam o fluxo da circulação venosa e diminuem a resistência vascular sistêmica, levando ao aumento do consumo de oxigênio e baixa resistência vascular sistêmica, respectivamente.<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B4">4</xref></sup></p>
					<p>De acordo com um estudo de Anand de mais 16.000 pacientes as principais causas de IC de alto débitos são: obesidade 31%, doença hepática (cirrose) 23%, shuts arteriovenosos (fistulas arteriovenosas sistêmicas (FAV)), fistulas para hemodiálise e telangiectasia hemorrágica hereditária) 22%, doença pulmonar (doença pulmonar obstrutiva crônica, bronquiectasia bronquiolite obliterante, doença intersticial) 16% e doença mieloproliferativa 8%. Outras causas que podem levar a IC de alto débito incluem deficiência de tiamina, causando uma doença conhecida por Beribéri e finalmente a tireotoxicose.<sup><xref ref-type="bibr" rid="B5">5</xref></sup></p>
					<p>O tratamento pode ser dividido em duas partes. Primeiro começa com a intervenção aguda da insuficiência cardíaca. Dependendo da gravidade, o tratamento deve ser direcionado à insuficiência respiratória aguda por sobrecarga de volume e se presente, à hipotensão. A conduta inicial pode variar desde terapia diurética intermitente e suplementação de oxigênio até infusão contínua de diurético, ventilação não invasiva com pressão positiva ou intubação. Se a hipotensão e a diminuição da perfusão de órgãos forem evidentes, são necessários medicamentos inotrópicos. Depois que os pacientes estejam estabilizados e não estejam ais em estado descompensado, o tratamento pode ser direcionado à etiologia subjacente.<sup><xref ref-type="bibr" rid="B6">6</xref>,<xref ref-type="bibr" rid="B7">7</xref></sup></p>
					<p>O tratamento do hipertireoidismo é focado na terapia sintomática com o objetivo de diminuir os hormônios tireoidianos circulantes, seja por meio de medicamentos e/ou uso de radioterapia ou cirurgia se necessário. As doenças mieloproliferativas são tratadas de acordo com a doença subjacente específica e podem envolver transplante de células hematopoiéticas dependendo da gravidade. O tratamento é amplamente variável, dependendo da doença e da gravidade dos sintomas. O tratamento da sepse é orientado pelas diretrizes da Surviving Sepsis Campaign e envolve reconhecimento precoce, reanimação imediata e agressiva com fluidos intravenosos e terapia antibiótica com investigação para determinar a fonte da infecção. A deficiência de tiamina que causa beribéri é tratada com reposição de tiamina por no mínimo duas semanas. A doença pulmonar crônica é uma doença progressiva com tratamento direcionado à doença pulmonar subjacente. Em geral, a hipóxia e a hipercapnia são abordadas e o manejo é a terapia sintomática que retarda a progressão da doença subjacente. As FAV adquiridas são tratadas com fechamento ou redução do fluxo sanguíneo. É mais pertinente em pacientes em hemodiálise, que necessitam de acesso; entretanto, se apresentar ICAD, pode ser necessário fechar e locais de acesso alternativos devem ser obtidos. O tratamento das FAV congênitas pode envolver terapia médica, embolização invasiva ou excisão cirúrgica, dependendo da causa exata. A cirrose hepática avançada o suficiente para causar ICAD está em estágio terminal e o tratamento envolve transplante de fígado. A terapia médica tem um papel no manejo de fluidos para hipervolemia, envolvendo o uso combinado de diuréticos de alça e antimineralocorticoides, que podem limitar o fluxo através dos shunts.</p>
				</sec>
				<sec>
					<title>Diagnóstico diferencial</title>
					<p>A insuficiência cardíaca clínica é um diagnóstico baseado na história do paciente e no exame físico na avaliação inicial. Embora o tipo possa não ser claro, a maioria dos pacientes apresenta sintomas muito semelhantes, se não iguais. Hipervolemia, dispneia em repouso ou esforço, ortopneia e fadiga são os sintomas gerais de insuficiência cardíaca. Diferentes tipos de insuficiência cardíaca incluem insuficiência cardíaca com fração de ejeção reduzida e insuficiência cardíaca com fração de ejeção preservada e podem ser diferenciadas da ICAD pela mensuração do débito cardíaco e/ou índice cardíaco e baixa resistência vascular sistêmica.</p>
				</sec>
				<sec>
					<title>Prognóstico</title>
					<p>O prognóstico da ICAD depende da causa da doença. Reddy publicou uma análise retrospectiva de pacientes com ICAD, relatando um aumento na taxa de mortalidade de três pacientes em comparação com o grupo controle (indivíduos livres de insuficiência cardíaca). O estudo relatou uma taxa de risco de 3,4 (1,6 a 7,6). Este estudo afirmou ainda que entre os pacientes com ICAD, as causas relacionadas à obesidade tiveram a menor mortalidade em 5 anos, 19%, em comparação com a doença hepática (58%) e a insuficiência cardíaca associada à formação de shunt (59%) que apresentou a maior mortalidade em 5 anos.<sup><xref ref-type="bibr" rid="B1">1</xref></sup></p>
					<p>A ICAD é uma complicação cardiovascular raramente relatada associada a doenças não cardiovasculares e é encontrada em 0,07% de todos os casos de IC. Embora tenha sido observada mortalidade hospitalar comparável entre as coortes estudadas, é necessário aumentar a conscientização e o reconhecimento oportuno dessa entidade.</p>
					<p>
						<fig id="f01002">
							<label>Figura 1</label>
							<caption>
								<title>– Etiologias de IC de alto débito.</title>
							</caption>
							<graphic xlink:href="2764-3107-abchf-003-02-e20230093-gf01-pt.tif"/>
						</fig>
					</p>
					<p>
						<fig id="f02002">
							<label>Figura 2</label>
							<caption>
								<title>– Fisiopatologia da doença. Adaptado Reddy et al.1</title>
							</caption>
							<graphic xlink:href="2764-3107-abchf-003-02-e20230093-gf02-pt.tif"/>
						</fig>
					</p>
				</sec>
			</sec>
		</body>
		<back>
			<fn-group>
				<fn fn-type="other">
					<label/>
					<p>Vinculação acadêmica</p>
					<p>Não há vinculação deste estudo a programas de pós-graduação.</p>
				</fn>
				<fn fn-type="other">
					<label/>
					<p>Aprovação ética e consentimento informado</p>
					<p>Este artigo não contém estudos com humanos ou animais realizados por nenhum dos autores.</p>
				</fn>
			</fn-group>
			<fn-group>
				<fn fn-type="financial-disclosure">
					<p>Fontes de financiamento: O presente estudo não teve fontes de financiamento externas.</p>
				</fn>
			</fn-group>
		</back>
	</sub-article>
</article>