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<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="publisher-id">abcimg</journal-id>
			<journal-title-group>
				<journal-title>ABC Imagem Cardiovascular</journal-title>
				<abbrev-journal-title abbrev-type="publisher">Arq Bras Cardiol: Imagem cardiovasc.</abbrev-journal-title>
			</journal-title-group>
			<issn pub-type="epub">2675-312X</issn>
			<publisher>
				<publisher-name>Sociedade Brasileira de Cardiologia</publisher-name>
			</publisher>
		</journal-meta>
		<article-meta>
			<article-id pub-id-type="publisher-id">abcimg.20240049i</article-id>
			<article-id pub-id-type="doi">10.36660/abcimg.20240049i</article-id>
			<article-categories>
				<subj-group subj-group-type="heading">
					<subject>Review Article</subject>
				</subj-group>
			</article-categories>
			<title-group>
				<article-title>Hemodynamic Assessment In Exercise Stress Echocardiography</article-title>
			</title-group>
			<contrib-group>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0003-0056-4378</contrib-id>
					<name>
						<surname>Vilela</surname>
						<given-names>Andrea de Andrade</given-names>
					</name>
					<role>Conception and design of the research and acquisition of data</role>
					<role>writing of the manuscript</role>
					<role>critical revision of the manuscript for intellectual content</role>
					<xref ref-type="aff" rid="aff1"><sup>1</sup></xref>
					<xref ref-type="aff" rid="aff2"><sup>2</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0002-2634-4632</contrib-id>
					<name>
						<surname>Otto</surname>
						<given-names>Maria Estefania</given-names>
					</name>
					<role>writing of the manuscript</role>
					<role>critical revision of the manuscript for intellectual content</role>
					<xref ref-type="aff" rid="aff3"><sup>3</sup></xref>
					<xref ref-type="aff" rid="aff4"><sup>4</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0002-7053-3684</contrib-id>
					<name>
						<surname>Nishida</surname>
						<given-names>Gustavo</given-names>
					</name>
					<role>organization of references</role>
					<xref ref-type="aff" rid="aff1"><sup>1</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0002-5153-8420</contrib-id>
					<name>
						<surname>Assef</surname>
						<given-names>Jorge Eduardo</given-names>
					</name>
					<role>critical revision of the manuscript for intellectual 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>
			<aff id="aff2">
				<label>2</label>
				<institution content-type="orgname">Hospital Israelita Albert Einsten</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">Hospital Israelita Albert Einsten, São Paulo, SP – Brazil</institution>
			</aff>
			<aff id="aff3">
				<label>3</label>
				<institution content-type="orgname">Instituto de Cardiologia do Distrito Federal </institution>
				<addr-line>
					<named-content content-type="city">Brasília</named-content>
					<named-content content-type="state">DF</named-content>
				</addr-line>
				<country country="BR">Brazil</country>
				<institution content-type="original">Instituto de Cardiologia do Distrito Federal (ICDF), Brasília, DF – Brazil</institution>
			</aff>
			<aff id="aff4">
				<label>4</label>
				<institution content-type="orgname">Instituto de Cardiologia e Transplantes do Distrito Federal</institution>
				<addr-line>
					<named-content content-type="city">Brasília</named-content>
					<named-content content-type="state">DF</named-content>
				</addr-line>
				<country country="BR">Brazil</country>
				<institution content-type="original">Instituto de Cardiologia e Transplantes do Distrito Federal (ICTDF), Brasília, DF – Brazil</institution>
			</aff>
			<author-notes>
				<corresp id="c01">
					<label>Mailing Address</label>: Andrea de Andrade Vilela Instituto Dante Pazzanese de Cardiologia. Av. Dante Pazzanese, 500. Postal Code: 04012-909. São Paulo, SP – Brazil E-mail: <email>andrea_de_andrade@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>
				<fn fn-type="edited-by">
					<p>Editor responsible for the review: Marcelo Tavares</p>
				</fn>
			</author-notes>
			<pub-date date-type="pub" publication-format="electronic">
				<day>27</day>
				<month>08</month>
				<year>2024</year>
			</pub-date>
			<pub-date date-type="collection" publication-format="electronic">
				<month>08</month>
				<year>2024</year>
			</pub-date>
			<volume>37</volume>
			<issue>3</issue>
			<elocation-id>e20240049</elocation-id>
			<history>
				<date date-type="received">
					<day>30</day>
					<month>05</month>
					<year>2024</year>
				</date>
				<date date-type="rev-recd">
					<day>3</day>
					<month>06</month>
					<year>2024</year>
				</date>
				<date date-type="accepted">
					<day>3</day>
					<month>06</month>
					<year>2024</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</license-p>
				</license>
			</permissions>
			<abstract>
				<title>Abstract</title>
				<p>Cycle ergometer stress echocardiography is an important technique to provides information of cardiac chambers dynamics and cardiovascular hemodynamics during exercise. This method identifies patients who present hemodynamic congestion during exertion, assessment of different causes of dyspnea, through the analysis of diastolic filling pressures and pulmonary artery systolic pressure. Recently, with the incorporation of lung ultrasound, it was possible to add the pulmonary congestion parameter with the identification of the appearance of “B” lines during the exam, increasing the sensivity of the protocol.</p>
				<p>However, Cycle ergometer stress echocardiography is still little used in our country. This reality is probably due, in part, to the need for appropriate training of the medical and nursing staff; in addition to the lack of knowledge of the method among the medical community, which rarely requests this test for hemodynamic assessment and research into exertional dyspnea. Therefore, the objective of this document is not only to disseminate the method, but also to describe in a practical and didactic way the step-by-step hemodynamic evaluation of the echocardiogram with physical stress on a Cycle ergometer. We suggest a protocol that is easy to apply and capable of distinguishing between the findings of patients with normal hemodynamics and those with an inappropriate hemodynamic response to physical effort. Additionally, two clinical cases are reported with multiple images and hemodynamic changes, with a description of the correct interpretation of the findings to better understand the method and its diagnostic capacity.</p>
			</abstract>
			<kwd-group xml:lang="en">
				<kwd>Diastolic stress</kwd>
				<kwd>Exercise stress echocardiography</kwd>
				<kwd>Hemodynamics</kwd>
				<kwd>Echocardiopraphy</kwd>
			</kwd-group>
			<counts>
				<fig-count count="20"/>
				<table-count count="2"/>
				<equation-count count="0"/>
				<ref-count count="28"/>
			</counts>
		</article-meta>
	</front>
	<body>
		<p>
					<fig id="f01">
						<label>Central Illustration</label>
						<caption>
							<title>: Hemodynamic Assessment In Exercise Stress Echocardiography</title>
							<p>Arq Bras Cardiol: Imagem cardiovasc. 2024;37(3):e20240049</p>
						</caption>
						<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf01.tif"/>
					</fig>
				</p>
		<sec sec-type="intro">
			<title>Introduction</title>
			<p>Among the many indications for exercise echocardiography in nonischemic heart disease, hemodynamic assessment has emerged as a fundamental part of the examination, providing both diagnostic and prognostic information. Currently, one of the primary scenarios in which exercise echocardiography is highly applicable is in the evaluation of heart failure with preserved ejection fraction (HFpEF), in which the main complaint is exertional dyspnea. Hemodynamic assessment is part of the study protocol, evaluating the presence or absence of signs of hemodynamic and/or pulmonary congestion during exercise.</p>
			<p>Cycle ergometer stress echocardiography (CESE) has an advantage over treadmill stress echocardiography. CESE allows for real-time detection of the pathological increase in the E/e’ ratio, which is indicative of hemodynamic congestion, as well as the moment when B-lines appear on lung ultrasound (LUS), which is indicative of pulmonary congestion.</p>
			<p>In the present study, we will describe the echocardiography findings of hemodynamic congestion, the ultrasound findings of pulmonary congestion, and the step-by-step process of hemodynamic assessment by using CESE. We also aim to suggest an examination protocol for the evaluation of exertional dyspnea using clinical cases. We will not discuss hemodynamic assessment in valvular heart disease.</p>
			<sec>
				<title>Echocardiography evidence of hemodynamic congestion in CESE</title>
				<p>Left ventricular (LV) filling pressures may be estimated from the ratio of the peak velocity of the E wave of mitral valve diastolic flow (estimated by pulsed Doppler) to the velocity of the e’ wave of the mitral annulus (estimated by tissue Doppler).<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B2">2</xref></sup> During exercise, the velocities of the E and e’ waves typically increase proportionally with increasing transmitral gradient (<xref ref-type="fig" rid="f02">Figure 1</xref>). In healthy hearts, despite the shortening of the diastolic period (because of the increase in heart rate during exercise), diastolic filling pressures remain unchanged or increase minimally. This is due to increased LV suction at the beginning of diastole, which allows for more efficient atrial emptying and an increase in stroke volume.<sup><xref ref-type="bibr" rid="B3">3</xref></sup> Individuals with HFpEF have an increase in the velocity of the E wave while the velocity of the e’ wave remains unchanged, leading to a peak in the E/e’ ratio. In these patients, there is an increase in afterload with slowed myocardial relaxation and reduced ventricular suction during exercise; there is also an increase in heart rate, which, in the presence of a less compliant myocardium, leads to increased LV diastolic pressure and left atrial (LA) pressure, leading to increased pulmonary capillary pressure (PCP) with pulmonary congestion and dyspnea (<xref ref-type="fig" rid="f03">Figure 2</xref>).<sup><xref ref-type="bibr" rid="B4">4</xref></sup></p>
				<p>
					<fig id="f02">
						<label>Figure 1</label>
						<caption>
							<title>– Increase in E and e’ velocities in individuals with normal filling pressure response to exercise (source: image bank of the Dante Pazzanese Institute of Cardiology [IDPC]). E: mitral inflow velocity during the rapid filling phase; e’: tissue Doppler velocity during the rapid filling phase.</title>
						</caption>
						<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf02.tif"/>
					</fig>
				</p>
				<p>
					<fig id="f03">
						<label>Figure 2</label>
						<caption>
							<title>– Algorithm of the pathophysiology of stress-induced congestion (source: personal collection of the author Assef JE). PCWP: pulmonary capillary wedge pressure; PA: arterial pressure; LV: left ventricle; HR: heart rate; DP: diastolic pressure; LA: left atrium.</title>
						</caption>
						<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf03.tif"/>
					</fig>
				</p>
				<p>Diastolic stress testing refers to the use of Doppler echocardiography to detect reduced LV diastolic functional reserve and the resulting increase in LV filling pressures during exercise in patients with dyspnea of unknown origin or subclinical diastolic dysfunction (a common finding in diabetic cardiomyopathy, obesity, and hypertension).<sup><xref ref-type="bibr" rid="B5">5</xref>- <xref ref-type="bibr" rid="B8">8</xref></sup> Studies have shown Doppler echocardiography is a viable technique for noninvasive detection of pathologic increases in exercise-induced diastolic filling pressures (<xref ref-type="table" rid="t1">Table 1</xref>), allowing the differentiation between dyspnea of cardiac and noncardiac origin.<sup><xref ref-type="bibr" rid="B4">4</xref></sup></p>
				<p>
					<table-wrap id="t1">
						<label>Table 1</label>
						<caption>
							<title>– Studies validating stress echocardiography for evaluation of dyspnea of undetermined origin, correlating E/e’ parameter with invasive measures of diastolic filling pressures (adapted from Ha et al.<bold>4</bold>)</title>
						</caption>
						<table frame="hsides" rules="groups">
							<colgroup width="20%">
								<col/>
								<col/>
								<col/>
								<col/>
								<col/>
							</colgroup>
							<thead>
								<tr>
									<th align="left" style="font-weight:normal"> </th>
									<th>Burgess et al., 2006<sup><bold>7</bold></sup></th>
									<th>Talreja et al., 2007<sup><bold>8</bold></sup></th>
									<th>Obokata et al., 2017<sup><bold>9</bold></sup></th>
									<th>Hong et al., 2018<sup><bold>10</bold></sup></th>
								</tr>
							</thead>
							<tbody>
								<tr>
									<td>Study design</td>
									<td align="center">Prospective</td>
									<td align="center">Prospective</td>
									<td align="center">Prospective</td>
									<td align="center">Prospective</td>
								</tr>
								<tr>
									<td>Casuistry</td>
									<td align="center">37</td>
									<td align="center">12</td>
									<td align="center">74</td>
									<td align="center">21</td>
								</tr>
								<tr>
									<td>Effort mode</td>
									<td align="center">Cycle ergometer</td>
									<td align="center">Cycle ergometer</td>
									<td align="center">Cycle ergometer</td>
									<td align="center">Cycle ergometer</td>
								</tr>
								<tr>
									<td>Invasive measure to assess LV filling pressure</td>
									<td align="center">Mean LVEDP</td>
									<td align="center">PCP</td>
									<td align="center">PCP</td>
									<td align="center">Mean LVEDP</td>
								</tr>
								<tr>
									<td>Noninvasive parameter to assess LV filling pressure</td>
									<td align="center">Average E/e’ ratio</td>
									<td align="center">Average E/e’ ratio</td>
									<td align="center">Average E/e’ ratio</td>
									<td align="center">Average E/e’ ratio</td>
								</tr>
								<tr>
									<td>Sensitivity/Specificity</td>
									<td align="center">73/96</td>
									<td align="center">89/100</td>
									<td align="center">-----</td>
									<td align="center">----</td>
								</tr>
								<tr>
									<td>Correlation coefficient</td>
									<td align="center">0.59</td>
									<td align="center">-----</td>
									<td align="center">0.57</td>
									<td align="center">0.51</td>
								</tr>
							</tbody>
						</table>
						<table-wrap-foot>
							<fn id="TFN1">
								<p>LVEDP: LV end-diastolic pressure; PCP: pulmonary capillary pressure</p>
							</fn>
						</table-wrap-foot>
					</table-wrap>
				</p>
			</sec>
			<sec>
				<title>Ultrasound signs of pulmonary congestion in CESE</title>
				<p>LUS was introduced in intensive care units and emergency departments more than 20 years ago, primarily as an assessment tool for patients with acute dyspnea.<sup><xref ref-type="bibr" rid="B9">9</xref>-<xref ref-type="bibr" rid="B11">11</xref></sup> Over the past decade, the cardiology community has recognized the potential of LUS to detect pulmonary congestion and has expanded its use in the diagnosis and management of patients with heart failure.<sup><xref ref-type="bibr" rid="B12">12</xref></sup></p>
				<p>LUS is a versatile examination with high sensitivity for detecting pulmonary deaeration due to increased extravascular water in the pulmonary interstitium. Its integration with echocardiography allows for a comprehensive analysis, facilitating better management of patients with exertional dyspnea suspected of having heart failure.<sup><xref ref-type="bibr" rid="B13">13</xref>,<xref ref-type="bibr" rid="B14">14</xref></sup></p>
				<p>In a fully aerated lung, the pleura is the only anatomical structure that can be visualized, appearing as a smooth, hyperechoic horizontal plane moving synchronously with respiration. This line is called the pleural line, and its movement is known as lung sliding, which allows assessment of lung excursion during ventilation. The ultrasound pattern of a ventilated lung also includes horizontal, parallel, hyperechoic lines that are seen at regular intervals from the pleural line (A-lines, <xref ref-type="fig" rid="f04">Figure 3</xref>).</p>
				<p>
					<fig id="f04">
						<label>Figure 3</label>
						<caption>
							<title>– A) Lung ultrasound image with A lines. B) Lung ultrasound image with B lines (arrow) (source: personal collection of the author Otto ME).</title>
						</caption>
						<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf04.tif"/>
					</fig>
				</p>
				<p>As the air content in the lungs decreases and lung density increases, vertical reverberation artifacts (B-lines, <xref ref-type="fig" rid="f04">Figure 3</xref>) appear. B-lines originate from the pleural line and move in sync with respiration, appearing as laser-like lines extending toward the bottom of the ultrasound image sector. These lines are present in patients with heart failure (cardiogenic pulmonary edema) and lung disease (noncardiogenic pulmonary edema).<sup><xref ref-type="bibr" rid="B13">13</xref></sup> Otto and Andrioli describe in detail the technique for image acquisition and interpretation of LUS for congestion.<sup><xref ref-type="bibr" rid="B15">15</xref></sup></p>
				<p>By integrating LUS with stress echocardiography, a simplified approach can be performed by evaluating four zones by placing the sector transducer in the third intercostal space along the anterior and midaxillary lines.<sup><xref ref-type="bibr" rid="B16">16</xref>;<xref ref-type="bibr" rid="B17">17</xref></sup></p>
				<p>This simplified protocol has shown a good correlation between practicality and accuracy when performed at rest, at peak exercise, and immediately after exercise is completed.<sup><xref ref-type="bibr" rid="B16">16</xref></sup></p>
				<p>In patients with HFpEF, the appearance of B-lines on LUS is because of pulmonary congestion and correlates with worsening diastolic function induced by exercise, as assessed by peak E/e’ ratio and reduced global strain rate values at the end of diastole.<sup><xref ref-type="bibr" rid="B18">18</xref></sup> Based on an invasive hemodynamic study (using high-fidelity micromanometers), acute pulmonary congestion during exercise is because of both increased pulmonary capillary hydrostatic pressure and systemic venous hypertension, which can be assessed by the decoupling between right ventricular function and pulmonary artery (RV-PA) pressure.<sup><xref ref-type="bibr" rid="B19">19</xref></sup> Assessment of RV-PA decoupling during CESE, calculated by the ratio of tricuspid annular plane systolic excursion (TAPSE) to peak tricuspid regurgitation velocity (TRV), is a parameter that can help identify the cause of exertional pulmonary congestion with a normal E/e’ ratio, likely indicating systemic venous hypertension, often associated with pulmonary disease. According to the literature, values below 0.36 mm.cm/s correlate with greater RV-PA uncoupling in patients with postcapillary pulmonary hypertension (PH)<sup><xref ref-type="bibr" rid="B20">20</xref></sup> and values below 0.31 mm.cm/s are associated with greater RV-PA uncoupling in individuals with precapillary PH due to idiopathic and thromboembolic pulmonary disease.<sup><xref ref-type="bibr" rid="B21">21</xref></sup></p>
				<p>The appearance of B-lines on CESE, even if there is only one per field evaluated, should be taken seriously. The number of B-lines at peak exercise is directly related to rehospitalization and death from heart failure in patients with preserved or reduced ejection fraction.<sup><xref ref-type="bibr" rid="B22">22</xref></sup></p>
			</sec>
			<sec>
				<title>Protocol for physical stress test</title>
				<p>The expected normal response to exercise on a treadmill or cycle is a two- to threefold increase in heart rate, a three- to fourfold increase in contractility, an increase in systolic blood pressure of at least 50%, and a decrease in systemic vascular resistance with maintenance or reduction of diastolic blood pressure.<sup><xref ref-type="bibr" rid="B23">23</xref></sup> In terms of cardiac volume, there is initially an increase in end-diastolic volume because of the increased venous return, resulting in an increase in stroke volume, initially because of the Frank-Starling mechanism and subsequently because of the increased heart rate.</p>
				<p>If the objective of the test is the hemodynamic assessment of filling pressures during exercise, the cycle ergometer is more sensitive to the increase in these pressures than the upright bicycle because diastolic volume and mean arterial pressure are greater in the supine position because of the increased venous return. Thus, the supine position contributes to greater wall stress, increased myocardial oxygen demand, and higher filling pressures compared to the upright bicycle test.<sup><xref ref-type="bibr" rid="B23">23</xref>,<xref ref-type="bibr" rid="B24">24</xref></sup></p>
				<p>The profile of patients undergoing hemodynamic assessment on the cycle ergometer is often complex and accompanied by multiple comorbidities. The evaluation of dyspnea includes various pathologies such as ischemic cardiomyopathy, hypertrophic cardiomyopathy, diastolic dysfunction and pulmonary disease. Therefore, the evaluation protocol must include all the necessary information for a wide variety of diagnoses. <xref ref-type="fig" rid="f05">Figure 4</xref> shows an example of the protocol used in our service. In the initial views, corresponding to the baseline examination, it is necessary to obtain data on increased filling pressures and pulmonary congestion: pulsed Doppler of the mitral valve to estimate the E wave velocity, septal and lateral tissue Doppler of the mitral annulus to estimate the e’ wave, continuous Doppler of the tricuspid regurgitation (TR) to estimate the peak velocity, LUS to assess pulmonary congestion, and in the final views, at least three LV views to analyze segmental contractility of the 17 segments and to study ischemia. In the <xref ref-type="fig" rid="f01">central figure</xref>, we have an image showing the arrangement of the cycle ergometer/patient and the echocardiography machine as well as images with criteria defining hemodynamic congestion and pulmonary congestion.</p>
				<p>
					<fig id="f05">
						<label>Figure 4</label>
						<caption>
							<title>– Example of an ergometric bed protocol with assessment of filling pressures, pulmonary congestion, and segmental contraction analysis (source: IDPC image bank).</title>
						</caption>
						<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf05.tif"/>
					</fig>
				</p>
			</sec>
			<sec>
				<title>Interpretation of hemodynamic data</title>
				<p>For the correct interpretation of hemodynamic data during exercise, it is important to consider the workload (generated in watts by the calculation in the ergometry module coupled to the ergometer bed) and the age of the patient, since there is an increase in pulmonary artery systolic pressure (PSAP) with advancing age both at rest and during exercise, a finding also observed in athletes.<sup><xref ref-type="bibr" rid="B24">24</xref></sup> In patients aged ≥ 70 years, the increase in pulmonary systolic pressure is associated with decreased transpulmonary flow and increased systemic pulse pressure, which is explained by increased arterial stiffness in older people<sup><xref ref-type="bibr" rid="B24">24</xref></sup>. A higher stroke volume compared to normal subjects justifies the increase in PSAP during exercise in athletes.<sup><xref ref-type="bibr" rid="B25">25</xref></sup></p>
				<p>In healthy individuals, exercise increases cardiac output and decreases pulmonary vascular resistance (PVR). A PSAP value of &lt; 43 mmHg during exercise is considered normal.<sup><xref ref-type="bibr" rid="B26">26</xref></sup> Pathologically, based on the fundamental flow equation (flow [F] = pressure change [∆P] / resistance [R]), the abnormal increase in pulmonary artery pressure during exercise can be attributed to supranormal cardiac output (e.g., in athletes) or an increase in resistance because of the limited capacity of the pulmonary vascular bed (as occurs in chronic obstructive pulmonary disease or congenital heart disease). In this context, the relationship between pressure change (estimated by the TR velocity) and flow (estimated by the right ventricular outflow tract [RVOT] velocity time integral [VTI]) can help differentiate whether the pressure increase is due to increased flow or resistance. The PVR is calculated by the formula: (maximum TR velocity/RVOT VTI) X 10 + 0.16. Calculation of PVR also helps to identify patients with postcapillary pulmonary hypertension (PVR &lt; 3 WU) and patients with precapillary or mixed pulmonary hypertension (PVR &gt; 3 WU).</p>
				<p>Shim CY et al.<sup><xref ref-type="bibr" rid="B28">28</xref></sup> followed 498 patients who underwent diastolic stress echocardiography for 41 months and found patients with exercise-induced PH had a worse prognosis. Patients with a pathological increase in the E/e’ ratio and exercise-induced PH had a significantly worse outcome compared with the normal diastolic stress group and the group with only exercise-induced PH.<sup><xref ref-type="bibr" rid="B28">28</xref></sup></p>
			</sec>
		</sec>
		<sec sec-type="cases">
			<title>Case reports</title>
			<p>
				<underline>Case report 1:</underline> A 45-year-old woman with nonobstructive hypertrophic cardiomyopathy presents with complaints of fatigue and moderate exertional dyspnea. The purpose of the requested study was to evaluate the intraventricular gradient during exercise (resting study: <xref ref-type="fig" rid="f06">Figure 5</xref>).</p>
			<p>
				<fig id="f06">
					<label>Figure 5</label>
					<caption>
						<title>– Resting assessment of a patient with hypertrophic cardiomyopathy with septal predominance. For Review Only: Left images: resting gradient and right images: assessment of global longitudinal strain with reduction of the septal wall (source: IDPC image bank).</title>
					</caption>
					<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf06.tif"/>
				</fig>
			</p>
			<p>She underwent CESE. The following hemodynamic data were assessed: E/e’ ratio, peak TRV, LUS, and LV outflow tract gradient (<xref ref-type="fig" rid="f07">Figure 6</xref>).</p>
			<p>
				<fig id="f07">
					<label>Figure 6</label>
					<caption>
						<title>– Exercise evaluation of a patient with hypertrophic cardiomyopathy with septal predominance. Upper left images: gradients measured in the LV outflow tract at rest: 17.1 mmHg; at 25W: 22.8 mmHg; at 50W: 19.6 mmHg; and during recovery: 19.9 mmHg. Upper right images: Resting E/e’ ratio: 9.7; E/e’ at 25W: 15.2; E/e’ at 50W: not evaluated because of fusion of E and A waves, and E/e’ during recovery: 12.4. Bottom left images: Peak TRV at rest: 3.27 m/s; at 25W: 4.32 mmHg; at 50W: 4.07 mmHg, and during recovery: 2.32 mmHg. Bottom right images: LUS analysis at rest and at 50W (source: IDPC image bank).</title>
					</caption>
					<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf07.tif"/>
				</fig>
			</p>
			<p>As observed in the analysis of the study described in <xref ref-type="fig" rid="f07">Figure 6</xref>, patient did not have LV outflow tract obstruction during exercise. However, there was a pathological increase in the E/e’ ratio during low-load exercise (E/e’ ratio = 15.2 at 25W) associated with PH and the appearance of B-lines on LUS, consistent with HFpEF. In this case, the patient had hemodynamic and pulmonary congestion during exercise. At 50 W, we observed fusion of the E and A waves at a heart rate of 100 bpm, a common finding that prevents evaluation of the E/e’ ratio. However, the acquisition of pulsed Doppler of the mitral flow during immediate recovery, when the E and A waves separate, allows an accurate assessment of the filling pressures modified by exercise.</p>
			<p>
				<underline>Case report 2:</underline> A 62-year-old hypertensive, diabetic, former smoker man presents with complaints of moderate exertional dyspnea. Clinically, he was classified as obese grade I. In addition, B-type natriuretic peptide level was normal, estimated at 65 pg/ml. A transthoracic echocardiography (<xref ref-type="fig" rid="f08">Figure 7</xref>) and CESE (<xref ref-type="fig" rid="f09">Figure 8</xref>) were performed.</p>
			<p>
				<fig id="f08">
					<label>Figure 7</label>
					<caption>
						<title>– Resting echocardiogram of a hypertensive, diabetic, ex-smoker patient complaining of moderate exertional dyspnea (source: IDPC image bank).</title>
					</caption>
					<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf08.tif"/>
				</fig>
			</p>
			<p>
				<fig id="f09">
					<label>Figure 8</label>
					<caption>
						<title>– Exertional assessment of a hypertensive, diabetic, former smoker with complaints of moderate exertional dyspnea. Upper half images: Normal E/e’ ratio during exercise. Lower left images: Peak TRV at rest: 2.67 m/s; at 25 W: 3.22 m/s; at 75 W: 3.64 m/s, and during recovery: 3.26 m/s, respectively. Bottom right images: LUS analysis at 75W (source: IDPC image bank).</title>
					</caption>
					<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf09.tif"/>
				</fig>
			</p>
			<p>In contrast to clinical case 1, he did not show increased filling pressures during exercise (normal E/e’ ratio). However, at 75W he experienced dyspnea with a slight decrease in O<sub>2</sub> saturation (initially 98% on room air, dropping to 93% at 75W) associated with pulmonary congestion. Based on these findings, the TAPSE/TRV ratio was evaluated and found to be decreased (<xref ref-type="fig" rid="f10">Figure 9</xref>). The conclusion from these changes in saturation and right ventricular function was pulmonary congestion was likely because of systemic venous hypertension associated with ventriculo-arterial uncoupling. In addition, the patient’s history of smoking with chronic obstructive pulmonary disease supports the findings of decreased saturation and “hidden” right ventricular dysfunction.</p>
			<p>
				<fig id="f10">
					<label>Figure 9</label>
					<caption>
						<title>– Assessment of right ventricle-pulmonary artery uncoupling. TAPSE/TR velocity ratio estimated at 0.35 mm.cm/s</title>
					</caption>
					<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf10.tif"/>
				</fig>
			</p>
		</sec>
		<sec sec-type="conclusions">
			<title>Conclusion</title>
			<p>Exercise stress echocardiography using a cycle ergometer allows detailed assessment of several parameters beyond segmental contraction of the LV. This method allows the investigation of the cause of dyspnea by describing the ventricular hemodynamic behavior during exercise by detecting dynamic intraventricular gradients, the evaluation of increased filling pressures by analyzing the E/e’ ratio during exercise, the increased PSAP in the presence of TR, and the appearance of B-lines on lung ultrasound (pulmonary congestion). Although financially accessible, this method requires extensive training of the involved team and the development of specific protocols on the echocardiography equipment, as well as knowledge of the use of a specific ergometry system to apply the appropriate protocol with progressive loads on the cycle ergometer. Thus, although the cycle ergometer offers a wide range of possibilities for the study of dyspnea, it remains underutilized in our setting.</p>
		</sec>
	</body>
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		</ref-list>
		<fn-group>
			<fn fn-type="other">
				<label/>
				<p>Study Association</p>
				<p>This study is not associated with any thesis or dissertation work.</p>
			</fn>
			<fn fn-type="other">
				<label/>
				<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</p>
				<p>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-id pub-id-type="doi">10.36660/abcimg.20240049</article-id>
			<article-categories>
				<subj-group subj-group-type="heading">
					<subject>Artigo de Revisão</subject>
				</subj-group>
			</article-categories>
			<title-group>
				<article-title>Avaliação Hemodinâmica na Ecocardiografia sob Estresse Físico</article-title>
			</title-group>
			<contrib-group>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0003-0056-4378</contrib-id>
					<name>
						<surname>Vilela</surname>
						<given-names>Andrea de Andrade</given-names>
					</name>
					<role>Concepção e desenho da pesquisa e obtenção de dados</role>
					<role>redação do manuscrito</role>
					<role>revisão crítica do manuscrito quanto ao conteúdo intelectual importante</role>
					<xref ref-type="aff" rid="aff1002"><sup>1</sup></xref>
					<xref ref-type="aff" rid="aff2002"><sup>2</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0002-2634-4632</contrib-id>
					<name>
						<surname>Otto</surname>
						<given-names>Maria Estefania</given-names>
					</name>
					<role>redação do manuscrito</role>
					<role>revisão crítica do manuscrito quanto ao conteúdo intelectual importante</role>
					<xref ref-type="aff" rid="aff3002"><sup>3</sup></xref>
					<xref ref-type="aff" rid="aff4002"><sup>4</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0002-7053-3684</contrib-id>
					<name>
						<surname>Nishida</surname>
						<given-names>Gustavo</given-names>
					</name>
					<role>organização das referências</role>
					<xref ref-type="aff" rid="aff1002"><sup>1</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0002-5153-8420</contrib-id>
					<name>
						<surname>Assef</surname>
						<given-names>Jorge Eduardo</given-names>
					</name>
					<role>revisão crítica do manuscrito quanto ao conteúdo intelectual importante</role>
					<xref ref-type="aff" rid="aff1002"><sup>1</sup></xref>
				</contrib>
			</contrib-group>
			<aff id="aff1002">
				<label>1</label>
				<country country="">Brasil</country>
				<institution content-type="original">Instituto Dante Pazzanese de Cardiologia, São Paulo, SP – Brasil</institution>
			</aff>
			<aff id="aff2002">
				<label>2</label>
				<country country="">Brasil</country>
				<institution content-type="original">Hospital Israelita Albert Einsten, São Paulo, SP – Brasil</institution>
			</aff>
			<aff id="aff3002">
				<label>3</label>
				<country country="">Brasil</country>
				<institution content-type="original">Instituto de Cardiologia do Distrito Federal (ICDF), Brasília, DF – Brasil</institution>
			</aff>
			<aff id="aff4002">
				<label>4</label>
				<country country="">Brasil</country>
				<institution content-type="original">Instituto de Cardiologia e Transplantes do Distrito Federal (ICTDF), Brasília, DF – Brasil</institution>
			</aff>
			<author-notes>
				<corresp id="c01002">
					<label>Correspondência</label>: Andrea de Andrade Vilela Instituto Dante Pazzanese de Cardiologia. Av. Dante Pazzanese, 500. CEP: 04012-909. São Paulo, SP – Brasil E-mail: andrea_de_andrade@hotmail.com </corresp>
				<fn fn-type="conflict">
					<p>Potencial Conflito de Interesse</p>
					<p>Declaro não haver conflito de interesses pertinentes.</p>
				</fn>
				<fn fn-type="edited-by">
					<p>Editor responsável pela revisão: Marcelo Tavares</p>
				</fn>
			</author-notes>
			<abstract>
				<title>Resumo</title>
				<p>O ecocardiograma com esforço físico em ciclomaca é uma técnica de grande importância pois provê informações da dinâmica das câmaras cardíacas e da hemodinâmica cardiovascular durante o exercício. Este método possibilita a investigação de diversas causas de dispneia, por meio da análise das pressões de enchimento diastólico e pressão sistólica da artéria pulmonar, identificando os pacientes que apresentam congestão hemodinâmica ao esforço. Recentemente, com a incorporação do ultrassom de pulmão, foi possível agregar o parâmetro de congestão pulmonar com a identificação do aparecimento de linhas “B” durante o exame, sensibilizando o protocolo. Entretanto, o ecocardiograma em ciclomaca ainda é pouco utilizado em nosso meio. Provavelmente, essa realidade se deve, em parte, a necessidade de um treinamento apropriado da equipe médica e enfermagem; além do desconhecimento do método entre a comunidade médica que pouco solicita esse exame para avaliação hemodinâmica e pesquisa de dispnéia aos esforços. Dessa forma, o objetivo do presente documento é não apenas difundir o método, mas também descrever de forma prática e didática o passo a passo da avaliação hemodinâmica do ecocardiograma com estresse físico em ciclomaca. Sugerimos protocolo de fácil aplicabilidade e capaz de distinguir entre os achados de pacientes com hemodinâmica normal daqueles com resposta hemodinâmica inapropriada ao esforço físico. Adicionalmente, dois casos clínicos são relatados com múltiplas imagens e alterações hemodinâmicas, com a descrição da correta interpretação dos achados para melhor compreensão do método e de sua capacidade diagnóstica.</p>
			</abstract>
			<kwd-group xml:lang="pt">
				<kwd>Estresse Diastólico</kwd>
				<kwd>Estresse Fisico</kwd>
				<kwd>Ecocardiografia</kwd>
				<kwd>Hemodinâmica</kwd>
			</kwd-group>
		</front-stub>
		<body>
			<p>
					<fig id="f01002">
						<label>Figura Central</label>
						<caption>
							<title>: Avaliação Hemodinâmica na Ecocardiografia sob Estresse Físico</title>
							<p>Arq Bras Cardiol: Imagem cardiovasc. 2024;37(3):e20240049</p>
						</caption>
						<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf01-pt.tif"/>
					</fig>
				</p>
			<sec sec-type="intro">
				<title>Introdução</title>
				<p>Dentre as inúmeras indicações da ecocardiografia sob estresse físico para cardiopatia não isquêmica, a avaliação hemodinâmica tem se destacado como parte fundamental do exame, pois provê informações diagnósticas e prognósticas. Atualmente, um dos principais cenários com importante aplicabilidade da ecocardiografia sob estresse físico é na pesquisa de insuficiência cardíaca com fração de ejeção preservada (ICFEP), cuja queixa principal é a dispneia ao esforço. A avaliação hemodinâmica faz parte do protocolo do exame, sendo avaliada a presença ou não dos sinais de congestão hemodinâmica e/ou congestão pulmonar ao esforço físico.</p>
				<p>A ecocardiografia com estresse físico em cicloergômetro (ECOCICLO) tem vantagem sobre a ecocardiografia com estresse em esteira ergométrica. A ECOCICLO possibilita a detecção em tempo real do aumento patológico da relação E/e’, que sugere congestão hemodinâmica, bem como o momento do aparecimento de linhas B no ultrassom pulmonar (USP), que sugere congestão pulmonar.</p>
				<p>No presente estudo, iremos descrever os achados ecocardiográficos de congestão hemodinâmica, os achados ultrassonográficos de congestão pulmonar e o passo a passo da avaliação hemodinâmica com ECOCICLO. Também objetivamos sugerir um protocolo de exame para avaliação de dispneia ao esforço por meio de casos clínicos. Não abordaremos a avaliação hemodinâmica na doença cardíaca valvar.</p>
				<sec>
					<title>Sinais ecocardiográficos de congestão hemodinâmica no ECOCICLO</title>
					<p>As pressões de enchimento do ventrículo esquerdo (VE) podem ser estimadas por meio da razão entre o pico de velocidade da <underline>onda E</underline> do fluxo diastólico da valva mitral (estimada via Doppler pulsátil) e a velocidade da <underline>onda e’</underline> do anel mitral (estimada via Doppler tecidual).<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B2">2</xref></sup> Durante o esforço físico, normalmente, as velocidades das ondas E e e’ aumentam proporcionalmente à medida que o gradiente transmitral se eleva (<xref ref-type="fig" rid="f02002">Figura 1</xref>). Em corações saudáveis, a despeito da redução do período diastólico (decorrente do aumento da frequência cardíaca no exercício), as pressões de enchimento diastólico permanecem inalteradas, ou com mínimo aumento. Isso se deve ao aumento da sucção do VE no início da diástole, possibilitando um esvaziamento atrial mais eficiente e o aumento do volume sistólico.<sup><xref ref-type="bibr" rid="B3">3</xref></sup> Já nos pacientes com ICFEP, há elevação da velocidade da onda E e manutenção da velocidade da onda e’, determinando assim um pico da razão E/e’. Nesses pacientes, há aumento da pós carga com “alentecimento” do relaxamento miocárdico associado a menor sucção ventricular durante o esforço físico; além disso, há aumento da frequência cardíaca, que, na vigência de um miocárdio menos complacente, gera elevação da pressão diastólica do VE e da pressão do átrio esquerdo (AE), resultando assim no aumento da pressão capilar pulmonar (PCP) com congestão pulmonar e dispneia (<xref ref-type="fig" rid="f03002">Figura 2</xref>).<sup><xref ref-type="bibr" rid="B4">4</xref></sup></p>
					<p>
						<fig id="f02002">
							<label>Figura 1</label>
							<caption>
								<title>– Aumento as velocidades de E e e’ em indivíduos com resposta normal das pressões de enchimento ao esforço (fonte: banco de imagens do Instituto Dante Pazzanese de Cardiologia [IDPC]). E: velocidade do influxo mitral no período de esvaziamento rápido; e’: velocidade do Doppler tecidual no período de esvaziamento rápido.</title>
							</caption>
							<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf02-pt.tif"/>
						</fig>
					</p>
					<p>
						<fig id="f03002">
							<label>Figura 2</label>
							<caption>
								<title>– Algoritmo da fisiopatologia do surgimento de congestão ao estresse físico (fonte: acervo pessoal do autor Assef JE). PCWP: pressão capilar pulmonar em cunha; PA: pressão arterial; VE: ventrículo esquerdo; FC: frequência cardíaca; PD: pressão diastólica; AE: átrio esquerdo.</title>
							</caption>
							<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf03-pt.tif"/>
						</fig>
					</p>
					<p>O exame de estresse diastólico refere-se ao uso de ecocardiografia com Doppler para detectar reserva funcional diastólica do VE reduzida e o aumento resultante nas pressões de enchimento do VE durante o esforço físico em pacientes com dispneia de origem indeterminada ou disfunção diastólica subclínica (achado frequente na cardiomiopatia diabética, na obesidade e na hipertensão).<sup><xref ref-type="bibr" rid="B5">5</xref>-<xref ref-type="bibr" rid="B8">8</xref></sup> Estudos mostraram que a ecocardiografia com Doppler é uma técnica viável que permite a detecção do aumento patológico das pressões de enchimento diastólico esforço induzido de forma não invasiva (<xref ref-type="table" rid="t1002">Tabela 1</xref>), sendo capaz de distinguir entre dispneia de origem cardíaca e não cardíaca.<sup><xref ref-type="bibr" rid="B4">4</xref></sup></p>
					<p>
						<table-wrap id="t1002">
							<label>Tabela 1</label>
							<caption>
								<title>– Estudos que validaram o ecocardiografia de estresse para avaliação de dispneia de origem indeterminada, correlacionando o parâmetro E/e’ com as medidas invasivas das pressões de enchimento diastólico (adaptado de Ha et al.<bold>4</bold>)</title>
							</caption>
							<table frame="hsides" rules="groups">
								<colgroup width="20%">
									<col/>
									<col/>
									<col/>
									<col/>
									<col/>
								</colgroup>
								<thead>
									<tr>
										<th align="left" style="font-weight:normal"> </th>
										<th>Burgess et al., 2006<sup><bold>7</bold></sup></th>
										<th>Talreja et al., 2007<sup><bold>8</bold></sup></th>
										<th>Obokata et al., 2017<sup><bold>9</bold></sup></th>
										<th>Hong et al., 2018<sup><bold>10</bold></sup></th>
									</tr>
								</thead>
								<tbody>
									<tr>
										<td>Desenho do estudo</td>
										<td align="center">Prospectivo</td>
										<td align="center">Prospectivo</td>
										<td align="center">Prospectivo</td>
										<td align="center">Prospectivo</td>
									</tr>
									<tr>
										<td>Casuística</td>
										<td align="center">37</td>
										<td align="center">12</td>
										<td align="center">74</td>
										<td align="center">21</td>
									</tr>
									<tr>
										<td>Modo de esforço</td>
										<td align="center">Bicicleta supina</td>
										<td align="center">Bicicleta supina</td>
										<td align="center">Bicicleta supina</td>
										<td align="center">Bicicleta supina</td>
									</tr>
									<tr>
										<td>Medida invasiva para avaliar a pressão de enchimento do VE</td>
										<td align="center">PDVE média</td>
										<td align="center">PCP</td>
										<td align="center">PCP</td>
										<td align="center">Variação da PDVE</td>
									</tr>
									<tr>
										<td>Parâmetro não invasivo para avaliar a pressão de enchimento do VE</td>
										<td align="center">E/e’ média</td>
										<td align="center">E/e’ média</td>
										<td align="center">E/e’ média</td>
										<td align="center">E/e’ média</td>
									</tr>
									<tr>
										<td>Sensibilidade/especificidade</td>
										<td align="center">73/96</td>
										<td align="center">89/100</td>
										<td align="center">-----</td>
										<td align="center">----</td>
									</tr>
									<tr>
										<td>Coeficiente de correlação</td>
										<td align="center">0,59</td>
										<td align="center">-----</td>
										<td align="center">0,57</td>
										<td align="center">0,51</td>
									</tr>
								</tbody>
							</table>
							<table-wrap-foot>
								<fn id="TFN1002">
									<p>PDVE: pressão diastólica final do VE; PCP: pressão capilar pulmonar</p>
								</fn>
							</table-wrap-foot>
						</table-wrap>
					</p>
				</sec>
				<sec>
					<title>Sinais ultrassonográficos de congestão pulmonar no ECOCICLO</title>
					<p>O USP foi introduzido nas unidades de terapia intensiva e departamentos de emergência há mais de 20 anos, principalmente como uma ferramenta de avaliação para pacientes com dispneia aguda.<sup><xref ref-type="bibr" rid="B9">9</xref>-<xref ref-type="bibr" rid="B11">11</xref></sup> Na última década, a comunidade cardiológica reconheceu o potencial do USP na detecção de congestão pulmonar e expandiu seu uso para o diagnóstico e manejo de pacientes com insuficiência cardíaca.<sup><xref ref-type="bibr" rid="B12">12</xref></sup></p>
					<p>O USP é um exame versátil, de alta sensibilidade para detectar desaeração pulmonar devido ao aumento da água extravascular no interstício pulmonar. Seu uso integrado à ecocardiografia possibilita uma análise completa para melhor manejo do paciente com queixa de dispneia ao esforço na suspeita de insuficiência cardíaca.<sup><xref ref-type="bibr" rid="B13">13</xref>,<xref ref-type="bibr" rid="B14">14</xref></sup></p>
					<p>Num pulmão totalmente aerado, a única estrutura anatômica que pode ser visualizada é a pleura, que aparece como uma superfície horizontal lisa e hiperecóica, uma linha que se move em sincronia com a respiração. Esta linha é chamada linha pleural e seu movimento é o deslizamento pulmonar, o que possibilita a avaliação da excursão pulmonar durante a ventilação. O padrão ultrassonográfico do pulmão aerado também inclui linhas horizontais, paralelas e hiperecóicas que podem ser vistas em intervalos regulares a partir da linha pleural (linhas A, <xref ref-type="fig" rid="f04002">Figura 3</xref>).</p>
					<p>
						<fig id="f04002">
							<label>Figura 3</label>
							<caption>
								<title>– A) Imagem de ultrassom pulmonar com linhas A. B) Imagem de ultrassom pulmonar com linhas B (seta) (fonte: acervo pessoal do autor Otto ME)</title>
							</caption>
							<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf04-pt.tif"/>
						</fig>
					</p>
					<p>Quando o conteúdo de ar nos pulmões diminui e a densidade pulmonar aumenta, surgem artefatos de reverberação vertical (linhas B, <xref ref-type="fig" rid="f04002">Figura 3</xref>). As linhas B se originam da linha pleural e se movem em sincronia com a respiração, têm formato de laser e se estendem em direção à parte inferior do setor da imagem ultrassonográfica. Essas linhas estão presentes em pacientes com insuficiência cardíaca (edema pulmonar cardiogênico) e em doenças pulmonares (edema pulmonar não cardiogênico).<sup><xref ref-type="bibr" rid="B13">13</xref></sup> Otto e Andrioli descrevem em detalhes a técnica de obtenção de imagens e interpretação do USP para congestão.<sup><xref ref-type="bibr" rid="B15">15</xref></sup></p>
					<p>Ao integrar o USP à ecocardiografia com estresse, pode-se realizar uma abordagem simplificada, avaliando quatro zonas, colocando o transdutor setorial no terceiro espaço intercostal ao longo das linhas axilares anterior e média.<sup><xref ref-type="bibr" rid="B16">16</xref>,<xref ref-type="bibr" rid="B17">17</xref></sup></p>
					<p>Esta simplificação no protocolo mostrou uma boa correlação entre praticidade e acurácia quando realizada no repouso, no pico do esforço e logo após a finalização do esforço.<sup><xref ref-type="bibr" rid="B16">16</xref></sup></p>
					<p>Em pacientes com ICFEP, o aparecimento de linhas B ao USP ocorre por congestão pulmonar e se correlaciona com a piora da função diastólica induzida pelo esforço físico, avaliada pelo pico da relação E/e’ e pelos valores reduzidos do <italic>strain rate</italic> global no final da diástole.<sup><xref ref-type="bibr" rid="B18">18</xref></sup> Com base em estudo hemodinâmico invasivo (por meio de micromanômetros de alta fidelidade), a congestão pulmonar aguda durante o estresse físico ocorre tanto pelo aumento da pressão hidrostática no capilar pulmonar quanto pela hipertensão venosa sistêmica, que pode ser avaliada pelo desacoplamento entre a função do ventrículo direito e a pressão da artéria pulmonar (VD-AP).<sup><xref ref-type="bibr" rid="B19">19</xref></sup> A avaliação do desacoplamento VD-AP durante o ECOCICLO, calculado pela razão do deslocamento sistólico do anel tricúspide (TAPSE) pela velocidade máxima do refluxo tricúspide (VTri), é um parâmetro que pode auxiliar na identificação da causa da congestão pulmonar ao esforço com relação E/e’ normal, tratando-se provavelmente de hipertensão venosa sistêmica, muitas vezes associada a doença pulmonar. De acordo com a literatura, valores inferiores a 0,36 mm.cm/s correlacionam-se com maior desacoplamento VD-AP em pacientes com hipertensão pulmonar (HP) pós-capilar,<sup><xref ref-type="bibr" rid="B20">20</xref></sup> e valores inferiores a 0,31 mm.cm/s estão associados a maior desacoplamento VD-AP nos pacientes com HPpré-capilar, devido à doença pulmonar idiopática e tromboembólica.<sup><xref ref-type="bibr" rid="B21">21</xref></sup></p>
					<p>O surgimento de linhas B durante o ECOCICLO, mesmo que apenas uma por campo avaliado, deve ser valorizado. O número de linhas B no pico do exercício tem correlação direta com reinternação e morte por insuficiência cardíaca em pacientes com fração de ejeção preservada ou reduzida.<sup><xref ref-type="bibr" rid="B22">22</xref></sup></p>
				</sec>
				<sec>
					<title>Protocolo do exame de estresse físico</title>
					<p>A resposta normal esperada durante o estresse físico em esteira ou bicicleta é um aumento da frequência cardíaca de duas a três vezes, maior contratilidade de três a quatro vezes, elevação da pressão arterial sistólica em pelo menos 50% e queda da resistência vascular sistêmica, com manutenção ou redução da pressão arterial diastólica.<sup><xref ref-type="bibr" rid="B23">23</xref></sup> Em relação aos volumes cardíacos, inicialmente ocorre um aumento do volume diastólico final devido ao aumento no retorno venoso, o que resulta em um aumento do volume sistólico decorrente do mecanismo de <italic>Frank-Starling</italic> num primeiro momento e do aumento da frequência cardíaca posteriormente.</p>
					<p>Quando o objetivo do exame é a avaliação hemodinâmica das pressões de enchimento durante o esforço, a bicicleta supina é mais sensível em detectar o aumento dessas pressões em comparação com a bicicleta vertical, pois os volumes diastólicos e a pressão arterial média são maiores na posição supina devido ao aumento do retorno venoso. Dessa forma, a posição supina contribui para uma maior tensão na parede, um aumento na demanda miocárdica de oxigênio e nas pressões de enchimento em comparação com um teste de bicicleta vertical.<sup><xref ref-type="bibr" rid="B23">23</xref>,<xref ref-type="bibr" rid="B24">24</xref></sup></p>
					<p>Frequentemente, o perfil dos pacientes submetidos à avaliação hemodinâmica no cicloergômetro é complexo e acompanhado de múltiplas comorbidades. A investigação da dispneia engloba diversas patologias, como cardiomiopatia isquêmica, cardiomiopatia hipertrófica, disfunção diastólica e doença pulmonar. Por tal motivo, o protocolo de avaliação deve incluir todas as informações necessárias para os mais diversos diagnósticos. Na <xref ref-type="fig" rid="f05002">Figura 4</xref>, temos o exemplo do protocolo que adotamos em nosso serviço. Nas projeções iniciais, que correspondem ao exame basal, é necessário que dados de aumento das pressões de enchimento e congestão pulmonar sejam obtidos: o fluxo pulsátil da valva mitral para estimativa da velocidade da onda E, o Doppler tecidual septal e lateral do anel mitral para estimativa da onda e’, o Doppler contínuo do refluxo tricúspide para estimativa da velocidade de pico, o USP para avaliação da congestão pulmonar e, nas últimas projeções, pelo menos três incidências do VE para analisar a contratilidade segmentar dos 17 segmentos e pesquisar isquemia. Na <xref ref-type="fig" rid="f01002">Figura Central</xref>, temos a imagem da disposição do cicloergômetro/paciente e aparelho de ecocardiografia, além de imagens com os critérios definidores de congestão hemodinâmica e congestão pulmonar.</p>
					<p>
						<fig id="f05002">
							<label>Figura 4</label>
							<caption>
								<title>– Exemplo de protocolo para maca ergométrica com avaliação de pressões de enchimento, congestão pulmonar e análise da contração segmentar (fonte: banco de imagens do IDPC).</title>
							</caption>
							<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf05-pt.tif"/>
						</fig>
					</p>
				</sec>
				<sec>
					<title>Interpretação dos dados hemodinâmicos</title>
					<p>Para uma correta interpretação dos dados hemodinâmicos durante o esforço físico, é importante considerar a carga de trabalho (gerada em <italic>Watts</italic> pelo cálculo no módulo de ergometria acoplado à maca ergométrica) e a idade do paciente, por haver um aumento da pressão sistólica da artéria pulmonar (PSAP) com o avançar da idade, tanto em repouso quanto no exercício, achado também verificado em atletas<sup><xref ref-type="bibr" rid="B24">24</xref></sup>. Em pacientes com idade ≥ 70 anos, o aumento da pressão sistólica pulmonar está associado à diminuição do fluxo transpulmonar e ao aumento da pressão de pulso sistêmica, explicado pelo aumento da rigidez arterial no idoso.<sup><xref ref-type="bibr" rid="B24">24</xref></sup> Um maior volume sistólico em comparação aos indivíduos normais é o que justifica o aumento da PSAP durante o esforço em atletas.<sup><xref ref-type="bibr" rid="B25">25</xref></sup></p>
					<p>Em indivíduos saudáveis, o exercício aumenta o débito cardíaco e reduz a resistência vascular pulmonar (RVP). Um valor de PSAP &lt; 43 mmHg durante o exercício é considerado normal.<sup><xref ref-type="bibr" rid="B26">26</xref></sup> Do ponto de vista patológico, baseado na equação fundamental do fluxo (Fluxo [F] = variação de pressão [∆P] / resistência [R]), o aumento anormal da pressão da artéria pulmonar durante o exercício pode ser atribuído ao débito cardíaco supranormal (por exemplo, em atletas) ou a um aumento da resistência devido à capacidade limitada do leito vascular pulmonar (como ocorre na doença pulmonar obstrutiva crônica ou cardiopatia congênita). Neste contexto, a relação entre ∆P (estimada pela velocidade da insuficiência tricúspide [IT]) e o fluxo (estimado pela integral da velocidade pelo tempo do fluxo [VTI] na via de saída do ventrículo direito [VSVD]) pode ajudar a diferenciar quando o aumento da pressão está relacionado ao aumento do fluxo ou da resistência, sendo esta última calculada pela fórmula: (velocidade máxima da IT÷VTI VSVD)×10 + 0,16.<sup><xref ref-type="bibr" rid="B27">27</xref></sup> O cálculo da RVP também auxilia na identificação dos pacientes com HP pós-capilar (RVP &lt; 3 UW) e pacientes com HP pré-capilar ou HP mista (RVP &gt; 3 UW).</p>
					<p>Shim et al.<sup><xref ref-type="bibr" rid="B28">28</xref></sup> seguiram 498 pacientes submetidos à ecocardiografia com estresse diastólico por 41 meses e observaram que os pacientes que apresentaram HP induzida pelo esforço tiveram pior prognóstico. Nos pacientes com elevação patológica da relação E/e’ e HP induzida pelo esforço, a evolução foi significativamente desfavorável em comparação ao grupo de pacientes com estresse diastólico normal e ao grupo que apresentou apenas HP induzida pelo esforço.<sup><xref ref-type="bibr" rid="B28">28</xref></sup></p>
				</sec>
			</sec>
			<sec sec-type="cases">
				<title>Relatos dos Casos Clínicos</title>
				<p>
					<underline>Caso Clínico 1</underline>
					<underline>:</underline> Paciente do gênero feminino, 45 anos, com diagnóstico de cardiomiopatia hipertrófica não obstrutiva, apresenta queixa de fadiga e dispneia ao esforço moderado. O objetivo do exame solicitado era a investigação do gradiente intraventricular durante o esforço físico (exame de repouso: <xref ref-type="fig" rid="f06002">Figura 5</xref>).</p>
				<p>
					<fig id="f06002">
						<label>Figura 5</label>
						<caption>
							<title>– Avaliação em repouso de paciente com cardiomiopatia hipertrófica com predomínio septal. For Review Only Imagens a esquerda: gradiente em repouso e à direita avaliação do Strain Global Longitudinal com redução na parede septal. (fonte: banco de imagens do IDPC).</title>
						</caption>
						<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf06-pt.tif"/>
					</fig>
				</p>
				<p>A paciente foi submetida ao ECOCICLO e foram avaliados os seguintes dados hemodinâmicos: relação E/e’, pico de VTri, USP e gradiente na via de saída do VE (<xref ref-type="fig" rid="f07002">Figura 6</xref>).</p>
				<p>
					<fig id="f07002">
						<label>Figura 6</label>
						<caption>
							<title>– Avaliação durante o esforço de paciente com cardiomiopatia hipertrófica com predomínio septal. Imagens superior a esquerda: gradientes medidos na via de saída do VE no repouso: 17,1 mmHg; com 25W: 22,8 mmHg; com 50W:19,6 mmHg e na recuperação: 19,9 mmHg, respectivamente. Imagens superior a direita: relação E/e’ em repouso: 9,7; E/e’ 25W: 15,2; E/e’ 50W: Não Avaliado por fusão das ondas E e A e E/e’ recuperação: 12,4. Imagens inferior a esquerda: velocidade de pico do refluxo tricuspídeo em repouso: 3,27 m/s; com 25W: 4,32 mmHg; com 50W: 4,07 mmHg e na recuperação: 2,32 mmHg. Imagens inferior a direita: análise do USP em repouso e com 50W. (fonte: banco de imagens do IDPC).</title>
						</caption>
						<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf07-pt.tif"/>
					</fig>
				</p>
				<p>Conforme observado na análise do exame descrito na <xref ref-type="fig" rid="f07002">Figura 6</xref>, a paciente não apresentava obstrução na via de saída do VE durante o esforço. No entanto, houve elevação patológica da relação E/e’ durante o esforço com baixa carga (relação E/e’ = 15,2 com 25W), associada à HP e ao aparecimento de linhas B no USP, compatível com ICFEP. Nesse caso, a paciente apresentou congestão hemodinâmica e pulmonar ao esforço físico. É interessante ressaltar que, na potência de 50W, observamos o fenômeno de fusão das ondas E e A a uma frequência cardíaca de 100 bpm, um achado habitual que impossibilita a avaliação da relação E/e’. Entretanto, a aquisição do Doppler pulsátil do fluxo mitral na recuperação imediata, quando há a separação das ondas E e A, permite avaliar com precisão as pressões de enchimento modificadas pelo esforço físico.</p>
				<p>
					<underline>Caso Clínico 2</underline>
					<underline>:</underline> Paciente de 62 anos, sexo masculino, hipertenso, diabético, ex-tabagista, com queixa de dispneia ao esforço moderado. Na avaliação clínica, apresentava obesidade grau I. Adicionalmente, o nível de peptídeo natriurético cerebral tipo B (BNP) estava normal, estimado em 65 pg/ml. Foi realizado ecocardiografia transtorácica (<xref ref-type="fig" rid="f08002">Figura 7</xref>) e ECOCICLO (<xref ref-type="fig" rid="f09002">Figura 8</xref>).</p>
				<p>
					<fig id="f08002">
						<label>Figura 7</label>
						<caption>
							<title>– Ecocardiografia de repouso de paciente hipertenso, diabético, ex-tabagista com queixa de dispneia aos esforços moderados (fonte: banco de imagens do IDPC).</title>
						</caption>
						<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf08-pt.tif"/>
					</fig>
				</p>
				<p>
					<fig id="f09002">
						<label>Figura 8</label>
						<caption>
							<title>– Avaliação durante o esforço de paciente hipertenso, diabético, ex-tabagista com queixa de dispneia ao esforço moderado. Imagens na metade superior: Relação E/e’ normal ao esforço. Imagens inferior a esquerda: velocidade de pico do refluxo tricuspídeo em repouso: 2,67 m/s; com 25W: 3,22 m/s; com 75W: 3,64 m/s e na recuperação: 3,26 m/s; respectivamente. Imagens inferior a direita: análise do USP com 75W (fonte: banco de imagens do IDPC).</title>
						</caption>
						<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf09-pt.tif"/>
					</fig>
				</p>
				<p>Contrapondo o caso clínico 1, este paciente não apresentou aumento das pressões de enchimento durante o esforço (relação E/e’ normal). Entretanto, com 75W, apresentou dispneia com discreta queda na saturação de O<sub>2</sub> (inicialmente saturava 98% em ar ambiente, caindo para 93% com 75W de potência), associada à congestão pulmonar. Baseado nesses achados, foi realizada a avaliação da relação TAPSE/VTri, a qual se mostrou reduzida (<xref ref-type="fig" rid="f10002">Figura 9</xref>). A conclusão dessas alterações de saturação e função ventricular direita foi que a congestão pulmonar ocorreu provavelmente por hipertensão venosa sistêmica associada ao desacoplamento ventrículo-arterial. Adicionalmente, o paciente apresentava histórico de tabagismo, com possível doença pulmonar obstrutiva crônica, condições que corroboram os achados de queda de saturação e disfunção do ventrículo direito “oculta”.</p>
				<p>
					<fig id="f10002">
						<label>Figura 9</label>
						<caption>
							<title>– Avaliação do desacoplamento VD-AP: TAPSE/Velocidade máxima refluxo tricúspide = 0.35mm.cm/s.</title>
						</caption>
						<graphic xlink:href="2675-312X-abcimg-37-03-e20240049-gf10-pt.tif"/>
					</fig>
				</p>
			</sec>
			<sec sec-type="conclusions">
				<title>Conclusão</title>
				<p>A ECOCICLO permite uma avaliação detalhada de diversos parâmetros que vão muito além da contração segmentar do VE. Este método possibilita a investigação da causa de dispneia, descrevendo o comportamento hemodinâmico ventricular durante o esforço por meio da detecção de gradientes intraventriculares dinâmicos, avaliação do aumento das pressões de enchimento pela análise da relação E/e’ no esforço, aumento da PSAP na presença de regurgitação tricúspide e o aparecimento de linhas B ara aplicação do protocolo adequado com cargas progressivas no cicloergômetro. Dessa forma, apesar de oferecer uma ampla possibilidade de aplicação na investigação de dispneia, o cicloergômetro ainda é subutilizada no nosso meio.</p>
			</sec>
		</body>
		<back>
			<fn-group>
				<fn fn-type="other">
					<p>Vinculação Acadêmica</p>
					<p>Não há vinculação deste estudo a programas de pós-graduação.</p>
				</fn>
				<fn fn-type="other">
					<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</p>
					<p>O presente estudo não teve fontes de financiamento externas.</p>
				</fn>
			</fn-group>
		</back>
	</sub-article>
</article>