Glossary

Premature Atrial Contraction (PAC) occurs when ectopic electrical cells in the atria begin to fire an electrical signal telling the muscle in the atria to contract before it’s supposed to, versus the electrical impulse normally received from the SA node.

ECG rhythm strip showing Premature Atrial Contraction (PAC).

Most times this premature signal is conducted through to the ventricles making it a full, perfusing heartbeat. Occasionally the premature atrial contraction does not result in a complete beat. Whether the contraction results in a complete, perfusing heartbeat or not, there is usually a “compensatory pause” or pause in electrical impulse generation, giving the heart a chance to reset itself electrically before the next beat. During this pause the heart continues to fill with blood, making the first beat after the pause stronger than normal because the heart is pushing a greater volume of blood during this contraction.

The entire episode of PAC, compensatory pause and the next, stronger beat is often described by patients as a skipped beat, flutter or heart stoppage followed by a “thud” or “thump.”

Premature atrial contractions occur in normal, disease-free hearts. Medical care is usually not required and the prognosis for most people with PACs is excellent.

Paroxysmal Atrial Tachycardia (PAT) consists of bouts of rapid, regular heart beating originating in the atrium (upper chamber of the heart).  Often due to abnormalities in the AV node “relay station” that lead to rapid firing of electrical impulses from the atrium which bypass the AV node under certain conditions.  These conditions include alcohol excess, stress, caffeine, overactive thyroid or excessive thyroid hormone intake, and certain drugs.

PAT is an example of an arrhythmia where the abnormality is in the electrical system of the heart, while the heart muscle and valves may be normal.

PAT is a form of tachycardia that begins and ends abruptly.  Though seldom life-threatening, paroxysmal atrial tachycardia produces annoying symptoms which can include lightheadedness, chest pain, anxiety, sweating and shortness of breath.

Postural orthostatic tachycardia syndrome (often referred to as just postural tachycardia syndrome or POTS) is a condition of dysautonomia, and more specifically, orthostatic inolerance, in which a change from the supine position to an upright position causes an abnormally large increase in heart rate, called tachycardia. This is often, but not always, accompanied by a fall in blood pressure. Several studies show a decrease in cerebral blood flow with systolic and diastolic CBF velocity decreased 44 and 60%, respectively.  Patients with POTS have problems maintaining homeostasis when changing position, i.e. moving from one chair to another or reaching above their heads. Many patients also experience symptoms when stationary or even while lying down.

Symptoms present in various degrees of severity depending on the patient. POTS is a serious, though non-life threatening, medical condition that can be severely disabling and debilitating. Some patients are unable to attend school or work, and especially severe cases can completely incapacitate the patient.

Paroxysmal Supraventricular Tachycardia (PSVT) is a rapid heart rate, which begins and ends suddenly (paroxysmal).  PSVT starts with events taking place above the ventricle.  Normally, the chambers of the heart (atria and ventricles) contract in a coordinated manner.  The contractions are caused by an electrical signal that begins in the sinoatrial node (also called the sinus node or SA node).  The signal is conducted through the atria (the upper chambers) and stimulates the atria to contract.

Paroxysmal supraventricular tachycardia can be initiated in the SA node, in the atria or the atrial conduction pathways,  or in the AV node.  It occurs most often in young people and infants.

To be able to understand the term pulseless electrical activity (PEA), it’s important to first recognize the difference between a tactile pulse and the indication of a heartbeat on an ECG tracing. Just because it appears that the heart is beating as it should on an ECG does not necessarily mean blood is being pumped throughout the body. It simply means that the electrochemical signals sent out by the sinoatrial node are propagating throughout the heart and being captured by the ECG machine.

Being able to feel a person’s pulse means that blood is actually being pumped; when you place your fingers on the inside of your wrist, you’re feeling the rush of blood being pushed through the artery by your heart’s contraction.

So in the case of pulseless electrical activity, depolarization and repolarization of heart tissue is occuring but blood isn’t being pumped.

How does this happen? Most often it occurs when there has been a significant loss of fluid volume in the body, to the point that such small amounts of blood are being pumped with each contraction as to not be able to detect the pulsing of the blood through arteries and veins. Called hypovolemia, the loss of fluid volume could be from blood loss due to an injury, or surgery, severe dehydration or the use of diuretics (causing excessive urination).

Other causes for PEA include:

Hypoxia
Hydrogen ion (acidosis)
Hypokalemia/hyperkalemia
Hypoglycemia
Hypothermia
Toxins
Tamponade, cardiac
Tension Pneumothorax
Thrombosis (coronary or pulmonary)
Trauma

Premature ventricular contractions (PVC) are premature heartbeats originating from the ventricles of the heart.  PVC’s are premature because they occur before the regular heartbeat.  Symptoms are often not presented with premature ventricular contractions.

During a pvc, the ventricle electrically discharges (and contracts) prematurely before the normal electrical signals arrive from the SA node.  These premature discharges are due to electrical “irritability” of the heart muscle of the ventricles, and can be caused by heart attacks, electrolyte imbalances, lack of oxygen, or medications.  Immediately after a premature ventricular contraction, the electrical system of the heart resets.  This resetting causes a brief pause (called a ‘compensatory pause’) in the heartbeat and some patients report feeling the heart briefly stopping after a pvc.  PVC’s without any other electrical or structural abnormality are of virtually no diagnostic nor prognostic value at all.  They occur in everyone in various sorts of patterns, and again, absent any structural or neurocardiological disease, they have no real meaning.  They can, however, be very alarming when they occur, and can provoke a good deal of anxiety which, unfortunately causes the release of adrenaline, which in turn makes the heart muscle more irritable, and often thus sets off yet more PVC’s sometimes making the sufferer a nervous wreck. This is truly unfortunate, because without significant left ventricular dysfunction PVC’s have no meaning at all (and even with LV dysfunction they are only an indicator, not a cause, of potential trouble).