| Keywords [eng] |
cardiogenic shock (CS), acute myocardial infarction cardiogenic shock (AMI- CS), heart failure cardiogenic shock (HF-CS), mechanical circulatory support (MCS), hemodynamic instability, prognosis of cardiogenic shock, risk stratification, early diagnosis, vasopressors and inotropes, percutaneous coronary intervention (PCI), extracorporeal membrane oxygenation (ECMO) |
| Abstract [eng] |
Background. Cardiogenic shock (CS) is a clinical syndrome characterized by clinical and biochemical signs of tissue hypoperfusion resulting from reduced cardiac output (CO), possibly causing multi-organ dysfunction and death. The occurrence of CS varies according to its definition and clinical situation. 2-5% of patients with acute heart failure (HF) develop CS, but the most frequent cause is ventricular failure after acute myocardial infarction (AMI). The diagnosis is based on presenting clinical signs of hypoperfusion, such as oliguria, cold extremities and narrow pulse pressure. Other typical clinical features include biochemical signs of hypoperfusion, including elevated serum creatinine, metabolic acidosis and elevated serum lactate. Hypotension (systolic blood pressure (SBP) <90 mmHg) is often the first clinical manifestation of CS but not present in all patients since BP could be maintained by compensatory vasoconstriction leading to impaired tissue perfusion and oxygenation. CS is described by five stages in The Society for Cardiovascular Angiography and Interventions classification (SCAI). This includes patients at risk of developing CS (stage A), pre-shock (stage B), to severe state of shock (stages C, D and E). The prognosis of CS is extremely poor with in-hospital mortality ranging from 30% to 60%, despite advances in the management of CS. The key features of CS management include immediate stabilization in intensive care unit (ICU), recognition and treatment of the underlying cause, possible initiation of mechanical circulatory support (MCS) and correction of end-organ hypoperfusion to prevent or reverse organ failure. Materials and methods. A review based on scientific literature was conducted using the international database PubMed, Scopus, Google Scholar and the guidelines of European Society of Cardiology (ESC). All articles used in the review are published during the last 10 years. Study types involved in the review include RCTs, meta-analyses and cohort studies. Clinical case description. The patient presented with dyspnea, general weakness, and chest pain. The patient had been diagnosed with pulmonary arterial hypertension (PAH), hyperlipidemia and hypertension. The patient was brought to the emergency room in Utena hospital and diagnosed with AMI. TnI was highly elevated and ECG presented with STEMI. The chest x-ray showed signs of HF. Echo presented signs of ischemic myocardial damage of all left ventricle (LV) walls, significantly reduced left ventricle ejection fraction (LVEF), functional leakage of the mitral valve (MV) and tricuspid valve (TV). The patient developed CS and signs of multiple organ failure. The patient was sedated in the ICU and extracorporeal membrane oxygenation (ECMO) was initiated, but there were no signs of improvement. The patient deteriorated and resuscitation was initiated without success. Death was confirmed. Discussion, conclusions and recommendations. This clinical case emphasizes the importance of early recognition of patients at risk of developing CS. Inspection for signs of tissue perfusion and volume status assessment should be included in the initial evaluation of all patients presenting with suspicion of shock. Invasive hemodynamic monitoring methods, such as pulmonary artery catheterization (PAC) may be performed in critically ill patients to establish a diagnosis of shock, differentiate causes of shock, assess volume status and assist with therapy. Early management of CS focuses on immediate cardiopulmonary stabilization, reversing the underlying cause and restoring the end-organ perfusion. Early initiation of MCS should be considered in eligible patients and when there are no contraindications. However, further research is required to improve current guidelines on optimal management approaches, particularly regarding effectiveness of different MCS devices and early identification of patients who are eligible for MCS therapy. |
