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Pathology
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Atrial fibrillation
Atrial flutter
Atrioventricular nodal reentrant tachycardia (AVNRT)
Premature atrial contraction
Wolff-Parkinson-White syndrome
Brugada syndrome
Long QT syndrome and Torsade de pointes
Premature ventricular contraction
Ventricular fibrillation
Ventricular tachycardia
Cardiac tumors
Shock
Arterial disease
Aneurysms
Aortic dissection
Angina pectoris
Coronary steal syndrome
Myocardial infarction
Prinzmetal angina
Stable angina
Unstable angina
Abetalipoproteinemia
Familial hypercholesterolemia
Hyperlipidemia
Hypertriglyceridemia
Coarctation of the aorta
Conn syndrome
Cushing syndrome
Hypertension
Hypertensive emergency
Pheochromocytoma
Polycystic kidney disease
Renal artery stenosis
Hypotension
Orthostatic hypotension
Lymphangioma
Lymphedema
Peripheral artery disease
Subclavian steal syndrome
Nutcracker syndrome
Superior mesenteric artery syndrome
Angiosarcomas
Human herpesvirus 8 (Kaposi sarcoma)
Vascular tumors
Behcet's disease
Kawasaki disease
Vasculitis
Chronic venous insufficiency
Deep vein thrombosis
Thrombophlebitis
Acyanotic congenital heart defects: Pathology review
Aortic dissections and aneurysms: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Cardiac and vascular tumors: Pathology review
Cardiomyopathies: Pathology review
Coronary artery disease: Pathology review
Cyanotic congenital heart defects: Pathology review
Dyslipidemias: Pathology review
Endocarditis: Pathology review
Heart blocks: Pathology review
Heart failure: Pathology review
Hypertension: Pathology review
Pericardial disease: Pathology review
Peripheral artery disease: Pathology review
Shock: Pathology review
Supraventricular arrhythmias: Pathology review
Valvular heart disease: Pathology review
Vasculitis: Pathology review
Ventricular arrhythmias: Pathology review
Premature ventricular contraction
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The heart has two lower chambers, called the ventricles, so a premature ventricular contraction is when the ventricles contract earlier than normal in the cardiac cycle. This happens because an abnormal contraction signal, called a depolarization, originates from somewhere in the ventricles rather than coming from the pacemaker cells.
So, if we simplify this heart a little bit, normally, the sinoatrial node or SA node sends an electrical signal that propagates out through the walls of the heart and contracts both upper chambers. Then that signal moves to the atrioventricular node or AV node, where the signal is delayed for a split second, and then it goes down into the ventricles or lower chambers where it moves down the bundle of His and into the left and right bundle branches and into each ventricle’s Purkinje fibers, causing them to contract as well. So, in a healthy heart the upper chambers contract first, then shortly after, the lower chambers contract. On an electrocardiogram or ECG, which measures the electrical activity of the heart via electrodes that are placed on the skin, the atrial depolarization, and therefore its contraction, is seen as a p-wave; the ventricular contraction is seen as a QRS complex; and the ventricular repolarization, and therefore its relaxation, is seen as a T-wave.
This empty space here is called the PR segment, and it corresponds to the pause in the AV node, and this one is called the ST segment, and it corresponds to the interval between ventricular depolarization and repolarization, and this one is called the TP segment, which represents the heart’s quiet time when the cells are finished repolarizing and are ready for another signal.
Now, if we just look at the QRS complex, which normally lasts less than 100 milliseconds or 2-and-a-half little boxes, it’s usually made up of three smaller waves, also called deflections. If the first wave after the p-wave is downwards, or negative, it’s called a Q wave - which you can remember by the letter Q having a downward tail. If the next deflection is upward, or positive, then it’s called the R wave. If, though, the first wave after the p-wave is upwards, instead, or positive, you basically skip the Q and just call it an R wave. Finally, any downward deflection after the R wave is called the S wave.
Now, the interesting thing is that in addition to the pacemaker cells in the SA node, cells in the AV node, the Bundle of His, and the Purkinje fibers, all have the ability to generate an electrical potential. Those last three are called latent pacemakers, and they have slower depolarization rates—which is the rate at which they fire off electrical signals—and they get slower as you move further down. Let’s use this bar to visualize the SA node’s depolarization rate, which is the fastest, and then each one below is slightly slower. Notice that each time the SA node fires, it resets all the slower ones, and this is exactly how it works. If, for example, the SA node stopped altogether, then the AV node would take over at its slightly slower pace. Now, though, let’s say you have a ventricular ectopic focus somewhere in the ventricles, which is a cell or area of tissue that sends off an early depolarization wave, before even the SA node gets to fire. This is what leads to a premature ventricular contraction, or PVC.
Premature ventricular contractions are abnormal heartbeats that originate in the ventricles and show up as tall and wide QRS complexes on an ECG. They occur when an extra beat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node, the normal heartbeat initiator. PVCs are usually asymptomatic, but when they're a sign of an underlying disorder, treatment including a radiofrequency ablation may be necessary.
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