Heart Rhythm Guide
Heart Rhythm Guide
All Rhythms
Home Normal Rhythm Rapid Heart Rate Slow Heart Rate Premature Heart Beat Pacemakers Automatic Defibrillator Atrial Fribrillation Sinus Rhythms Conduction Defects Supraventricular Defects About

Normal Heart Rhythms

   The heart has its own electric conductionsystem, which drives the rate and timing of the heart beat. This electricalconduction system adjusts the timing of the contraction patterns of the two atria and two ventricles to provide optimal pumping of the heart to maximize cardiac output. The electrical conduction system also automatically adjusts the heart rate to provide faster heart rates when the body needs more blood flow anda slower heart rate when at rest.

Normal Sinus Rhythm

Normal Sinus Rhythm
Each P-wave (caused by atrial contraction) is followed by a QRS-complex (caused by ventricular contraction) which is followed by a T-wave (ventricular repolarization). HR = 65 beats/min.

   Cardiac output, which is the quantity of blood pumped by the heart per minute, is equal to the volume of blood pumped by each heart beat (stroke volume) multiplied by the heart rate per minute. Thus, in the normal heart, doubling the heart rate doubles the cardiac output. The normal heart rate at rest ranges from 60 beats per minute to 100 beats perminute, but wide variations are common.

   For example the heart rate frequently declines to 45-60 beats per minute when you are asleep, particularly in young adults. The heart rate may be even slower during deep sleep. Trained athletes frequently have slower heart rates at rest because their left ventricles enlarge to pump more blood during exercise. The resulting increase in stroke volume means that their hearts pump more blood with slower heart rates. A few highly trained athletes will have heart rates at rest as slow as 35 beats perminute.

   During exercise, the electrical system of the heart increases the heart rate steadily to match the needs of the muscles for more blood flow. The maximum heart rate for adult patients at peak exercises typically 180 beats per minute.  Only in young patients during extreme exercise does the heart rate go higher. The maximum heart rate during peak exercise is also influenced significantly by age. For example older individuals in their eighties rarely elevate their heart rates over 150 beats per minute during exercise. Individuals who are out of shape due to sedentary lifestyles often have faster heart rates during lowlevel exercise, whereas, highly trained individual have slower heart rates during high levels of exercise.

Normal Heart Rhythm

Normal Heart Rhythm
Source: Male, 48 years old, Heart Rate: 65bpm, PR: 188ms, QRS: 92ms

   The human heart rate is adjusted minute by minute by a small clump of specialized cardiac cells located in the upperportion of the right atrium. These cells, referred to as the sinoatrial node,emit a regular pulsed electrical signal which triggers the heart beat. The sinoatrial node, influenced by neuro-humeral factors and by pressures in the rightatrium, adjusts the heart rate up or down to adjust the cardiac output to match the needs of the body for blood flow and oxygen requirements.

   Like all body organs the heart requires rest to remain healthy. Typically your heart rate and blood pressure diminish at night during sleep, lowering the work of the heart and permitting it to recover.

   The heart cannot tolerate being driven athigh rates for weeks without rest. Experiments in laboratory animals show that if high heart rates averaging 150 beats per minute are maintained continuously by an electric pacemaker for weeks, the heart begins to weaken and heart failure ensues.

   On the other hand, abnormally slow heart rates result in inadequate blood pumped by the heart causing patients to experience weakness, dizziness, and poor endurance. Extremely low heart rates reduce cardiac output further and can result in low blood pressure and eventually loss of consciousness. Irreversible death ensues when the heart rate is zero for more than a few minutes.

   The heart is comprised of two atria and two ventricles, which must contract in a synchronized pattern to optimize thepumping performance of the heart. Normally the two atriae contract first, filling the two ventricles which are the main pumps of the heart. The thick walled left ventricle generates high pressures to propel blood through the arteries throughout the body.  The thin-walled right ventricle pumps blood under much lower pressure to the pulmonary artery, which distributes blood to the right and left lungs, where it is oxygenated and returned to the left atrium to be re-circulated to the left ventricle.Simultaneous contraction of the two atria ensures that the two ventricles are fully filled before they contract; thus, contraction of the two atriae primes the pumping of the ventricles, optimizing the performance of the heart.

   The timing of the rhythmical synchronized contraction pattern of the atriae followed by contraction of the ventricles is set by the atrial-ventricular node, which establishes a delay between atrial and ventricular contraction, referred to as the A-V internal. This delay provides time for the atria to completely fill the ventricles before ventricular contraction. At rest the AV interval typically is approximately 0.14 to 0.18 seconds. When the heart rate increases during exercise, the AVinterval shortens to maintain optimal filling of the ventricles. Abnormal function of the AV node results in desynchronized or independent contraction of the atriae and ventricles which is referred to as AV dissociation, and causes suboptimal performance of the heart.

   The human heart beat begins with an electrical spark generated by the clump of specialized cells in the upper right atrium referred to as the SA node. This electrical signal passes quickly through the right and left atriae activating the AV node, which slows electrical conduction, providing time for atrial contraction to fill the ventricles. Next the electrical signal travels to the HIS bundle, where it is transmitted down the right and left bundles which activitates contraction of the right and left ventricles, respectively. The bundles are strands of specialized conduction cells, which transmit theelectrical signal rapidly and simultaneously to the right and left ventricles to trigger simultaneous contraction of the two ventricles. The large electrical signal resulting from contraction of the ventricles produces the R-wave on the electrocardiogram. After left ventricular contraction, the T-wave is generated during recovery of the ventricles.

Lead2 P QRS T U

   In summary the normal heart rhythm, referred to as normal sinus rhythm, is characterized by first a P-wave created electrical activation of the two atria, next a larger R-wave caused byelectrical activation of the two ventricles and lastly a T-wave resulting from recovery of the ventricles. Normal sinus rhythm is usually very regular with equally spaced intervals between heart beats. Occasionally, however, the heart rate will vary slightly with respiration causing a slight variation in the intervals between beats. This variation of the normal heart rhythm is referred to sinus arrhythmia and is more common in younger individuals.

Premature Heart Beats

   Although the normal heart beat is triggered by the SA node, any heart muscle tissue in either the atria or the ventricles can trigger cardiac contraction by emitting an electrical discharge. Ectopic beats arising from the atrium are referred to as premature atrial beats (PAB’s), and ectopics beats arising from either ventricle are referred to as premature ventricular beats (VPB’s).

Atrial Premature Beats

Atrial Premature Beats
In this patient with NSR and a heart rate of 61 beats/min, the third beat is a premature atrial beat. Note that the configuration of the ectopic P-wave differs from the configuration of the other P-waves.

   PAB’s are characterized by premature P-waves, which come early or prematurely in the cardiac cycle and differ slightly in configuration from the normal P-waves. These early P-waves are usually followed by a QRS complex, resulting from ventricular contraction. Occasionally, however, the premature P-waves arrive so early that the ventricles are still recovering from the previous beat and are refractory to the premature atrial beat. This phenomenon results in a dropped beat which causes a pause in the heart rhythm. These very early premature atrial beats, not followed by ventricular contraction, are referred to as blocked premature beats. Premature atrial beats are common and are virtually always benign. Often PAB’s are asymptomatic,but occasional patients, especially individuals with thin chests, will experience each and every PAB as an early beat interrupting the normal regularly sequenced heart rhythm.

   Usually patients with symptomatic PAB’s can be reassured by their physician that PAB’s are never life-threatening and do not require treatment with antiarrhythmic agents. Occasionally patients with very frequent PAB’s will develop symptoms due to the palpitations caused by multiple PAB’s and will require treatment with antiarrhythmic agents which suppress the PAB’s.

   Ventricular premature beats (VPB’s) arising from the right or left ventricles are also common. VPB’s are characterized by early wide QRS complexes with a T-wave usually directed in the opposite direction from the QRS. VPB’s can be associated with any type of heart disease but are also common in patients with completely normal hearts. VPB’s are commonly seen in normal individuals who consume large quantities of caffeinated beverages or who became exhausted from lack of sleep.

Ventricular Premature Beats

Ventricular Premature Beats
VPB's are wide premature beats (QRS greater than 0.14 sec) arising from either ventricle that are not proceeded by P-waves. Shown are two unifocal VPB's with identical morphologies. The pause following each VPB is compensatory because VPB's do not reset the rhytmicity of the sinoatrial node.

   VPB’s in patients with congestive heart failure are more ominous and are associated with a worse prognosis. In patients suffering an acute myocardial infarction, VPB’s are an indication that the heart may fibrillate or arrest. Studies have shown that in individuals with normal hearts, based on echocardiography and cardiac catheterization, VPB’s are harmless and are not associated with a poor cardiac prognosis. In fact a few individuals have frequent VPB’s all their lives with no adverse effects. The most important determinant of the clinical significance of VPB’s is the structural condition of the heart. Thus, VPB’s in a patient with a dilated weak heart are associated with a poor prognosis. Whereas, VPB’s in a patient with a structurally normal heart are nearly always benign.  It is the cardiologist’s responsibility to detect structural heart disease in a patient with frequent VPB’s and to advise the patient regarding prognosis associated with the VPB’s.  Occasionally, VPB’s result from inadequate blood flow to the heart muscle.  Thus, VPB’s may be a helpful clue in the detection of coronary artery disease.

   VPB’s, however, do not generate a full left ventricular stroke volume because the left ventricle is incompletely filled due to the prematurity of the beat and lack of atrial contraction preceding ventricular contraction. Thus, a weak pulse usually results from each VPB.  In patients with frequent VPB’s, the heart rate determined by feeling the wrist pulse is often reduced because the weak pulses resulting from VPB’s are not detectable at the wrist.  In a patient with ventricular bigeminy, each normal heart beat is followed by a VPB. Since only the normal beats produce a pulse, detection at the wrist will be one-half the patient’s actual heart rate. Weak peripheral pulses resulting from VPB’s can cause some patients with frequent VPB’s to feel fatigue and asensation of loss of energy.

Atrial Bigeminy

Atrial Bigeminy
Typically atrial flutter is characterized by rapid regular atrial rates ranging from 250 to 350 beats/minute. Atrial flutter waves have a sawtooth appearance.

   Whether patients with frequent VPB’s should be started on antiarrhythmic medications, which may suppress VPB’s, is a complex issue which is best decided by a cardiologist who is familiar with the patient’s underlying structural heart disease and with the symptoms the patient experiences from the VPB’s.  The antiarrhythmic medications currently available for suppressing VPB’s are effective in only slightly more than half of patients and occasionally cause adverse side effects, which may rarely be severe.  Thus, the decision to treat a patientwith frequent VPB’s is best made by a cardiologist familiar with the patient’s symptoms, physical examination, and heart disease assessed by non-invasive cardiac tests, including a 12 lead EKG echocardiogram, treadmill study, nuclear stress test, and/or stress echocardiogram.