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Coronary steal syndrome
Peripheral artery disease
Subclavian steal syndrome
Renal artery stenosis
Coarctation of the aorta
Polycystic kidney disease
Chronic venous insufficiency
Deep vein thrombosis
Human herpesvirus 8 (Kaposi sarcoma)
Transposition of the great vessels
Total anomalous pulmonary venous return
Tetralogy of Fallot
Hypoplastic left heart syndrome
Patent ductus arteriosus
Ventricular septal defect
Coarctation of the aorta
Atrial septal defect
Premature atrial contraction
Atrioventricular nodal reentrant tachycardia (AVNRT)
Premature ventricular contraction
Long QT syndrome and Torsade de pointes
Bundle branch block
Pulseless electrical activity
Tricuspid valve disease
Pulmonary valve disease
Mitral valve disease
Aortic valve disease
Rheumatic heart disease
Pericarditis and pericardial effusion
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
0 / 13 complete
0 / 2 complete
β -blockers for p. 329
ECG tracing of p. 300
potassium channel blockers for p. 329
Tanner Marshall, MSVincent Waldman, PhD
The heart has four chambers, two upper chambers—the left and right atrium, or together the atria, and two lower chambers—the left and right ventricles.
Atrial flutter is used to describe when the atria contract at really high rates—about 300 beats per minute, but sometimes as high as 400 beats per minute. Why flutter?
Well there’s a wave of muscle contraction that flows through the atria that looks like its flapping or fluttering, hence the name.
Normally, an electrical signal is sent out from the sinus node in the right atrium, but then propagates out through both atria super fast, causing the atria to contract.
Usually, that signal moves in one direction from the atria to the ventricles through the AV node, it then moves down to the ventricles, and causes them to contract shortly after.
After each ventricular contraction, the ventricle has to wait for another signal from the sinus node. With atrial flutter, a reentrant rhythm starts in either the right or left atrium.
Reentrant signals loop back on themselves, overriding the sinus node and setting up an endless cycle that causes the atria to contract again and again and again—at really fast rates.
There are actually two types, type 1 or typical atrial flutter is more common and is caused by a single reentrant circuit that moves around the annulus, or the ring of the tricuspid valve of the right atrium, usually in a counterclockwise direction when viewed looking up through the tricuspid valve.
Ok so imagine you’re this eyeball looking up through the valve, you’ll see the superior vena cava or SVC, the inferior vena cava or IVC, and the coronary sinus, or CS.
In this case, a stretch of tissue along the pathway called the cavotricuspid isthmus propagates the signal more slowly than the surrounding tissue.
Tissue that was just activated can’t be activated again until a certain amount of time has passed, which is called the refractory period; so that slow propagation gives the tissue enough time to be out of refractory, and therefore the circuit can loop on itself.
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