Cardiogenic Shock

Abstract

ardiogenic shock (CS) occurs in Ϸ5% to 8% of patients hospitalized with ST-elevation myocardial infarction (STEMI). Recent research has suggested that the peripheral vasculature and neurohormonal and cytokine systems play a role in the pathogenesis and persistence of CS. Early revascularization for CS improves survival substantially. New mechanical approaches to treatment are available, and clinical trials are feasible even in this high-risk population. Most importantly, hospital survivors have an excellent chance for long-term survival with good quality of life. This review will outline the causes, pathophysiology, and treatment of CS with a focus on CS complicating myocardial infarction (MI.) The case will be made for viewing CS as a serious disorder with a high early death rate, but one that is treatable and that, if approached aggressively, can result in full recovery. The diagnosis is usually made with the help of pulmonary artery (PA) catheterization; however, Doppler echocardiography may also be used to confirm elevation of LV filling pressures. 1 Hypoperfusion may be manifest clinically by cool extremities, decreased urine output, and/or alteration in mental status. Hemodynamic abnormalities form a spectrum that ranges from mild hypoperfusion to profound shock, and the short-term outcome is directly related to the severity of hemodynamic derangement. MI with LV failure remains the most common cause of CS. It is critical to exclude complicating factors that may cause shock in MI patients. Chief among these are the mechanical complications: ventricular septal rupture, contained free wall rupture, and papillary muscle rupture. Mechanical complications must be strongly suspected in patients with CS complicating nonanterior MI, particularly a first MI. Echocardiography is the technique of choice to rule out these entities and should be performed early unless the diagnosis is extensive anterior MI and the patient is undergoing prompt percutaneous coronary intervention (PCI). In addition, the detection of valvular disease before angiography may alter the revascularization approach. Diagnosis and CausesHemorrhage, infection, and/or bowel ischemia may contribute to shock in the setting of MI. As with mechanical complications, a high index of suspicion is required to make these diagnoses in MI patients, and survival may depend on timely recognition and treatment.Any cause of acute, severe LV or RV dysfunction may lead to CS. Acute myopericarditis, tako-tsubo cardiomyopathy, and hypertrophic cardiomyopathy may all present with ST elevation, release of cardiac markers, and shock in the absence of significant coronary artery disease. Stress-induced cardiomyopathy, also known as apical ballooning or takotsubo cardiomyopathy, is a syndrome of acute LV dysfunction after emotional or respiratory distress that leads to CS in 4.2% of cases. 2 Acute valvular regurgitation, typically caused by endocarditis or chordal rupture due to trauma or degenerative disease, may also cause CS. Aortic dissection may lead to CS via acute,...

Ten‐Year (2001–2011) Trends in the Incidence Rates and Short‐Term Outcomes of Early Versus Late Onset Cardiogenic Shock After Hospitalization for Acute Myocardial Infarction

“…Previous studies have suggested that the declining trend in mortality associated with CS complicating AMI was mainly attributed to the early and aggressive use of evidence‐based medications and coronary interventions, including the use of balloon pumps 7, 8, 9, 10, 11, 25, 26, 28, 35. However, a recent report from the National Cardiovascular Database Registry Cath‐PCI registry, which included more than 56 000 patients with CS complicating AMI who underwent a PCI within 24 hours from acute symptom onset, showed that the hospital death rate for this patient group increased between 2005–2006 (27.6%) and 2011–2013 (30.6%) 36.…”

Vascular phenotypes of acute decompensated vs. new‐onset heart failure: treatment implications

“…The Frank–Starling mechanism is limited to the venoconstriction‐based increase in the preload, because retention of sodium and water needs time to expand the volemia . The absence of cardiac remodelling exacerbates the reduction of CO even in patients with moderately reduced ejection fraction 25. The deficiency of these adaptive mechanisms can be amplified by inappropriate responses of the hypoperfused endothelium, such as overexpression of inducible nitric oxide synthase and inflammatory cytokines (tumour necrosis factor‐alpha and interleukin‐6)23, 26 that reduce catecholamine responsivity, decrease myocardial contractility, and further depress perfusion pressure.…”

“…The deficiency of these adaptive mechanisms can be amplified by inappropriate responses of the hypoperfused endothelium, such as overexpression of inducible nitric oxide synthase and inflammatory cytokines (tumour necrosis factor‐alpha and interleukin‐6)23, 26 that reduce catecholamine responsivity, decrease myocardial contractility, and further depress perfusion pressure. Consequently, many patients have impending or even cardiogenic shock8 with a vicious circle of ischaemia, hypotension, and myocardial dysfunction 25…”

Extracorporeal Membrane Oxygenation in Adults

“…Sljedeća najvažnija indikacija jest kardiogeni šok, bilo koje etiologije, koji perzistira unatoč odgovarajućoj nadoknadi intravaskularnog volumena, visokim dozama inotropnih lijekova i primjeni intraaortne balonske pumpe 18-20 . Kardiogeni je šok definiran srčanim indeksom < 2 L/min/m 2 i perzistirajućom hipotenzijom (sistolički tlak < 90 mmHg), unatoč normalnim ili povišenim tlakovima punjenja klijetki 21 . Mogući su uzroci akutna zbivanja poput velikog infarkta miokarda, fulminantnog miokarditisa ili pak masivne plućne tromboembolije s akutnim zatajivanjem desnoga srca.…”