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Cardiovascular Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Cyanosis is a blue discoloration of skin and mucous membranes. It can either be central (with a blue tongue) caused by heart and lung disease, or peripheral because of poor peripheral perfusion.
Paper 2
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
Truncus arteriosus is due to a failure of the normal division of the primitive truncus arteriosus into the aorta and pulmonary artery. A single vessel leaves the heart giving rise to the pulmonary, coronary and systemic arteries. The condition causes cyanosis and cardiac failure. Chest radiograph commonly demonstrates cardiomegaly, pulmonary plethora and forked ribs. The aortic arch is right-sided in around a third of cases.
The patient with acute respiratory problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
If nursed in a level 1 area of care, ongoing monitoring of the patient during non-invasive ventilation remains very important, and the following parameters must be monitored: Heart rate and respiratory rate.Blood pressure.Oxygen saturation.Cardiac monitoring, where necessary.Degree of respiratory distress.Accessory muscle use.Presence of cyanosis.Orientation.Risk of aspiration.
Fatal Sodium Nitrite Poisoning: Key Considerations for Prehospital Providers
Published in Prehospital Emergency Care, 2021
Matthew R. Neth, Jennifer S. Love, B. Zane Horowitz, Michael D. Shertz, Ritu Sahni, Mohamud R. Daya
During a normal physiologic state, methemoglobin levels are less than 1% (31). This steady state is primarily achieved through the enzymatic action of cytochrome-b5 reductase, which reduces methemoglobin back to functional hemoglobin (31). Methemoglobinemia can develop when the body is exposed to an oxidant stress and reduction though cytochrome-b5 reductase is overwhelmed (31,32). Cyanosis, the blue discoloration of the skin, is ordinarily apparent to an observer when deoxygenated hemoglobin represents 15% of the available hemoglobin. However, in methemoglobinemia, only 5% of the abnormal hemoglobin is needed for the patient to appear cyanotic. At lower concentrations, the patient is generally not truly hypoxic. However, the pulse oximeter will misread the abnormal hemoglobin and give a reading of 85%, which will not change despite supplemental oxygen. As methemoglobin concentrations rise above 30%, other symptoms appear that are related to inadequate oxygen delivery to the central nervous system (headache, lightheadedness, confusion, seizure, coma, death) and the heart (dysrhythmias, hypotension, pulseless electrical activity). These progressively worsen with increasing concentrations (8–10).
Preventing disease progression in Eisenmenger syndrome
Published in Expert Review of Cardiovascular Therapy, 2021
Ana Barradas-Pires, Andrew Constantine, Konstantinos Dimopoulos
Most contemporary patients with large post-tricuspid shunts and PVD leading to ES are diagnosed in infancy and early childhood, even though the full ES phenotype (with cyanosis at rest) may not become obvious until the second decade of life. Few undiagnosed cases present late with complications of disease, such as arrhythmia, bleeding or thromboembolism, triggered by a stressor, for example, pregnancy or infection. The symptoms of PAH are rather nonspecific, e.g. fatigue, dizziness, chest pain, shortness of breath or syncope. In ES, central cyanosis due to desaturated blood entering the systemic circulation and clubbing are the key clinical signs. Clubbing and low oxygen saturations might only be present in the toes (differential cyanosis and clubbing) in patients with ES due to a PDA: deoxygenated blood enters the aorta through the PDA at or after the origin of the left subclavian artery. ES should also be suspected in patients with exercise intolerance and unexplained erythrocytosis, in whom the central cyanosis may not be obvious.
Pulmonary arteriovenous malformation revealed by a chronic cyanosis
Published in Acta Cardiologica, 2019
Martial M. Massin, Marc Laureys, Nasroolla Damry
An eight-year-old female presented with a history of intermittent acrocyanosis and progressive effort dyspnoea. Family and personal history was otherwise uneventful. Clinical examination showed central cyanosis and oxygen saturation was 80%. Echocardiogram was normal. Chest X-ray showed opacities in the right lower and upper lobes (Figure 1(A)). Chest computed tomography revealed major pulmonary arteriovenous malformations in the right lung (Figure 2) and minor lesions in the left lung. The patient did not fulfil the Curaçao criteria for hereditary haemorrhagic telangiectasia but the disease was confirmed by genetic analysis which revealed a mutation in endoglin, a major gene encoding endothelial surface proteins. Coils were used for the embolisation of the main lesions (Figure 1(B)) and oxygen saturation improved to 96%. Three years later, oxygen saturation was 90% and control CT showed partial reperfusion of the same lesions that required a second procedure.