1
Basic
Acute coronary syndrome: A group of clinical syndromes caused by acute myocardial ischemia, including unstable angina, non-ST-segment elevation myocardial infarction, and ST-segment elevation myocardial infarction.
Syndrome X: Patients with angina pectoris or angina-like symptoms and no abnormalities on coronary angiography with ST-segment shift on exercise plate test.
These patients account for 10% to 30% of all patients who undergo coronary angiography for chest pain. The etiology of this disease is unknown and may be related to endothelial abnormalities and microvascular dysfunction.
Atrial fibrillation triad: first heart sound of unequal intensity, absolute arrhythmia, and pulse dystocia.
Beck’s triad: a clinical feature of cardiac tamponade, characterized by hypotension, weak heart sounds, and jugular venous anger.
Ewart’s sign: a sign of pericardial effusion with distant heart sounds, a turbid sound under the left scapula and bronchial breath sounds in the left lung.
Kussmaul’s sign: a characteristic sign of constrictive pericarditis. Jugular venous dilatation is more pronounced during inspiration.
Aortic stenosis triad: Patients with aortic stenosis have a long asymptomatic period until the orifice area ≤ 1.0 cm2 becomes symptomatic. Dyspnea, angina, and syncope are typical of the common triad of aortic stenosis.
De Musset (nodding) sign: aortic valve closure insufficiency with nodding in response to heartbeat.
Traube sign: aortic valve insufficiency with femoral artery gunshot sound.
Duroziez sign: aortic valve insufficiency with a two-phase murmur heard in the femoral artery.
Tetralogy of Fallot: A combined congenital cardiovascular anomaly that includes four anomalies: pulmonary stenosis, ventricular septal defect, right aortic position (aorta riding over the defective septum), and right ventricular hypertrophy.
Embolic 5P sign: In the case of arterial embolism or thrombosis of the limb, the characteristic manifestation is persistent pain (Pain), accompanied by signs and symptoms such as pallor, pulselessness, abnormal sensation (Paresthesia) and dyskinesia (Paralysis) of the affected limb.
Pulmonary chorea: Also known as “pulmonary pulsation”. Pulmonary artery and its branches are obviously dilated and thickened, the pulmonary valve is relatively incompetent to close, and the pulmonary artery and the hilar vessels are obviously dilated during ventricular contraction, and the pulsation is obvious under X-ray fluoroscopy.
Pulmonary hilar butterfly sign: Also known as butterfly wing sign. It is a description of alveolar pulmonary edema on X-ray. The distribution and morphology of alveolar solid shadows are central, showing a large patchy shadow symmetrically distributed in the middle and inner bands of both lungs, with a higher density in the hilar region, shaped like a butterfly wing. It is commonly seen in chronic heart failure.
2
Advanced
Dewinter syndrome: The electrocardiogram manifests as follows.
① J-point depression in chest V₁~₆ leads of 1~3 mm, ST-segment is upward-sloping downward, followed by symmetrical hyperacute T-wave.
② QRS waves are usually not wide or mildly widened.
(3) Some patients have poor R-wave rise in the anterior chest leads.
④ Most patients have mild ST-segment elevation in the aVR leads. It is a manifestation of ACS.
Wellens syndrome: The electrocardiographic manifestations are as follows.
(1) The characteristic changes of T wave mainly appear in the anterior chest leads, mainly in V₂~₃ leads, sometimes it can be extended to V₁~₆ leads, and in a few cases, there are also characteristic changes in Ⅱ, Ⅲ and aVF leads.
(ii) Decrease or disappearance of the amplitude of the original abnormal Q wave or R wave.
(iii) Shift or mild elevation (< 0.1 mV) of the original ST segment.
(4) The dynamic evolution of symmetrical deep inversion or bidirectional T waves after angina relief, followed by a gradual shift to upright, lasting from a few hours to several weeks.
⑤ The characteristic T-wave changes described above can be repeated after another episode of angina pectoris.
Heartbreak syndrome (heartbreak syndrome/apical balloon-like syndrome): also known as octopus pot cardiomyopathy, stress cardiomyopathy.
The clinical presentation is sudden onset of retrosternal pain with elevated or depressed ECG ST-segment with or without T-wave inversion after a sharp emotional or psychological stimulus. Stenosis is not present on coronary angiography. Impaired left ventricular function with ventriculography or echocardiography showing mid-ventricular and apical dilatation. The clinical course is transient.
A-S syndrome: Adams-Stokes syndrome, also known as cardiogenic ischemic syndrome. It refers to a sudden onset of severe, fatal slow or rapid arrhythmia that causes a sharp decrease in cardiac output over a short period of Time, producing symptoms such as severe cerebral ischemia, loss of consciousness, and syncope.
A-S syndrome is a group of clinical syndromes in which acute ischemic attacks are caused by sudden changes in heart rate. The syndrome is not associated with postural changes and often causes syncope due to sudden and severe tachycardia or bradycardia.
Pre-excitation syndrome: A syndrome in which some of the atrial excitation is transmitted down a congenital additional channel (bypass) outside the normal atrioventricular conduction system, causing pre-excitation (pre-excitation) of a part of the ventricular myocardium, resulting in abnormal cardiac electrophysiology and/or multiple tachyarrhythmias.
The Kent bundle-induced ventricular preexcitation with tachyarrhythmias is called classic preexcitation syndrome, also known as WPW syndrome.
Morbid sinus node syndrome: This is a combination of sinus node lesions leading to hypofunction and multiple arrhythmias. Patients may have more than one arrhythmia at different times, often combined with abnormal atrial autoregulation and, in some cases, with atrioventricular conduction dysfunction.
Slow-fast syndrome: Bradycardia-tachycardia syndrome, also known as slow-fast syndrome, is a subtype of sick sinus node syndrome and is the most common and typical manifestation of this syndrome.
It is characterized by bradycardia, which is a disorder of sinus node excitation or sinus impulse transmission to the atria, causing a slow sinus rhythm (sinus block or sinus arrest), which is accompanied by tachyarrhythmia. Occasionally, rapid ventricular arrhythmias occur, with paroxysmal atrial fibrillation being the most common.
Fast-slow syndrome: Patients with preexcitation syndrome or paroxysmal atrial fibrillation without organic heart disease and normal sinus node function have severe sinus bradycardia, sinus block, sinus arrest and other slow arrhythmias when termination of tachyarrhythmia occurs, which can cause transient acute cerebral ischemia, syncope, A-Syndrome attack, and even sudden death, called fast-slow syndrome.
Some scholars call it pseudosinus syndrome, which is a primary fast atrial arrhythmia leading to secondary transient sinus node dysfunction.
Long QT interval syndrome: The majority of these syndromes are inherited ion channel abnormalities caused by mutations in one or more genes. The clinical manifestation is recurrent syncope and sudden death due to tip-twist ventricular tachycardia.
Short QT interval syndrome: an autosomal dominant ion channel disorder caused by a single mutation. Clinical manifestations include palpitations, dizziness, and recurrent syncope and/or sudden cardiac death.
Early repolarization syndrome: a type of cardiac repolarization abnormality, which is a physiological ECG variant. Early repolarization is manifested when there are 2 or more consecutive inferior and/or lateral wall leads with J-point elevation ≥ 1 mm on the ECG; when accompanied by ventricular tachycardia, it is considered early repolarization syndrome.
Brugada syndrome: Mutations in the sodium and calcium channels have been identified in familial Brugada syndrome.
It presents clinically as recurrent syncope and is one of the leading causes of sudden death in young and middle-aged people with nonorganic heart disease. The cardiac structure is normal and the electrocardiogram shows a downward sloping or saddle elevation of the ST segment in V₁~₃ leads.
Pacemaker syndrome: It refers to a group of clinical syndromes caused by abnormal hemodynamics and electrophysiology after pacemaker implantation. The main manifestations are neurological symptoms, low cardiac output and congestive heart failure, with syncope occurring in approximately 38% of cases.
Eisenmenger syndrome: Strictly speaking, it cannot be called congenital heart disease, but is a group of consequences of the development of congenital heart disease. If a congenital ventricular septal defect persists, pulmonary hypertension develops progressively, the original left-to-right shunt becomes a right-to-left shunt, and when it progresses from no cyanosis to cyanosis, it is called Eisenmenger syndrome.
Marfan syndrome: It is an autosomal dominant connective tissue disorder with familial aggregation and is also often referred to as Marfan syndrome. The disease can affect connective tissue throughout the body, including eye, cardiovascular and skeletal muscle lesions, which are the most common sites of damage, and can also lead to pulmonary, cutaneous and central nervous system involvement.
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