P Wave Definition
A P wave is a period of electrical activity on an ECG that causes the atria of the heart to contract. The P wave is a summation wave, which means that it is electrical activity caused by many places signalling simultaneously, resulting in wave-like contractions. Pacemaker cells are present in a variety of locations and generate action potentials independently of the central nervous system. The P wave is the very first wave on an ECG of a healthy individual.
What Does the P Wave Represent?
The P wave is the electrical activity (in volts) that causes the atria’s heart muscle to contract. which are the top two chambers of the heart. When a P wave is defined as representing atrial contraction, this isn’t totally accurate.
The voltage that precisely initiates atrial muscle cell contraction is shown as a P wave (over time). As a result, an ECG depicts electrical activity rather than muscular action.
By examining ECG waves and analysing changes or anomalies in electrical voltage at various places, we can ascertain when and where the heart muscle contracts or relaxes. as well as whether or not this is a healthy activity.
P Wave on the ECG
On an electrocardiogram, the P wave is the first one (ECG). The PR interval, the QRS complex, and the ST interval are all examples of intervals, and ultimately, the T wave comes next.
Cardiologists may interpret the findings of an ECG P wave as good or unhealthy heart function. Atria issues are indicated by abnormal P waves and the absence of P waves.
Voltage and time are shown on an ECG. It may either be printed on graph paper or seen on a computer screen. The gaps between the T wave (the last wave) and the P wave may be used to determine if a heartbeat is rapid or slow. Conductivity difficulties are indicated by irregular gaps between the P and T waves; nonetheless, they have little effect on heart rate.
A regular P wave has a duration of less than 0.12 seconds (120ms), or around three squares on an ECG printout. The P wave’s peak height varies between 1.5 and 2.5 millimetres, based on the quantity of leads and the location of the ECG electrodes. This corresponds to a voltage range of 0.15 to 0.25 millivolts.
P Wave and Conduction
A healthy P wave begins in the right atrium’s sinoatrial node. The atria were filled with action potentials produced at this node. This suggests that the right atrium shrinks somewhat earlier than the left.
The sinoatrial node, Thorel’s bundle, Wenckebach’s bundle, Bachmann’s bundle, and the atrioventricular node make up the cardiac conduction route in the atria. Wenchebach’s bundle transmits action potentials from the SA node across the right side and front of the right atrium, whereas Thorel’s bundle conducts them along the rear of the right atrium. Bachmann’s bundle is the result of a collection of fibres crossing deep into the left atrial muscle.
P Wave and Automaticity
The brain is not required for heart conduction or contraction. The medulla oblongata of the brainstem governs the pace at which the heart muscle contracts (heart rate in beats per minute) and the amount of blood pumped through it; nonetheless, the myocardium is self-contained. This implies that cardiac cells create their own action potentials rather than relying on those generated by the central nervous system.
In the heart, action potentials are generated by specialised pacemaker cells. These are cardiomyocytes or myocardiocytes, which are heart muscle cells. They have a secondary role of generating action potentials. Only a tiny fraction of people are capable of generating action potential.
Pacemaker cells should be present only in the sinoatrial node (SAN) and atrioventricular node (AVN) (AVN). These cells serve as the cardiac pacemaker’s captains. Automaticity is not present in normal (healthy) heart muscle cells. Nevertheless, once the ions associated with heart muscle contraction (sodium, potassium, and calcium) are out of balance, normal cardiomyocytes may begin to produce action potentials.
These atypical signals are referred to as ectopic (not passing from the areas where pacemaker cells are normally identified). Irregular P wave anomalies in the atria are frequently caused by irregular automaticity.
Role of the Central Nervous System
The pace at which the SA node fires is consistent—roughly 100 times every minute. It is a consistent rate (native rate) that will continue indefinitely… or until cardiac arrest occurs. The heart generates the natural heart rate, which the autonomic nervous system then regulates through the medulla oblongata.
For example, while the sympathetic nervous system’s nerves outnumber those of the SA node, the heart rate rises. While the body is at rest, parasympathetic nerves dominate action potential creation in the SA node. resulting in a drop in heart rate. The autonomic nervous system regulates heart rate, notwithstanding the fact that the heart doesn’t ever stop beating (unless a huge quantity of cardiomyocytes die).
The heart has a backup mechanism in the form of pacemaker cells in the AV node. The main pacemaker is the SA node, but when it is destroyed or malfunctions, the AV node takes control. This is an ectopic rhythm with aberrant P waves.
The AV node, the auxiliary pacemaker, also continuously generates action potentials, albeit at a lesser rate than the SA node. The SA node’s rapid firings take precedence over the AV node’s slower impulses. As a result, if the SA node fails, the heart rate is likely to slow down (bradycardia).
Heart Conduction Pathway
The sino-atrial node, located near the apex of the right atrium, is where pacemaker cells develop and transmit action potentials. These spread across both atria and cause the apex of the heart muscle to constrict.
Electrical impulses originate at the bottom of the right atrium’s atrioventricular node and flow through the cardiac septum’s bundle of His from top to bottom. The His bundle’s right and left bundle branches transmit action potentials along the septum’s right and left sides and into the right and left ventricle walls, accordingly.
The right and left bundles combine to form a large number of Purkinje fibres. Purkinje fibres run vertically across each ventricle’s muscles. They cause blood vessels to constrict more, so blood is pushed toward the aorta and pulmonary artery.
On an ECG, the QRS complex and T wave are generated by the voltages that cause depolarization from the AV node forward.
The waves on an electrocardiogram reveal to us what is going on within the heart. Even if this article focuses on the P wave, it’s still vital to obtain the whole picture and comprehend anomalous P wave pathology.
- Atrial depolarization (P wave). Gravity facilitates blood flow into the ventricles. Fewer muscular contractions are necessary. As a result, the P wave is shorter than the R and T waves.
- A brief gap before the QRS complex is called the PR interval.
- The bundle of His depolarizes the apex of the ventricular septum, resulting in a Q wave. A little wave with a downward slant,
- R wave: depolarization of the ventricles through bundle branches in their thickest section; this is why the R wave is the greatest (more voltage is needed).
- Purkinje fibre depolarization (S wave). The signals ascend from the base of the ventricles in the reverse curve direction of the R wave.
- ST-segment: the amount of time it takes for every ventricle to depolarize entirely (relax).
- T wave: full ventricular repolarization (relaxation).
On the University of Utah School of Medicine website, you may test your comprehension of ECG readings. Heart conductivity abnormalities and P-wave abnormalities are among the tests performed.
P Wave Abnormalities
On an ECG, P wave abnormalities might be seen. Most textbook ECG examples are rather apparent; nevertheless, a skilled eye is usually required in the hospital.
Inverted P Wave (ECG)
Generally, an ECG with an inverted P wave indicates an ectopic atrial beat. When particular electrolytes are out of equilibrium, the AV node, regular cardiomyocytes, or ectopic pacemaker cells may all produce action potentials that cause myocardiocyte depolarization. An inverted P wave is the opposite of a normal P wave.
Retrograde P wave
The AV node takes control if the SA node isn’t working correctly. Due to the fact that action potentials propagate back to the SA node, the atria continue to contract. A retrograde P wave is the outcome.
ECG printouts with retrograde P waves may lead a cardiologist to suspect junctional rhythm, a kind of ectopic rhythm. The atria usually take longer to contract, and the P wave may be near to or inside the QRS complex. The backward migration of action potentials is referred to as retrograde.
Notched P Wave
A notched or bifid P wave implies expansion of the left atrium, which is almost typically caused by a constricted mitral valve. The mitral valve directs blood flow from the left atrium to the left ventricle. If this valve is constricted, the atrium will not get enough time to drain before relaxing (mitral stenosis). As they relax, the atria draw blood from the venae cavae and pulmonary veins. Mitral stenosis requires the left atrium to extend (enlarge) to accommodate the increased blood volume.
Because there is more tissue to travel through, a notched P wave is generally broader (slower). Right atrial contraction is represented by the first half of the P wave prior to the notch, whereas left atrial contraction is represented by the second half of the P wave. The biphasic P wave is a subtype of the notched P wave.
No P Wave on ECG
The lack of a P wave on an ECG does not mean the heart has stopped beating; the QRS complex and T wave that follow show that the ventricles remain functional.
In certain cases, such as atrial fibrillation, the P wave may simply be exceedingly erratic and undetectable. Other options include the arrest of the SA node or the blocking of the many bundles that link the SA and AV nodes. These illnesses would result in mortality if ordinary myocardiocytes were unable to adjust and produce impulses on their own.
If the SA node fails to function, the heart has one more defendant’s act up its sleeve: escape rhythm. If one component of the cardiac conductivity system malfunctions, the other components take control. In junctional rhythm, the AV node assumes the role of the primary pacemaker.
Myocardiocytes in the ventricles may cause an ectopic ventricular beat if the AV node collapses as well. Because they take a second or two to produce, the heart rate is reduced to between twenty and forty beats per minute. If there is no atrial electrical activity, there is no P wave on the ECG or monitor.
Although atrial flutter may seem to be a deadly condition, it is extremely common. Multiple P waves and a fast heart rate are also common symptoms. Atrial fibrillation may develop from this condition.
Atrial flutter occurs when the atria contract many times. These numerous contractions are not as hazardous as you would assume, since most blood travels from the atria to the ventricles through gravity. Despite this, atrial flutter may induce turbulence and tiny blood clots.
On ECG printouts, due to the near proximity of flutter P waves, rates of up to 300 beats per minute are possible. The ventricles contract at a slower rate than the atria; in fact, they normally contract at a rate less than half that of the atria. Apart from being overly rapid, the atrial flutter rhythm is regular. The saw-tooth pattern of the P waves (plural) is characteristic.
AFib, or atrial fibrillation, affects up to 6.1 million individuals in the United States. It might manifest as symptoms or remain unnoticed (without symptoms).
The rhythm and appearance of the P wave vary between atrial flutter and atrial fibrillation. The pulse is erratic in AFib, and P waves are shallow, wavy lines; to the untrained eye, the ECG may seem to have no P wave.
Multiple ectopic action potentials originating from diverse places sprinkled across the atria generate atrial fibrillation. Atrial fibrillation affects around one-third of people with AFib.
Blood clots are more likely to occur in people with AFib. The heart rate is generally fast, but the pulse is usually irregular. However, in mixed flutter/fibrillation disease, this is not always the case.
- Ashley EA, Niebauer J. (2004). Cardiology Explained. Chapter 3, Conquering the ECG. London Remedica. Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK2214/
- Mohrman DE, Heller L. (2018). Cardiovascular Physiology, Ninth Edition. New York, McGraw Hill Education.
- Jevon P, Gupta J. (2020). Medical Student Survival Skills: ECG. Oxford, Wiley Blackwell.