Percutaneous coronary intervention: cardiogenic shock
cardiogenic shock.A 65 year old man with a 3-4 hour history of acute
anterior myocardial infarction had cardiogenic shock and acute pulmonary oedema, requiring mechanical ventilation and inotropic support.He underwent emergency angiography(left), which showed a
totally occluded proximal left anterior descending artery (arrow). A soft tipped guidewire was passed across the occlusive thrombotic lesion, which was
successfully stented (center). Restoration of brisk antegrade flow down this artery (right) followed by insertion of an intra-aortic balloon
pump markedly improved blood pressure and organ perfusion. The next day he was extubated and weaned off all inotropic drugs, and the intra-aortic balloon pump was
removed
Effects of cardiogenic shock
Cardiac effects
In an attempt to maintain cardiac output, the remaining non-ischaemic myocardium becomes hypercontractile, and its oxygen consumption increases. The effectiveness of this response depends on the extent of current and previous left ventricular damage, the severity of coexisting coronary artery disease, and the presence of other cardiac pathology such as valve disease.Three possible outcomes may occur:
Systemic effects
The falling blood pressure increases catecholamine levels, leading to systemic arterial and venous constriction. In time, activation of the renin-aldosterone-angiotensin axis causes further vasoconstriction, with subsequent sodium and water retention. These responses have the effect of increasing left ventricular filling pressure and volume. Although this partly compensates for the decline in left ventricular function, a high left ventricular filling pressure leads to pulmonary oedema, which impairs gas exchange. The ensuing respiratory acidosis exacerbates cardiac ischaemia, left ventricular dysfunction, and intravascular thrombosis.Time course of cardiogenic shock
The onset of cardiogenic shock is variable. In the GUSTO-I study, of patients with acute myocardial infarction, 7% developed cardiogenic shock—11% on admission and 89% in the subsequent two weeks. Almost all of those who developed cardiogenic shock did so by 48 hours after the onset of symptoms, and their overall 30 day mortality was 57%, compared with an overall study group mortality of just 7%.Differential diagnosis
Hypotension can complicate acute myocardial infarction in other settings.Right coronary artery occlusion
An occluded right coronary artery (which usually supplies a smaller proportion of the left ventricular muscle than the left coronary artery) may lead to hypotension in various ways: cardiac output can fall due to vagally mediated reflex venodilatation and bradycardia, and right ventricular dilation may displace the intraventricular septum towards the left ventricular cavity, preventing proper filling.In addition, the right coronary artery occasionally supplies a sizeable portion of left ventricular myocardium. In this case right ventricular myocardial infarction produces a unique set of physical findings, haemodynamic characteristics, and ST segment elevation in lead V4R. When this occurs aggressive treatment is indicated as the mortality exceeds 30%.
Ventricular septal defect, mitral regurgitation, or myocardial rupture
In 10% of patients with cardiogenic shock, hypotension arises from a ventricular septal defect induced by myocardial infarction or severe mitral regurgitation after papillary muscle rupture. Such a condition should be suspected if a patient develops a new systolic murmur, and is readily confirmed by echocardiography—which should be urgently requested. Such patients have high mortality, and urgent referral for surgery may be needed. Even with surgery, the survival rate can be low.Myocardial rupture of the free wall may cause low cardiac output as a result of cardiac compression due to tamponade. It is more difficult to diagnose clinically (raised venous pressure, pulsus paradoxus), but the presence of haemopericardium can be readily confirmed by echocardiography. Pericardial aspiration often leads to rapid increase in cardiac output, and surgery may be necessary.
Hallmarks of right ventricular infarction
- Rising jugular venous pressure, Kassmaul sign, pulsus paradoxus
- Low output with little pulmonary congestion
- Right atrial pressure > 10 mm Hg and > 80% of pulmonary Right atrial prominent Y descentcapillary wedge pressure
- Right ventricle shows dip and plateau pattern of pressure
- Profound hypoxia with right to left shunt through a patent foramen ovale
- ST segment elevation in lead V4R
Main indications and contraindications for intra-aortic balloon pump counterpulsation
Indications- Cardiogenic shock.cardiogenic shock
- Unstable and refractory angina
- Cardiac support for high risk percutaneous intervention
- Hypoperfusion after coronary artery bypass graft surgery
- Septic shock
- Enhancement of coronary flow after succesful recanalisation by percutaneous intervention
- Ventricular septal defect and papillary muscle rupture after myocardial infarction
- Intractable ischaemic ventricular tachycardia
- Severe aortic regurgitation
- Abdominal or aortic aneurysm
- Severe aorto-iliac disease or peripheral vascular disease
Management
The left ventricular filling volume should be optimised, and in the absence of pulmonary congestion a saline fluid challenge of at least 250 ml should be administered over 10 minutes. Adequate oxygenation is crucial, and intubation or ventilation should be used early if gas exchange abnormalities are present. Ongoing hypotension induces respiratory muscle failure, and this is prevented with mechanical ventilation. Antithrombotic treatment (aspirin and intravenous heparin) is appropriate.Supporting systemic blood pressure
Blood pressure support maintains perfusion of vital organs and slows or reverses the metabolic effects of organ hypoperfusion. Inotropes stimulate myocardial function and increase vascular tone, allowing perfusion pressures to increase. Intra-aortic balloon pump counterpulsation often has a dramatic effect on systemic blood pressure. Inflation occurs in early diastole, greatly increasing aortic diastolic pressure to levels above aortic systolic pressure. In addition, balloon deflation during the start of systole reduces the aortic pressure, thereby decreasing myocardial oxygen demand and forward resistance (afterload).Reperfusion
Although inotropic drugs and mechanical support increase systemic blood pressure, these measures are temporary and have no effect on long term survival unless they are combined with coronary artery recanalisation and myocardial reperfusion.Thrombolysis is currently the commonest form of treatment for myocardial infarction. However, successful fibrinolysis probably depends on drug delivery to the clot, and as blood pressure falls, so reperfusion becomes less likely. One study (GISSI) showed that, in patients with cardiogenic shock, streptokinase conferred no benefit compared with placebo.
The GUSTO-I investigators examined data on 2200 patients who either presented with cardiogenic shock or who developed it after enrolment and survived for at least an hour after its onset. Thirty day mortality was considerably less in those undergoing early angiography (38%) than in patients with late or no angiography (62%). Further analysis suggested that early angiography was independently associated with a 43% reduction in 30 day mortality.
In the SHOCK trial, patients with cardiogenic shock were treated aggressively with inotropic drugs, intra-aortic balloon pump counterpulsation, and thrombolytic drugs. Patients were also randomised to either coronary angiography plus percutaneous intervention or bypass surgery within six hours, or medical stabilisation (with revascularisation only permitted after 54 hours). Although the 30 day primary end point did not achieve statistical significance, the death rates progressively diverged, and by 12 months the early revascularisation group showed a significant mortality benefit (55%) compared with the medical stabilisation group (70%). The greatest benefit was seen in those aged < 75 years and those treated early ( < 6 hours). Given an absolute risk reduction of 15% at 12 months, one life would be saved for only seven patients treated by aggressive, early revascularisation.
Support and reperfusion: impact on survival
Over the past 10 years, specific measures to improve blood pressure and restore arterial perfusion have been instituted. Mortality data collected since the 1970s show a significant fall in mortality in the 1990s corresponding with increased use of combinations of thrombolytic drugs, the intra-aortic balloon pump, and coronary angiography with revascularisation by either percutaneous intervention or bypass surgery. Before these measures, death rates of 80% were consistently observed.Cardiogenic shock is the commonest cause of death in acute myocardial infarction. Although thrombolysis can be attempted with inotropic support or augmentation of blood pressure with the intra-aortic balloon pump, the greatest mortality benefit is seen after urgent coronary angiography and revascularisation. Cardiogenic shock is a catheter laboratory emergency.
Names of trials
cardiogenic shock