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Can epinephrine therapy be detrimental to patients with hypertrophic cardiomyopathy with hypotension or cardiac arrest? A systematic review

Ilicki, Jonathana; Bruchfeld, Samuela; Djärv, Theresea,b

European Journal of Emergency Medicine: June 2019 - Volume 26 - Issue 3 - p 150–157
doi: 10.1097/MEJ.0000000000000573
Review article
Free
SDC

Approximately 10% of sudden cardiac deaths among patients under 35 years of age is owing to hypertrophic cardiomyopathy (HCM)-related cardiac arrest (CA). CA is often associated with pre-arrest or peri-arrest hypotension and is treated by a set of interventions, including the administration of epinephrine. It is debated whether epinephrine increases or decreases survival to discharge following CA. HCM is associated with septal hypertrophy with a dynamic left ventricular outflow tract obstruction and impaired peripheral vasoconstriction in response to α1-adrenergic stimulation, both of which could cause epinephrine to have a different effect than in the general population. This systematic review of the literature aimed to investigate if patients with HCM in CA have a detrimental hemodynamic response to epinephrine. A literature search was performed in October 2016 using Medline (OVID), Embase (Elsevier), and Cochrane Library (Wiley). The initial search generated 2429 articles, of which 22 articles were found to meet inclusion criteria: four physiology studies, 13 case reports of hypotensive HCM patients, and five case reports of HCM patients in CA. The reviewed studies demonstrate that epinephrine effect varies in patients with HCM: in some cases, the expected hypertensive effect was obtained, but in others, a paradoxical hypotensive effect, or no effect, was observed. The probable mechanism of this effect is an increased left ventricular outflow tract obstruction. Other drugs were considered in several of these cases. In summary, the retrieved studies jointly suggest that patients with HCM may respond differently to epinephrine than patients without HCM. The suitability of epinephrine in HCM-associated CA is questionable.

aFunction of Emergency Medicine, Karolinska University Hospital

bDepartment of Medicine Solna, Center for Resuscitation Science, Karolinska Institutet, Stockholm, Sweden

Received 12 October 2017 Accepted 25 August 2018

Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website, www.euro-emergencymed.com.

Correspondence to Therese Djärv, MD, PhD, Karolinska Institutet, Stockholm 17100, Sweden Tel: + 46 851 770 000; fax: + 46 851 770 000; e-mail: therese.djarv@ki.se

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Introduction

Approximately 10% of sudden cardiac deaths among patients under 35 years of age are owing to hypertrophic cardiomyopathy (HCM) [1–3]. Patients with HCM are prone to malignant cardiac arrhythmias leading to cardiac arrest (CA) and have a 0.7% annual mortality rate of sudden cardiac death [4].

CA is treated by advanced life support, a set of interventions including, among other things, cardiopulmonary resuscitation (CPR) and the administration of drugs, aiming to maintain enough cardiac output and coronary and cerebral perfusion pressure to enable return of spontaneous circulation (ROSC) and save neurological function [56].

Epinephrine is a nonselective α-adrenergic and β-adrenergic agonist. It is the main drug recommended in advanced life support and has been used in conjunction with CPR and hypotension since 1896 [7–9]. Epinephrine’s key beneficial effect in CA is believed to be the stimulation of vascular α1-adrenergic receptors, causing a peripheral vasoconstriction in nonvital organs, thus increasing the coronary and cerebral blood flow [9].

However, despite increasing rates of ROSC, it is still debated whether epinephrine increases or decreases survival to discharge or improves neurological function among survivors following CA [10–14]. Several putative mechanisms have been suggested, such as increased postresuscitation myocardial dysfunction and cerebral ischemia associated with epinephrine usage [1516]. Using pure α-agonists or epinephrine combined with β-blockers has been shown to lessen these adverse effects in animals [17]. The summation of beneficial and harmful effects likely differs among different patient subgroups, and identifying patient groups that respond differently to epinephrine could enable a more judicious administration of epinephrine to the subgroups that benefit the most.

HCM is associated with septal hypertrophy with a dynamic left ventricular outflow tract (LVOT) obstruction [18] and impaired peripheral vasoconstriction in response to α1-adrenergic stimulation [19]. Both of these properties could cause epinephrine to have a different effect than in the general population, which could be detrimental for patients with HCM with CA or pre-arrest/peri-arrest hypotension. This systematic review of the literature aims to investigate if patients with HCM in CA have a detrimental hemodynamic response to epinephrine.

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Methods

The research question was ‘Can epinephrine therapy be harmful in patients with HCM in CA with regards to effects on cardiac perfusion?’

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Search strategy

A literature search was performed in the following databases: Medline (OVID), Embase (Elsevier), and Cochrane Library (Wiley). The MeSH-terms identified for searching Medline (OVID) were adapted in accordance to corresponding vocabulary in Embase. Each search concept was also complemented with relevant free-text terms like: hypertrophic cardiomyopathy, epinephrine, and adrenaline. In the search ‘catecholamines’, a term comprising of epinephrine, norepinephrine and dopamine, was used to conduct a wider search. The free-text terms were, if appropriate, truncated and/or combined with proximity operators. No language restriction was applied during the search and retrieval of articles. Databases were searched from inception. The searches were performed by two librarians at the Karolinska Institutet University Library in October 2016. The full search strategies are available in the Supplementary Appendix (Supplemental digital content 1, http://links.lww.com/EJEM/A227).

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Selection criteria

After the initial search and removal of duplicates, the remaining article titles and abstracts were screened by two of the authors (J.I. and S.B.). We included full articles, abstracts and posters with no restriction on date of publication. Articles were included for full-text review if their abstract reported either (a) administration of any catecholamine to a patient with HCM or (b) CPR of a patient with HCM. During full-text review, articles were excluded from data extraction if they were not in English, did not include a patient with HCM, did not include the administration of catecholamines, or did not report any clinical or physiological outcome in humans. These criteria allowed cases of patients with HCM with hypotension to be included. As hypotension often precedes CA or can be indistinguishable from CA, such cases were deemed relevant for understanding epinephrine’s hemodynamic effects in CA. Any disagreement regarding inclusion was discussed until consensus was reached. The search and selection process is depicted in Fig. 1.

Fig. 1

Fig. 1

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Data extraction and synthesis

Data from the included studies were extracted independently, without the use of piloted forms. Extracted data included patient characteristics (age and sex of patient/cohort, type of HCM), intervention parameters (dose and type of catecholamine used, other sympathomimetic drugs used), and outcome parameters (clinical outcome and/or physiological responses deemed relevant to the research question).

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Results

Categorization of results

The search strategy generated 2429 articles, from which 510 duplicates were removed. The abstracts of the remaining 1919 articles were screened and 1842 articles were excluded per the aforementioned criteria. The remaining 77 articles underwent full-text review. Of these, 55 articles were excluded and 22 articles were found to meet the inclusion criteria (Fig. 1). The 22 studies included are grouped into three groups: (a) physiology studies in which patients with HCM received epinephrine or norepinephrine (Table 1), (b) 13 case reports in which hypotensive patients with HCM received epinephrine or norepinephrine (Table 2), and (c) five case reports in which patients with HCM in CA received epinephrine (Table 3).

Table 1

Table 1

Table 2

Table 2

Table 3

Table 3

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Physiology studies

Two studies entailed epinephrine administration [2021] and two studies included the administration of norepinephrine [2223] in hemodynamically stable patients with HCM (Table 1). Salzman et al. [20] gave epinephrine to nine patients with HCM and 14 controls. Epinephrine increased blood pressure in controls, but not in the HCM group. Moreover, epinephrine seemed to worsen LVOT obstruction. This effect was reduced by β-blockers [20]. Koga et al. [21] compared low-dose and high-dose epinephrine in 21 patients with nonobstructive HCM and 21 controls. Patients with HCM responded more to low-dose infusion than the controls, but both groups responded similarly to high-dose infusion. Furthermore, epinephrine decreased diastolic blood pressure more in the patients with HCM. The authors suggest that patients with HCM may have more sensitive cardiac β-receptors.

Brush et al. [22] gave tracer-labelled norepinephrine and tracer-labelled isoproterenol to 11 patients with HCM and 10 controls. The infusion doses were relatively low and given without any hemodynamic effects. Koga et al. [23] studied norepinephrine levels and effects in 26 patients with nonobstructive HCM and 26 controls in rest, after exercise and during norepinephrine infusion. Norepinephrine infusion induced a greater increase in peripheral vascular resistance, blood pressure, and left ventricular contractility in patients with HCM than in controls.

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Case reports of hypotensive patients with hypertrophic cardiomyopathy

Thirteen case reports describe administration of epinephrine or norepinephrine to hypotensive patients with HCM (Table 2). Four cases describe the administration of epinephrine: three following intraoperative hypotension [262737] and one persistent hypotension following CA [33]. In one case, epinephrine produced a transient increase of blood pressure and heart rate [26]. In the other cases, epinephrine and norepinephrine resulted in an insufficient increase in blood pressure [273337]. In two of these cases, intraoperative echocardiography revealed previously undiagnosed HCM [2737]. In one case, epinephrine was observed, by transoesophageal echocardiography, to repeatedly have a direct worsening effect on the LVOT obstruction [37]. In the other case, the identification of HCM guided management away from epinephrine to esmolol, intravenous fluids and phenylephrine, with a subsequent increase in the patient’s blood pressure [27].

The remainder of the case reports in Table 2 describe administration of norepinephrine to hypotensive patients with HCM. In two cases, it is difficult to comment on the effect of norepinephrine owing to how clinical outcomes are described [2528]. In four cases (three cases of cardiogenic shock and one case of septic vasoplegic shock), norepinephrine was administered without improvement [29303236]. The three patients in cardiogenic shock improved only following septal ablation [2930] or mitral valve replacement [32], whereas the septic patient improved following administration of methylene blue [36].

The remaining three case reports describe one case of hypotension in the ICU and two cases of intraoperative hypotension [313435]. In the first case, norepinephrine had a negligible effect on the blood pressure. Instead, decreasing inotropic agents and administering fluid therapy improved the blood pressure [31]. In one case of intraoperative hypotension, norepinephrine had a sufficient hypertensive effect [34]. In the other case, norepinephrine, together with phenylephrine and vasopressin, improved the blood pressure and decreased the LVOT obstruction seen in echocardiography [35].

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Case reports of patients with hypertrophic cardiomyopathy in cardiac arrest

Five articles describe treating patients with HCM in CA with epinephrine (Table 3). One case series describes perioperative ventricular fibrillation in four children with Pompe’s disease. All were given epinephrine and three had ROSC and survived [38]. Another case study describes severe intraoperative anaphylaxis and arrest, which was successfully resuscitated with epinephrine [42].

Two reports describe out-of-hospital CA in patients with HCM [4041]. Despite bystander CPR, initial ventricular fibrillation and prehospital defibrillation, early ROSC was not achieved. One patient died, whereas the other received mechanical CPR and extracorporeal membrane oxygenation, and survived with discrete neurological deficits.

The final report describes how an intraoperative intranasal epinephrine induced ventricular fibrillation [39]. Refractory hypotension and ventricular fibrillation persisted despite chest compressions and epinephrine but was successfully treated with norepinephrine and esmolol.

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Discussion

This was a systematic review of the literature aiming to investigate the effects of epinephrine on patients with HCM in CA. Despite broad inclusion criteria, only physiology studies and case reports were found. However, the retrieved studies jointly suggest that patients with HCM with hypotension or CA may respond differently from patients without HCM. The suitability of epinephrine in HCM-associated CA is questionable.

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Limited data suggest different hemodynamic profile in hypertrophic cardiomyopathy

This review included eight case reports of patients with HCM in CA who received epinephrine, of whom six survived. It is difficult to evaluate the effects of epinephrine in these cases as several interventions were performed simultaneously and limited physiological and clinical outcome data was reported. However, inferring from the case reports of hypotensive patients with HCM, and from the physiological studies reviewed, administering epinephrine to patients with HCM with hypotension or CA may have three key adverse effects: an increased LVOT obstruction, a greater increase in cardiac oxygen demand and a lesser increase in total peripheral resistance than among patients without HCM.

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Epinephrine may increase peri-arrest left ventricular outflow tract obstruction

In several of the reviewed case reports, epinephrine administration did not increase mean arterial pressure, especially in cases with intraoperative hypovolemia and/or severe vasoplegia [273739]. The lack of a hypertensive effect, combined with a chronotropic and inotropic effect, suggests that such agents may worsen the dynamic hypotension-mediated component of the LVOT obstruction in the peri-arrest phase. This is relevant as post-ROSC hypotension is seen in 65% of non-HCM CA patients [43] and is probably more common in patients with HCM considering the pre-existing LVOT obstruction.

Interestingly, epinephrine and other sympathomimetic drugs have had paradoxical hypotensive effects on patients with HCM in several studies [373944], most likely mainly by worsening a pre-existent LVOT obstruction [203744], as seen with real-time transoesophageal echocardiography in the case report by Yee and colleagues. In summary, although it is unlikely that epinephrine has a significant inotropic effect on a nonbeating heart, it seems likely that epinephrine may increase LVOT obstruction in the critical peri-arrest/post-arrest phase, which in turn may decrease cardiac output and impede sustained ROSC.

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Epinephrine may cause myocardial ischemia

Patients with HCM showed higher sensitivity to low-dose epinephrine in one study [21]. Another study, not included in the review, demonstrated that the specific β1-agonist isoproterenol increases cardiac oxygen demand and in some cases induced ischemic ECG changes and even angina in a subgroup of patients with HCM [44].

HCM is known to be associated with an increased risk for ischemia, as illustrated by several cases of myocardial infarction without any coronary artery stenosis [4546]. Furthermore, high-dose epinephrine has been shown to increase cardiac ischemia during CPR in animal studies [1547]. It is possible that this effect is augmented in patients with HCM owing to increased epinephrine sensitivity and ischemic predisposition.

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Epinephrine may cause less peripheral vasoconstriction

Epinephrine did not increase blood pressure in patients with HCM in one study [20] and caused a greater drop in diastolic blood pressure in patients with HCM in another study [21]. This could partly be owing to an increased LVOT obstruction, but a different peripheral response seems likely as well. Patients with HCM seem to have an impaired peripheral α-mediated vasoconstriction [19].

Epinephrine can have a sufficient hypertensive effect in anaesthesia-induced or anaphylactic peripheral vasodilation [262742]. However, this differs from the peri-arrest phase, which typically does not resemble distributive shock. A high afterload and diastolic blood pressure is needed to achieve a sufficient CPP [56] but epinephrine does not seem to be as successful in generating this in patients with HCM [44]. In summary, epinephrine may not cause as great an increase in afterload in patients with HCM as in patients without HCM.

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Practical implications: identify and monitor

In conjunction, the included articles in this review suggest possible negative effects of epinephrine in patients with HCM in CA. These possible harms can be mitigated in several ways.

First, one should consider underlying HCM in young patients presenting with CA. Family and previous medical history, ECG findings and intra-arrest or peri-arrest echocardiography can aid in the diagnosis [2448]. Second, if a patient with HCM in CA is resuscitated in the ED or in hospital, one should consider using invasive blood pressure monitoring to allow early detection of paradoxical or deleterious responses.

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Other drugs

β-Blockers have been used successfully in several cases to ameliorate abnormal outflow gradients in patients with HCM in shock [273949]. In the two cases where β-blockers did not have a sufficient effect, acute surgical intervention was needed to relieve the LVOT obstruction [2932]. β-Blockers could be considered as an adjunct therapy in HCM CA to decrease epinephrine-mediated increases in LVOT obstruction and cardiac ischemia.

In three cases, norepinephrine successfully stabilized patients with HCM in shock [343539], but in three other cases, norepinephrine was insufficient [293032]. In the latter three cases, the patients did not respond to any medical therapy and first improved following surgical removal of the LVOT obstruction by either septal ablation or mitral valve replacement [293032]. Norepinephrine is predominantly vasoconstrictive rather than inotropic and therefore may be advantageous over epinephrine in HCM CA [23].

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Limitations

First, our search strategy was limited to studies in humans in English, which excludes many potentially relevant studies in other languages and in animal models. Second, the search yielded a heterogeneous mix of studies. This limits a joint assessment as it is difficult to extrapolate findings from hemodynamically stable patients with HCM and patients with HCM in shock to patients with HCM in CA. Third, the intrinsic selection and publication bias of case reports limits comparability to other patient subgroups, and furthermore, causality cannot be inferred from individual case reports.

Fourth, HCM is a heterogeneous condition, and it is unlikely that epinephrine administration has the same benefits or harms for all patients with HCM in CA.

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Conclusion

The heterogeneity and limited number of articles identified in this review indicate a paucity of evidence for what effect epinephrine has in patients with HCM in CA. However, the retrieved studies jointly suggest that patients with HCM may respond differently to epinephrine than non-HCM patients. Until more studies are performed on this patient group, it seems prudent to utilize hemodynamic monitoring to allow a more judicious and individualized pharmacological approach to patients with HCM in CA, which may involve, for example, norepinephrine and/or β-blockers rather than solely epinephrine.

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Acknowledgements

Klas Moberg and Susanne Gustafsson, at the Karolinska Institutet University Library for data acquisition help. T.D. was supported by the Stockholm County Council.

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Conflicts of interest

There are no conflicts of interest.

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Keywords:

cardiac arrest; cardiomyopathy; cardiopulmonary resuscitation; epinephrine; hypertrophic; shock

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