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Małgorzata Kobusiak-Prokopowicz, Andrzej Mysiak

Cardiogenic Shock in Acute Coronary Syndrome

– the Management of Procedures

Wstrząs kardiogenny w ostrym zespole wieńcowym – postępowanie

Department of Cardiology, Wroclaw Medical University, Poland

Abstract

Cardiogenic shock is caused by mechanical cardiac failure, which results in poor tissue perfusion, below the level necessary to meet the basic metabolic needs of tissue at rest. It is the most common cause of death in subjects with an acute coronary syndrome (ACS). According to the clinical definition, cardiogenic shock is characterized by decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. Cardiogenic shock usually occurs during the course of an acute myocardial infarction (AMI) involving at least 40% of left ventricular mass. Despite advances in cardiology, the frequency of and mortality rates from cardiogenic shock remained unchanged for 25 years, but it has recently been found that the frequency of cardiogenic shock and mortality rates related to it have dropped slightly. Most probably this is connected with more frequent and faster decisions to perform primary percutaneous coronary intervention (PCI) during ACS. Prompt restoration of blood flow in the infarct-related artery is basic to the treatment of cardiogenic shock. Cardiogenic shock complicating ACS, its etiopathogenesis and the principles of monitoring and treatment are discussed in the article. Present-day procedures, tactics and logistics in subjects with cardiogenic shock are also presented (Adv Clin Exp Med 2011, 20, 6, 661-665).

Key words: cardiogenic shock, acute coronary syndrome, door-to-balloon time, acute heart failure, acute myocar-dial infarction.

Streszczenie

Leczenie pacjentów ze wstrząsem kardiogennym, mimo rozwoju kardiologii i intensywnej terapii, jest nadal zna-czącym wyzwaniem. W ocenie klinicznej dochodzi do zmniejszenia rzutu serca i hipoksji tkankowej, przy speł-nieniu warunku odpowiedniego wypełnienia łożyska naczyniowego. Wstrząs kardiogenny stwierdza się u 8,6% pacjentów z zawałem serca z uniesieniem odcinka ST (STEMI) oraz u 2% chorych z zawałem serca bez uniesie-nia odcinka ST (NSTEMI). Najczęściej wstrząs kardiogenny rozwija się w przebiegu zawału mięśuniesie-nia sercowego obejmującego przynajmniej 40% masy lewej komory. Warto podkreślić, że częstość występowania i śmiertelność z powodu wstrząsu kardiogennego pozostawały niezmienne od 25 lat, który był główną przyczyną zgonu u chorych z ostrymi zespołami wieńcowymi (o.z.w.). W ostatnim okresie stwierdzono jednak nieznaczne zmniejszenie często-ści występowania wstrząsu kardiogennego oraz zgonów powstałych w jego następstwie. Wiąże się to najprawdo-podobniej z częstszym i szybszym, niż wcześniej, podejmowaniem zabiegów pierwotnej przezskórnej angioplastyki wieńcowej (PCI) w przebiegu leczenia o.z.w. Badanie SHOCK to pierwsze zakończone randomizowane badanie, które porównywało leczenie zachowawcze i wczesną rewaskularyzację u chorych ze wstrząsem kardiogennym, ale już wcześniejsze nierandomizowane studia wykazywały nawet 40% zmniejszenie śmiertelności we wstrząsie kar-diogennym po zastosowaniu pierwotnej PCI. Podczas transportu do szpitala postępowanie u chorych we wstrząsie powinno uwzględniać wytyczne Europejskiej Rady Resuscytacji. Należy podkreślić, że kluczem do poprawy rezul-tatów w leczeniu wstrząsu kardiogennego jest dobra logistyka postępowania, uwzględniająca szybką diagnostykę i natychmiastową terapię skierowaną na zwiększenie ciśnienia tętniczego i rzutu serca. Natychmiastowa korona-rografia i rewaskularyzacja przezskórna, a w koniecznych przypadkach kardiochirurgiczna, są obecnie uznawane za standardowe metody poprawiające rokowanie we wstrząsie kardiogennym (Adv Clin Exp Med 2011, 20, 6, 661-665).

Słowa kluczowe: wstrząs kardiogenny, ostry zespół wieńcowy, czas drzwi–balon, ostra niewydolność serca, ostry zawał serca.

Adv Clin Exp Med 2011, 20, 6, 661–665 ISSN 1230-025X

EDITORIAL

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In many subjects with acute heart failure (AHF), the clinical picture and lab results reveal an acute coronary syndrome (ACS). About 15% of subjects with ACS show both subjective and objective AHF symptoms [1]. According to the clinical classifica-tion, AHF involves pulmonary edema (with acute respiratory failure and an oxygen saturation level below 90%), hypertensive crisis (a rapid elevation of arterial blood flow with concomitant left ven-tricular function at rest), cardiogenic shock (evi-dence of tissue hypoperfusion at normal preload), right ventricular failure and chronic heart failure exacerbation.

Cardiogenic shock usually occursin the course

of an acute myocardial infarction (AMI) involving at least 40% of the left ventricular mass [2, 3]. Dur-ing the initial stage of AMI, extensive myocardial necrosis with concomitant widespread ischemia accompany cardiogenic shock. Cardiogenic shock that takes place at later stages is mostly caused by adverse mechanical events following myocardial infarction, secondary thrombosis in a previously patent vessel or the closing of sequential coronary arteries. As a result, coronary hypoperfusion and radical worsening of left ventricular function con-nected with increased end-diastolic pressure and systemic hypotension occur [4].

It is worth emphasizing that the incidence of cardiac shock and the associated death rate re-mained invariable for 25 years as the leading cause of death in patients with acute myocardial infarc-tion [2]. However, it has recently been found that the frequency of and mortality rates from cardio-genic shock have dropped [3]. Most probably, this is connected with more frequent and faster deci-sions to perform primary percutaneous coronary intervention (PCI) during ACS [5]. The strategy of early revascularization in patients with cardiogenic shock due to AMI is thought to be more advanta-geous than aggressive pharmacological treatment, including thrombolysis (which is currently consid-ered an alternative). Prompt restoration of blood flow in the infarct-related artery is basic to the treatment of cardiogenic shock [6].

Even though the 2005 SHOCK trial was the first completed randomized trial that compared conventional therapy and early revasculariza-tion in patients with cardiogenic shock, there had been some earlier non-randomized studies which showed a 40% lower mortality in cardiogenic shock after PCI [7]. As the result of primary PCI, both six-month and twelve-month survival rates improve, although one-month survival does not [4]. It is worth mentioning that coronary artery bypass graft surgery (CABG) can bring positive re-sults in certain selected situations associated with ACS, but intraoperative mortality is high. In the

SHOCK trial, it was concluded that urgent revas-cularization in cardiogenic shock did not signifi-cantly influence 30-day mortality, but diminished mortality by 20% within one year of the onset; the greatest advantage from urgent revascularization was among subjects under 75 years in age [8].

Cardiogenic Shock

Management in Intensive

Cardiology Care Units

Making the decision to perform, on an urgent basis, a diagnostic procedure and PCI in patients with cardiogenic shock does not replace other in-dispensable intensive-therapy steps [9].

The death rate among patients with cardiogenic shock in whom no aggressive techniques typical of highly advanced intensive care units were applied is 70-90%. Difficulties with the proper choice of an effective pharmacological method for patients with cardiogenic shock arise from a shortage of random-ized controlled trials in this field. It is worth not-ing that the European Society of Cardiology (ESC) guidelines list the majority of pharmacological treat-ment methods used for cardiogenic shock as class IIa or IIb and level of evidence B or C [10].

During the initial phase of cariogenic shock the use of high concentrations of oxygen in the oxygen mixture is recommended, and – if necessary – con-trolled mechanical ventilation should be applied. Pharmacological procedures carried out concur-rently with revascularization methods aim mainly at maintaining adequate perfusion of the heart and other internal organs. The aim of such treatment is to stabilize circulation by optimizing preload and afterload, and restoring, ipso facto, normal balance between potential cardiac power (estimated by the Cardiac Power Index) and afterload [10].

In order to obtain optimal vascular bed filling one should first measure central blood pressure. Patients with right ventricular infarction leading to AHF are particularly susceptible to hypovolemia and they tend to show symptoms of bradycardia and atrioventricular conduction disturbances.

Treatmentaims concurrently at achieving normal

left ventricular pressure-volume and normal sinus rhythm in compliance with A-V synchronized stimulation; dobutamine is also administered to improve right ventricular function.

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treatment. Some evidence indicates that a ven-tricular assist device (VAD) for mechanical sup-port can substantially remodel an unloaded heart muscle and facilitate its functioning much better than an IABP [12].

Door-to-Balloon Time

When AHF takes place in ACS, either percu-taneous coronary intervention (PCI) or coronary artery bypass graft (CABG) should be performed within the first hours after the onset of the symp-toms (within two to four hours is most advisable) [1]. For PCI intervention, the ESC currently rec-ommends a door-to-balloon time (d2b time) of

90 minutes or less [2].While transporting the

pa-tient to the hospital the European Resuscitation Council (ERC) guidelines should be followed [13]. Adequate permeability of the respiratory duct must be ensured, including tracheal intubation with mechanical ventilation if necessary, since the evoked pressure changes in the thoracic cavity may substantially influence preload and afterload. The key element to a better outcome in treating AHF is a course of action that allows for a quick diagno-sis and immediate arterial blood pressure-oriented and cardiac output-oriented therapy [4].

Although evidence suggests that primary PCI is a justified reperfusion strategy in the majority of patients with ST segment elevation myocardial infarction (STEMI), only a minority of patients re-ceive this treatment within the recommended d2b time of 90 minutes after entry into the medical system [2]. This happens in spite of the fact that ACC/AHA guidelines prefer aggressive activities in order to minimize the time for applying a reper-fusion strategy [3].

The reasons for the difficulty in limiting d2b time to the recommended 90 minutes are complex. Pressure to shorten the time from the first contact with medical personnel to the coronary vessel in-tervention undoubtedly results in positive logistic and organizational changes, but it is the authors’ view that it leads at the same time to simplification of decision-making procedures, which in practice may result in underestimating the significance of basic diagnostic and therapeutic treatment. Al-though the d2b time is especially important in high-risk groups, it is in these cases that patients should be provided with the highest possible de-gree of safety during the operation, which may to various degrees extend the time between the onset of symptoms and the initiation of reperfusion. At-tention should be paid to the fact that pressure to shorten d2b time may result in worse initial pro-tection of patients with destabilized circulation,

including cardiogenic shock. Inappropriate clini-cal decisions made with the intention of shorten-ing d2b time in the treatment of cardiogenic shock, such as neglecting to stabilize the patient, are a side effect of focusing the attention only on the coro-nary arteries [5].

Also, if shortening d2b time is treated as an

overriding priority, it may result in the

disqualifi-cation of patients for PCI when it is assumed that their treatment will be connected with complica-tions and delays in conducting the operation.

In the authors’ view, it is worth considering whether imposing unrealistic principles causes more harm than benefit. The recommendation that the door-to-balloon time should not exceed 90 minutes should be replaced by a suggestion that PCI should be conducted as early as possi-ble, preferably within 90 minutes of the onset of

symptoms. The phrase as early as possible allows

the basic conditions of patient safety to be met and creates the highest chances for survival and for successful PCI.

The evidence indicating that prolonging d2b time to more than two hours is associated with an increase in mortality suggests that doctors and health care systems should aim at minimizing d2b time. However, d2b time should be carefully used as a quality-of-care indicator, as there are cases in which a longer d2b time must be considered justi-fied [14].

The SHOCK trial demonstrated that a patient can be brought out of shock by delaying coronary intervention [8]. The 30-day mortality rate among patients who had undergone medical treatment did not differ from that of patients who had ear-ly revascularization. Considerable improvement in the survival rates of patients undergoing early revascularization was, however, demonstrated in observations lasting six months and one year. These observations were also confirmed by an analysis of the SHOCK registry, which included a group of patients who, for various reasons, were not qualified for the SHOCK trial. In this group too early coronary intervention improved survival rates, including the 30-day rate as well as later ones [15, 16].

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during cardiac arrest or immediately after the re-turn of spontaneous circulation (ROSC). PCI at-tempts conducted during resuscitation operations regardless of the risks are not justified.

There seems to be an assumption among

car-diologists thatcontroversies regarding the

assess-ment of the effectiveness of PCI as compared with intensive care (sometimes unfortunately referred

to by the overly broad term medical treatment)

in patients with acute myocardial infarction and cardiogenic shock result from a failure to take into consideration the methodological aspects of the trials on the basis of which the guidelines were for-mulated. The lack of differences in early mortality between patients treated with immediate PCI and patients in which PCI was not used or was deferred may suggest that PCI does not impact the effective-ness of treatment of cardiogenic shock. Patients with acute myocardial infarction and cardiogenic shock should be treated in rigorous accordance with the principles for treating patients with life-threatening conditions. The treatment of patients with cardiogenic shock, modified appropriately to the location and circumstances and performed in an interdisciplinary way, should start at the pre-hospital stage and should be continued during the coronarography and PCI. In this sense PCI con-stitutes an element of intensive care, and not an alternative to it [18].

The other important condition which limits the universality of conclusions based on polycen-tric randomized clinical programs is the sophis-tication of procedures for including patients in trials. Many patients would never be qualified for any clinical program – but obviously doctors must make decisions regarding such patients as well. An interesting elaboration related to such dilemmas is the research by Hordijk-Trion et al., who evaluated methods for including patients in trials compar-ing the effectiveness of PCI and CABG [19]. In one study they looked at, as many as 64% of the patients initially assessed did not meet the quali-fication criteria, which means that a research pro-gram used as a basis for establishing guidelines in

accordance with theprinciples of evidence-based

medicine, was conducted with the participation of only 36% of the patients from the real world. Other programs that Hordijk-Trion et al. analyzed excluded from 58% to 96% of the patients initially evaluated.

It is the current authors’ view that the moment of the patient’s first contact with medical personnel should activate universal procedures, adjusted to the patient’s condition, which must be performed so that the patient survives and is effectively read-ied for further specialist procedures, including the most urgent ones. The mechanical application of universal guidelines is more logically justified dur-ing the early stage of the patient’s entry into the medical system, while on more advanced levels of specialist care it may pose a considerable threat to patients. Not perceiving this truth inevitably re-sults in the creation of unrealistic “virtual guide-lines” that cannot be adhered to in practice.

It is clear that improving the effectiveness of the treatment of patients with ACS requires pro-fessional methods of work management and or-ganization, psychology and sociology. Experience shows that it is at the initial stages of the patients’ entry into the medical system that d2b time can be effectively shortened. Nurses and assistants may also play an important role in providing more rapid treatment of STEMI [20], given effective management of human resources, particularly in-tellectual capital. Imposing d2b time frames cre-ates a number of dangers along with the benefits. Interventional cardiology is a relatively new field, and its practitioners frequently have no experience treating patients in an emergency. With a superfi-cial understanding of the ESC recommendations, stabilizing the general condition of such patients may be perceived as an obstacle to fulfilling d2b

guidelines. The expression time is muscle – which

implies that in patients with any symptom spec-trum accompanying STEMI the primary issue is a simple correlation between the time of revas-cularization and recovery – has the hallmarks of demagogy.

References

[1] Dickstein K, Cohen-Solal A, Filippatos G, McMurray JJV, Ponikowski P, Poole-Wilson PA, Stroemberg A, van Veldhuisen DJ, Atar D, Hoes AW, Keren A, Mebazaa A, Nieminen M, Priori SG, Swedberg K: ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008. Eur Heart J 2008, 29, 2388–2442.

[2] Eagle KA, Nallamothu BK, Mehta RH, Granger CB, Steg PG, Van de Werf F, Lopez-Sendon J, Goodman SG, Quill A, Fox KA: For the Global Registry of Acute Coronary Events (Grace) Investigators. Trends in acute reperfu-sion therapy for ST-segment elevation myocardial infarction from 1999 to 2006: we are getting better but have got a long way to go. Eur Heart J 2008, 29, 609–617.

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[4] Hochman JS: Cardiogenic shock complicating acute myocardial infarction. Circulation 2003, 107: 2998–3002.

[5] Kern M: Door-to-balloon time (DTB) – putting the cath lab’s role in perspective. Cath Lab Digest 2006, 14, 6–8.

[6] Jacobs AK, Sleeper LA, Forman R: Cardiogenic shock caused by right ventricular infarction: a report from SHOCK Trial Registry. Am Heart J 2001, 141, 964–970.

[7] Gibson CM: Has my patient achieved adequate myocardial reperfusion? Circulation 2003, 108, 504–-507.

[8] Hochman JS, Sleeper LA, White HD, Dzavik V, Wong SC, Menon V, Webb JG, Steingart R, Picard MH, Menegus MA, Boland J, Sanborn T, Buller CE, Modur S, Forman R, Desvigne-Nickens P, Jacobs AK, Slater JN, LeJemtel TH: SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. One-year survival following early revscularization for cardiogenic shock. JAMA 2001, 10, 285, 190–192. Am Heart J 2001, 141, 964–970.

[9] Fincke R, Hochman JS, Lowe AM, Menon V, Slater JN, Webb JG, LeJemtel TH, Cotter G: SHOCK Investigators. J Am Coll Cardiol 2004, 2, 340–348.

[10] Nieminen MS: Key issues of European Society of Cardiology guidelines on acute heart failure. Eur Heart J 2006, 8, Suppl. E, E6–E11.

[11] Tan LB, Williams SG, Wright DJ: Ventriculo-arterial function curves – a new dimension in characterizing acute heart failure. Eur J Heart Fail 2003, 5, 407–410.

[12] Thiele H, Sick P, Boudriot E, Diederich KW, Hambrecht R, Niebauer J, Schuler G: Randomized comparison of intra-aortic balloon support with a percutaneous left ventricular assist device in patients with revascularized acute myocardial infarction complicated by cardiogenic shock. Eur Heart J 2005, 26, 1276–1283.

[13] Nolan JP, Deakin CD, Soar J, Böttiger BW, Smith G: European Resuscitation Council guidelines for resuscitation 2005. Section 4. Adult advanced life support. Resuscitation 2005, 67, Suppl 1, S39–86.

[14] Cannon ChP, Gibson CM, Lambrew CT, Shoultz DA, Levy D,French WJ, Gore JM, Weaver WD, Rogers WJ, Tiefenbrunn AJ: Relationship of symptom-onset-to-balloon time and door-to-balloon time with mortality in patients undergoing angioplasty for acute myocardial infarction. JAMA 2000, 283, 2941–-2947.

[15] Dzavik V, Sleeper LA, Cocke TP, Moscucci M, Saucedo J, Hosat S, Jiang X, Slater J, LeJemtel T, Hochman JS:

SHOCK Investigators: Early revascularization is associated with improved survival in elderly patients with acute myocardial infarction complicated by cardiogenic shock: a report from the SHOCK trial. Eur Heart J 2003, 24, 828–837.

[16] Jeger RV, Harkness SM, Ramanathan K, Buller CE, Pfisterer ME, Sleeper LA, Hochman JS, SHOCK Investigators: Emergency revascularization in patients with cardiogenic shock on admission: a report from the SHOCK trial and registry. Eur Heart J 2006, 27, 664–670.

[17] Van de Werf F, Ardissino D, Betriu A, Cokkinos DV, Falk E, Fox KA, Julian D, Lengyel M, Neumann FJ, Ruzyllo W, Thygesen C, Underwood SR, Vahanian A, Verheugt FW, Wijns W: Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J 2003, 24, 28–66.

[18] The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Guidelines on myocardial revascularization. Eur Heart J 2010, 31, 2501–2555.

[19] Hordijk-Trion M, Lenzen M, Wijns W, de Jaegere P, Simoons ML, Scholte op Reimer WJ, Bertrand ME, Mercado N, Boersma E, EHS-CR Investigators: Patients enrolled in coronary intervention trials are not represen-tative of patients in clinical practice: results from the Euro Heart Survey on Coronary Revascularization. Eur Heart J 2006, 27, 671–678.

[20] The Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology. Management of acute myocardial infarction in patients presenting with persistent ST-segment ele-vation. Eur Heart J 2008, 29, 2909–2945.

Address for correspondence:

Małgorzata Kobusiak-Prokopowicz Department of Cardiology

Wroclaw Medical University Pasteura 4

50-367 Wrocław Poland

Tel.: +48 71 784 2611, +48 71 784 2612 E-mail: [email protected]

Conflict of interest: None declared

References

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