Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 122

In the SHOCK trial, LVEF was ~30 ± 12%, implying that at least half the patients only had a moderate LV insult and a moderate reduction of LV systolic function.⁷³ Also, ~40% of patients had non-anterior MI, mainly inferior MI.^73,102 Thus, an EF that is well tolerated in chronic HF may be associated with cardiogenic shock in acute MI. In a way, this is similar to tolerating chronic MR or AI vs. developing shock with acute MR or AI. Beside systolic dysfunction, several mechanisms explain cardiogenic shock in acute MI:

 While the progressive LV dilatation that occurs chronically raises afterload and is maladaptive, some early degree of LV dilatation is adaptive and increases stroke volume at a given LV contractility. Also, some degree of LA dilatation is adaptive and lessens the rise in backward pressure. This is similar to the chronic LV adaptation to MR or AI. In fact, half of patients with cardiogenic shock have a small or normal-size LV, which represents failure of the mechanism of acute LV dilatation.103,104

Table 2.4 Differential diagnosis of shock in MI.

LV-related cardiogenic shock: anterior MI, MI with a prior history of MI or LV dysfunction, or MI in a patient with multivessel CAD. Cardiogenic shock occurs in 4–7% of STEMI (vs. 2.5% of NSTEMI). It is occasionally present on admission, and more typically develops soon after admission, at a median of 5.5 hours after MI onset (vs. a later shock development, at ~3 days, in NSTEMI with three-vessel disease).RV infarct: RV-related shock should be considered whenever hypotension occurs in inferior MI. RV infarct occurs in 30% of inferior MIs, mainly with proximal RCA occlusion. Only one-half of RV infarcts produce clinical RV failure.Mechanical complications (mitral regurgitation, ventricular septal rupture, free wall rupture) or tamponade.Arrhythmias (inappropriate bradycardia, advanced AV block, VT).Vagal stimulation and vagal shock in inferior MI. It manifests as bradycardia with clear lungs and low JVP. It is treated with atropine and fluid administration.Hypovolemic hypotension: hypotension with clear lungs, low JVP, and no bradycardia. May attempt small fluid challenge in this situation.

During or after PCI, shock may develop from the use of sedative and vasodilatory drugs in a patient with limited cardiac output reserve, or from myocardial reperfusion injury that aggravates myocardial depression. Coronary reocclusion, coronary perforation with tamponade, and bleeding complications are also considered.

 For a given LV contractility, the more severe impairment of LV compliance in acute MI leads to a more severe rise of LV filling pressure, which further reduces coronary perfusion pressure.

 Transient hypotension (drugs, arrhythmia, sedation) in an initially stable patient may transiently reduce coronary blood flow and thus initiate a vicious circle of progressive myocardial ischemia that sustains the hypotension. Furthermore, since the pulmonary edema of MI results from volume redistribution rather than florid volume overload, aggressive diuresis may precipitate shock in MI. Also, β-blockers, ACE-Is, and other vasodilators, including sedatives administered during PCI or during intubation, may precipitate shock in a pre-shock patient who depends on the compensatory vasoconstriction and tachycardia. This partly explains why cardiogenic shock often develops after hospital admission.While mild hypotension unloads the LV and may be tolerated in chronic LV failure, it is not well tolerated in a patient with acute ischemia and unstable CAD or in a patient with RV failure.

 In over 25% of MI-associated cardiogenic shock, SVR is inappropriately low or normal rather than elevated, despite the use of vasopres-sors (SVR ≤1000 dyn.s.cm–5).¹⁰⁵ This mismatch between myocardial depression and inappropriate vasodilatation (or lack of compensa- tory vasoconstriction) may result in cardiogenic shock. Also, 18% of patients, mainly those with a low initial SVR, go on to develop a clinical picture of sepsis with fever or leukocytosis 2–4 days later, mostly with positive bacterial cultures. Thus, inappropriate vasodilata- tion is initiated by a systemic inflammatory response syndrome (SIRS) secondary to MI early on, then a septic process later on, and contributes to shock in a substantial proportion of patients. This implies a role for vasopressors in this subset of patients. High levels of cytokines and inducible nitric oxide synthase, beyond the healthy levels of endothelial nitric oxide synthase, precipitate vasodilatation and further myocardial depression. The initial vasodilatation, per se, is associated with an increased risk of later sepsis (bacterial translocation?).¹⁰⁵

Some patients with a pre-shock state before PCI develop a full-blown shock after PCI. PCI may initiate a reperfusion injury with further activation of inducible nitric oxide synthase, and thus vasodilatation and myocardial depression. This is a temporary phenomenon, as the benefit from PCI eventually takes over. Also, the use of sedatives and supine positioning may precipitate shock during PCI.