affecting flow to the acute marginal branches (RV free wall) and the PDA (inferior septum). The left coronary is responsible for RV infarction in 4% of the cases, and up to a third of anterior infarcts have some degree of RV infarction; this occurs when the left coronary supplies collaterals to a chronically occluded RCA, when the septal infarction affects the septal contribution to RV function as well as the anterior RV, but also when RV MI leads to ST elevation beyond V1 and V2, falsely creating an ECG impression of anterior MI.
Treatment of RV shock (beside emergent reperfusion):
1 Fluid administration. In patients without significant pulmonary hypertension, one may increase the RA pressure to passively force flow through the PA and therefore increase the cardiac output. However, this is only effective as long as the RV does not dilate. Once the RV dilates, fluid administration worsens ventricular interdependence, further reduces LV output, and increases TR. Thus, 500 ml fluid boluses are provided while carefully assessing the hemodynamic response to each bolus, and preferably the RV size on echo. Boluses are stopped if RV is significantly dilated or if no improvement in SBP and pulse pressure is noted.While RA pressure may not correlate with volume responsiveness of the stiff RV, a study has suggested that in RV MI, the best stroke volume is seen when RA pressure is 10–14 mmHg (13-18 cmH2O), beyond which the stroke volume declines.117
2 Inotropes/vasopressors. After RV preload has been optimized, the patient with persistent hypotension is treated with inotropes/ vasopressors. Since at least half of the RV coronary flow occurs in systole, RV coronary flow depends on the driving gradient between SBP and RV systolic pressure. Thus, the RV is very sensitive to decreased SBP, more so than the LV, which may thrive with a slightly reduced SBP.Inotropes used in RV MI should be able to increase SBP, and thus norepinephrine is often the agent of choice.118
3 Maintenance of AV synchrony is critical in acute RV failure, as the RV but also the underfilled LV are dependent on the extra-filling provided by the atrial contraction, more so than a failing, overfilled LV.119 AF may need to be DC cardioverted. Patients with AV block or AV dissociation from an accelerated junctional rhythm need to have atrial and ventricular sequential pacing. Transvenous atrial and ventricular leads are placed through separate venous accesses (e.g., bilateral femoral accesses).As in any shock, a “normal” heart rate of 60–70 bpm is inappropriate and dictates pacing to a rate >80 bpm.
4 Hypoxemia should be aggressively treated with mechanical ventilation if necessary, as hypoxemia increases pulmonary vascular resist- ance and RV afterload.
5 IABP may be useful to increase RV perfusion through the reperfused RCA, lessening RV ischemia. It is reserved for RV shock refractory to inotropes, or concomitant LV failure (pulmonary edema).
6 Inhaled NO may be used in refractory RV shock and has been shown to reduce RA pressure and pulmonary vascular resistance, and increase stroke volume, in RV MI.120
Beware of two processes that may mimic RV infarct: pulmonary embolism and tamponade.
II. Mechanical complications
Mechanical complications occur within the first 14 days of STEMI and have two peaks (24 hours and 3–5 days). They are responsible for 12% of cases of cardiogenic shock (severe mitral regurgitation, 7%; ventricular septal rupture, 3.9%).102 Myocardial rupture usually results from the shear stress at the border between the live and the infarcted area. In the reperfusion era, myocardial rupture is most frequently seen in the first 24 hours (SHOCK registry).121,122 It may occur at 3–5 days, particularly in non-reperfused patients, when the forming scar thins, expands, and exerts excessive tension at the border. In the second week, the rupture may involve the thin necrotic area itself.
A. Severe mitral regurgitation (MR)
Posterior leaflet tethering – A degree of ischemic MR is seen in ~30% of acute MI. Inferior MI with localized inferior/posterior akinesis pulls the posterior papillary muscle posterolaterally, with subsequent tethering of the posterior mitral leaflet (predominantly). This tether- ing may lead to severe MR, a dynamic form of MR that may be mild at rest and severe with increased ventricular loading. Tethering may also occur with anterior MI and is usually a posterior tethering as well. In anterior MI, posterior tethering is secondary to global LV dilatation.
Papillary muscle rupture – Severe MR may result from rupture of a papillary muscle head, usually the posterior papillary muscle in the context of an inferior or posterior MI (two-thirds of severe MR cases in the SHOCK registry).121 The posterior papillary muscle is supplied by one artery, the PDA (from a dominant RCA or LCx), whereas the anterolateral muscle has a dual blood supply from the LAD (usuallyfirst diagonal) and the LCx. Papillary muscle rupture occurs in ~1% of MIs, and, unlike ventricular septal rupture, the infarct is relatively small in 50% of the cases. Each papillary muscle extends chordae to both leaflets, and therefore flailing of either or both leaflets may occur with rupture of either papillary muscle.Echo distinguishes papillary muscle rupture (treated surgically) from leaflet tethering (initially treated with revascularization and supportive measures). In the former, the leaflet(s) are flail, prolapsed, with flailing of chordae and flailing of an echogenic piece of papillary muscle; in the latter, the posterior leaflet is restricted and the jet is usually posterior.
B.Ventricular septal rupture (VSR) occurs in ~1% of MIs (only 0.2% of reperfused MIs). Anterior MI (LAD) and inferior MI (mainly RCA) were equally common causes of VSR in the SHOCK registry, while other registries suggest that anterior MI is slightly more common.122 Patients with a wrap-around LAD have less septal collaterals and are at a higher risk of septal rupture with anterior MI. The location is apical septal in anterior MI and basal inferior in inferior MI. VSR leads to a severe left-to-right shunting with severe hypotension and LV volume overload.
C.Free wall rupture occurs in ~2% of MIs and is the most common and most underdiagnosed mechanical complication (≤1.5% of patients treated with PCI, 3% of patients treated with thrombolysis, 6% of patients not reperfused).123,124 The most common location is anterior MI (LAD culprit); the second most common location is lateral MI (LCx culprit).125
Free wall rupture often leads to tamponade and a bradycardic pulseless electrical activity. It commonly has one of the following pro- dromes: chest pain, re-elevation of ST segments, bradycardia, or syncope from a vagal shock.124 In ~30% of the cases, it is preceded by a concealed rupture and a moderate pericardial effusion, where the pericardium temporarily seals the rupture.124
Risk factors for VSR and free wall rupture: female sex, older age, first MI, absence of collaterals, history of HTN, anterior MI. Also, the use of NSAIDs or steroids increases the risk of rupture. Anticoagulants do not clearly increase the risk of rupture.
Reperfusion with thrombolysis or PCI reduces the incidence of all mechanical complications. While early thrombolysis reduces the risk of free wall rupture, late thrombolysis >12 hours, particularly in elderly patients, may increase the risk of free wall rupture according to a meta-analysis of thrombolytic trials.126,127
The majority of patients with VSR have multivessel disease, while patients with papillary muscle or free wall rupture usually have a single-vessel disease with good LV function.
D. Clinical manifestations
Patients with either MR or VSR present with cardiogenic shock and pulmonary edema.
Pulmonary edema is less marked with VSR than with MR. Patients with VSR can typically lie supine, which is not the case with MR.
The
