Practical Cardiovascular Medicine. Elias B. Hanna

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 the cases, usually proximal RCA 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.