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<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.20240033i</article-id>
<article-id pub-id-type="doi">10.36660/abchf.20240033i</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Viewpoint</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Non-Ischemic Cardiogenic Shock: How to Improve Outcomes – From Early Recognition to Distinctive Management</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name><surname>Amantéa</surname><given-names>Rodrigo P.</given-names></name>
<role>Conception and design of the research and Acquisition of data</role>
<role>Writing of the manuscript</role>
<xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0000-0003-2022-7512</contrib-id>
<name><surname>Hastenteufel</surname><given-names>Laura</given-names></name>
<role>Writing of the manuscript</role>
<role>Critical revision of the manuscript for content</role>
<xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0000-0003-2150-6337</contrib-id>
<name><surname>Scolari</surname><given-names>Fernando Luís</given-names></name>
<role>Writing of the manuscript</role>
<role>Critical revision of the manuscript for content</role>
<xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0000-0002-1523-4286</contrib-id>
<name><surname>Goldraich</surname><given-names>Lívia A.</given-names></name>
<role>Writing of the manuscript</role>
<role>Critical revision of the manuscript for content</role>
<xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0000-0003-4207-3809</contrib-id>
<name><surname>Clausell</surname><given-names>Nadine</given-names></name>
<role>Conception and design of the research and Acquisition of data</role>
<role>Writing of the manuscript</role>
<xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="corresp" rid="c1"/></contrib>
<aff id="aff1">
<label>1</label>
<institution content-type="orgname">Hospital de Clínicas de Porto Alegre</institution>
<addr-line>
<named-content content-type="city">Porto Alegre</named-content>
<named-content content-type="state">RS</named-content>
</addr-line>
<country country="BR">Brazil</country>
<institution content-type="original">Hospital de Clínicas de Porto Alegre, Porto Alegre, RS – Brazil</institution>
</aff>
</contrib-group>
<author-notes>
<corresp id="c1"><label>Mailing Address:</label> <bold>Nadine Clausell</bold> • Programa de transplante cardíaco – Serviço de cardiologia – Hospital de Clínicas de Porto Alegre – Rua Ramiro Barcellos, 2350. Postal Code <postal-code>90035-903</postal-code>, Porto Alegre, RS – Brazil E-mail: <email>nclausell@hcpa.edu.br</email></corresp>
<fn fn-type="edited-by"><label>Editor responsible for the review:</label> <p>Luis Beck-da-Silva</p></fn>
<fn fn-type="conflict"><label>Potential conflict of interest</label>
<p>No potential conflict of interest relevant to this article was reported.</p></fn>
</author-notes>
<pub-date publication-format="electronic" date-type="pub">
<day>18</day>
<month>10</month>
<year>2024</year></pub-date>
<pub-date publication-format="electronic" date-type="collection">
<year>2024</year></pub-date>
<volume>4</volume>
<issue>1</issue>
<elocation-id>e20240033</elocation-id>
<history>
<date date-type="received">
<day>02</day>
<month>06</month>
<year>2024</year></date>
<date date-type="rev-recd">
<day>12</day>
<month>08</month>
<year>2024</year></date>
<date date-type="accepted">
<day>26</day>
<month>08</month>
<year>2024</year></date>
</history>
<permissions>
<license license-type="open-access" xml:lang="en" xlink:href="http://creativecommons.org/licenses/by/4.0/">
<license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License</license-p>
</license>
</permissions>
<kwd-group xml:lang="en">
<title>Keywords</title>
<kwd>Cardiogenic Shock</kwd>
<kwd>Heart Failure</kwd>
<kwd>Intensive Care Unit</kwd>
</kwd-group>
<counts>
<fig-count count="2"/>
<table-count count="2"/>
<equation-count count="0"/>
<ref-count count="40"/>
</counts>
</article-meta>
</front>
<body>
<sec sec-type="intro">
<title>Introduction</title>
<p>Cardiogenic shock is a clinical condition with an increasing incidence that presents with tissue hypoperfusion, leading to multiorgan dysfunction with a high mortality rate.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> Non-ischemic cardiogenic shock has been recognized as an important cause of shock in emergency rooms, with an incidence exceeding that of shock related to acute myocardial infarction (AMI) in some populations.<sup><xref ref-type="bibr" rid="B2">2</xref></sup> Recent data from the Cardiogenic Shock Working Group (CSWG), an international multicenter registry, reveals that the mortality rate for this condition varies from 22 to 32%, depending on the type of institution.<sup><xref ref-type="bibr" rid="B3">3</xref></sup></p>
<p>Unlike cardiogenic shock of ischemic origin, in which an index event marks the beginning of myocardial injury, potentially leading to the state of shock, in cardiogenic shock of non-ischemic origin the presentation represents the continuum of advanced heart failure. For the purposes of this article, we will be focusing exclusively on shock related to advanced heart failure, since it is the most prevalent type and often presents with a wide range of symptoms, which can delay diagnosis and contribute to poorer outcomes. The following topics will be covered: definitions pertinent to diagnosing cardiogenic shock and its various clinical presentations; initial systematic evaluation of these patients, including recent updates on the use of pulmonary artery catheters and individualized risk stratification for morbidity and mortality; and management strategies for non-ischemic cardiogenic shock, including pharmacological treatments, mechanical devices, and the role of &quot;Shock Teams&quot; in coordinated care.</p>
</sec>
<sec>
<title>Definitions and clinical presentation</title>
<p>Most societies include the following factors in the definition of shock: systolic blood pressure (SBP) &lt; 90 mmHg for more than 30 min and/or requiring vasopressor drugs to maintain SBP ≥ 90 mmHg, associated with changes suggesting hypoperfusion (cold extremities, altered mental status, slowed capillary refill) and lactate levels ≥ 2 mmol/L.<sup><xref ref-type="bibr" rid="B4">4</xref></sup> However, there is no clear consensus to define the presence of non-ischemic cardiogenic shock. The clinical presentation of patients with advanced heart failure who progress to a state of shock with classic signs of hypoperfusion and multiorgan dysfunction can be slow and often elusive. Many patients have lower baseline blood pressure levels, and this may not be a major sign of impending shock; hypoperfusion often does not require hypotension.<sup><xref ref-type="bibr" rid="B5">5</xref></sup> The physical examination may not be exuberant, and concomitant congestion, observed in many cases, may not be evident. Thus, point-of-care ultrasound (POCUS) has become increasingly important in evaluating patients with advanced heart failure,<sup><xref ref-type="bibr" rid="B6">6</xref></sup> as it allows for objective stratification of the patient&apos;s hemodynamic profile and aids in guiding the initial therapeutic approach. Moreover, due to the variability in presentations and pre-existing conditions, it is crucial to emphasize the need for dynamic, serial assessments, as relying solely on single-point evaluations can lead to missed early signs of shock and, consequently, delay necessary treatment measures.</p>
<sec>
<title>Assessment with exams</title>
<p>Alongside the physical examination and point-of-care ultrasound, performing an electrocardiogram is essential, just as it is important to collect the following tests: coagulation, renal function, and liver function tests to swiftly identify the presence and extent of multiorgan dysfunction; inflammatory markers such as C-reactive protein and leukogram; and markers of tissue perfusion and cardiac output, including lactate, bicarbonate, and central venous saturation. Lactate clearance within the first 24 hours of assessment has been studied as a predictor of mortality in patients with cardiogenic shock, and it may serve as an objective therapeutic target and an important factor in the decision-making process when managing this patient population.<sup><xref ref-type="bibr" rid="B7">7</xref>,<xref ref-type="bibr" rid="B8">8</xref></sup></p>
</sec>
<sec>
<title>Use of pulmonary artery catheter</title>
<p>Although data from the ESCAPE study<sup><xref ref-type="bibr" rid="B9">9</xref></sup> and other reports question or even contraindicate the use of the Swan-Ganz catheter (pulmonary artery catheter/PAC) in the past, contemporary management of cardiogenic shock unequivocally includes this resource. This shift in perspective may be attributed to improved indications for the method&apos;s use, as well as a better understanding and application of the information it provides.<sup><xref ref-type="bibr" rid="B10">10</xref>-<xref ref-type="bibr" rid="B12">12</xref></sup> Currently, the use of the Swan-Ganz catheter is crucial for the diagnosis and management of non-ischemic cardiogenic shock, and its early use should be promoted. Recent studies have associated the use of PAC with greater use of ventricular assist devices and reduced mortality.<sup><xref ref-type="bibr" rid="B12">12</xref></sup> More specifically, a study by Kanwar et al. demonstrated that the use of CAP in the first six hours of hospitalization for non-ischemic cardiogenic shock was associated with reduced in-hospital mortality compared with later use of PAC or no use of this resource (OR 0.37; 95% CI, 017-0.82).<sup><xref ref-type="bibr" rid="B13">13</xref></sup> To maximize the benefits of the Swan-Ganz catheter in shock management, healthcare teams must be well-trained in its use, measurements should be taken at least 2 to 3 times daily, and the data should be integrated into daily patient discussions and reassessments.</p>
</sec>
<sec>
<title>Risk stratification</title>
<p>In recent years, more than 30 scores for predicting the risk and severity of cardiogenic shock have been created.<sup><xref ref-type="bibr" rid="B14">14</xref></sup> The SCAI (Society for Cardiovascular Angiography and Interventions) indicator of cardiogenic shock, developed in 2019,<sup><xref ref-type="bibr" rid="B15">15</xref></sup> has been widely used to stratify severity and serve as a basis for implementing therapies and defining prognosis. This ranges from &quot;A&quot; (at risk) to &quot;E&quot; (extremis) on a scale that covers clinical, hemodynamic, and laboratory parameters.<sup><xref ref-type="bibr" rid="B16">16</xref></sup> Since its inception, this indicator has gained significant importance in non-ischemic cardiogenic shock due to its practical application, reproducibility, and widespread acceptance in academic circles. The SCAI classification was recently refined by the CSWG, including progression of shock and worsening of hemodynamic parameters, as well as clinical recovery. The dynamic profile of this classification thus became clearer, with a progressively increased risk of mortality between phases &quot;B&quot; and &quot;E&quot;.<sup><xref ref-type="bibr" rid="B17">17</xref></sup></p>
</sec>
</sec>
<sec>
<title>Management</title>
<p>The initial stage of managing non-ischemic cardiogenic shock involves accurately identifying and understanding the patient&apos;s hemodynamic profile to enable effective hemodynamic resuscitation and clinical stabilization.<sup><xref ref-type="bibr" rid="B4">4</xref></sup> Simultaneously, medications aimed at optimizing cardiac function, such as vasopressors and inotropes, should be considered as established practices. These represent the main tools in the initial management of non-ischemic cardiogenic shock.<sup><xref ref-type="bibr" rid="B18">18</xref></sup></p>
<p>The use of oxygen support is indicated for hypoxemic patients with peripheral O<sub>2</sub> saturation &lt; 90% or PaO<sub>2</sub> &lt; 60 mmHg in order to correct hypoxemia. Its routine use is not recommended since it causes vasoconstriction and a reduction in cardiac output.<sup><xref ref-type="bibr" rid="B19">19</xref></sup> The use of non-invasive positive pressure ventilation (NIV) is also indicated for certain patients with ventilatory dysfunction, which potentially reduces the need for orotracheal intubation.<sup><xref ref-type="bibr" rid="B20">20</xref></sup> Blood pressure (BP) should be monitored during NIV therapy, as the increase in intrathoracic pressure reduces venous return and ventricular preload. There may also be impairment of right ventricular (RV) function due to the increased pulmonary vascular resistance and RV afterload. In patients with progressive ventilatory dysfunction, orotracheal intubation is recommended. For patients who do not respond to initial treatment, the use of temporary mechanical circulatory support (MCS) devices should be assessed, with increasing benefits observed when care is guided by decisions from a dedicated &quot;Shock Team.&quot; These topics will be discussed in greater detail below.</p>
<sec>
<title>Pharmacological therapies</title>
<p>In our routine, the initial management of non-ischemic cardiogenic shock essentially comprises the use of vasoactive and inotropic drugs, considering the state of systemic hypoperfusion and insufficient cardiac output for metabolic demand. The main representatives of these pharmacological classes and their main characteristics are presented in <xref ref-type="table" rid="t1">Table 1</xref>. The main objective of treating this condition is restoring cardiac output, followed by relieving congestion, if present. In addition to drugs that act to regulate cardiovascular hemodynamics, loop diuretics are also key to the management of patients with acutely decompensated advanced heart failure by improving volume overload and systemic and pulmonary congestion resulting from increased renal excretion of water and sodium.<sup><xref ref-type="bibr" rid="B5">5</xref></sup> Therefore, it is indicated when there is evidence of congestion, as determined by Swan-Ganz catheter measurements and POCUS assessment.</p>
<table-wrap id="t1">
<label>Table 1</label>
<caption><title>Main medications used in cardiogenic shock and characteristics</title></caption>
<table frame="hsides" rules="groups">
<colgroup width="14%">
<col/>
<col/>
<col/>
<col/>
<col/>
<col/>
<col/>
</colgroup>
<thead style="border-top: thin solid; border-bottom: thin solid; border-color: #000000">
<tr style="background-color:#98ADCA">
<th align="left" valign="middle">Medication</th>
<th align="center" valign="middle">Mechanism of action</th>
<th align="center" valign="middle">Dose</th>
<th align="center" valign="middle">SVR</th>
<th align="center" valign="middle">BP</th>
<th align="center" valign="middle">CO</th>
<th align="center" valign="middle">HR</th>
</tr>
</thead>
<tbody style="border-bottom: thin solid; border-color: #000000">
<tr>
<td align="left" valign="middle">Norepinephrine</td>
<td align="center" valign="middle">α1 &gt;&gt; β1 &gt;β2</td>
<td align="center" valign="middle">0,05-1 μg/kg/min</td>
<td align="center" valign="middle">↑↑</td>
<td align="center" valign="middle">↑↑</td>
<td align="center" valign="middle">↑</td>
<td align="center" valign="middle">↓↔</td>
</tr>
<tr style="background-color:#E8CCBF">
<td align="left" valign="middle">Vasopressin</td>
<td align="center" valign="middle">V1</td>
<td align="center" valign="middle">0,01 - 0,06 U/min</td>
<td align="center" valign="middle">↑↑</td>
<td align="center" valign="middle">↑↑</td>
<td align="center" valign="middle">-</td>
<td align="center" valign="middle">-</td>
</tr>
<tr>
<td align="left" valign="middle">Sodium nitroprusside</td>
<td align="center" valign="middle">NO</td>
<td align="center" valign="middle">0,1 - 3 μg/kg/min</td>
<td align="center" valign="middle">↓↓</td>
<td align="center" valign="middle">↓↔</td>
<td align="center" valign="middle">↔↑</td>
<td align="center" valign="middle">↔</td>
</tr>
<tr style="background-color:#E8CCBF">
<td align="left" valign="middle">Dobutamine</td>
<td align="center" valign="middle">β1 &gt;&gt; β2 &gt; α1</td>
<td align="center" valign="middle">2-20 μg/kg/min</td>
<td align="center" valign="middle">↓↔</td>
<td align="center" valign="middle">↓↔</td>
<td align="center" valign="middle">↑↑</td>
<td align="center" valign="middle">↑</td>
</tr>
<tr>
<td align="left" valign="middle">Milrinone</td>
<td align="center" valign="middle">PDE3 - Inhibitor</td>
<td align="center" valign="middle">0,125-0,75 μg/kg/min</td>
<td align="center" valign="middle">↓↓</td>
<td align="center" valign="middle">↓↓</td>
<td align="center" valign="middle">↑↑</td>
<td align="center" valign="middle">↔</td>
</tr>
</tbody>
</table>
<table-wrap-foot>
<fn id="TFN1"><p>α1: alpha-1 adrenergic receptor; α2: alpha-2 adrenergic receptor; β1: beta-1 adrenergic receptor; β2: beta-2 adrenergic receptor; CO: cardiac output; HR: heart rate; NO: nitric oxide; BP: blood pressure; PDE3: phosphodiesterase 3; SVR: systemic vascular resistance; VR1: vasopressin V1 receptor.</p></fn>
</table-wrap-foot>
</table-wrap>
<p>The initial pharmacological therapy for non-ischemic cardiogenic shock depends on the patient&apos;s pressure threshold. In patients with permissive BP (usually systolic blood pressure [SBP] of at least 90 mmHg or mean arterial pressure [MAP] of 65 mmHg), we opt for an initial strategy of intravenous vasodilators, with sodium nitroprusside (SNP) being the preferred drug. This should be administered as a slow infusion, with a low initial dose and strict observation of BP behavior immediately after the start of administration. The usual expected response is a slight increase in BP, improvement in peripheral perfusion, increased diuresis and clinical improvement.<sup><xref ref-type="bibr" rid="B21">21</xref></sup> In case of a hypotensive response, excessive NPS dose or hypovolemia should be considered. As an alternative to NPS, nitroglycerin (NTG) can be used, but with a lower arterial vasodilatory effect and less robust evidence supporting its use.</p>
<p>In patients with hypotension at initial presentation, a vasopressor can be started, especially norepinephrine, considered a first-line agent in this clinical context. Previous studies have demonstrated that this catecholamine is more effective than both dopamine and epinephrine. A recommendation IIb/B supports its use for maintaining organic perfusion pressure in recent guidelines.<sup><xref ref-type="bibr" rid="B20">20</xref></sup> The effect of norepinephrine on vital organ perfusion is accompanied by an increased left ventricular (LV) afterload, with a potential reduction in cardiac output. Therefore, the combination of norepinephrine with inotropes should be considered, especially in the population of patients with non-ischemic cardiogenic shock.<sup><xref ref-type="bibr" rid="B20">20</xref></sup></p>
<p>Vasopressin, a non-sympathomimetic vasoconstrictor, increases systemic vascular resistance through a mechanism similar to the vasodilation effect of milrinone, and it is used alongside this inotropic agent to counterbalance hypotension, which allows for reduced use of norepinephrine.<sup><xref ref-type="bibr" rid="B22">22</xref></sup></p>
<p>Inotropic therapy is commonly used in cardiogenic shock due to its effectiveness in increasing cardiac output. However, its application is not strongly supported by large-scale studies, with only a class IIb/C recommendation for use in this setting. Therefore, inotropic agents such as dobutamine or milrinone should be considered for patients with shock who do not respond to initial management.<sup><xref ref-type="bibr" rid="B20">20</xref></sup> These agents should be used for a short period, with ongoing hemodynamic reassessment and transition to vasodilator therapy as soon as feasible.</p>
<p>The DOREMI randomized clinical trial (RCT) compared the treatment of patients in cardiogenic shock with dobutamine versus milrinone.<sup><xref ref-type="bibr" rid="B23">23</xref></sup> This study included mostly ischemic patients and revealed a neutral result in the primary composite outcome involving in-hospital death, aborted cardiopulmonary arrest, heart transplantation, use of mechanical circulatory support devices, or cardiac or cerebral ischemic event. However, an observational study suggests that there may be a benefit in using milrinone as the inotropic therapy of choice in non-ischemic cardiogenic shock,<sup><xref ref-type="bibr" rid="B24">24</xref></sup> requiring an RCT involving this specific population.</p>
</sec>
<sec>
<title>Temporary mechanical circulatory support devices</title>
<p>For patients with persistent organ dysfunction despite initial treatment, the use of MCS devices should be evaluated. The choice of device depends on equipment availability, the care team&apos;s familiarity, and the specific needs of the patient. In Brazil, we can use the intra-aortic balloon pump (IABP), an extracorporeal membrane oxygenation (ECMO) device, and, more rarely, a microaxial flow pump (Impella).</p>
<p>The decision to escalate treatment to temporary circulatory support devices is critical and sensitive when managing patients at SCAI stage B or higher. Just as the early use of these devices can expose the patient to the risk of complications, a delayed indication may provide results below expectations. The concept of &quot;door-to-support time&quot; in the management of shock has gained strength, as was the case in the past with the &quot;door-to-balloon&quot; parameter in primary angioplasty for infarction.<sup><xref ref-type="bibr" rid="B25">25</xref></sup> Therefore, the ideal indication for MCS should occur according to the use of vasoactive drugs while considering, for example, the vasoactive drug score.<sup><xref ref-type="bibr" rid="B26">26</xref></sup> Before installing these devices, it is essential to define their objectives, such as achieving hemodynamic stabilization and improving perfusion parameters.<sup><xref ref-type="bibr" rid="B27">27</xref></sup> The main potential complications of MCS devices include vascular injury leading to limb ischemia, infection at the vascular access site, damage to heart valves, thromboembolic events, and bleeding.<sup><xref ref-type="bibr" rid="B28">28</xref></sup></p>
<p>In cases of non-ischemic cardiogenic shock, the IABP is the most commonly used temporary circulatory support device. It serves as a bridge to definitive treatment, which typically involves transitioning to a ventricular assist device or heart transplantation.<sup><xref ref-type="bibr" rid="B29">29</xref></sup> The IABP works through a counterpulsation mechanism that reduces afterload, increases MAP, and optimizes coronary perfusion pressure, resulting in an average improvement of approximately 1 L/min in cardiac output, along with reductions in left ventricular end-diastolic pressure and myocardial oxygen consumption.<sup><xref ref-type="bibr" rid="B29">29</xref></sup> Currently, the multicenter RCT &quot;Altshock 2 trial&quot; is underway to evaluate early IABP implantation vs. standard optimized medical therapy in patients with non-ischemic cardiogenic shock. The primary outcome will be 60-day survival or successful bridge to heart transplantation.<sup><xref ref-type="bibr" rid="B30">30</xref></sup></p>
<p>In the context of ischemic cardiogenic shock, on the other hand, the use of IABP should be considered only for exceptional cases since the – IABP - SHOCK - II – study showed no difference in mortality rates between the use of this device vs. optimized medical therapy.<sup><xref ref-type="bibr" rid="B31">31</xref></sup> It is important to recognize the limitations of this RCT, including the inclusion of patients with mild to moderate cardiogenic shock, a low rate of device insertion before primary coronary intervention, and a high crossover rate in the IABP group.</p>
<p>In the context of ischemic cardiogenic shock, the &quot;DanGer Shock&quot; study was recently published. This study compared the use of Impella CP combined with optimized clinical treatment against optimized clinical treatment alone in patients with AMI and cardiogenic shock.<sup><xref ref-type="bibr" rid="B32">32</xref></sup> A total of 360 patients were randomized, and 45.8% from any cause were recorded in the Impella CP group vs. 58.5% in the clinical treatment group, with a hazard ratio of 0.74 (95% CI, 0.55-0.99, p = 0.04). The Impella is implanted percutaneously through the femoral artery and continuously transfers blood from the LV to the aorta, thus ensuring improvement in cardiac output and reduction in LV wall tension, with a positive effect on myocardial O<sub>2</sub> consumption. Depending on the device, it can provide up to 2.5 - 5 L/min of blood flow.<sup><xref ref-type="bibr" rid="B29">29</xref></sup></p>
<p>Venoarterial ECMO consists of a percutaneous ventricular assist device comprised of a circuit between the venous and arterial systems, interposed by a centrifugal propulsion pump and an external membrane blood oxygenation system. Its effect is the result of a reduction in RV preload, pulmonary flow, LV end-diastolic pressure, and LV end-diastolic volume.<sup><xref ref-type="bibr" rid="B29">29</xref></sup> The use of ECMO in cardiogenic shock is based mainly on observational studies. The 2023 ECLS VA-ECMO study, which included patients with cardiogenic shock regardless of etiology, found no benefit from the technology.<sup><xref ref-type="bibr" rid="B33">33</xref></sup> In a recent meta-analysis that included four RCTs addressing the use of venoarterial ECMO in patients with AMI-related cardiogenic shock, the result was also negative, without benefit in 30-day mortality and with an increased risk of major bleeding or vascular complications.<sup><xref ref-type="bibr" rid="B34">34</xref></sup></p>
<p>Despite unfavorable results in RCTs, the use of MCS devices continues to be popular as rescue therapy in patients with cardiogenic shock refractory to clinical management.<sup><xref ref-type="bibr" rid="B35">35</xref></sup> It is noteworthy that the studies evaluating these devices have not accurately reflected real-world clinical scenarios, and there are currently no studies specifically focused on non-ischemic cardiogenic shock. Many RCTs compared the use of MCS devices as part of a protocol with optimized medical therapy combined with the device if deemed necessary by the attending physician, with a rescue ECMO use rate of up to 39% in the control group.<sup><xref ref-type="bibr" rid="B36">36</xref></sup> Additionally, the clinical study protocols for MCS device use may be less flexible, potentially leading to less optimal device selection for individual patients.</p>
<p>In a prospective cohort study of 49 patients with cardiogenic shock treated with venoarterial ECMO or Impella CP in Brazil, the average mortality rate was 61%, with no significant difference between the devices used.<sup><xref ref-type="bibr" rid="B39">39</xref></sup> In these patients, the etiology of shock in 45% of cases was acute myocardial infarction (AMI) and, in 20%, advanced HF. In patients with non-ischemic cardiogenic shock, the mortality rate was 70%. In patients with AMI as the etiology for shock, the mortality rate was 59%.</p>
</sec>
<sec>
<title>Shock team</title>
<p>For the best results in the management of patients with cardiogenic shock, including the appropriate indication of circulatory support devices, it is essential to apply a concept that has been gaining international traction, although little discussed in national literature: the &quot;shock team&quot; (<xref ref-type="fig" rid="f1">Figure 1</xref>). This involves a team with interventional cardiologists, cardiologists specialized in advanced heart failure, cardiac surgeons, and intensive care specialists, and it seeks early recognition and diagnosis of cardiogenic shock, in addition to rapid coordination between the professionals involved for streamlined decision-making.<sup><xref ref-type="bibr" rid="B38">38</xref></sup> Several studies have demonstrated better outcomes when shock management is performed with a shock team approach,<sup><xref ref-type="bibr" rid="B39">39</xref></sup> with increased survival rates in 30 and up to 240 days.</p>
<fig id="f1">
<label>Figure 1</label>
<caption><title>General approach to the patient with non-ischemic cardiogenic shock.</title></caption>
<graphic xlink:href="2764-3107-abchf-004-01-e20240033-gf01.tif"/>
</fig>
<p>In cardiology, there are other examples of an interdisciplinary approach to the treatment of specific diseases. The concept of a &quot;Heart Team&quot; is consolidated in the literature for decision-making in structural heart disease and advanced coronary disease. This team approach in cardiogenic shock is especially relevant considering the high morbidity and mortality rates associated with this condition and the complex set of interventions involved in its treatment, including percutaneous, surgical and clinical procedures.<sup><xref ref-type="bibr" rid="B40">40</xref></sup> Thus, the management of these patients involves good communication and interdisciplinary coordination.</p>
<p>It is becoming increasingly evident that early use of MCS devices is proving to be a strategy that leads to better outcomes for patients with cardiogenic shock. However, to determine these interventions precisely and swiftly, a specialized and cohesive team is essential, as it requires careful consideration of the risk of complications versus potential benefits. The greater the personal and institutional experience with this profile of patients and interventions, the better the outcomes. A learning curve effect has been reported, with improvement in clinical outcomes after the implantation of 40 MCS devices by the care team. The average mortality rate in the first period of this study was 83%, compared to a mortality rate of 40% in the final period of the study (p = 0.002).<sup><xref ref-type="bibr" rid="B37">37</xref></sup></p>
</sec>
</sec>
<sec sec-type="conclusions">
<title>Conclusion</title>
<p>The increased focus on non-ischemic cardiogenic shock has led to a rise in scientific research, gradually establishing key principles that guide modern management. Notable practices include adopting a team-based approach for rapid and integrated decision-making; utilizing a combination of clinical, hemodynamic, and radiological assessments efficiently and sequentially to determine the optimal timing for escalating to mechanical support; employing risk scores to guide the escalation or de-escalation of mechanical support; and aligning the management strategy, which should be patient-centered, with institutional capabilities, including expertise in mechanical support, to maximize benefits and minimize complications.</p>
</sec>
</body>
<back>
<fn-group>
<fn fn-type="financial-disclosure" id="fn1">
<label>Sources of funding</label>
<p>There were no external funding sources for this study.</p></fn>
<fn fn-type="other" id="fn2">
<label>Study association</label>
<p>This study is not associated with any thesis or dissertation work.</p></fn>
<fn fn-type="other" id="fn3">
<label>Ethics approval and consent to participate</label>
<p>This article does not contain any studies with human participants or animals performed by any of the authors.</p></fn>
</fn-group>
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</ref-list>
</back>
<sub-article article-type="translation" id="S1" xml:lang="pt">
<front-stub>
<article-id pub-id-type="doi">10.36660/abchf.20240033</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Ponto de Vista</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Choque Cardiogênico Não Isquêmico: Como Melhorar Desfechos – Do Reconhecimento Precoce ao Manejo Diferenciado</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name><surname>Amantéa</surname><given-names>Rodrigo P.</given-names></name>
<role>Concepção e desenho da pesquisa e Obtenção de dados</role>
<role>Redação do manuscrito</role>
<xref ref-type="aff" rid="aff2"><sup>1</sup></xref></contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0000-0003-2022-7512</contrib-id>
<name><surname>Hastenteufel</surname><given-names>Laura</given-names></name>
<role>Redação do manuscrito</role>
<role>Revisão crítica do manuscrito quanto ao conteúdo</role>
<xref ref-type="aff" rid="aff2"><sup>1</sup></xref></contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0000-0003-2150-6337</contrib-id>
<name><surname>Scolari</surname><given-names>Fernando Luís</given-names></name>
<role>Redação do manuscrito</role>
<role>Revisão crítica do manuscrito quanto ao conteúdo</role>
<xref ref-type="aff" rid="aff2"><sup>1</sup></xref></contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0000-0002-1523-4286</contrib-id>
<name><surname>Goldraich</surname><given-names>Lívia A.</given-names></name>
<role>Redação do manuscrito</role>
<role>Revisão crítica do manuscrito quanto ao conteúdo</role>
<xref ref-type="aff" rid="aff2"><sup>1</sup></xref></contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0000-0003-4207-3809</contrib-id>
<name><surname>Clausell</surname><given-names>Nadine</given-names></name>
<role>Concepção e desenho da pesquisa e Obtenção de dados</role>
<role>Redação do manuscrito</role>
<xref ref-type="aff" rid="aff2"><sup>1</sup></xref><xref ref-type="corresp" rid="c2"/></contrib>
<aff id="aff2">
<label>1</label>
<addr-line>
<named-content content-type="city">Porto Alegre</named-content>
<named-content content-type="state">RS</named-content>
</addr-line>
<country country="BR">Brasil</country>
<institution content-type="original">Hospital de Clínicas de Porto Alegre, Porto Alegre, RS – Brasil</institution>
</aff>
</contrib-group>
<author-notes>
<corresp id="c2"><label>Correspondência:</label> <bold>Nadine Clausell</bold> • Programa de transplante cardíaco – Serviço de cardiologia – Hospital de Clínicas de Porto Alegre – Rua Ramiro Barcellos, 2350. CEP <postal-code>90035-903</postal-code>, Porto Alegre, RS – Brasil E-mail: <email>nclausell@hcpa.edu.br</email></corresp>
<fn fn-type="edited-by"><label>Editor responsável pela revisão:</label> <p>Luis Beck-da-Silva</p></fn>
<fn fn-type="conflict"><label>Potencial conflito de interesse</label>
<p>Não há conflito com o presente artigo</p></fn>
</author-notes>
<kwd-group xml:lang="pt">
<title>Palavras-chave</title>
<kwd>Choque Cardiogênico</kwd>
<kwd>Insuficiência Cardíaca</kwd>
<kwd>Unidades de Terapia Intensiva</kwd>
</kwd-group>
</front-stub>
<body>
<sec sec-type="intro">
<title>Introdução</title>
<p>O choque cardiogênico é uma condição clínica de crescente incidência que cursa com hipoperfusão tecidual levando à disfunção multiorgânica com elevada taxa de mortalidade.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> Choque cardiogênico não isquêmico vem sendo reconhecido como uma importante causa de choque nas salas de emergência, com incidência ultrapassando o choque relacionado ao infarto agudo do miocárdio (IAM) em algumas populações.<sup><xref ref-type="bibr" rid="B2">2</xref></sup> Dados recentes do Cardiogenic Shock Working Group (CSWG), um registro internacional multicêntrico, apontam que a taxa de mortalidade para esta condição varia de 22 a 32%, dependendo do tipo de instituição.<sup><xref ref-type="bibr" rid="B3">3</xref></sup></p>
<p>Diferentemente do choque cardiogênico de origem isquêmica, no qual um evento índice marca o início da injúria miocárdica que pode levar ao estado de choque, no choque cardiogênico de origem não isquêmica a apresentação representa o <italic>continuum</italic> da insuficiência cardíaca avançada. Para fins deste artigo, abordaremos apenas o choque associado à insuficiência cardíaca avançada por se constituir na causa mais comum, também pela grande variabilidade de apresentações, levando frequentemente a atraso na identificação, que contribui para desfechos desfavoráveis. Discutiremos os seguintes temas: definições relacionadas ao diagnóstico do choque cardiogênico e formas de apresentação clínica; avaliação inicial sistematizada destes pacientes, incluindo últimas atualizações quanto ao uso do cateter de artéria pulmonar nesta população e quanto à estratificação individualizada do risco de morbimortalidade; e o manejo do choque cardiogênico não isquêmico, passando por terapias farmacológicas, dispositivos mecânicos, e atuação em equipe nos &quot;Times de Choque&quot;.</p>
</sec>
<sec>
<title>Definições e apresentação clínica</title>
<p>A maioria das sociedades engloba os seguintes fatores na definição de choque: pressão arterial sistólica (PAS) &lt; 90 mmHg por mais de 30 min e/ou a necessidade de drogas vasopressoras para manter PAS ≥ 90 mmHg, associada a alterações que sugerem hipoperfusão (extremidades frias, alteração de status mental, enchimento capilar lentificado) e níveis de lactato ≥ 2 mmol/L.<sup><xref ref-type="bibr" rid="B4">4</xref></sup> No entanto, não existe um consenso claro para definir a presença de choque cardiogênico não isquêmico. A apresentação clínica do paciente com insuficiência cardíaca avançada que evolui para estado de choque com sinais clássicos de hipoperfusão e disfunção multiorgânica pode ser lenta e, por vezes, elusiva. Muitos pacientes já apresentam níveis de pressão arterial (PA) mais baixos no dia a dia e este pode não ser o maior sinal de choque iminente; muitas vezes, hipoperfusão não exige hipotensão.<sup><xref ref-type="bibr" rid="B5">5</xref></sup> O exame físico pode não ser exuberante e a concomitância de congestão, presente em muitos casos, pode não ser evidente. Assim, o uso da ultrassonografia à beira do leito <italic>(POCUS)</italic> vem ganhando força e tornando-se cada vez mais parte do exame do paciente com insuficiência cardíaca avançada,<sup><xref ref-type="bibr" rid="B6">6</xref></sup> possibilitando estratificar com objetividade o perfil hemodinâmico do paciente e auxiliando a guiar de forma inicial a abordagem terapêutica. Por fim, dada a heterogeneidade de apresentações e condições pré-existentes, vale salientar a importância de avaliações dinâmicas, seriadas, capturando mais do que um ponto no tempo: avaliações pontuais podem induzir a falhas de identificação precoce do choque e, com isto, atrasar medidas terapêuticas.</p>
<sec>
<title>Avaliação com exames</title>
<p>Concomitante ao exame físico e uso da ultrassonografia à beira do leito, a realização do eletrocardiograma é parte integral da avaliação, assim como coleta dos seguintes exames: provas de coagulação, de função renal e de função hepática para rapidamente identificar a presença e grau de disfunção multiorgânica; marcadores inflamatórios (proteína C reativa e leucograma); e marcadores de perfusão tecidual e de débito cardíaco como lactato, bicarbonato e saturação venosa central. O clearance de lactato ao longo das primeiras 24 horas de avaliação do paciente já foi estudado como marcador para predição de mortalidade em pacientes com choque cardiogênico, podendo representar alvo terapêutico objetivo e mais um componente presente na tomada de decisão envolvendo manejo destes pacientes.<sup><xref ref-type="bibr" rid="B7">7</xref>,<xref ref-type="bibr" rid="B8">8</xref></sup></p>
</sec>
<sec>
<title>Uso do cateter de artéria pulmonar</title>
<p>Apesar de dados oriundos do estudo ESCAPE<sup><xref ref-type="bibr" rid="B9">9</xref></sup> e outros relatos questionarem, ou até contraindicarem, o uso do cateter de Swan-Ganz (cateter de artéria pulmonar / CAP) no passado, o manejo contemporâneo do choque cardiogênico inequivocamente inclui o uso deste recurso. É possível que esta mudança de conceito se deva à melhor indicação de uso do método, e melhor entendimento e aplicação das informações obtidas por meio do mesmo.<sup><xref ref-type="bibr" rid="B10">10</xref>-<xref ref-type="bibr" rid="B12">12</xref></sup> Atualmente, o uso do cateter de Swan-Ganz representa peça fundamental na definição e manejo do choque cardiogênico não isquêmico, e seu uso precoce deve ser encorajado. Estudos recentes têm associado o uso do CAP com maior uso de dispositivos de assistência ventricular e redução de mortalidade.<sup><xref ref-type="bibr" rid="B12">12</xref></sup> Mais especificamente, estudo de Kanwar et al. demonstrou que o uso do CAP nas primeiras seis horas de internação por choque cardiogênico não isquêmico associou-se com redução de mortalidade intra-hospitalar em comparação com o uso mais tardio do CAP ou ausência do uso deste recurso (OR 0,37; IC de 95%, 017-0,82).<sup><xref ref-type="bibr" rid="B13">13</xref></sup> Importante salientar que, para que o uso do cateter de Swan-Ganz possa ser um aliado no manejo do paciente com choque, as equipes precisam estar capacitadas para sua utilização, as medidas devem ser realizadas ao menos 2 a 3 vezes ao dia e suas informações devem ser incorporadas nas discussões e reavaliações diárias dos pacientes.</p>
</sec>
<sec>
<title>Estratificação de risco</title>
<p>Nos últimos anos, mais de 30 escores para predição de risco e gravidade do choque cardiogênico foram criados.<sup><xref ref-type="bibr" rid="B14">14</xref></sup> O indicador da SCAI <italic>(Society for Cardiovascular Angiography and Interventions)</italic> de choque cardiogênico, elaborado em 2019,<sup><xref ref-type="bibr" rid="B15">15</xref></sup> tem sido muito utilizado para estratificar gravidade e servir de base para implantação de terapias e definição de prognóstico. Este varia de &quot;A&quot; (<italic>at risk</italic>) a &quot;E&quot; (<italic>extremis</italic>) em uma escala que leva em consideração parâmetros clínicos, hemodinâmicos e laboratoriais.<sup><xref ref-type="bibr" rid="B16">16</xref></sup> Desde sua criação, este indicador assumiu grande importância no choque cardiogênico não isquêmico, devido em grande monta à sua aplicabilidade prática e simples, reprodutibilidade, e ampla aceitação dentro do cenário acadêmico. Recentemente, a classificação SCAI foi refinada pelo CSWG envolvendo progressão de choque e piora de parâmetros hemodinâmicos, além de recuperação clínica. Assim, ficou mais claro o perfil dinâmico desta classificação, com um aumento progressivo no risco de mortalidade entre as fases &quot;B&quot; e &quot;E&quot;.<sup><xref ref-type="bibr" rid="B17">17</xref></sup></p>
</sec>
</sec>
<sec>
<title>Manejo</title>
<p>A primeira etapa do manejo de choque cardiogênico não isquêmico envolve adequada identificação e compreensão do perfil hemodinâmico do paciente, possibilitando ressuscitação hemodinâmica e estabilização clínica.<sup><xref ref-type="bibr" rid="B4">4</xref></sup> Concomitantemente, deve ser considerado o uso de medicamentos direcionados à otimização da função cardíaca e consolidados na prática clínica: vasopressores e inotrópicos. Estes representam as principais ferramentas no manejo inicial do choque cardiogênico não isquêmico.<sup><xref ref-type="bibr" rid="B18">18</xref></sup></p>
<p>O uso de suporte de oxigênio é recomendado em pacientes hipoxêmicos, com saturação periférica de O<sub>2</sub> &lt; 90% ou PaO<sub>2</sub> &lt; 60mmHg, com o intuito de corrigir hipoxemia. Seu uso não é recomendado como rotina, uma vez que causa vasoconstrição e redução no débito cardíaco.<sup><xref ref-type="bibr" rid="B19">19</xref></sup> O uso de ventilação não-invasiva com pressão positiva (VNI) também está indicado em determinados pacientes com disfunção ventilatória, com o potencial benefício de reduzir a necessidade de intubação orotraqueal.<sup><xref ref-type="bibr" rid="B20">20</xref></sup> A PA deve ser monitorizada durante terapia com VNI, uma vez que o aumento na pressão intratorácica reduz o retorno venoso e a pré-carga ventricular. Pode haver também prejuízo à função de ventrículo direito (VD) devido ao aumento na resistência vascular pulmonar e na pós-carga de VD. Em pacientes com disfunção ventilatória progressiva, recomenda-se a intubação orotraqueal. Em pacientes que apresentam refratariedade ao tratamento inicial, deve ser avaliada a indicação de dispositivos de suporte circulatório mecânico temporário (SCM), e cada vez mais benefícios na assistência direcionada a estes pacientes são observados com base em decisões tomadas pelo &quot;Time de Choque&quot;. A seguir discutiremos estes tópicos em maiores detalhes.</p>
<sec>
<title>Terapias farmacológicas</title>
<p>Em nossa rotina, o manejo inicial do choque cardiogênico não isquêmico passa fundamentalmente pelo uso de drogas vasoativas e inotrópicos, considerando o estado de hipoperfusão sistêmica e débito cardíaco insuficiente para a demanda metabólica. Os principais representantes dessas classes farmacológicas e suas principais características são apresentados na <xref ref-type="table" rid="t2">Tabela 1</xref>. O principal objetivo do tratamento desta condição é o restabelecimento do débito cardíaco, seguido pelo alívio de congestão, se presente. Além de drogas com atuação na regulação da hemodinâmica cardiovascular, diuréticos de alça também são fundamentais no manejo do paciente com insuficiência cardíaca avançada agudamente descompensada, por meio da melhora na sobrecarga volêmica e congestão sistêmica e pulmonar resultante do aumento na excreção renal de água e sódio.<sup><xref ref-type="bibr" rid="B5">5</xref></sup> Sendo assim, seu uso é indicado quando houver evidência de congestão constatada por medidas do cateter de Swan-Ganz e da avaliação com POCUS.</p>
<table-wrap id="t2">
<label>Tabela 1</label>
<caption><title>Principais drogas usadas no choque cardiogênico e características</title></caption>
<table frame="hsides" rules="groups">
<colgroup width="16%">
<col/>
<col/>
<col/>
<col/>
<col/>
<col/>
</colgroup>
<thead style="border-top: thin solid; border-bottom: thin solid; border-color: #000000">
<tr style="background-color:#98ADCA">
<th align="left" valign="middle">Medicamento</th>
<th align="center" valign="middle">Mecanismo de ação</th>
<th align="center" valign="middle">Dose</th>
<th align="center" valign="middle">RVS</th>
<th align="center" valign="middle">PA</th>
<th align="center" valign="middle">DC</th>
<th align="center" valign="middle">FC</th>
</tr>
</thead>
<tbody style="border-bottom: thin solid; border-color: #000000">
<tr>
<td align="left" valign="middle">Noradrenalina</td>
<td align="center" valign="middle">α1 &gt;&gt; β1 &gt;β2</td>
<td align="center" valign="middle">0,05-1 μg/kg/min</td>
<td align="center" valign="middle">↑↑</td>
<td align="center" valign="middle">↑↑</td>
<td align="center" valign="middle">↑</td>
<td align="center" valign="middle">↓↔</td>
</tr>
<tr style="background-color:#E8CCBF">
<td align="left" valign="middle">Vasopressina</td>
<td align="center" valign="middle">V1</td>
<td align="center" valign="middle">0,01 - 0,06 U/min</td>
<td align="center" valign="middle">↑↑</td>
<td align="center" valign="middle">↑↑</td>
<td align="center" valign="middle">-</td>
<td align="center" valign="middle">-</td>
</tr>
<tr>
<td align="left" valign="middle">Nitroprussiato de sódio</td>
<td align="center" valign="middle">NO</td>
<td align="center" valign="middle">0,1 - 3 μg/kg/min</td>
<td align="center" valign="middle">↓↓</td>
<td align="center" valign="middle">↓↔</td>
<td align="center" valign="middle">↔↑</td>
<td align="center" valign="middle">↔</td>
</tr>
<tr style="background-color:#E8CCBF">
<td align="left" valign="middle">Dobutamina</td>
<td align="center" valign="middle">β1 &gt;&gt; β2 &gt; α1</td>
<td align="center" valign="middle">2-20 μg/kg/min</td>
<td align="center" valign="middle">↓↔</td>
<td align="center" valign="middle">↓↔</td>
<td align="center" valign="middle">↑↑</td>
<td align="center" valign="middle">↑</td>
</tr>
<tr>
<td align="left" valign="middle">Milrinone</td>
<td align="center" valign="middle">Inibidor - PDE3</td>
<td align="center" valign="middle">0,125-0,75 μg/kg/min</td>
<td align="center" valign="middle">↓↓</td>
<td align="center" valign="middle">↓↓</td>
<td align="center" valign="middle">↑↑</td>
<td align="center" valign="middle">↔</td>
</tr>
</tbody>
</table>
<table-wrap-foot>
<fn id="TFN2"><p>α1: receptor alfa-1 adrenérgico; α2: receptor alfa-2 adrenérgico; β1: receptor beta-1 adrenérgico; β2: receptor beta-2 adrenérgico; DC: débito cardíaco; FC: frequência cardíaca; NO: Óxido nítrico; PA: pressão arterial; PDE3: fosfodiesterase 3; RVS: resistência vascular sistêmica; VR1: receptor V1 de vasopressina.</p></fn>
</table-wrap-foot>
</table-wrap>
<p>A terapia farmacológica inicial do choque cardiogênico não isquêmico, depende do limiar pressórico do paciente. Em pacientes com PA permissiva (geralmente, PAS de pelo menos 90 mmHg ou pressão arterial média [PAM] de 65 mmHg) optamos por estratégia inicial de vasodilatadores endovenosos, sendo o nitroprussiato de sódio (NPS) a droga de escolha. Este deve ser administrado em infusão lenta, com dose baixa inicial e observação rigorosa do comportamento da PA logo após o início da administração. A resposta comum esperada é o aumento discreto da PA, melhora da perfusão periférica, aumento da diurese e melhora clínica.<sup><xref ref-type="bibr" rid="B21">21</xref></sup> Em caso de resposta hipotensora, deve-se pensar em dose excessiva de NPS ou hipovolemia. Como alternativa ao NPS, nitroglicerina (NTG) pode ser usada, porém com menor efeito vasodilatador arterial e evidências menos robustas suportando seu uso.</p>
<p>Em pacientes com hipotensão à apresentação inicial, pode ser iniciado um vasopressor, especialmente a noradrenalina, considerado um agente de primeira linha neste contexto clínico. Em estudos prévios, esta catecolamina mostrou-se superior tanto à dopamina quanto à adrenalina, sendo seu uso com o objetivo de manter a pressão de perfusão orgânica suportado por recomendação IIb/B em diretrizes recentes.<sup><xref ref-type="bibr" rid="B20">20</xref></sup> O efeito da noradrenalina sobre a perfusão de órgãos vitais vem acompanhado de aumento na pós-carga do ventrículo esquerdo (VE), com potencial redução no débito cardíaco. Assim, a combinação de noradrenalina com inotrópicos deve ser considerada, especialmente na população de pacientes com choque cardiogênico não isquêmico.<sup><xref ref-type="bibr" rid="B20">20</xref></sup></p>
<p>Vasopressina, um vasoconstritor não simpatomimético, aumenta a resistência vascular sistêmica por meio da mesma via de ação da vasodilatação promovida pelo milrinone, sendo usada em conjunto com este inotrópico para contrabalançar o efeito hipotensivo, permitindo redução no uso de noradrenalina.<sup><xref ref-type="bibr" rid="B22">22</xref></sup></p>
<p>O uso de terapia inotrópica no choque cardiogênico é prática amplamente difundida, dada sua eficácia em promover aumento do débito cardíaco, mas ainda pouco embasada em estudos de grande porte, apresentando classe de recomendação IIb/C para o uso neste contexto. Assim, o uso de inotrópicos como dobutamina ou milrinone deve ser considerado em pacientes com choque e refratariedade ao manejo inicial,<sup><xref ref-type="bibr" rid="B20">20</xref></sup> com o objetivo de usá-los por curto período de tempo, sempre envolvendo reavaliação hemodinâmica seriada, e com troca para terapia vasodilatadora assim que possível.</p>
<p>O ensaio clínico randomizado (ECR) DOREMI comparou o tratamento de pacientes em choque cardiogênico com dobutamina versus milrinone.<sup><xref ref-type="bibr" rid="B23">23</xref></sup> Este estudo incluiu majoritariamente pacientes isquêmicos, e apresentou resultado neutro em desfecho primário composto envolvendo óbito intra-hospitalar, parada cardiorrespiratória abortada, transplante cardíaco, uso de dispositivos de SCM, ou evento isquêmico cardíaco ou cerebral. No entanto, um estudo observacional sugere que pode haver benefício em uso de milrinone como terapia inotrópica de escolha no choque cardiogênico não isquêmico,<sup><xref ref-type="bibr" rid="B24">24</xref></sup> sendo necessário ECR envolvendo essa população específica.</p>
</sec>
<sec>
<title>Dispositivos de suporte circulatório mecânico temporário</title>
<p>Em pacientes com disfunção orgânica persistente a despeito do manejo inicial, deve ser avaliada a instalação de dispositivos de SCM, e sua escolha depende de disponibilidade de equipamentos, familiaridade da equipe assistencial, e particularidades relacionadas ao paciente em avaliação. No Brasil, podemos lançar mão do balão intra-aórtico (BIA), do uso de dispositivo de oxigenação por membrana extracorpórea <italic>(ECMO),</italic> e, mais raramente, de bomba de fluxo microaxial (Impella).</p>
<p>A decisão de escalonar o tratamento para dispositivos de suporte circulatório temporário representa ponto crucial e sensível do manejo destes pacientes, sobretudo em pacientes SCAI estágio B ou superior. Assim como o uso precoce destes dispositivos pode expor o paciente ao risco de complicações, o atraso em sua indicação pode resultar em resultados inferiores ao esperado. O conceito &quot;tempo porta-suporte&quot; no manejo do choque tem ganhado força, como foi no passado com o parâmetro &quot;porta-balão&quot; na angioplastia primária do infarto.<sup><xref ref-type="bibr" rid="B25">25</xref></sup> Desta forma, a indicação ideal de SCM deve ocorrer conforme uso de drogas vasoativas, levando em conta por exemplo o escore de drogas vasoativas.<sup><xref ref-type="bibr" rid="B26">26</xref></sup> Além disso, é fundamental que sejam definidos os objetivos dos dispositivos antes da instalação, tais como a estabilização hemodinâmica e a melhora de parâmetros perfusionais.<sup><xref ref-type="bibr" rid="B27">27</xref></sup> Destacam-se como principais potenciais complicações de dispositivos de SCM os seguintes: lesão vascular com isquemia de membro, infecção de sítio de acesso vascular, lesão de valvas cardíacas, eventos tromboembólicos e sangramento.<sup><xref ref-type="bibr" rid="B28">28</xref></sup></p>
<p>Em pacientes com choque cardiogênico não isquêmico, o BIA representa o dispositivo de suporte circulatório temporário mais usado em nosso contexto, funcionando como ponte para decisão terapêutica definitiva, a qual geralmente envolve a transição para dispositivo definitivo de assistência ventricular ou transplante cardíaco.<sup><xref ref-type="bibr" rid="B29">29</xref></sup> Por meio de mecanismo de contrapulsação, o BIA promove redução da pós-carga, aumento da PAM e otimização da pressão de perfusão coronariana, com consequente melhora média de cerca de 1L/min no débito cardíaco e redução na pressão diastólica final do VE e no consumo miocárdico de oxigênio.<sup><xref ref-type="bibr" rid="B29">29</xref></sup> Atualmente, está em curso o ECR multicêntrico <italic>&quot;Altshock 2 trial&quot;</italic> que avaliará o implante precoce de BIA vs. terapia médica otimizada padrão em pacientes com choque cardiogênico não isquêmico. O desfecho primário será sobrevida em 60 dias ou ponte com sucesso até a realização de transplante cardíaco.<sup><xref ref-type="bibr" rid="B30">30</xref></sup></p>
<p>No contexto do choque cardiogênico isquêmico, por outro lado, o uso do BIA deve ser considerado apenas para casos excepcionais, uma vez que o estudo – IABP - SHOCK - II – não mostrou diferença em mortalidade entre uso deste dispositivo vs. terapia médica otimizada.<sup><xref ref-type="bibr" rid="B31">31</xref></sup> Vale lembrar que existem limitações na interpretação deste ECR, tais como população com choque cardiogênico leve/moderado, baixa taxa de inserção do dispositivo antes da intervenção coronariana primária, e alta taxa de crossover para o grupo do BIA.</p>
<p>Ainda no contexto do choque cardiogênico isquêmico, recentemente foi publicado o estudo <italic>&quot;DanGer Shock&quot;,</italic> que comparou o tratamento de pacientes com IAM e choque cardiogênico por meio do uso de Impella CP associado a tratamento clínico otimizado vs. tratamento clínico otimizado apenas.<sup><xref ref-type="bibr" rid="B32">32</xref></sup> Um total de 360 pacientes foram randomizados, e houve 45,8% de óbitos por qualquer causa no grupo Impella CP vs. 58,5% no grupo de tratamento clínico, <italic>hazard ratio</italic> 0,74 (IC de 95%, 0,55-0,99, p = 0,04). O Impella é implantado de forma percutânea por meio da artéria femoral, e continuamente transfere sangue do VE para a aorta, garantindo melhora no débito cardíaco e redução na tensão de parede do VE, com efeito positivo no consumo de O<sub>2</sub> do miocárdio. A depender do dispositivo, pode fornecer até 2,5 - 5L/min de fluxo de sangue.<sup><xref ref-type="bibr" rid="B29">29</xref></sup></p>
<p>O ECMO veno-arterial consiste em um dispositivo de assistência ventricular percutâneo formado por um circuito entre o sistema venoso e arterial, interposto por uma bomba de propulsão centrífuga e um sistema externo de oxigenação sanguínea por membrana. Seu efeito é resultado de redução de pré-carga de VD, fluxo pulmonar, pressão diastólica final de VE e volume diastólico final de VE.<sup><xref ref-type="bibr" rid="B29">29</xref></sup> O uso do ECMO no choque cardiogênico é embasado principalmente em estudos observacionais. Em 2023 foi publicado o estudo ECLS VA-ECMO que não mostrou benefício com a tecnologia, embora tenham sido incluídos pacientes com choque cardiogênico, independente da etiologia.<sup><xref ref-type="bibr" rid="B33">33</xref></sup> Em metanálise recente, que incluiu quatro ECRs abordando o uso de ECMO veno-arterial em pacientes com choque cardiogênico relacionado a IAM, o resultado também foi negativo, sem benefício em mortalidade em 30 dias, e com aumento no risco de sangramento maior ou complicações vasculares.<sup><xref ref-type="bibr" rid="B34">34</xref></sup></p>
<p>Apesar de resultados não favoráveis em ECRs, o uso de dispositivo de SCM segue tendo espaço como terapia de resgate em pacientes com choque cardiogênico refratário ao manejo clínico.<sup><xref ref-type="bibr" rid="B35">35</xref></sup> Vale ressaltar que os estudos realizados para testar estes dispositivos apresentam falhas em reproduzir o contexto clínico real, além de não haver até o momento estudos focados exclusivamente em pacientes com choque cardiogênico não isquêmico. Em primeiro lugar, em muitos ECRs o uso de dispositivos de SCM como protocolo foi comparado ao uso de terapia médica otimizada associada a dispositivo se indicado pelo médico assistente, apresentando taxa de uso de ECMO de resgate de até 39% no grupo controle.<sup><xref ref-type="bibr" rid="B36">36</xref></sup> Além disso, a indicação do uso de dispositivo de SCM guiada pelo protocolo de estudos clínicos, pode ser menos consistente, e pode haver menor flexibilidade na escolha do dispositivo mais adequado ao paciente em tratamento.</p>
<p>Em coorte prospectiva de 49 pacientes com choque cardiogênico tratados com ECMO veno-arterial ou Impella CP no Brasil, a mortalidade média foi de 61%, sem diferença com relação ao dispositivo empregado.<sup><xref ref-type="bibr" rid="B37">37</xref></sup> Nestes pacientes, a etiologia do choque em 45% dos casos era IAM e, em 20%, IC avançada. Em pacientes com choque cardiogênico não isquêmico, a taxa de mortalidade foi de 70%. Em pacientes com IAM como etiologia para o choque, a taxa de mortalidade foi de 59%.</p>
</sec>
<sec>
<title>Time de choque</title>
<p>Para os melhores resultados no manejo de pacientes com choque cardiogênico, incluindo a adequada indicação de dispositivos de suporte circulatório, torna-se fundamental a aplicação de um conceito que vem ganhando força internacionalmente, ainda que pouco discutido em literatura nacional: o &quot;time de choque&quot; (<xref ref-type="fig" rid="f2">Figura 1</xref>). Este envolve uma equipe com cardiologistas intervencionistas, cardiologistas especialistas em insuficiência cardíaca avançada, cirurgiões cardíacos e intensivistas, e busca o reconhecimento e diagnóstico precoce do choque cardiogênico, além da rápida articulação entre os profissionais envolvidos na assistência para a tomada de decisão.<sup><xref ref-type="bibr" rid="B38">38</xref></sup> Vários estudos têm demonstrado melhores desfechos quando o manejo do choque é feito na lógica de atuação com time de choque,<sup><xref ref-type="bibr" rid="B39">39</xref></sup> com aumento na sobrevida em 30 e até 240 dias.</p>
<fig id="f2">
<label>Figura 1</label>
<caption><title>Abordagem geral do paciente com choque cardiogênico não isquêmico.</title></caption>
<graphic xlink:href="2764-3107-abchf-004-01-e20240033-gf01-pt.tif"/>
</fig>
<p>Na cardiologia existem outros exemplos de abordagem interdisciplinar para o tratamento de doenças específicas. O conceito de &quot;Heart Team&quot; já é consolidado na literatura para a tomada de decisão em cardiopatias estruturais e em doença coronariana avançada. Esta abordagem em time no choque cardiogênico é especialmente relevante considerando-se a alta morbidade e mortalidade associadas a esta condição, e o conjunto complexo de intervenções envolvidas no seu tratamento, abrangendo procedimentos percutâneos, cirúrgicos e clínicos.<sup><xref ref-type="bibr" rid="B40">40</xref></sup> Assim, o manejo destes pacientes necessariamente passa pela boa comunicação e coordenação interdisciplinar.</p>
<p>Cada vez se torna mais claro que o uso precoce de dispositivos de SCM consolida-se como estratégia que resulta em melhores desfechos em pacientes com choque cardiogênico. No entanto, para a indicação ágil e precisa destas intervenções, a qual envolve ponderação quanto a risco de complicações e potenciais benefícios, exige-se a presença de equipe especializada e coesa. Quanto maior a experiência pessoal e institucional com este perfil de pacientes e intervenções, melhores tornam-se os desfechos. Já foi relatado efeito de curva de aprendizado, com melhora nos desfechos clínicos após implante de 40 dispositivos de SCM pela equipe assistencial. A taxa de mortalidade média no primeiro período deste estudo foi de 83%, em comparação com taxa de mortalidade de 40% no período final do estudo (p = 0,002).<sup><xref ref-type="bibr" rid="B37">37</xref></sup></p>
</sec>
</sec>
<sec sec-type="conclusions">
<title>Conclusões</title>
<p>A crescente atenção dada ao choque cardiogênico não isquêmico tem contribuído para maior produção científica na área, a qual vem paulatinamente consolidando algumas premissas que norteiam seu manejo contemporâneo. Destacam-se principalmente as seguintes: a abordagem de time para tomada de decisão rápida e integrada; o uso de um conjunto de exames e avaliações clínica, hemodinâmica e radiológica de forma ágil e seriada para guiar decisões – especialmente a definição temporal ideal de escalonar para suporte mecânico; a importância de usar escores de risco para guiar escalonamento/desescalonamento de suporte mecânico; e, por fim, o alinhamento da estratégia do manejo, a qual deve ser centrada no paciente, às condições institucionais existentes, incluindo a expertise com uso de suporte mecânico no sentido de otimizar benefícios e reduzir complicações.</p>
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<label>Fontes de financiamento</label>
<p>O presente estudo não teve fontes de financiamento externas.</p></fn>
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<label>Vinculação acadêmica</label>
<p>Não há vinculação deste estudo a programas de pós-graduação.</p></fn>
<fn fn-type="other" id="fn6">
<label>Aprovação ética e consentimento informado</label>
<p>Este artigo não contém estudos com humanos ou animais realizados por nenhum dos autores.</p></fn>
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