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Cardiovascular Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Sinus tachycardia is defined as a sinus rate of more than 100 beats/min. It is usually secondary to other causes (Table 7.13). Rarely, a primary sinus tachycardia can result from a sinus node re-entry mechanism.
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Sinus tachycardia is a regular heart beat that originates from the sinoatrial node, but at a rate faster than 100 beats per minute (please see Figure 6.27). The resting heart rate will not normally be above 100 beats per minute, so the patient should be carefully assessed to determine the cause of the tachycardia. Sinus tachycardia is non-paroxysmal, that is, it doesn’t start or end abruptly, which is a feature of other tachy-arrhythmias. It would seem logical that an increased heart rate would always improve cardiac output and tissue perfusion, but this is not always the case. You may remember that the heart spends a larger proportion of the cardiac cycle in diastole, the filling phase. As the heart rate increases, it is the diastolic phase which shortens, and as the rate moves towards 140, the time for ventricular filling significantly reduces, so cardiac output may fall. Shortened diastole can also lead to a reduction in coronary artery blood flow, resulting in angina, increasing areas of myocardial ischaemia and infarction as the oxygen supply cannot meet the demand of the rapidly contracting myocardium. Ensuring that the patient is not hypoxaemic and is adequately filled, or not dehydrated, is a good starting point.
Arrhythmias in acute coronary syndrome
Published in K Sarat Chandra, AJ Swamy, Acute Coronary Syndromes, 2020
This rhythm is a poor prognostic marker as it may denote heart failure, persistent angina or hypotension. It can precipitate heart failure by increasing myocardial oxygen demand. The treatment is correction of primary causes which lead to sinus tachycardia. Beta-blockers are the most effective drugs. In patients with contraindications to beta-blockers, ivabradine may be useful for persisting sinus tachycardia despite correction of primary causes.
“Popper” induced methemoglobinemia
Published in Baylor University Medical Center Proceedings, 2022
Fares Elgendy, Gaspar Del Rio-Pertuz, Dalena Nguyen, Drew Payne
During the first medical assessment, the patient was anxious-appearing, alert, and oriented, moving all extremities normally, and had prominent cyanosis of his lips and bilateral palms (Figure 1a). Vital signs included a blood pressure of 128/95 mm Hg, a heart rate of 120 beats/min, a respiratory rate of 20 breaths/min, a temperature of 98°F, and an oxygen saturation of 88% measured by pulse oximetry. The remainder of the physical exam was unremarkable. Electrocardiogram revealed sinus tachycardia. Arterial blood gas (ABG) analysis on 6 L nasal cannula showed a pH of 7.51, partial pressure of carbon dioxide of 14 mm Hg, partial pressure of oxygen of 179 mm Hg, bicarbonate of 12 mmol/L, and methemoglobin of 19.8%. A urine toxicology screen was negative. Oxygen supplementation was started via nasal cannula of up to 6 L with no improvement of oxygen saturation.
Intractable cardiac inflammatory myofibroblastic tumour causing refractory right heart failure: a case report
Published in Acta Cardiologica, 2020
Irfan Veysel Duzen, Yasemin Akca, Hale Colakoglu, Mehmet Adnan Celkan, Mert Deniz Savcilioglu, Enes Alıc, Ugur Sener, Murat Sucu
A 37-year-old male patient was referred to our clinic due to refractory right-sided heart failure. Physical examination showed generalised oedema in lower extremities bilaterally, ascites and hepatomegaly. Electrocardiography showed sinus tachycardia. A confluencing tumour-like mass occupying the right atrium and ventricle with restricted motion of the tricuspid valve and pulmonary valve was observed on echocardiography (Figure 1). CT scan confirmed the heterogeneous mass involving the lateral wall of the right atrium, tricuspid valve up to the right ventricle that caused obstruction at both tricuspid and pulmonary artery levels (Figure 2). He was referred to cardiovascular surgery. During surgery, incomplete resection of the tumour tissue could be achieved which was attached to the heart, totally occluding the tricuspid valve (Figure 3). He was admitted to the intensive care unit and died postoperatively due to right ventricular dysfunction, hypotension and cardiogenic shock. Histological examination of the tumour sample demonstrated a lesion which was partly attached to the striated muscle fibres and partly invading the striated muscle cells and composed of many chronic active inflammatory cells and spindle cells with oval nuclei and distinct nucleoli, rich in inflammatory cells embedded in a myxoid matrix (Figure 4). Obvious pleomorphism, atypical mitosis and necrosis were absent. Immunohistochemical staining revealed positive staining with smooth muscle actin and vimentin. A cardiac inflammatory myofibroblastic tumour (IMFT) was diagnosed based on these findings.
Acute myocardial infarction triggered by use of synthetic cannabis
Published in Baylor University Medical Center Proceedings, 2018
Brooke Mills, Emma Dishner, Carlos E. Velasco
SCBs are associated with cardiovascular toxicity. The most common cardiovascular effect is sinus tachycardia, often in conjunction with hypertension, as seen in our patient.3,6 These illicit drugs have also been associated with myocardial infarction. In 2011, there were four reported cases of STEMIs in 16-year-old boys after K2 use.4,5 The subjects of these cases were young teenagers without other cardiovascular risk factors or past medical history. All of the above cases that underwent coronary angiography showed no evidence of coronary artery disease; therefore, their myocardial infarctions were attributed to coronary vasospasm related to SCB use rather than occlusive disease. To our knowledge, this is the first case that describes significant coronary artery disease following the use of SCBs.