CABG was performed briskly, at a median of 2.7 hours after randomization. CABG was associated with the same survival as PCI, despite the higher prevalence of extensive CAD.110 However, this quick CABG is not feasible at many institutions and the CABG rate in the community is lower.
IABP was recommended in all SHOCK trial patients, including medically treated patients and those initially presenting to a non-PCI hospital, and was used in 86% of patients. In the SHOCK registry, IABP was associated with a reduced mortality.109 However, randomized trials such as CRISP-AMI failed to show a benefit of IABP in STEMI patients with LV failure,111 and the IABP-SHOCK II trial failed to show a benefit of IABP even in MI patients with cardiogenic shock.112 The failure of the IABP-SHOCK II trial may be due to the heterogeneity of cardiogenic shock and the inclusion of patients whose shock was not purely related to LV dysfunction (median EF was 35%, 33% of patients had NSTEMI), or whose organ failure was advanced (45% had post-cardiac arrest shock); also, IABP was mostly placed after rather than before PCI. In patients with true LV shock, it is reasonable to place the IABP before PCI as an early measure to stabilize the patient, unload the LV and reduce O2 demands, and perform a safer PCI with potentially less reperfusion injury. Also, outside shock, IABP is useful in patients with a large STEMI who have persistent ischemia/slow coronary flow after primary PCI.
In sum, the following strategy is recommended in cardiogenic shock:
1 Emergent revascularization of the infarct-related artery only, irrespective of the time of presentation (even >24 hours after MI onset). Ongoing ischemia and necrosis are typical of the vicious cycle that characterizes shock, even late shock. Non-culprit artery PCI is preferably avoided as it adds contrast load and procedural time and therefore worsens LV volume overload and possibly myocardial injury (CULPRIT-SHOCK trial, STEMI [62%] or NSTEMI).69 Even patients with RCA culprit and severe LAD non-culprit do not appear to benefit from non-culprit PCI. This does not apply to cases without a clearly identifiable culprit, especially NSTEMI, where multivessel PCI may be required. Also, non-culprit PCI may be required in the patient with severe and refractory cardiogenic shock requiring multiple vasopressors despite culprit PCI, although a ventricular assist device is probably more useful in this case.
2 In patients presenting to non-PCI-capable hospitals within 12 hours of MI onset, administer fibrinolytics whenever transfer delays are expected. Also, IABP may be placed before transfer. Augmentation of blood pressure with IABP or vasopressors may increase coronary flow and facilitate fibrinolysis.
3 In patients with multivessel CAD on angiography:Severe three-vessel CAD (>90%) or critical left main disease dictates immediate CABG if possible. Alternatively, PCI of only the infarct-related artery is performed. Balloon angioplasty of the culprit artery followed by early CABG is another alternative.
4 IABP may be placed during or before the revascularization procedure and may be tailored to patients who continue to decline and require higher inopressor doses, yet are not in extremis and are not post-cardiac arrest.
5 Mechanical ventilation is often necessary to reduce the respiratory work, improve oxygenation, and reduce LV preload and afterload.
6 Inotropic support: dobutamine is used in patients whose SBP is >80 mmHg, while norepinephrine is required in patients with SBP <80 mmHg or inappropriately low or normal SVR. While vasoconstriction may be harmful, the maintenance of an appropriate systemic perfusion pressure, including coronary perfusion pressure, is a priority and justifies the use of norepinephrine in severely hypotensive patients; in fact, afterload remains low in hypotensive patients, even if vasopressors are used. Also, norepinephrine stimulates the myocardial release of local coronary vasodilators which counteract its direct α1-constrictive effect. Patients whose shock has been precipitated by vasodilators or sedation may also be temporarily treated with vasopressors, until the effect of the drugs wears off.
7 Temporary pacing, usually at a rate over 80–100 bpm, is required if the heart rate is inappropriately low or even “normal” (60–70 bpm).
8 PA catheter is generally placed to support the diagnosis and guide management, unless the patient quickly improves with revascularization; the finding of a low SVR may dictate the use of vasopressors.Echo should be done to rule out mechanical complications and to assess left-sided filling pressures.Alternatively, LV pressure measurement and LV angiography are performed during the emergent cardiac catheterization.
9 LV assist device, such as percutaneous Impella or TandemHeart, may be considered in patients with refractory shock as it provides better hemodynamic support than IABP. The survival benefit in patients with irreversible stage of shock and multiple organ failure is, however, uncertain, and is compounded by these devices’ high complication rates. In 3 large retrospective analyses, including two analyses of shock patients, Impella was associated with worse outcomes vs IABP, worse outcomes compared to the pre-Impella era, and worse outcomes vs matched patients from IABP-SHOCK II trial: more major bleeding (absolute risk >20%), death (1.25 times higher), vascular complications, hemolysis and stroke.113-115
D. Management of severe acute left heart failure without shock
In acute MI, pulmonary edema results from volume redistribution to the lungs without overt volume overload and sometimes without LV dilatation. Treatment consists of small doses of furosemide (e.g., 20–40 mg IV), along with a low dose of intravenous NTG to reduce preload. Excessive preload or afterload reduction may, however, precipitate shock.
Severe HF (Killip class III), i.e., massive pulmonary edema that frequently requires mechanical ventilation, is an indication for primary PCI of the culprit artery irrespective of the delay to presentation (approach similar to cardiogenic shock).1,2
Conversely, less severe HF with late presentation (>24 hours) and no residual angina does not dictate urgent PCI. Coronary angiography and PCI may be performed on a non-urgent basis if HF, i.e., severe functional limitation, persists after initial diuresis; otherwise, stress testing may be performed first to assess for residual ischemia.
E. RV-related cardiogenic shock: characteristics and management
If the patient survives the acute phase of RV MI, RV function usually improves spontaneously within 1 month, as RV ischemia is usually reversible and does not lead to chronic RV failure, even if the RV is not reperfused.116 In fact, the long-term survival is excellent in survivors of the acute phase. RV is thin (less O2 demands), is able to increase its transcoronary O2 extraction (which is 50% at baseline vs. 75% for the LV), easily recruits collaterals because of its lower coronary microvascular resistance, and may derive O2 from the RV cavity through the deep trabeculations; thus, RV usually recovers most of its contractile function. Acutely, however, RV shock is associated with a very high mortality, almost similar to LV shock (~50%), despite a younger age, a higher LVEF, and a much lower likelihood of three-vessel CAD.101 Similarly to LV shock, RV shock benefits from emergent reperfusion with PCI or CABG. In fact, reperfusion promptly improves RV function within 1 hour and normalizes it within 3–5 days, dramatically and quickly improving the survival and the clinical status.116 Non-reperfused patients continue to have a poor RV function and poor hemodynamics at 3–5 days; RV function eventually normalizes at 1 month, which may be too late.
In the SHOCK registry, PCWP was equally elevated in RV shock as in LV shock (23 ± 11 mmHg), and was equalized with RA pressure.101 This is mainly related to the RV–LV interdependence. The dilated RV pushes the septum, forcing the LV diastolic pressure to equalize with the RV diastolic pressure and reducing LV output. RV is thin, intolerant to the increased afterload, and thus intolerant to RV dilatation which begets more dilatation. The LV is underfilled, yet LA and LV diastolic pressures are elevated.
The usual culprit of RV shock is RCA in 96% of
