Rối loạn nhịp thất trong nhồi máu cơ tim cấp

Là bệnh lý tim mạch có tỷ lệ mắc ngày càng tăng và tỷ lệ tử vong cao

•  Tỷ lệ mới mắc tại Hoa Kỳ: 735.000 người/năm

•  Yếu tố nguy cơ: Tăng huyết áp, ĐTĐ2, Rối loạn lipid máu, Béo phì, ít vận

động thể chất, cuộc sống căng thẳng .

pdf44 trang | Chia sẻ: tieuaka001 | Lượt xem: 495 | Lượt tải: 0download
Bạn đang xem trước 20 trang nội dung tài liệu Rối loạn nhịp thất trong nhồi máu cơ tim cấp, để xem tài liệu hoàn chỉnh bạn click vào nút DOWNLOAD ở trên
ACS Cardioversion/defibrillation Overdrive pacing Attempt complete revascularization Treat ischaemia Correct electrolyte imbalance β-blocker therapy Deep sedation Recurrent VT/VF Amiodarone Lidocaine Consider catheter ablation Electrical Storm Amiodarone Consider ICD reprogramming Consider catheter ablation Consider LVAD implantation Figure 2 Treatment recommendations for recurrent VT/VF and electrical storm in ACS. ACS: acute coronary syndrome; ICD: implantable cardioverter-defibrillator; LVAD: left ventricular assist device; VF: ventricular fibrillation; VT: ventricular tachycardia – If antiarrhythmic drug therapy is necessary on top of these measures for the acute treatment of recurrent ventricular arrhythmias related to ACS after failure or non-availability of other treatment capabilities, administration of intravenous amiodarone is reasonable, followed by intravenous lidocaine, if necessary (Figure 2). – When experience is available, early catheter ablation should be considered when other treatments fail (see below). – Ventricular tachyarrhythmia in the first minutes after suc- cessful reperfusion therapy can be transient without need for treatment, known as reperfusion arrhythmias. – If frequent premature ventricular complexes and non-sus- tained ventricular tachycardia continue despite successful reperfusion therapy under sufficient beta-blocker therapy, they should only be treated if hemodynamically important. This treatment should follow the same principles as the treat- ment of sustained VA. How to manage electrical storm and inappropriate implantable cardioverter- defibrillator shocks in patients with acute coronary syndrome In patients with ACS, electrical storm and inappropriate implanta- ble cardioverter-defibrillator (ICD) shocks are associated with poor prognosis.46-49 Electrical storm is defined as the three or more episodes of VT or VF in any 24-hour period.46,50 It results from interplay between pre-existing vulnerable substrate and acute triggers. It is a rare but Phác đồ điều trị rối loạn nhịp thất trong ACS EuroIntervention 2014;10-online publish-ahead-of-print August 2014 Phòng ngừa đột tử trong hội chứng vành cấp trong viện: Tái thông ĐMV Phòng ngừa đột tử t rong hộ i chứng vành cấp trong viện: Tái thông ĐMV ST-Elevatio n M yo card ial In farctio n : M an ag em en t 52 1129 FIGURE 52-29 Cardiac rupture syndromes complicating STEMI. A, Anterior myocardial rupture in an acute infarct. B, Rupture of the ventricular septum. C, Complete rupture of a necrotic papillary muscle. (From Schoen FJ: The heart. In Kumar V, Abbas AK, Fausto N [eds]: Robbins & Cotran Pathologic Basis of Disease. 7th ed. Philadelphia, WB Saunders, 2005.) A B C TABLE 52-12 Cardiac Arrhythmias and Their Management During Acute Myocardial Infarction CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT THERAPEUTIC OPTIONS 1. Electrical instability Ventricular premature beats Correction of electrolyte deficits and increased sympathetic tone Potassium and magnesium solutions, beta blocker Ventricular tachycardia Prophylaxis against ventricular fibrillation, restoration of hemodynamic stability Antiarrhythmic agents, beta blocker; cardioversion/defibrillation Ventricular fibrillation Urgent reversion to sinus rhythm Defibrillation; amiodarone, lidocaine Accelerated idioventricular rhythm Observation unless hemodynamic function is compromised Increase sinus rate (atropine, atrial pacing); antiarrhythmic agents Nonparoxysmal AV junctional tachycardia Search for precipitating cause (e.g., digitalis intoxication); suppress arrhythmia only if hemodynamic function is compromised Atrial overdrive pacing; antiarrhythmic agents; cardioversion relatively contraindicated if digitalis intoxication present 2. Pump failure/ excessive sympathetic stimulation Sinus tachycardia Reduce heart rate to diminish myocardial oxygen demands Antipyretics; analgesics; consider beta- blocking agent unless congestive heart failure present Atrial fibrillation and/or atrial flutter Reduce ventricular rate; restore sinus rhythm Verapamil, digitalis glycosides; amiodarone; treat heart failure; cardioversion Paroxysmal supraventricular tachycardia Reduce ventricular rate; restore sinus rhythm Vagal maneuvers; verapamil, cardiac glycosides, beta-adrenergic blocking agents; cardioversion 3. Bradyarrhythmias and conduction disturbances Sinus bradycardia Acceleration of the heart rate only if hemodynamic function is compromised Atropine; atrial pacing Junctional escape rhythm Acceleration of the sinus rate only if loss of atrial “kick” causes hemodynamic compromise Atropine; atrial pacing AV block and intraventricular block Insertion of a pacemaker Modified from Antman EM, Rutherford JD (eds): Coronary Care Medicine: A Practical Approach. Boston, Martinus Nijhoff, 1986, p 78. imaging (Fig. 52-30) or by insertion of a pulmonary artery balloon catheter to document the left-to-right shunt. Rupture of the interven- tricular septum after STEMI confers high 30-day mortality.152 The likeli- hood of survival depends on the degree of impairment of ventricular function and the size of the defect, but because the rupture site can expand, prompt surgical repair is necessary even in hemodynami- cally stable patients.1,154 Rupture of a Papillary Muscle Partial or total rupture of a papillary muscle is a rare but often fatal complication of transmural MI (see Fig. 52-29).155 Complete transec- tion of a left ventricular papillary muscle is incompatible with life because the sudden massive mitral regurgitation that develops cannot be tolerated. Rupture of a portion of a papillary muscle, usually the tip or head of the muscle, that results in severe, although Điều trị rối loạn nhịp thất và mục tiêu Why get worked up about electrolytes? Nordrehaug JE, van der Lippe G: Hypokalemia and ventricular fibrillation in acute myocardial infarction. Br Heart J 50:525, 1983. NOTE: Pre-lytic study Rối loạn Kali tăng nguy cơ rung thất Phòng ngừa đột tử trong hội chứng vành cấp trong viện: Điều trị rối loạn nhịp Phòng ngừa đột t ử t r o n g h ộ i chứng vành cấp trong viện: Điều trị rối loạn nhịp 8EuroIntervention 2014;10-online publish-ahead-of-print A ugust 2014 ventricular tachycardia and fibrillation should be managed accord- ing to ESC guidelines.7 In patients with cardiac arrest and who are unresponsive to conventional cardiopulmonary resuscitation, it is reasonable to use mechanical chest compression devices and emergency cardiopulmonary bypass support is reported to be fea- sible. In hemodynamically unstable patients with refractory inces- sant VT, percutaneous left ventricular assist devices (LVADs) may be appropriate (see below). Following intervention, the incidence of arrhythmias ranges from 6% to 28% for new-onset AF, 7-13% IRUQRQVXVWDLQHG97IRUKLJKGHJUHH$9EORFN ”EHDWV PLQODVWLQJIRU•V IRUVLQXVEUDG\FDUGLD ”EHDWVPLQ Catheter ablation of sustained VA in ACS Indications: Patients with sustained VT refractory to other non-pharmacological and AAD treatment Patients with ES Setting: Catheter ablation procedure requires experienced electrophysiologists Consider transer to high volume VT ablation centre when experienced operators are not available Technique: Suppression of the triggering PVC and loss of Purkinje potentials Substrate-guided ablation in un-mappable VA Figure 4. Catheter ablation of VA in patients with ACS. AAD: antiarrhythmic drug; ACS: acute coronary syndrome; ES: electrical storm; PVC: premature ventricular complex; VA: ventricular arrhythmia; VT: ventricular tachycardia Table 1. Occurrence of arrhythmias in STEMI patients during and immediately after primary PCI.71 Accelerated idioventricular rhythm (50-120 b.p.m.) 15-42% Sinus bradycardia (<50 b.p.m.) 28% Non-sustained VT 26% Sinus tachycardia (>100 b.p.m.) 22% Atrial fibrillation 9% High-degree AV block 5-10% Sustained VT 2-4% VF 2-5% AV: atrioventricular; b.p.m.: beats per minute; PCI: percutaneous coronary intervention; STEMI: ST-elevation myocardial infarction; VF: ventricular fibrillation; VT: ventricular tachycardia ODVWLQJIRU•V IRUVLQXVDUUHVW •V IRUVXVWDLQHG97 and 3-6% for VF according to retrospective registry data or pro- spective recordings from cardiac monitors implanted soon during an acute MI.73 The occurrence of AF is frequently associated with severe LV damage and heart failure. Episodes may last from minutes to hours and are often repetitive. The arrhythmia is most often well toler- ated and no specific treatment is required, other than anticoagu- lation. In some instances, the fast ventricular rate contributes to heart failure, requiring prompt treatment using direct current car- dioversion (DCCV) with further management as indicated below. Several studies have suggested that development of AF in the set- ting of acute MI is an independent predictor of all-cause mortal- ity, irrespective of the treatment given.74,75 Atrial fibrillation not only increases the risk for ischaemic stroke during hospitalization but also during follow-up, and this includes patients with paroxys- mal AF that has reverted to sinus rhythm at the time of discharge. Accordingly, patients with AF and risk factors for thromboem- bolism should be adequately treated with oral anticoagulation. Because AF will generally require anticoagulation, when choosing a stent in these patients, the benefits of drug-eluting stents on reste- nosis should be weighed carefully against the substantial bleeding risks that are associated with the prolonged combination of triple antithrombotic therapy (see below). Other supraventricular tachy- cardias are uncommon and are usually self-limiting. Ventricular premature beats are almost universal on the first day of the acute phase and more complex arrhythmias (multiform complexes, short runs, or the R-on-T phenomenon) are common. Their value as predictors of VF is questionable. No specific therapy is required. The long-term prognostic significance of early (<48 h) VF or sustained VT in patients with acute MI is still controversial. In the APEX-AMI trial, VT/VF occurred in ~6% of patients with STEMI presenting for primary PCI.15 Two-thirds of these events occurred before the end of cardiac catheterization (defined as early events) and 90% within 48 h. Ventricular tachycardia/VF was not benign and was associated with substantially increased morbidity and mortality. Some of this association was related to older age, greater prevalence of comorbid conditions, and adverse presenting and post-cardiac catheterization features (ST resolution and TIMI flow) as shown by the attenuation of the risk with adjustment of these factors in a multivariate model. However, even after account- ing for these variables, any VT/VF remained associated with a more than 3-fold higher risk of 90-day mortality in patients undergoing primary PCI. The prognostic significance of late VT/VF appeared to be greater than early VT/VF with more than 5- and 2-fold higher risks of 90-day mortality, respectively. Thus, these data support the prognostic importance of (any, early, or late) VT/VF as an inde- pendent and incremental risk marker, although this does not prove a cause-andeffect relationship. However, sustained VT/VF after primary PCI in the HORIZONS-AMI trial was not significantly associated with 3-year mortality or major adverse clinical events.76 Clinical management of sustained VT and VF after primary PCI is according to ESC guidelines.7 Chỉ định điều trị RF trong rối loạn nhịp thất do ACS EuroIntervention 2014;10-online publish-ahead-of-print August 2014 Chỉ định ICD p h ò n g n gừa n h ị p n h a n h thất / rung thất và đột tử sau NMCT Máy phá rung tự động trong buồng tim Máy phá rung tự động cấy dưới da Máy phá rung tự động cấy dưới da Máy phá rung tự động dạng áo Máy phá rung tự động dạng áo Phòng ngừa và xử t r í độ t tử trong hội chứng vành cấp trong viện: Máy tạo nhịp/ phá rung tự động Phòng ngừa và xử t r í độ t tử trong hội chứng vành cấp trong viện: Máy tạo nhịp/ phá rung tự động Phân tầng sớm nguy cơ đột tử sau NMCT (trong vòng 10 ngày) Đánh giá chức năng thất trái xét ICD Khuyến cáo ICD sau NMCT EHRA/HRS/APHRS Expert Consensus on Ventricular Arrhythmias Heart Rhythm, Vol 11, No 10, October 2014 LVEF should be assessed 6–12 weeks after myocardial infarction in stable patients and in those on optimized HF medication to assess a potential indication for a primary preventive defibrillator implant- ation. This evaluation should be structured and offered to all patients.271,286–288 5.3 Stable coronary artery disease after myocardial infarction with preserved ejection fraction Modern revascularization and secondary prevention therapy allows preservation of LVEF in most patients presenting early with an acute myocardial infarction. Although the risk for SCD in these patients is substantially lower compared with patients with severely impaired LVEF, the absolute number of SCD victims with preserved LVEF is high. Improved SCD risk-detection strategies in the intermediate-risk population are needed. 5.3.1 Risk stratification Risk stratification in patients with stable coronary artery disease after myocardial infarction with preserved ejection fraction Recommendations Classa Levelb Ref.c PVS should be considered in survivors of a myocardial infarction with preserved LV function and otherwise unexplained syncope. IIa C 280– 282 LV ¼ left ventricular; PVS ¼ programmed ventricular stimulation. aClass of recommendation. bLevel of evidence. cReference(s) supporting recommendations. Most studies that have evaluated the usefulness of non-invasive risk stratification have been performed in patients with severely im- paired LVEF (,40%) or in mixed populations. In these studies, ei- ther the outcome in the subgroup of patients with LVEF .40% has not been reported or the subgroups were too small to allow analysis and interpretation of the data. To date, in patients with re- mote myocardial infarction and preserved LVEF, no non-invasive risk stratification technique has demonstrated sufficient specificity and sensitivity. There is limited evidence from subgroups of large-scale studies that programmed ventricular stimulation is helpful for risk stratifica- tion in patients after myocardial infarction with intermediate LVEF values or with an LVEF .40%.280 – 282 This question is currently being addressed in the ongoing Risk Stratification in Patients With Preserved Ejection Fraction (PRESERVE-EF) trial (NCT02124018). 5.3.2 Recommendations for optimal strategy Revascularization in patients with stable coronary artery disease after myocardial infarction with preserved ejection fraction Recommendations Classa Levelb Ref.c Coronary revascularization is recommended to reduce the risk of SCD in patients with VF when acute myocardial ischaemia precedes the onset of VF. I B 289, 290 SCD ¼ sudden cardiac death; VF ¼ ventricular fibrillation. aClass of recommendation. bLevel of evidence. cReference(s) supporting recommendations. Guidelines for coronary revascularization have been published re- cently.13 They provide clear management information and the read- er is referred to the source documents for details. In patients with CAD and VAs, assessment of obstructive coronary disease and ischaemia is essential. Surgical revascularization may in- crease survival and prevent SCD. Implantation of an epicardial ICD lead at the time of coronary artery bypass grafting is not associated with an overall mortality benefit. Percutaneous coronary intervention is also associated with a marked decline in cardiac mortality driven by fewer deaths from myocardial infarction or sudden death. Revascularization may be associated with an increase in LVEF of ≥5–6% in 15–65% of stable patients. This is particularly true for those with evidence of ischaemic or hibernating myocardium on preoperative imaging studies.291,292 The majority of patients with se- verely depressed LVEF immediately after STEMI show significantly improved systolic function after 3 months.286 LVEF should be re- evaluated 6–12 weeks after coronary revascularization to assess potential indications for primary prevention ICD implantation. In patients who survive SCD, revascularization can reduce the re- currence of life-threatening arrhythmias and SCD and also improve patient outcomes, particularly if there is evidence of ischaemia pre- ceding SCD. Sustained monomorphic VT in patients with previous myocardial infarction is less likely to be affected by revascularization. Myocardial revascularization is unlikely to prevent recurrent SCD in patients with extensive myocardial scarring and markedly depressed LVEF. 5.3.3 Use of anti-arrhythmic drugs Use of anti-arrhythmic drugs Recommendations Classa Levelb Ref.c Amiodarone may be considered for relief of symptoms from VAs in survivors of a myocardial infarction but it has no effect on mortality. IIb B 293, 294 ESC GuidelinesPage 28 of 87 by guest on November 21, 2016 Downloaded from LVEF should be assessed 6–12 weeks after myocardial infarction in stable patients and in those on optimized HF medication to assess a potential indication for a primary preventive defibrillator implant- ation. This evaluation should be structured and offered to all patients.271,286–288 5.3 Stable coronary artery disease after myocardial infarction with preserved ejection fraction Modern revascularization and secondary prevention therapy allows preservation of LVEF in most patients presenting early with an acute myocardial infarction. Although the risk for SCD in these patients is substantially lower compared with patients with severely impaired LVEF, the absolute number of SCD victims with preserved LVEF is high. Improved SCD risk-detection strategies in the intermediate-risk population are needed. 5.3.1 Risk stratification Risk stratification in patients with stable coronary artery disease after myocardial infarction with preserved ejection fraction Recommendations Classa Levelb Ref.c PVS should be considered in survivors of a myocardial infarction with preserved LV function and otherwise unexplained syncope. IIa C 280– 282 LV ¼ left ventricular; PVS ¼ programmed ventricular stimulation. aClass of recommendation. bLevel of evidence. cReference(s) supporting recommendations. Most studies that have evaluated the usefulness of non-invasive risk stratification have been performed in patients with severely im- paired LVEF (,40%) or in mixed populations. In these studies, ei- ther the outcome in the subgroup of patients with LVEF .40% has not been reported or the subgroups were too small to allow analysis and interpretation of the data. To date, in patients with re- mote myocardial infarction and preserved LVEF, no non-invasive risk stratification technique has demonstrated sufficient specificity and sensitivity. There is limited evidence from subgroups of large-scale studies that programmed ventricular stimulation is helpful for risk stratifica- tion in patients after myocardial infarction with intermediate LVEF values or with an LVEF .40%.280 – 282 This question is currently being addressed in the ongoing Risk Stratification in Patients With Preserved Ejection Fraction (PRESERVE-EF) trial (NCT02124018). 5.3.2 Recommendations for optimal strategy Revascularization in patients with stable coronary artery disease aft r myocardial infarction with preserved ejection fraction Recommendations Classa Levelb Ref.c Coronary revascularization is recommended to reduce the risk of SCD in patients with VF when acute myocardial ischaemia precedes the onset of VF. I B 289, 290 SCD ¼ sudden cardiac death; VF ¼ ventricular fibrillation. aClass of r commendation. bLevel of evidence. cReference(s) supporting recommendations. Guidelines for coronary revascularization have been published re- cently.13 They provide clear management information and the read- er is referred to the source documents for details. In patients with CAD and VAs, assessment of obstructive coronary disease and ischaemia is essential. Surgical revascularization may in- crease survival and prevent SCD. Implantation of an epicardial ICD lead at the time of coronary artery bypass grafting is not associated with an overall mortality benefit. Percutaneous coronary intervention is also associated with a marked decline in cardiac mortality driven by fewer deaths from myocardial infarction or sudden death. Revascularization may be associated with an increase in LVEF of ≥5–6% in 15–65% of stable patients. This is particularly true for those with evidence of ischaemic or hibernating myocardium on preoperative imaging studies.291,292 The majority of patients with se- verely depressed LVEF immediately after STEMI show significantly improved systolic function after 3 months.286 LVEF should be re- evaluated 6–12 weeks after coronary revascularization to assess potential indications for primary prevention ICD implantation. In patients who survive SCD, revascularization can reduce the re- currence of life-threatening arrhythmias and SCD and also improve patient outcomes, particularly if there is evidence of ischaemia pre- ceding SCD. Sustained monomorphic VT in patients with previous myocardial infarction is less likely to be affected by revascularization. Myocardial revascularization is unlikely to prevent recurrent SCD in patients with extensive myocardial scarring and markedly depressed LVEF. 5.3.3 Use of anti-arrhythmic drugs Use of anti-arrhythmic drugs Recommendations Classa Levelb Ref.c Amiodarone may be considered for relief of symptoms from VAs in survivors of a myocardial infarction but it has no effect on mortality. IIb B 293, 294 ESC GuidelinesPage 28 of 87 by guest on November 21, 2016 Downloaded from Phân tầng và tái thông ĐMV ở bệnh ĐMV ổn định sau NMCT có CNTT bảo tồn Thuốc chống loạn nhịp điều trị bệnh ĐMV ổn định sau NMCT có CNTT bảo tồn Rối loạn nhịp thất trong NMCT cấp •  Bao gồm: ngoại tâm thu thất, nhịp nhanh thất, rung thất là một biến chứng hay gặp •  Hay xảy ra: STEMI trong 48 giờ đầu, NSTEMI sau 48 giờ •  Nếu xảy ra trong giai đoạn sớm (trong vòng 48 giờ) sẽ làm tỷ lệ tử vong tăng 4-5 lần •  Tái thông mạch vành sớm là một trong các biện pháp đầu tiên giúp làm giảm rối loạn nhịp thất, giảm tử vong •  Các biện pháp điều trị quan trọng: điều chỉnh điện giải, thuốc chẹn bêta, amiodarone, máy phá rung tự động. XIN CHÂN THÀNH CẢM ƠN !!!

Các file đính kèm theo tài liệu này:

  • pdfroi_loan_nhip_that_trong_nhoi_mau_co_tim_2783.pdf
Tài liệu liên quan