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這篇文章回顧了導致急性失代償性心衰竭(AHF)的醫源性原因,並提出基於證據的管理策略。隨著心衰患者年齡增長,合併症和多重用藥增加,他們更容易受到醫源性心衰的觸發。臨床情景包括心衰藥物中斷、癌症治療中的心臟毒性、血管內過度液體輸注等。醫源性心衰在文獻中記載不多,但臨床上日益常見,與高死亡率和發病率相關。透過對這些觸發因素的認識,醫源性AHF應該是預防而不是發生後才管理。
醫源性失代償性心力衰竭
Iatrogenic Decompensated Heart Failure
Tran P, Banerjee P. Iatrogenic Decompensated Heart Failure. Curr Heart Fail Rep. 2020;17(2):21-27. doi:10.1007/s11897-020-00452-4
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066273/
Abstract
Purpose of Review
To provide an overview of the potential iatrogenic causes of acute decompensated heart failure (AHF) and an evidence-based management strategy to address this.
Recent Findings
As the heart failure (HF) population continues to age and become burdened with greater comorbidities and polypharmacy, patients become more susceptible to the iatrogenic precipitants of HF. The following clinical scenarios are familiar to clinicians, but the sequelae to AHF are often unanticipated: HF medications withdrawn during an intercurrent illness and not restarted, cardiotoxic therapy prescribed for cancer without timely and regular monitoring of left ventricular function, excessive intravenous fluids administered for sepsis or postoperatively, a blood transfusion volume not adjusted for body weight, iatrogenic anaemia that goes unnoticed or an inappropriate type of pacemaker implanted in a patient with underlying left ventricular systolic dysfunction.
Summary
Iatrogenic decompensated HF is a phenomenon that is infrequently documented in the literature but increasingly confronted by clinicians of all specialties. It is associated with a high mortality and morbidity rate. By having greater awareness of these triggers, iatrogenic AHF should be one that is prevented rather than managed when it occurs.
Keywords: Iatrogenic, Decompensated heart failure, Pharmacotherapy, Fluid management, High-output heart failure, Pacemaker
摘要
審查目的
提供急性失代償性心衰(AHF)潛在的醫源性原因概覽,並提出基於證據的管理策略來解決這一問題。
近期發現
隨著心衰(HF)人群持續老化,並且負擔著更多的共病和多藥治療,患者對HF的醫源性誘因更易敏感。以下臨床情況對臨床醫生來說很熟悉,但導致AHF的後果往往是意想不到的:在間發性疾病期間停用HF藥物且未重新開始、為癌症治療開具心臟毒性療法而未及時和定期監測左心室功能、為敗血症或術後過量輸注靜脈液體、未根據體重調整輸血量、未察覺的醫源性貧血,或在患有潛在左心室收縮功能障礙的患者中植入不適當的起搏器。
總結
醫源性失代償性HF是一種在文獻中不常記錄但臨床醫生越來越常面對的現象。它與高死亡率和發病率相關。通過更加了解這些誘因,醫源性AHF應該是一種被預防而不是在發生時被管理的病症。
關鍵詞:醫源性,失代償性心衰,藥物治療,液體管理,高輸出心衰,起搏器
引言
管理急性失代償性心衰(AHF)的主要挑戰之一是識別和處理導致這種病症的觸發因素,這些因素往往是多因素的。歐洲心臟病學會(ESC)對心衰(HF)的指南強調識別內在心血管觸發因素(如急性冠狀動脈綜合徵、心律失常和高血壓)以及外部侵害,如感染、呼吸和腎功能障礙[1]。然而,日常實踐中越來越常見但描述較少的是由醫生的作為或不作為的無意間造成的傷害,或直接由某種醫療治療引起的觸發因素,我們統稱為醫源性失代償性HF(IAHF)。對其流行病學知之甚少,這類數據也未在英國國家心衰年度審計中收集,該審計分析了超過58,000例AHF住院病例[2]。1996年的一項觀察性研究發現,醫源性原因佔HF住院的7%,與非醫源性原因相比,與較高的死亡率和較長的住院時間有關[3],儘管這種死亡率差異很可能受到其他合併症、額外藥物或感染的混淆。隨著人口老化、合併症和多藥治療的增加以及新藥物和技術的結合,這些看似無害的治療可能在不知不覺中使這些患者的精細神經激素平衡失代償;因此,IAHF的當前流行率可能更高。這些觸發因素及其管理含義在以下四個主要類別中討論:藥物治療、液體管理、高輸出心衰和起搏器設備,總結於表1中。
表1 AHF潛在醫源性原因摘要
藥物治療
停用和延遲心衰藥物
已經確立,在心室射血分數降低的心衰(HFrEF)患者中,腎素-血管緊張素-醛固酮系統抑制劑(RAASi),例如ACE抑制劑(ACEi)和血管緊張素受體阻滯劑(ARBs),β-阻滯劑,礦質皮質激素受體拮抗劑(MRAs),近期組合藥物sacubitril/valsartan,以及鈉-葡萄糖轉運蛋白2抑制劑(無論是否有糖尿病)與安慰劑相比明顯改善存活率並減少心衰住院率[4, 5]。延遲開始、不適當中斷或未能重新開始這些對預後至關重要的藥物可能使這些患者面臨穩定慢性心衰的急性失代償風險,有時甚至會導致血液動力學惡化。
RAASi經常被誤解為腎毒性藥物。英國電子急性腎損傷警報(AKI e-alert)系統的引入加劇了這種焦慮,且當觀察到少量血尿素或肌酐(sCr)上升時,醫院和社區執業醫生會出現反射性停用RAASi的情況[6]。RAASi引起腎小球入口動脈的舒張,預期會導致腎小球內壓降低,反映在最初sCr上升和腎小球過濾率(GFR)在頭兩週的下降。此外,GFR依賴於血壓(BP)。在經常患有慢性腎病(CKD)和高血壓的心衰患者中,腎臟內自我調節的BP範圍變窄,因此BP的小幅下降可能導致通過RAASi介導的血管擴張而非固有腎損傷引起的GFR輕度下降[7]。新的國家指導意見建議,只有在sCr增加> 30%或鉀水平≥ 6.0時才暫停RAASi[8••]。這提醒醫生,AKI e-alert並不自動意味著停用RAASi,而是應該促使對可能包括AHF本身在內的其他潛在原因進行調查。AHF可通過抗利尿激素釋放、系統性靜脈充血時腎間質壓力升高或因緊張性腹水導致的功能性輸尿管梗阻而導致尿素不成比例上升[9, 10]。一項超過16,000名患者的研究發現,HFrEF患者中斷RAASi與30天、90天和1年時更高的死亡率和再入院率相關[11]。事實上,RAASi在基線時腎功能較差的HFrEF患者中提供了最大的死亡率降低[12]。因此,即使在中度-重度腎功能障礙的情況下,也有共識在收益大於風險時繼續使用RAASi[8••]。
β-阻滯劑也是出於同樣的原因:隨著HFrEF嚴重程度的增加,其益處更大,但在停用時風險最大。這通常是由於對其負性肌力效應的焦慮或在低血壓的情況下[13]。除非有嚴重的低血壓,ESC建議以降低劑量繼續使用β-阻滯劑[1]。此外,β-阻滯劑不可能是長期維持穩定劑量的患者AHF的原因[14]。中斷可能會引發反彈性心動過速、心室心律失常並加重心絞痛[15, 16]。這與更高的死亡率和再住院率相關[13]。相反,在AHF中繼續使用β-阻滯劑與較低的死亡率和入院率相關[13, 17]。
即使是計劃中的心衰藥物停用也可能導致看似無症狀的慢性心衰患者AHF。在一項針對穩定擴張型心肌病患者的前瞻性隨機試驗中,MRA、β-阻滯劑和RAASi被逐步撤離。然而,即使在這些藥物的受控撤離下,也導致了40%患者左心室射血分數的顯著下降,且在8週內被檢測到[18]。這強調了心衰藥物只有在絕對必要時才應暫時停用的觀點。
心臟毒性和不良藥物反應
直接心肌毒性和后負荷與前負荷波動是導致AHF的藥物常見的機制。一個已建立的現象是癌症治療相關的心臟功能障礙,其中左心室射血分數(LVEF)下降超過10至小於53%,表現為急性或延遲,甚至在治療完成後長達20年[19]。蒽環類藥物(例如多柔比星)可引起劑量依賴性心臟毒性,通常是不可逆的,而生物靶向藥物(例如HER-2陽性乳腺癌的曲妥珠單抗)可引起通常在迅速停藥或開始心衰藥物治療後可逆的心臟毒性[20, 21]。根據ESC指南,不論臨床病史如何,在開始此類治療前推薦進行基線心臟超聲檢查。對於基線心臟超聲圖正常且沒有心衰臨床風險因素的低風險患者,應每4個治療周期進行一次心臟超聲檢查,或在相當於200 mg/m2蒽環類藥物劑量後進行,而高風險患者應更頻繁地進行監測。治療結束後,應安排1年和5年的隨訪掃描,並根據患者最初的風險分層有時繼續進行更長時間的隨訪。如果在治療期間或之後發生臨床心衰,應根據當前ESC心衰指南進行治療,通常開始使用心臟保護藥物,如ACEi和β-阻滯劑[1, 19, 22]。
估計有50%的年齡≥65歲的心衰患者患有至少5種合併症。這導致患者接觸到更多其他藥物,如慢性阻塞性肺病的類固醇、骨關節炎的非類固醇抗炎藥(NSAIDs)和2型糖尿病的吡格列酮[23]。這些藥物可能會增加液體潴留、后負荷或前負荷,並可能破壞心衰患者的神經激素和血液動力學平衡。類固醇有引起高血壓和液體潴留的傾向,並與劑量依賴性引發或惡化心衰的風險相關[24]。NSAIDs通過抑制環氧合酶(COX)引起鈉和水潴留,從而產生類似效應。一項研究表明,在72個月的NSAID使用中,AHF的風險增加了十倍[25]。的確,COX-2抑制劑也會導致劑量依賴性增加心衰住院風險,ESC指南不鼓勵在患有缺血性心臟病的患者中使用[26, 27]。α1阻滯劑(例如阿福唑嗪和多沙唑嗪)和口服降糖藥,噻唑烷二酮(例如吡格列酮)也會引起液體潴留。前者與其他降壓藥相比,心衰風險增加了兩倍,而後者則發現會加重現有心衰並增加新發心衰的風險[28, 29]。因此,這些常見藥物經常被心衰患者用於其他合併症(例如骨關節炎和2型糖尿病),應該用更安全的替代藥物替代。
另一個經常共存的合併症是心房顫動。對於心率控制,HFrEF患者應避免使用非二氫吡啶類鈣通道阻滯劑,因為它們的負性肌力活性和與AHF的相關性[30]。對於節律控制,I類抗心律失常藥物,例如氟卡尼,可能顯著抑制左心室功能,並在CAST試驗中發現會在基線LVSD患者中誘發AHF[31]。另一個黑盒警告是III類抗心律失常藥物,多那拉酮,原因相似,對於有症狀心衰患者禁忌[32]。
最後,AHF可能在術後發生,其中一個解釋可能是全身麻醉。吸入劑,例如異氟醚和丙泊酚,可能導致心肌抑制。氯胺酮,一種非競爭性NDMA谷氨酸受體拮抗劑,表現出負性肌力和交感神經激活,可能抵消前者。然而,在有顯著基線左心室損傷的患者中,仍可能導致心衰失代償[33]。
液體管理
過量靜脈注射液體和未能充分利尿
首次生存敗血症倡議推薦快速靜脈注射液體高達30 ml/kg,以恢復由於第三空間液體損失造成的血壓下降[34]。然而,這種策略對心衰和敗血症患者來說是不安全的。在一些基線血壓低於平均水平的HFrEF患者中,實現平均動脈壓(MAP)65 mmHg可能不切實際,為達到30 ml/kg的目標而增加更多液體可能會導致肺水腫。這一點得到了敗血性休克患者的一項回顧性研究的支持,該研究發現作為早期目標導向治療的靜脈注射液體30 ml/kg與更高的液體超載率相關,導致利尿劑和胸腔穿刺引流胸腔積液的使用增加[35]。這種做法甚至可能延遲對血管加壓劑甚至機械循環支持的預期和啟動。在敗血性休克情況下,最初的寬鬆液體策略和限制性液體與早期使用血管加壓劑對生存的影響仍然不確定且有興趣;CLOVERS是一項正在進行的多中心隨機研究,正在調查這個問題[36]。目前,國際指南建議最初的液體挑戰為30分鐘內250毫升至500毫升的液體,並在考慮使用去甲腎上腺素或多巴酚丁胺支持重症監護時閾值低[37]。同樣,在術中和術後期間對手術患者進行謹慎的液體管理至關重要。除了肺水腫的明顯後果外,寬鬆的靜脈注射液體還與腸水腫相關,可能導致腸梗阻、腸吸收不良和細菌轉移[38]。這可能會延遲過渡到口服補水並延遲重新開始和吸收重要的抗心衰藥物,其中大多數沒有靜脈注射形式。最重要的是,定期臨床評估液體狀態。
然而,液體管理的準確性只能與液體狀態的臨床評估一樣準確,這可能具有挑戰性且在臨床醫生之間存在矛盾。頸靜脈壓可能主觀,心衰的胸部X光征象可能不具特異性[39, 40]。更糟糕的是,老年患者可能表現出亞臨床性充血[41]。因此,我們經常看到用利尿劑和靜脈注射液體同時治療的違反直覺的困境。一項研究發現,11%的AHF住院患者(沒有敗血症或出血)同時接受靜脈注射液體(中位數1000毫升)和利尿劑,可能是為了平衡過度利尿的任何損害。這會增加左心室充盈壓,延長AHF發作[42]。另一個需要解決的問題是靜脈利尿劑初期引起的sCr上升,使醫生減少呋塞米劑量,導致未能充分利尿。DOSE-AHF研究安慰我們,高劑量靜脈呋塞米與低劑量相比,在60天內對腎功能沒有差異;相反,前者策略提供了更大的利尿而不會造成顯著的腎損傷[43]。有液體潴留的患者應該增加利尿劑劑量以達到恢復正常體液量,而不應僅根據腎功能提前停止或減少。
越來越多的證據表明,N末端前B型利鈉肽(BNP)和超聲檢查可以幫助評估液體狀況。通過連續的BNP測量,下降的水平與趨向正常體液量的趨勢相關[44]。心臟超聲可以揭示下腔靜脈擴張和少量收縮,使醫生遠離進一步的液體管理,而肺部超聲(LUS)可以顯示双側擴散的垂直高回聲波稱為B線,可以識別亞臨床肺水腫。≥15條B線與NT-proBNP > 1000 pg/ml和E/e′比率> 15相關[45]。這甚至可能導致改善患者預後,正如一項小型隨機試驗LUS-HF發現的那樣,該試驗發現,最近出院的心衰患者在隨訪期間使用LUS進行評估,與顯著降低的心衰再入院率相關[46]。因此,臨床醫生應該將這些新技術與體格檢查結合起來,以更準確地判斷液體狀態。
輸血相關循環超載
心衰、慢性腎病(CKD)和高血壓可能是輸血相關循環超載(TACO)的相關風險因素,其在輸血後6小時內表現為肺水腫,與血壓升高、BNP升高和高死亡率相關[47]。體弱的老年成人理論上如果接受超過必要的輸血量,則可能面臨更大的液體超載風險。一個普通的濃縮紅細胞單位是280毫升,4毫升/公斤的劑量通常會使血紅蛋白增加10克/升[48]。因此,一位重50公斤的80歲老太太只需要200毫升就可以使血紅蛋白升高10克/升。然而,如果輸注了整個單位且存在基礎心衰,AHF可能會迅速隨之而來。儘管Cochrane評論表明證據不足,但在輸血前使用呋塞米預防藥物仍然是常見做法[49]。相比之下,在存在左心室流出道阻塞(LVOTO)的情況下,容積耗竭可能會誘發AHF。降低的左心室容積和心動過速可能會增加心室間隔梯度和舒張壓,導致肺水腫。這些主要是通過病例系列報告的。例如,一例報告了一名患有肥厚型心肌病的患者,在禁食並接受輕度鎮靜後出現顯著的LVOTO和肺水腫。隨後在靜脈注射液體和β-阻滯劑後好轉[50]。有趣的是,高達25%的患者在Takotsubo心肌病中也可能發生中腔LVOTO,這是由其基底心肌過度收縮、過度交感神經刺激引起的,在極端情況下,當使用強心藥時可能會導致心源性休克[51, 52]。總體而言,如果我們忽略臨床背景,過多或過少的靜脈注射液體可能會觸發AHF。
高輸出心衰
貧血
嚴重貧血也會加重上述的LVOTO,但它更為人所知的是揭示心肌缺血並導致高輸出心衰[53]。貧血可以促進腎臟一氧化氮合酶活性。這會導致外周血管擴張、神經激素活化,推動心輸出量(CO)超過8升/分鐘,隨時間導致左心室肥大和擴張。所有這些最終可能導致高輸出心衰[54, 55]。貧血是心衰死亡率的獨立預測因素,但它是一種可能被忽視的合併症[56]。它可能由外科手術失血、導管術後血尿或穿刺引起,被抗凝劑或抗血小板藥物加速,並因此加重由肝素調節上升引起的慢性疾病的原有貧血[57]。因此,應在心衰中定期檢查鐵蛋白和轉鐵蛋白飽和度。這可以指導靜脈注射鐵劑的處方,這可以減少心衰住院並改善運動能力,並且由於TACO風險而被推薦超過輸血[48, 58]。
動靜脈瘻管
不太常見的是,動靜脈分流引起的低系統血管阻力也可以類似地激活系統性神經激素系統。心輸出量的增加程度取決於分流大小和流量大小。腎科醫生應注意,由於存在貧血的附加效應,透析患者進一步面臨心衰風險[55]。在血管通路(例如在血管造影或臨時起搏)中,動靜脈瘻管可能會不經意地創建。一份病例報告描述了一名由於穿刺引起的髂動靜脈瘻管而患AHF的患者,發現其心輸出量>16升/分鐘,在分流閉合後解決[59]。因此,心臟科醫生應該警惕這種罕見的併發症。
起搏器相關心衰
心臟科醫生更熟悉的併發症之一是起搏器誘導的心肌病,其定義為起搏器植入後左心室射血分數(LVEF)降低超過10%(已排除其他原因)。這背後有幾種機制[60]。首先,起搏器導線可能影響三尖瓣的關閉,這可能導致對血液動力學有重大影響的三尖瓣返流。這種情況不常見。其次,對於VVI起搏,如果窦房結的放電速度快於設定的速率,心房將對關閉的房室瓣進行收縮,導致房室不同步(稱為起搏器綜合症),這可能引發AHF。這可以通過降低起搏速率或升級為雙腔起搏器(例如DDD)來緩解,後者支持更生理的AV順序起搏[61]。然而,雙腔起搏也可能在有基礎心衰的患者中誘發AHF。DAVID試驗發現,在有LVSD的患者中,DDD起搏(特別是當右心室心尖部起搏(RVP)超過40%時)導致更多的心衰住院或死亡,與心室後備起搏相比。這被認為是由電機械不同步和隨後的不良左心室重塑所驅動的。的確,當DDD導致<40% RVP時,心衰住院率較低[62]。BLOCK-HF試驗對此有所啟示。在高度AV阻塞和LVEF ≤50%的患者中,與RVP相比,雙腔起搏與死亡和AHF住院的絕對風險降低10%相關[63]。因此,無論嚴重程度如何,需要抗心動過緩起搏的HFrEF患者,建議進行新的雙腔起搏或升級[1, 61]。
結論
醫源性失代償性心衰是一種在文獻中不常記錄但臨床醫生越來越常面對的現象。它與高死亡率和發病率相關。隨著心衰人群持續老化並負擔著更多的合併症和多藥治療,患者對心衰的醫源性誘因更易敏感。可以理解的是,當伴隨的腎功能惡化,停止RAASi的需要超過其益處,或當發展出如癌症這樣的重要並發病時,IAHF有時是不可避免的。然而,只要臨床醫生警惕這些行為或遺漏的潛在AHF後果,我們可以預期並及時採取行動,及時監測左心室功能並開始心衰藥物治療,以防止AHF發生。當患者突然出現敗血症或嚴重貧血時,心衰的本已復雜的管理可能會變得更加複雜。一種有效而簡單的方法是定期臨床評估,結合使用肺部超聲和生化標記,如BNP。最重要的是,通過更加了解這些醫源性誘因,這種現象應該是
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