The patient with acute cardiovascular problems
Peate Ian, Dutton Helen in Acute Nursing Care, 2020
Acute coronary syndrome (ACS) (see Figure 6.23) is an umbrella term encompassing a spectrum of clinical presentations all caused by the same disease process, resulting in clot formation in the coronary arterial blood supply. This is triggered by the erosion or rupture of a fibrous plaque, disrupting coronary arterial blood flow to the myocardium. Myocardial injury and/or death is a medical emergency and results from flow disruption. These clinical presentations can be categorised as: Unstable angina, ischaemic pain without myocardial death.Non-ST segment elevation myocardial infarction (NSTEMI).ST segment elevation myocardial infarction (STEMI).
PCI post-thrombolysis
K Sarat Chandra, AJ Swamy in Acute Coronary Syndromes, 2020
ST-elevation myocardial infarction (STEMI) is a medical emergency and timely revascularisation is essential for reducing the infarct size and improving short-term and long-term outcomes. Thrombolysis and primary percutaneous coronary intervention (PCI) are the two most commonly used strategies to achieve timely reperfusion. Evidence from many trials underlines the superiority of primary PCI over thrombolysis in the management of ST-elevation myocardial infarction (STEMI) [1]. Primary PCI is superior to thrombolysis strategy in reducing myocardial ischaemia, reinfarction, death, intracranial bleeding and re-occlusion of the infarct-related artery in STEMI patients irrespective of the patient's risk or whether inter-hospital transfer for PCI is required [1]. As compared to thrombolysis, PCI is able to preserve the myocardium and improve clinical outcomes over a wider window period following symptom onset and is the treatment of choice for patients who present early or late after symptom onset.
Electrocardiography and arrhythmias
Neil Herring, David J. Paterson in Levick's Introduction to Cardiovascular Physiology, 2018
By contrast, a large ST-elevation myocardial infarction is caused by acute atherosclerotic plaque rupture, thrombus formation and complete occlusion of one of the main epicar dial coronary arteries (Figure 5.11b). This can be treated by emergency revascularization using a catheter and injection of dye (angiography) to identify the blockage, and passing a wire through the blockage and inflating a small balloon on the wire (angioplasty) surrounded by an expandable metal frame known as a stent. This is known as primary percutaneous coronary intervention and is indicated within 12 hours of the onset of pain if ST elevation occurs in 2 or more contiguous leads (>2 mm in the chest leads or >1 mm in the limb leads), or a new left bundle branch block develops, to minimize the amount of subsequent myocardial damage. This has been shown to improve morbidity and mortality in randomized clinical trials. If a large enough volume of ventricular tissue is infarcted, then broad, deep negative deflections in the ECG, known as Q waves, can develop over the subsequent days and remain permanently. These may represent endo-to-epicardial activation in the wall opposite to the scar ‘window', becoming more prominent in some ECG leads.
Brugada syndrome and the story of Dave
Published in Neuropsychological Rehabilitation, 2018
Samira Kashinath Dhamapurkar, Barbara A Wilson, Anita Rose, Gerhard Florschutz
There are several abnormal ECG patterns that identify BrS including a heart block affecting the right ventricle so that it is not directly activated by impulses travelling through the right bundle branch (known as the right bundle branch block). ST-segment elevations noted in leads v1–v3, prolonged PR and negative T wave may also indicate BrS (Brugada, 2016). This segment is part of the ECG. An ST segment elevation myocardial infarction (STEMI) is the name for one type of heart attack that arises from an acute interruption of blood supply to a part of the heart. Initially, it was believed that people with BrS had a structurally normal heart but this has been challenged (Frustaci et al., 2005) and the syndrome can also occur as a consequence of subtle structural changes in the right ventricular outflow tract (Antzelevitch, Brugada, Brugada, & Brugada, 2005; Nademanee et al., 2011). Other terms for this syndrome include sudden unexplained death syndrome; sudden unexplained nocturnal death syndrome and sudden arrhythmic death syndrome (Nademanee et al., 1997; Vatta et al., 2002). Symptoms vary from palpitations and giddiness to recurrent fainting, nocturnal agonal respiration (breathing with short, sporadic gasps) and sudden cardiac death (Antzelevitch & Patocskai, 2016; Wilde et al., 2002). The condition is accountable for 4% of all sudden deaths and 20% of sudden deaths reported to be in those without structural heart disease (Vohra & Rajagopalan, 2015). A family history is present in about 20 to 30% of patients.
Prehospital ST-Segment Elevation Myocardial Infarction (STEMI) in Queensland, Australia: Findings from 11 Years of the Statewide Prehospital Reperfusion Strategy
Published in Prehospital Emergency Care, 2020
Tan N. Doan, Brendan V. Schultz, Stephen Rashford, Brett Rogers, Marcus Prior, William Vollbon, Emma Bosley
ST-segment elevation myocardial infarction (STEMI) is a life-threatening medical emergency, and its prognosis is highly dependent on reperfusion times (1, 2). STEMI survival and long-term outcomes are improved when delays in reperfusion are minimal (1, 2). Treatment strategies aim to shorten reperfusion times as much as possible. Reperfusion treatment times within 90 minutes after STEMI diagnosis for pPCI and 30 minutes for fibrinolysis are widely adopted standards recommended by international guidelines (1–3). These figures have traditionally been used as key performance indicators for hospitals. However, it has been shown that these targets are ambitious and currently achieved in less than half of STEMI patients internationally (4–6). Accordingly, research has focused on strategies for reducing reperfusion times.
Citrate pretreatment attenuates hypoxia/reoxygenation-induced cardiomyocyte injury via regulating microRNA-142-3p/Rac1 aix
Published in Journal of Receptors and Signal Transduction, 2020
Haiyan Xiang, Juesheng Yang, Jin Li, Linhui Yuan, Fei Lu, Chen Liu, Yanhua Tang
In recent years, with the change of people’s lifestyle and dietary structure, the incidence of coronary atherosclerosis and heart disease is on the rise and tends to be younger [1]. Among them, acute ST-segment elevation myocardial infarction is the most serious clinical manifestation of coronary heart disease [2]. Recovering myocardial perfusion as early as possible is the most effective measure to resolve acute coronary heart disease. The wide application of powerful new technologies such as coronary artery bypass grafting and percutaneous coronary intervention has rapidly restored the blocked coronary artery perfusion, saved the dying myocardial cells, and significantly improved the clinical therapeutic effect [3]. However, myocardial injury induced by reperfusion itself, namely, myocardial ischemia reperfusion injury, has become a bottleneck restricting the treatment of coronary heart disease. How to effectively prevent and treat myocardial ischemia reperfusion injury has become one of the most important problems to be solved in clinical cardiovascular work [4].
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