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ECG in dogs and cats: how much does it cost and when to do an ECG?

ECG test

Electrocardiography (EKG) is a non-invasive diagnostic method that allows the analysis of the heart rhythm and its frequency, and may indirectly give indications about the enlargement of individual parts of the heart muscle.

Electrocardiographic examination is based on the assessment of the electrical activity of the heart (depolarization and repolarization of cardiac cells) using electrodes located (most often) on the body surface.

The course of electrical phenomena occurring in the heart is analyzed on the basis of the electrocardiographic (EKG) waveform.

  • The principle of operation of the electrocardiograph
  • The heart's conductive system
    • Centers of myocardial automatism
    • Innervation of the conducting system
  • What information can we get by ECG examination?
  • Indications for the ECG test
  • What does the ECG test look like??
    • Guidelines for carrying out an ECG test
    • Placing the animal for ECG testing
  • Shape of electrocardiogram curve
  • Assessment of the electrocardiogram by a veterinarian
    • Assessment of the heart rate
    • Determination of the heart rhythm
    • Determination of the electrical axis of the heart
    • Determining the values ​​of individual parameters
  • Normal ECG values ​​for dogs and cats
    • Normal ECG values ​​in a dog
    • Correct ECG values ​​in a cat
  • As evidenced by changes in individual values ​​of the ECG record?
    • P wave
    • QRS complex
    • ST segment
    • QT interval
    • T wave
    • Other changes visible in the ECG test:
  • Artifacts
  • Long-term recording of the heart rate
    • Cardiomonitoring
    • Holter test for ECG
  • How much does an ECG test cost?

The principle of operation of the electrocardiograph

The principle of operation of the electrocardiograph

ECG apparatus it is nothing but a kind of sensitive galvanometer that measures electric current values.

Connected to electrodes applied to two different points on the body surface, it forms a circuit (in electrocardiography this is called a lead).

The potentials detected on the surface of the body are then amplified by ecg apparatus and displayed on special graph paper or monitor screen.

The electrocardiogram is therefore a graphic record of the electrical potentials generated by the heart muscle during its work.

How is it possible that the heart rate is recorded from the surface of the body??

To answer this question, we must "enter" the heart muscle and observe what electrophysiological phenomena take place inside it.

Virtually all cells in the body that are surrounded by a cell membrane (and this membrane has the characteristic feature of semi-permeability, thanks to which it is possible to exchange various types of substances between the external and intracellular environment) are excitable cells.

This means that they are able to react to compounds that will penetrate inside them.

It is possible thanks to its properties cytoplasmic membrane surrounding cell and a very characteristic ion arrangement on both sides.

Well, it occurs in the intracellular environment very high concentration of potassium ions (K +) compared with the extracellular environment.

There are about 30 times more of them in the cell than outside.

In turn, in the extracellular environment there is a higher concentration (compared to the inside of the cell) sodium (Na +) and chloride (Cl-) ions.

This arrangement of individual ions causes a certain amount to be produced across the cell membrane electrochemical gradient.

The potential difference in the cell membrane of the heart muscle makes the interior of the myocyte (heart muscle cells) more negative than the extracellular environment.

Thanks to this, the cell is somehow "electrically charged ".

Such a resting potential (approximately - 90 mV in the working cells of the heart muscle) is "unstable" because - according to the laws of physics - there is a constant permeation of these ions through the membrane, aiming at equalizing the concentrations:

potassium ions accumulated inside the cell will go to the outside, and sodium and chloride ions from the extracellular environment will penetrate inside.

And it really does.

Therefore - in order to maintain the desired resting potential (and thus ensure excitability) there is a certain mechanism of active transport of these ions against the concentration gradient.

Magnesium-dependent is responsible for it sodium-potassium pump.

It is she who persistently throws back chloride and sodium ions to the outside, and transports potassium ions to the inside of the cell.

As a result, a resting excitable cell has a defined resting potential.

What happens when a cell is stimulated?

At the moment of the stimulus action on the cells of the heart muscle, the so-called. action potential.

Its first phase is called depolarization.

In it, sodium ion channels open, and a current of Na ions begins to flow into the cell+.

As a result, the membrane potential becomes less negative, increasing to the value of approx. -40 mV.

When the potential increases above this value, other ion channels (in particular calcium channels) are activated and Ca2 ions begin to flow into the cell (apart from sodium)+.

It is this inflow of calcium that stimulates the mechanical contractions of the heart.

This influx of ions into the cell and the associated action potential continues until the membrane potential reaches a value of about 20-40 mV.

Is it rapid depolarization phase, followed by initial repolarization phase.

During this time, the permeability to sodium ions decreases, while a slow calcium current continues to flow into the cell.

At the same time, the membrane permeability to potassium ions, which begins to flow out of the cell, increases.

An extracellular potassium current appears.

These changes in the permeability of the cell membrane to sodium, calcium and potassium result in a potential decrease to about 0 mV.

Now the cell enters the plateau phase - i.e. the potential remains at 0mV for a period of several dozen to several hundred milliseconds.

This is due to a certain balance between the intracellular calcium current and the extracellular potassium current.

In the final phase of repolarization, the membrane potential begins to decline to the baseline value.

This is due to the inactivation of calcium channels.

Calcium ions no longer flow into the cell, but potassium flows out of the cell all the time - hence reaching the resting value of the potential.

The membrane potential of a single cell during its depolarization is called monophasic action potential (MAP).

The sum of all such potentials generates an electric field, the effects of which radiate throughout the body.

And it is these small potential differences that can be measured with electrodes attached to the animal's skin.

They are recorded and enhanced by electrocardiograph.

The heart's conductive system

In order for the heart muscle to work efficiently, it is necessary to ensure a certain sequence of synchronized atrial contractions and subsequent ventricular contractions.

As it turns out in a moment, everything is based on a certain intricate system, built into the heart muscle - the so-called. conductive system.

The heart has its own automatism.

This means that it can work independently of the initiating stimuli from the nervous system.

Even more - in order for the heart muscle to work, stimulation from the nervous system is not necessary (the heart contracts - under appropriate conditions - even after isolating it from the body).

This system does - indeed - regulate and modulate the work of the heart in certain situations.

However, the heart itself has the ability to both generate and conduct impulses of active state to all its cells.

In other words - the heart muscle has its own starter, located in the structures of the so-called. the conductive system.

It is thanks to the presence of this complex structure that rhythmic, coordinated, consecutive and almost simultaneous contractions of the atria and then the ventricles are possible.

The tissue that makes up the heart's conductive system is made of specialized muscle cells, with a slightly different histological structure than the rest of the working cells of the heart muscle.

It is located in the four most important places, the so-called. centers of automatism.

Centers of myocardial automatism

  • I - row center - is the sinoatrial node (SA), called sinus node - located in the right atrium at the mouth of the main cranial vein.
    The physiological rhythm of the heartbeat transmitted by the sinoatrial node is the so-called. sinus rhythm.
    The heart works according to the rhythm imposed on it by this primary center of automatism.
    Why this node is a "pacemaker "?
    Well, because it is the fastest.
    The course of slow resting depolarization and the triggering of an active state impulse occurs most quickly right here.
    This means that the sinoatrial node is the superior center.
    However, in order for the entire heart muscle to be stimulated, the impulses must travel to the next centers of heart automatism.
    This is due to the presence of certain conduction paths.
    These include:

    • Interstitial road - running from the sinoatrial node to the atrioventricular node (another automatism center).
      It consists of the front, middle and rear interstitial roads.
      These conduction pathways increase the likelihood of excitation from the sinus node to the AV node and thus increase the likelihood of onset of ventricular depolarization.
      Why is it so important?
      Conduction disturbances may appear quite often at the right atrium level, which may result in blocking the conduction of the active impulse from this superior center of cardiac automatism.
      The interstitial pathway determines the correct transition of stimulation from the first-order to the second-order center of automatism.
    • It leads from the sinoatrial node (in the right atrium) to the left atrium vestibular road.
      It is a conduction beam, thanks to which both atria can be stimulated and contracted almost simultaneously.
      If for some reason the activity of the sinoatrial node is blocked, the second-order center of heart automatism, i.e atrioventricular node.
      But then the heart will slow down.
  • II - row center - atrioventricular node (AV).
    It is located subendocardium, in the right part of the atrial septum.
    It is an extremely important node because it is the only way for excitation to spread from the atria to the ventricles.
    Here, however, the conduction velocity is much slower than in the sinoatrial node.
    As a result, the depolarization of the ventricular muscle is slower by approx. 100-150 milliseconds compared to atrial depolarization.
    This slowing down of conduction is of great importance for the mechanics of the heart, because it allows the ventricles to contract only after contraction of the atria.
    The most important effect of this distribution over time is that the heart can fulfill its most important function - that is, to pump blood.
    Earlier contraction of the atria allows blood to be pushed into the ventricles.
    The delayed ventricular contraction, in turn, ejects blood to the periphery.
    If atrial and ventricular contraction occurred at the same time, it would be impossible to pump blood.
    The second aspect of this slowdown in conduction is that it allows the heart to work very quickly.
  • Third-row center - atrioventricular bundle Paladino - Hisa.
    It is divided into two branches: right and left.
    They run on both sides of the interventricular septum.
    The left leg is additionally divided into a front and rear beam.
    These branches run below the endocardium to the apex of the heart where they become Purkinje fibers.
    The ability to trigger active state impulses (physiologically) in the body is appropriate for the first two centers, i.e. the sinoatrial and atrioventricular nodes.
    In the His bundle, or even in Purkinje's fibers, pulses of the active state may also be triggered.
    However, if such an impulse is triggered at the level of one of these two centers, it is called a delayed pacemaker and it is a pathological situation.
  • IV row center - Purkinje fibers.
    They begin in the subendocardial plexuses, formed by the branches of the His bundle.
    They are characterized by the highest conduction velocity (up to 4 m / s), thanks to which both chambers contract almost simultaneously.
    This greatly increases the efficiency of the contraction.

The pacemaker cells, located in the sinoatrial node, determine the heart rate.

Apart from them, also cells located in other centers of cardiac automatism can also act as pacemakers.

Under normal circumstances, however, this does not happen because it is the sinoatrial node that generates the pulses at the highest frequency.

However, if the speed of "discharges " in the first-line center falls below the rate of stimulation of the other pacemakers, one of them will become the dominant pacemaker and will drive the heart rate.

These auxiliary stimulators are found in the His bundle, bundle branches, and Purkinje cells.

Other heart cells can become auxiliary pacemakers when the cytoplasmic membranes of the cells leak (usually as a result of damage to them).

This abnormal automatism is one of the main causes of arrhythmia, when the frequency of depolarization of damaged cells becomes dominant.

Innervation of the conducting system

Despite the fact that the heart "spontaneously" produces impulses of the active state (which somehow makes this organ independent of external factors), the work of the heart must meet the needs of the whole organism.

So the heart rate must be adapted to the current needs of the system - at the right moments the heart should work faster, and at other times - slow down.

The regulation of such changes takes place in the nervous and humoral way.

Sinoatrial node (which gives the heart a proper rhythm) is largely innervated by parasympathetic fibers (vagal fibers).

The influence of the sympathetic nervous system is much less at the level of this node.

The greater activity of the parasympathetic innervation causes the sinoatrial node to be constantly under its inhibitory effect.

At the level atrioventricular node the parasympathetic and sympathetic innervation are more or less evenly distributed.

When the parasympathetic system is stimulated, the heart rate slows down, and when the sympathetic system is stimulated - the heart rate accelerates.

Many drugs affect the work of the heart muscle in this way - by stimulating or inhibiting the vegetative system.

What information can we get by ECG examination?

What information can we get by ECG examination?

The normal heart rhythm comes from the sinoatrial node and propagates through the atria, atrioventricular node, His bundle, Purkinje fibers, up to the ventricular myositis.

Each generated waveform in the ECG record gives information about depolarization, repolarization, and conduction in the heart.

Electrocardiography provides information on:

  • heart rate,
  • heart rhythm,
  • conduction system in the heart,
  • ventricle size (potentially - can give some clues, but the final assessment of heart size should be based on other diagnostic methods such as radiography or echocardiography),
  • potential myocardial ischemia,
  • certain electrolyte disturbances (must be confirmed with a blood test).

Indications for the ECG test

Indications for the ECG test
  • diagnosis of arrhythmias suspected during the clinical examination of the patient (especially during auscultation),
  • fainting or fainting episodes - the ECG test is designed to detect possible arrhythmias that may cause fainting,
  • critical condition of the patient (e.g. after a traffic accident) is an important indication for ECG monitoring,
  • to optimize therapy in a patient with cardiological problems (monitoring the heart rate and its rhythm)
  • monitoring the patient for drug toxicity (e.g. digoxin, procainamide),
  • looking for electrolyte disturbances (e.g. hyperkalemia),
  • other medical conditions that may affect the heartbeat (e.g. hypothyroidism, uremia, cancer),
  • as one of the tests qualifying for anesthesia,
  • symptoms of cardiac problems, detected during other diagnostic tests (e.g. enlargement of the heart shape visible on X-ray),
  • monitoring the patient during anesthesia.

What can not be determined on the basis of ECG?

  • the strength of the contraction of the heart muscle,
  • the presence or absence of heart failure,
  • forecasting about the survival of an anesthetic procedure.

What does the ECG test look like??

The ECG test is an examination non-invasive and painless.

The pet is placed in the appropriate position (lying or standing), then electrodes are attached to the skin of the armpits, groin and sometimes the chest.

The entire examination usually continues from tens of seconds to several minutes (it may be longer - it all depends on the purpose of the examination and the irregularities found).

No special preparation of the patient is required to perform the ECG test.

However, there are some guidelines that should be followed in order for the test to be of adequate diagnostic value.

Guidelines for carrying out an ECG test

  • The test should be performed in a calm and quiet environment.
  • If possible, the patient should be relaxed and calm as panting, muscle tremors and movements cause artifacts.
  • The animal's skin and coat should be dry.
  • During the examination, the patient should be placed on a rubber mat or a thick, dry blanket.
  • The electrodes should fit snugly against the skin and should not touch each other.
    In order to reduce the electrical resistance between the body surface and the electrodes, a special ECG gel is used or the skin is degreased with alcohol.
  • The test should be carried out without the use of premedication measures (after all, we want to detect potential arrhythmias, and drugs used to calm animals pharmacologically affect the heart rate, which may "seem " disappear some abnormalities).
    The exception is ECG monitoring during surgery.
  • Cables should be positioned so that they do not lie on the patient's chest, as this may be a source of artifacts related to chest movement during breathing.
  • The test should be carried out at a suitable distance from other electrical devices due to possible recording disturbances.

Placing the animal for the ECG test

Patients for ECG testing are usually placed on their right side with their limbs perpendicular to the body.

Most dogs (and a large number of cats) allow this position and last for several dozen seconds without moving.

In a situation where it is not possible to put the patient in such a position, the ECG test can be performed with the animal standing, sitting or lying on the sternum.

There are strict, defined standards for placing the electrodes on the animal's body.

Electrodes come in several forms:

these can be disposable, self-adhesive overlays, glued on the skin, special crocodile clips (the most commonly used) or transdermal needles.

Such electrodes are connected to the ECG device by means of cables marked with appropriate colors.

When the heart beats, an electric field of varying voltage is created.

In order to register the potential differences in the form of an ECG recording, the registration should be made between two electrodes, placed in different parts of the tested body.

One of them is referred to as the positive electrode and the other as the negative electrode.

Such electrodes are placed on the animal's body in an appropriate manner.

Limb electrode attachment sites

  • the yellow electrode is attached to the skin of the left chest limb (above the left elbow tumor, "under the left armpit "),
  • the green electrode is placed on the skin fold of the left pelvic limb (above the knee joint),
  • red electrode - skin of the right thoracic limb (above the elbow tumor),
  • black electrode - on the skin fold of the right pelvic limb (above the knee joint).

Pre-cardiac electrodes attachment sites

  • white electrode CV1 - in the fifth right intercostal space, on the edge of the sternum, at the transition of the cartilage ribs to the sternum,
  • white electrode CV2 - at the level of the sixth intercostal space on the sternum,
  • white CV4 electrode - in the sixth intercostal space, on the left side, at the level of the transition between cartilage and bone ribs.

The ECG apparatus together with the electrodes form a lead, i.e. an electrical circuit.

In the graph, the signal from each such electrode pair is also called a lead and labeled accordingly.

Limb drains

These are the six leads that evaluate the depolarization of the heart in the frontal (horizontal) plane.

These are the main leads and are most often used in routine ECG testing.

Limb bipolar leads according to Einthoven

These leads record the electrical activity of the heart between two electrodes placed on the animal's limbs.

One of them is the reference electrode (i.e. the one against which the measurement is made) - it is the negative electrode.

The positive electrode is the "testing" electrode.

Due to this polarity, these leads are referred to as bipolar.

  • Lead I - right (-) and left (+) pectoral limb,
  • Lead II - right thoracic limb (-) and left pelvic limb (+),
  • Lead III - left thoracic limb (-) and left pelvic limb (+).

Unipolar limb leads according to Goldberger (reinforced lead system)

They use the same electrodes as the bipolar limb leads, but here the recording electrode is positive and the negative pole is formed by the sum of the electrodes attached to the left and right thoracic limbs and the left pelvic limb.

The names of these leads come from the location of the positive electrode:

  • aVR - Right arm,
  • aVL - Left arm i
  • aVL - left foot.

The letter "a " stands for augmented and "V " stands for vector.

  • aVR - collecting electrode: left thoracic limb and left pelvic limb (-) and right thoracic limb (+),
  • aVL - collecting electrode: right thoracic limb and left pelvic limb (-) and left thoracic limb (+),
  • aVF - collecting electrode: right and left thoracic limb (-) and left pelvic limb (+).

Precardiac drains

These leads "look" at the heart in a transverse plane.

The information obtained from precordial leads complements the data on the electrical activity of the heart obtained via limb leads.

They are used to perform a more detailed diagnosis of the heart rhythm (especially when intraventricular arrhythmias are suspected, they are also more sensitive to detect enlargement of individual parts of the heart muscle and enable better identification of P waves).

These leads can be marked with the letter "C ", denoting the location of the electrodes on the animal's chest (chest), or the letter "V " (from voltage).

There are also common signs "CV ".

The precordial leads are unipolar leads and the electrodes are located directly on the chest.

Unipolar precordial leads according to Wilson:

  • CV1 - collecting electrode: from limb leads (-) and precordial electrode CV1 (+)
  • CV2 - collecting electrode from limb leads (-) and precordial electrode CV2 (+)
  • CV4 - collecting electrode: from limb leads (-) and precordial electrode CV4 (+)

Measurement of the potential difference between two electrodes (forming a lead) enables electrical recording of myocardial activity.

Each lead identifies the points between which we measure the potential differences generated by the heart's electric field.

For example:

lead II measures the potential difference between the electrode attached to the patient's left leg and the electrode on the patient's right thoracic limb.

Each electrode is also assigned a specific polarity:

in lead II, the left pelvic limb is positive and the right pelvic limb is negative.

Thanks to the different leads, we are able to assess the electric field generated by the heart from several different perspectives.

It can be said that individual leads "look" at the heart from different angles.

As a result, a three-dimensional image of the electrical changes occurring in the heart muscle is obtained.

The complete electrocardiogram consists of six limb leads and several unipolar thoracic leads.

The most common is the frontal plane, which is defined by 6 leads - 3 bipolar (one electrode is positive and the other negative) and 3 reinforced unipolar leads.

Leads I, II, and III are bipolar (one electrode is positive and the other is negative).

Lead aVR, aVL, and aVF are unipolar enhanced leads, i.e. only one electrode has a certain polarity.

With these leads, the electrode in question (e.g. right arm in lead aVR) is positive and compared with the mean of the other two (left arm and left leg).

These six leads allow us to view the heart from six different perspectives in the plane defined by the electrode attachment points (frontal plane).

The other planes are defined by the shift of the electrode attachment point.

In veterinary medicine, these extra points are on the chest wall.

For this purpose, four unipolar leads on the chest are used.

In addition to the above-mentioned leads from the body surface, in some special cases also leads from the esophagus or from the heart cavities are used.

The purpose of using this type of lead is to bring the electrode closer to the source of the electric field.

Shape of electrocardiogram curve

Shape of electrocardiogram curve

Each wave, wave or ECG space gives information about depolarization or repolarization and the conduction of pulses in the heart muscle.

What will the ECG record look like, what will be the morphology of the particular shifts of the ECG curve, their amplitude or duration depends on the amount of activated muscle tissue at a given moment as well as the speed and direction of the excitation wave.

In individual leads, the depolarization wave towards the positive electrode gives a positive deflection of the isoelectric line (in the ECG record it is visible as upward deflection above the baseline), and the wave from the positive electrode gives a negative deflection.

Therefore, the electrocardiogram shows different waves, segments and intervals, and each of them is analyzed for possible abnormalities:

  • Isoelectric line - this is the baseline, horizontal line of the record, recorded when there is no electrical activity in the heart (to put it simply - it is visible in the intervals between individual waves).
    It is a benchmark against which other ECG values ​​are assessed.
  • The wave is the inclination of the ECG curve from the isoelectric line.
    Such a deflection may be directed downwards (below the line) - then it is called negative, or upwards (above the line) - then it is a positive wave.
    The folds are:

    • P wave,
    • QRS complex,
    • T wave.
  • Interval - is the time from the beginning of one wave to the beginning of the next.
    The ECG record evaluates:

    • PQ interval,
    • ST interval,
    • QT interval.
  • Segment - time from the end of one wave to the beginning of the next wave.
    We evaluate the PQ section and the ST section.

Characteristics of individual ECG waves

  1. The P wave is the result of depolarase in the atria.
    This is the first inclination of the ECG curve and indicates the activation of the atria.
    Their repolarization is hidden in the QRS complex.
  2. The PQ (PR) interval reflects the time it takes for an impulse to travel from the sino-atrial node through the AV node to the ventricles.
    Since the depolarization of cells within the atrioventricular node is slower, impulse conduction at this point is markedly slower.
    As a result, a short pause between atrial contraction and ventricular contraction is possible.
    In ECG, it is the distance from the beginning of the P wave to the beginning of the Q wave.
  3. The QRS complex is due to the depolarization of the ventricles.
    Arousal, starting from the AV node and running to the bundle of His, and then the Purkinje fibers accelerates again.
    Since a large mass of the ventricular muscle is depolarized, the variation in the ECG curve is quite significant.

    • The Q wave is the first negative P wave and represents the depolarization of the ventricular septum.
    • The R wave is the first positive wave after the P wave and represents a depolarization of the ventricles.
    • The S wave is the first negative wave after the R wave and represents the depolarization of the base of the ventricular walls.
    • Point J - transition of the ascending S-wave arm into the ST segment
  4. ST segment.
    After the stimulation has passed, the ventricular muscle is completely non-excitable (it cannot respond to the stimulation even if there is an impulse) - it remains in the phase of the so-called. refraction.
  5. The T wave is due to the repolarization of the ventricles.
    After a short time of refraction, the ventricular muscle returns to a resting state.
    At this time, the chambers are still partially non-excitable.
    The T wave can be positive, negative or biphasic, but it should not change direction (polarization) in serial ECG testing.
    Large T waves can be observed with:

    • myocardial hypoxia,
    • disturbances of interventricular conduction,
    • bradycardia,
    • chamber enlargement,
    • hyperkalemia.
  6. The QT interval represents the cumulative time of ventricular depolarization and repolarization (i.e. the duration of a ventricular contraction).
    It is measured from the beginning of the QRS complex to the end of the T wave.

Assessment of the electrocardiogram by a veterinarian

After obtaining the ECG curve, the veterinarian starts its assessment based on a standardized procedure.

Assessment of the heart rate

Since the heart rate is influenced by various factors, both external (e.g. stress, ambient temperature) and internal (e.g. patient's physiological condition, internal body temperature, excitability or age), it is difficult to clearly define physiological values.

Heart rate in dogs and cats

  • in dogs approx 70-160 beats per minute:
    • big dogs 60-80 beats per minute,
    • small dogs 80-120 beats per minute;
  • in cats 150-220 strokes per minute.

Where it is smaller, it is referred to as bradycardia (bradycardia), and when it is greater than correct - tachycardia (tachycardia).

Determination of the heart rhythm

As we know, the physiological heart rhythm in animals is the sinus rhythm, generated by the primary heart automatism center, i.e. the sinus node.

It starts every contraction of the heart.

Under normal conditions, in a healthy heart, the impulse goes from the sinus node, spreads to the atria, the atrioventricular node and the muscles of the ventricles.

In the ECG examination, the presence of normal sinus rhythm is determined by the presence of:

  • positive P waves in lead II,
  • correct shape of the QRS complexes (sometimes they can be widened in the case of intraventricular impulse conduction disorders,
  • constant value of the PQ interval.

At this stage, the veterinarian must determine that each QRS complex is preceded by a correct P wave, and both these curve deviations are at an appropriate, repeated distance from each other.

Thanks to this, it determines the source of the ventricular complexes and answers the question whether there are any unforeseen present ecg curve deviations.

If the heart rhythm is a normal sinus rhythm then the heartbeat will be preceded by a P wave and the PR interval will be relatively constant.

Arrhythmia (i.e., abnormal heart rhythm) found in ECG examination it may result from the incorrect production of the stimulus or from its incorrect conduction.

Rhythm disturbances are therefore a fairly broad term which can include:

  • irregularity of stimulation generation,
  • stimulus conduction abnormalities (e.g. blocks),
  • ectopic abnormalities.

So let's see what types of abnormal heart rhythms we may be dealing with.

Disturbances in generating excitations

  1. Sinus arrhythmia.
    It occurs when stimuli are generated in the sinus node at irregular intervals.
    Put simply - the heart beats irregularly. There are two types of sinus arrhythmia:

    • Respiratory sinus arrhythmia.
      It is associated with a change in the activity of the parasympathetic center in the medulla: respiration causes changes in the tone of the vegetative system.
      Then, during inhalation, the heart rate is reflexively accelerated, and during exhalation - slows down.
      The heart is dominated by the parasympathetic system.
      This tonic activity of the intracardiac branches of the vagus nerve inhibits the heart.
      During inspiration, the inspiratory neurons in the respiratory center are stimulated, which results in the inhibition of the activity of neurons in the dorsal vagus nerve.
      Then the heart "escapes" from the action of the vagus nerve and the heart rate reflexively accelerates.
      It is a physiological phenomenon that is often found in dogs (especially brachycephalic breeds).
      It also occurs in cats, but is usually not observed during routine ECG testing.
      It is characterized by normal QRS complexes and normal P-R and Q-T intervals, while RR intervals vary in certain ways.
    • Sinus arrhythmia disorderly - does not depend on breathing and is usually an expression of certain heart conditions.
  2. Bradycardia i.e. a slow sinus rhythm (sinus bradycardia).
    The sinus node generates impulses at a lower frequency than the physiological frequency for a given animal species.
    The heart rate is slowed down.
    It is assumed that in weighing dogs less than 20 kg bradycardia occurs with the heartbeat < 70 uderzeń na minutę, and in weighing dogs more than 20 kg - heart rate < 60 uderzeń na minutę.
    In cats < 100 uderzeń na minutę.

    • The cause of this condition is either excessive tension of the vagus nerve or reduced discharges in the primary center of cardiac automatism, i.e. the sinus node.
      The heart rate can also slow down reflexively, e.g. increased pressure on the eyeballs or pressure on the carotid sinus.
      Physiological release is seen in working, athletic and trained animals
      As a rule, bradycardia does not give any visible clinical symptoms, but in severe conditions it can lead to drowsiness and even syncope.
      Sinus heart rate depression may be a pathological symptom associated with clinical conditions such as:

      • hypothermia,
      • Hypothyroidism,
      • increased intracranial pressure,
      • brain stem injuries,
      • uraemia,
      • hyperkalemia,
      • diseases of the sinoatrial node,
      • when administering certain groups of drugs (n. tranquilizers, general anesthesia, beta-blockers, calcium channel blockers, digitalis glycosides),
      • before or after cardiac arrest.
  3. Tachycardia or accelerated sinus rhythm (tachycardia).
    The sinus node generates impulses at a higher frequency than the physiological frequency for a given animal species.
    The heart rate is accelerated.
    It is assumed that in weighing dogs less than 20 kg tachycardia occurs with the heartbeat > 180 beats per minute, in dogs weighing more than 20 kg -> 160 bpm, in puppies> 220 bpm, and in cats> 240 bpm.

    • Physiological sinus tachycardia occurs during physical exertion, during heat, but also with strong emotional arousal, excitement.
    • Sinus tachycardia most often accompanies such conditions as:
      • ache,
      • fever or hyperthermia,
      • anemia (as a compensation for insufficient blood oxygenation),
      • overactive thyroid gland,
      • respiratory failure,
      • circulatory failure,
      • shock,
      • hypotension,
      • sepsis,
      • anxiety, anxiety,
      • poisoning (e.g. chocolate),
      • electric shock,
      • increased sympathetic tone.
    • Certain medications can induce sinus tachycardia, e.g.:
      • ketamine,
      • atropine,
      • adrenalin.
  4. Sinus inhibition.
    The sinoatrial node does not generate pulses uniformly, but it stops working (inhibition) over time.
    Then there are breaks in the heart's work, visible on the ECG graph in the form of pauses between individual heart cycles.
    These breaks are longer than the multiples of the basic rhythm.
    If such sinus depression lasts longer, it can develop fainting the animal.
    Often, the function of the pacemaker is taken over by a lower-level center, which results in the formation of an extra-sinus rhythm.

    • Sinus inhibition may appear in states of severe vagal tone.
    • In pathological situations, it accompanies the following conditions:
      • increase in intracranial pressure,
      • poisoning,
      • myocarditis,
      • heart diseases,
      • administration of antiarrhythmic drugs (glycosides, beta-blockers).
  5. Sick sinus syndrome.
    This is a term that refers to a sinus node dysfunction in generating active state pulses.
    It includes various sinus node abnormalities including severe sinus bradycardia and severe sinus suppression.
    Sometimes bradycardia alternates with supraventricular tachycardia.
    This phenomenon is known as bradycardia-tachycardia syndrome.
    Sick sinus syndrome is common in adult (over 6 years old) female Miniature Schnauzers and West Highland White Terriers.
    Does not apply to cats.

    • The features of the ecg are quite variable:
      • Persistent bradycardia or episodes of sinus depression that do not respond to escape rhythms,
      • in bradycardia syndrome, persistent bradycardia (with sinus arrest) alternating with supraventricular tachycardia.

Disturbances in the heart conduction system

In virtually every stage of the impulse traveling from the sinoatrial node to the lower levels of the heart's conduction system, certain disorders may occur, consisting in either slowing down or interrupting the conduction of the stimulus from the atria to the ventricles.

Such irregularities are referred to as heart blocks.

  1. Sinoatrial block (sinus node block).
    It causes difficulties in the conduction of the stimulus from the sinoatrial node to the atrium, as a result of which the active state impulse is blocked.
    The ECG curve shows gaps between heart cycles, similar to sinus inhibition (without P waves and QRS-T complexes), but here they are equal to a multiple of the basic rhythm.
    Both sinus inhibition and sinus block can cause bradycardia and even electrical arrest of the heart (asystole).
  2. Atrioventricular block 1st degree (First-Degree AV Block / Block AV I °).
    This disorder is a delay in the conduction of an impulse from the atria to the ventricles (through the atrioventricular node).
    Usually there is a sinus rhythm.

    • On ECG, P waves and QRS complexes are normal, but the PR interval is prolonged.
    • I ° AV block may occur physiologically with excessive vagal tone.
      It can accompany heart disease as well as poisoning (e.g. heart medications such as beta-blockers or digitalis glycosides).
  3. Second degree AV block (Second-Degree AV Block / Block AV II °).
    Here, the conduction of the stimulus in the atrioventricular node is temporarily blocked.
    In other words, not all impulses are conducted from the atria to the ventricles.
    There are the following types of second degree AV block:

    • Weckenbach's periodical / Weckenbach's arrhythmia (Type Mobitz I).
      It consists in a gradual and regular extension of the PR interval (or conduction time) in successive heart beats until conduction to the ventricles is completely blocked (no QRS complex after the P wave, as if it had fallen out of the rhythm).
      This phenomenon can occur with excessive vagal tension (especially in brachycephalic breeds).
      It usually appears in the course of organic heart diseases, as well as in the case of drug poisoning (β-blockers, glycosides) or the administration of certain anesthetics (e.g. xylazine).
    • Type Mobitz II.
      It is a periodic interruption of conduction in the AV node, as a result of which not all stimuli pass to the ventricles.
      In this case, there is no gradual lengthening of the PQ intervals (as was the case in the Weckenbach period), but the characteristic is that the PQ interval is constant, and there is no QRS complex after the P wave periodically.
      A certain specific ratio of the atrial rhythm to the ventricles is established (e.g. 6: 5 or 8: 7), but such cycles are relatively long.
      When the ratio of atrial to ventricular rhythm is expressed in a small number (e.g. 2: 1 or 3: 2) and is permanent, it is a fixed block.
      The reasons for its formation are similar to those observed with the Mobitz I type.
      May result in complete heart block.
  4. 3rd degree AV block (total heart block) (Third-Degree AV Block / Block AV III °).
    It occurs when impulse conduction from the atria to the ventricles is completely interrupted.
    However, in order for the heart to perform its most important function, a second pacemaker is activated, located below the place where the depolarization failure occurred. It can arise:

    • or in the lower part or branches of the beam, leading to the formation of the normal QRS complex and the AV node rhythm (then the heart rate is set at 60-70 beats per minute),
    • or in Purkinje cells - then an abnormal QRS-T complex is formed with the heart rhythm of approx. 30-40 beats per minute.
      The ventricles work in a slow rhythm (emanating from the emergency pacemaker), completely independent of the atria, which contract to the rhythm of the supraventricular pacemaker (which is most often the sinus node).
      IN ECG recording you can see regular and fast P wave waves and much slower (but relatively regular) QRS-T complexes that appear independently of P waves.
      Total heart block represents severe damage to the heart's conductive system.
  5. Abnormalities of intraventricular conduction (ventricular aberration).
    Impulse conduction disturbances can also occur in the lower levels of the heart's conduction system.
    His bundle is divided into left and right branches, supplying the left and right ventricles respectively.
    The left branch of the bundle, in turn, is divided into front and rear tufts.
    Excitation may be blocked in these conduction pathways, resulting in a delay in depolarization in the part of the ventricular muscle that is served by the affected vascular tissue. The most common findings are:

    • In dogs:
      • Right bundle branch block (RBBB).
        It occurs as a result of damage to the conduction or delay in conduction of the impulse through the right branch of the bundle of His.
        Left ventricular muscle activation is normal, while in the right ventricle the depolarization is prolonged because depolarization does not occur properly - through the conductive tissue but through the working cells of the heart muscle.
        The ECG record then states:

        • prolonged QRS duration (usually> 0.07 sec.),
        • the QRS complex has deep S waves in leads I, II, III and aVF and is positive in aVR and aVL,
        • the heart axis is right-handed.
      • Left bundle branch block (LBBB - left bundle branch block).
        It occurs when conduction through the left bundle branch is disturbed.
        In this situation, it is the right ventricle that is properly depolarized, while the activation of the left ventricle takes much longer (the impulse is transmitted not through the conductive tissue, but from the cell to the cell) - the result is a prolongation of the QRS complex.
        The ECG record states:

        • prolonged duration of the QRS complex (> 0.07 sec),
        • a positive QRS complex is present in leads I, II, III and aVF,
        • negative QRS in leads aVR and aVL.
    • In cats:
      • Left anterior fascicular block (LAFB) as a result of a failure in conduction through this bundle.
        It is relatively common in cats and rare in dogs.
        In ECG, ORS is normal, but:

        • high R waves are present in leads I and aVL,
        • deep S waves (greater than R) in leads II, III, and aVF,
        • heart axis shifted to the left (approx - 60 ° in a cat).
  6. Stopping the atria, during which there is no activity in the atria.
    This is due to abnormalities in the depolarization of the atrial muscle during impulse transit.
    The sinus node can generate pulses, but the atrial muscles do not depolarize and remain inactive.

    • Such a state can be caused by, among others:
      • Diseases of the myocardium - conduction disturbances also occur as a result of disease processes in the atrial musculature.
        Then the node substitute rhythms are activated.
      • Hyperkalemia - impulses are conducted from the sino-atrial node through the interstitial pathways to the atrioventricular node, so there is a sino-ventricular rhythm.
    • Features of ECG:
      • no P waves,
      • usually slow (
      • QRS complexes are relatively normal in shape (nodal rhythm), often with mildly prolonged duration.
  7. Periodic ventricular aberration.
    This is an abnormality in the conduction of a stimulus that may mimic an existing heart block.
    It may appear in the presence of premature supraventricular beats (more on them later).
    Such premature, unplanned impulse reaches the branches of the His beam before the latter is ready for action.
    His bundle cells are in the refractory period (i.e. they are unable to respond to subsequent stimuli).
    Such a branch (most often the right) is partially depolarized, resulting in the occurrence of a functional block.
    On ECG, the QRS complex is dilated and atypical, often adopts a right bundle branch block morphology and is premature.

Cardiac arrhythmias related to ectopy

Ectopia, in the literal sense of the word means "in an abnormal place ".

This type of disorder consists in the fact that impulses of the active state are created in such an abnormal place, outside the sinus node (which is the primary stimulus-generating center of the heart).

Ectopic foci are places that generate electrical impulses (in an unpredictable manner) and are at the same time arrhythmogenic areas.

Your doctor will check for ventricular syndromes that appear too early or too late. whether premature beats are present and whether ventricular syndromes have normal morphology.

Ectopic arousal is characterized on the basis of:

  • The places of formation. Ectopic foci can arise both in the atria and ventricles, and can affect both the cardiac conductive tissue and the working cells of the heart muscle. Therefore, it has been adopted to divide this type of stimulation into:
    • Supraventricular stimulation:
      • vestibular,
      • from the atrioventricular junction,
    • Ventricular beats.
  • Time of creation:
    • Premature beats - appear earlier than the expected sinus rhythm.
      They are not from the sinus node.
      Premature beats can appear singly or in more numbers, regularly or irregularly:

      • If there is one premature beat after each normal QRS complex, it is known as twin rhythm (bigeminy).
      • WITH trigeminia We are dealing with two premature stimulations after each normal sinus stimulation.
      • Additional stimuli may also appear in groups. If there are more than 3 of them - we are dealing with tachycardia:
        • periodic if they are brief seizures,
        • extended,
        • fixed.
    • Intermediate beats - While such accessory beats occur during the expected sinus beat, they do not originate from the sinus node and are usually ventricular in origin.
      Interrupted rhythms may originate from heart automatism cells in the atria, atrioventricular junction, or in the ventricles.
      If the sinus node fails to take up its function, this focus keeps the stimulus generation at its own pace.
    • Delayed beats - if they occur later than the expected beat from the sinus node, they are called surrogate beats.
  • Morphology:
    • If the ectopic stimuli in a given ECG record have a similar morphology (they look similar), they are called monomorphic (monomorphic).
    • If the ectopic stimulations are of different shape - they are polymorphic (multi-shaped) stimuli.

Premature ventricular complexes

They are relatively common in dogs and cats.

They arise in an ectopic focal point or foci located in the ventricular stimulus system below the His bundle or in the ventricular myositis.

Ventricular depolarization does not occur properly, pulses travel directly from cell to cell (rather than via conductive tissue), resulting in abnormal ECG images.

Such a ventricular syndrome may appear too quickly - then it is called premature ventricular complex (VPC) or after a pause (with some delay) - then it is called a surrogate beat.

Monomorphic (or monomorphic) ventricular premature beats can occur in healthy dogs, and there should be no more than 500 per day.

The exceptions are breeds predisposed to dilated cardiomyopathy (dobermans) or arrhythmogenic right ventricular cardiomyopathy (boxers), in which the number of premature ventricular beats should not exceed 100 / day.

Polymorphic ventricular premature beats are always abnormal.

The ECG record most often states:

  • Abnormal shape of the QRS complex. Any QRS complex that is abnormal in shape compared to the sinus syndrome is an abnormality.
    If it differs from normal sinus syndrome, it is more than certain that the depolarization was not conducted through the AV node, but arose from an ectopic focus in the ventricles.
  • Broad QRS complex (extended in time usually by about 50%).
    Since the excitation has not passed the normal (fast) conduction path, the time required for ventricular depolarization is prolonged.
  • The T wave (following the ectopic QRS complex) is usually large and in the opposite direction to the QRS.
  • The occurrence of three or more ventricular beats consecutively is called ventricular tachycardia.

Ventricular tachycardia (tachycardia) is a series of premature ventricular beats where the heart rate is usually> 100 beats per minute.

The causes of ventricular additional beats include:

  • cardiomyopathies,
  • advanced endocardiosis,
  • myocarditis,
  • heart cancer,
  • heart muscle injury,
  • pericarditis,
  • congenital defects of the conductive system,
  • electrolyte disturbances,
  • hypoxia,
  • anemia,
  • pyomyxia,
  • digestive system diseases (e.g. parvovirosis),
  • Lyme disease,
  • drugs that act proarrhythmically, e.g. epinephrine, atropine, most anti-arrhythmic drugs.

Accelerated ventricular rhythm (idioventricular tachycardia)

This is an ectopic ventricular rhythm that is not very fast:

is lower than the tachycardia rhythm but higher than the escape rhythm.

Therefore, it is called slow ventricular tachycardia.

In the ECG trace it looks like slow ventricular tachycardia.

It may not have any clinical consequences, but there is a risk of developing it into ventricular tachycardia.

Ventricular fibrillation

It is a terminal cardiac arrest event.

In the ventricles, depolarization waves appear randomly, not causing the ventricles to contract effectively.

The ECG test shows irregular isoelectric line waves.

With such uncoordinated activity, the chambers are unable to function as a pump.

This rhythm is known as deadly heart rhythm.

Surrogate rhythms

They constitute a very important defense mechanism.

In a situation where, for some reason, there is a break in the physiological, sinus rhythm of the heart, the stimulation from another focus is generated.

Then the stimulatory tissue from the lower centers can take over the function of the pacemaker and "escape " from the dominant influence of the sinus node.

This is often seen with occurrence bradyarrhythmia, e.g.:

  • sinus bradycardia,
  • sinus inhibition,
  • AV block.

Such evacuation complexes are rescue rhythms - if they had not been activated in the event of a sinus node failure, the heart would inevitably have stopped beating and the animal would die.

If escape rhythms do not develop, this is known as asystole that is, the lack of electrical activity in the heart.

The knotic surrogate rhythms are relatively normal in shape, while the ventricular ones are morphologically abnormal.

Supraventricular premature complexes

They arise in the ectopic focus or foci located above the ventricles, i.e. in the tissue of the atria or in the atrioventricular junction.

In this case, depolarization is transmitted to the ventricles by conduction physiological, and thus usually results in a normal QRS complex of normal duration.

However, the activation on the ECG curve appears too early.

Premature complexes that form in the atria are usually preceded by an abnormal P wave, called the P 'wave.

Atrioventricular junction beats are usually not preceded by a P 'wave.

The term "supraventricular" is a broad term used when it is not known whether the premature beat comes from the atria or from the.

Features visible in the ECG trace:

  • normal QRS-T morphology (as stimulus conduction is via the normal pathway),
  • the QRS complex is premature,
  • P waves may be present, but may not be identifiable either,
  • if P waves are visible, they are usually abnormal (i.e., deviating from normal sinus morphology) and the P-R interval is not normal.

The presence of three or more supraventricular premature beats is known as supraventricular tachycardia.

Usually the heart rate is then about 200 beats per minute (it can go up to 400).

Due to the place of origin, the following can be distinguished:

  • Premature excitations of vestibular origin.
  • Agitations from the atrioventricular junction.

Atrioventricular dissociation

It may be that the atria and ventricles are depolarized by completely separate and independent foci.

This can happen with an accelerated nodal or ventricular rhythm, disturbed AV conduction, or when the function of the sinus node is impaired.

Features in the EKG:

  • ventricular rate slightly faster than atrial rate,
  • P waves may occur before, during, or after the QRS complex,
  • P waves and QRS complexes are independent of each other.

Atrial fibrillation

It is one of the most common arrhythmias in small animals.

It is a supraventricular arrhythmia in which numerous waves of depolarization appear randomly in the atria.

On ECG, the QRS complexes have normal morphology and occur with normal or rapid frequency:

  • normal morphology of QRS complexes,
  • R-R spacing is irregular and chaotic,
  • the amplitude of the QRS complexes often varies,
  • there are no recognizable P waves preceding the QRS complexes,
  • small, irregular isoelectric line undulations ( "f " waves) are often visible.

The causes of atrial fibrillation include:

  • valve defects, e.g.:
    • mitral valve regurgitation,
    • mitral stenosis,
    • tricuspid regurgitation and / or stenosis,
    • aortic stenosis,
  • organic heart disease:
    • Dilated or hypertrophic cardiomyopathy,
    • bacterial endocarditis,
    • myocarditis,
    • pulmonary hypertension,
    • defect of the atrial septum,
    • Wolf-Parkinson-White syndrome,
    • myocardial infarction,
    • sinus node disease,
  • other diseases:
  • overactive thyroid gland,
  • pulmonary embolism,
  • poisoning,
  • hypoglycemia,
  • hypothermia,
  • physical effort,
  • water-electrolyte and acid-base imbalances.

Wandering starter

Dominant pacemaker gradually jumps from the sinus node to the atria and / or the AV node.

As a result, in ECG recording P waves differ in morphology - they can be positive, negative, biphasic, or even difficult to identify.

A wandering pacemaker is found relatively frequently in dogs and is most often associated with excessive vagal tone.

The depolarization and repolarization of the ventricles is shown on the ECG chart by the QRS-T complex.

If the morphology of this QRS complex is normal, we know that the ventricular depolarization was due to impulse conduction through the AV node.

If the QRS-T complex is different from the normal sinus syndrome, it is not from the AV node (because then its morphology would be normal), but from some random ectopic site in the ventricles.

Additionally, such ectopic ventricular beats are not associated with the preceding P wave.

The QRS complex is not only reshaped, it is usually also wider than normal.

Ventricular pre-excitation

It may happen that an impulse from the sino-atrial node bypasses the AV node during its path and enters the ventricles through additional conduction pathways.

This "shortcut" of conduction causes such a stray impulse to prematurely depolarize the ventricular muscle.

Such stimulation acts on a specific part of the heart muscle, while the rest of the myocardium is activated in the correct rhythm by the atrioventricular node.

Among the additional conduction paths, the following are distinguished:

  • Kent bundles,
  • James fibers,
  • Mahaim fibers.

Pre-excitation occurs in the so-called. Wolff-Parkinson-White syndrome (WPW) accompanied by episodes of paroxysmal supraventricular tachycardia.

The ECG record states:

  • short episode of PR,
  • delta wave in the R wave,
  • a slight prolongation of the QRS complex,
  • the heart rhythm (except for WPW) remains unchanged and usually regular,
  • in a ventricular syndrome, tachycardia may exceed 300 beats per minute.

Atrial flutter

It is a rare arrhythmia in dogs, and in cats it has not been documented.

The ECG record states:

  • flutter waves (the so-called "F " waves), visible as regular deflections of the isoelectric line (in the shape of a sawtooth), usually with a frequency 300-400 / min (if visible),
  • supraventricular tachycardia as a result of a ventricular response,
  • at high speeds, a functional AV block can occur (with a conduction ratio of 2: 1 or 3: 1).

Mechanisms of arrhythmia in animals

In animals, arrhythmias can be caused by several mechanisms.

As a rule, arrhythmias are associated with the following disturbances in the heart's conductive system:

  1. Disorders of cardiac automatism:
    • Disorders of physiological automatism can lead to the development of supraventricular or ventricular accessory beats.
      They occur when slow resting depolarization in peripheral cells of automatism is accelerated in relation to the physiological pacemaker, which is the sinus node, getting out of its control (or other superior centers).
      The causes of this type of disorders may be abnormalities in the tone of the autonomic nervous system, a decrease in the extracellular concentration of K + ions, an overdose of digitalis glycosides, local ischemia.
    • Pathological automatism.
      In this case, abnormal activity of the pacemaker cells or other (working) cells of the heart muscle may be responsible for the development of arrhythmias.
      This type of disorder may be the result of ischemia, excessive stretching or pressure of the heart muscle, or inflammatory or degenerative changes within it.
      As a result of changes in the cell membrane of myocytes (and subsequent changes in the flow of ions), there is a decrease in the membrane resting potential (it becomes more positive).
      Thanks to this, it becomes possible to reach the threshold potential faster, which in turn may lead to arrhythmias.
    • Triggered Activity.
      In its course, the so-called. follow-up (depolarization) potentials: early and late.
      These are additional discharges that appear during the period of depolarization of the atria or ventricles.
      As a result, additional stimulation or tachycardia may appear.
      Triggered activity does not occur spontaneously - it requires a depolarization wave (usually a normal sinus stimulation) in order to trigger another.
  2. The phenomenon of the circulating recurrent wave (reentry) - i.e. the circulation of excitation pulses on closed circuits.
    It is a disturbance in the conduction of impulses in the heart that is one of the major mechanisms for the development of life-threatening supraventricular and ventricular arrhythmias.
    Under normal conditions, excitation that is initiated in the sinus node propagates in a strictly orderly manner.
    Thanks to this, depolarized cells remain in those places of the heart muscle through which the excitation wave has passed - they are for some time in the period of the so-called absolute refraction (they are completely non-excitable and do not respond to any stimuli).
    Thanks to this, there is no possibility of the wave of excitation receding, which disappears after a directed passage through the whole heart.
    A pulse from the sinus node is needed to initiate another excitation.
    This ordered pulse conduction, however, can be disturbed.
    The reason for this is the presence of groups of cells that differ in the speed of impulse conduction and the duration of absolute refraction.
    In order for the reentry to occur, the active state impulse must be conducted simultaneously by two paths: usually one of them is a fast path (with a high conduction velocity), and the other - a slow path (the conduction velocity is lower).
    Under normal conditions, the conduction takes place on the fast path.
    With the phenomenon reentry the state of excitation reaches both paths, but depolarization in the fast path occurs at a higher speed, leaving depolarized cells behind, in the period of absolute refraction.
    The impulse, conducted along a slow path, therefore hits the cells that are already stimulated (i.e. temporarily unable to stimulate again).
    The excitation wave cannot go back along the slow path (because it has depolarized, insensitive cells behind it), so it returns quickly.
    If it encounters cells that have become excitable again after previous depolarization, it stimulates them.
    If they are still in the refractory period, the impulse returns to its free path.
    As a result, the impulse may "loop", which circulates around a closed circuit, leading to non-physiological stimulations and, consequently, arrhythmia.

Determination of the electrical axis of the heart

After assessing the heart rhythm and identifying possible disturbances, the electrical axis of the heart is assessed.

The electrical axis of the heart describes the directions of the formation and conduction of electrical stimuli in the heart's conducting system in the horizontal plane.

The impulses in a healthy heart arise in an orderly manner and are conducted in this way.

The axis of the heart is the resultant of all vectors of spreading stimulation. It can be:

  • Correct, it is then referred to as the normogram.
    In dogs, the normal electrical axis of the heart is between +40 and + 100 °.
    In cats - 0 to +160 °.
  • Tilted to the left - the so-called. levogram.
  • Tilted to the right - the so-called. prescription.

Abnormalities in the electrical axis of the heart:

  • Right-hand axle.
    It may indicate an enlargement of the right ventricle, but it is also present when the heart shifts to the right side of the chest, or it is also an individual feature.
    Conduction disturbances (e.g. right bundle branch block) can also deflect the heart axis to the right.
  • Left-hand axle.
    Moving the axis to the left may suggest enlargement of the left ventricle, but it is also present when shifting the cheese in the chest to the left, and is also an individual feature.
    A conduction disorder, such as the left anterior bundle block, also deflects the heart axis to the left.

Determining the values ​​of individual parameters

The last step in the ECG assessment is the measurement of the duration and / or amplitude of individual waves, segments and intervals visible in the ECG record.

Normal ECG values ​​for dogs and cats

Normal ECG values ​​in a dog

  • Heart rate: 70-160 beats / minute (puppies 70-220 bpm)
  • Rhythm: sinus or sinus arrhythmia.
  • P wave (max): 0.04 sec and 0.4 mV
  • PQ Interval: 0.06-0.13 sec.
  • QRS (width): 0.04-0.05 sec.
  • R wave (max.): up to 3 mV (giant breeds or greyhounds up to 3.5 mV).
  • ST Spacing: Within 0.2 mV from the baseline.
  • T wave not> 1/4 R.
  • QT interval: 0.15-0.25 sec.
  • Electric axis (frontal plane) 40-100 degrees.
  • A slower heart rate tends to occur in larger dog breeds, while a smaller dog breed tends to have a faster heart rate.

Correct ECG values ​​in a cat

  • Heart rate: 150-220 beats / minute.
  • Rhythm: sinus.
  • P wave (max): 0.04 sec and 0.2 mV.
  • PQ Interval: 0.05-0.09 sec.
  • QRS (width): 0.04 sec.
  • R wave (max.): up to 0.9 mV (total QRS < 1,2 mV).
  • ST Spacing: No change from baseline.
  • T wave: 0.3 mV (max).
  • QT interval: 0.12-0.18 sec.
  • Electric axis (frontal plane) 0-160 degrees.
  • All measurements are referenced to lead II with a travel speed of 50 mm / s.

As evidenced by changes in individual values ​​of the ECG record?

P wave

Under normal conditions, it is symmetrical, positive, and single-peak.

He is the first wave by the QRS complex.

  • A high P wave (called. P pulmonale):
    • right atrium enlargement (dogs),
    • enlargement of the left or right atrium (cats),
    • Sinus tachycardia (dogs).
  • Wide P wave (P-mitral):
    • enlargement of the left atrium (dogs and cats).
  • Missing P wave:
    • hyperkalemia,
    • sinus inhibition,
    • stopping the atria,
    • atrial fibrillation (bumpy isoelectric line).
  • Variable height of the P wave:
    • wandering pacemaker (a frequent phenomenon, especially with sinus arrhythmias)
    • premature atrial or linkage beats.
  • Inverted or retrograde P waves:
    • premature nodal or atrial beats or escape rhythms.
  • Duration of PQ Interval (PR).
    This time is measured from the beginning of the P wave to the beginning of the Q wave.
    If the latter is missing, then the measurement is made to the R wave (hence the possible designation PR).
    Thanks to the assessment of this progress, e.g. atrioventricular blocks.

    • Abbreviated PQ:
      • high influence of the sympathetic nervous system,
      • an additional pathway that excitation passes through the atrioventricular node.
    • A prolonged PQ interval is usually the result of an excessive slowdown in impulse conduction from the AV node:
      • 1st degree atrioventricular block,
      • second degree atrioventricular block.

QRS complex

It is measured from the beginning of the Q wave to the end of the S wave.

  • Deep Q wave:
    • normal option for dogs with a deep chest,
    • bilateral ventricular enlargement (if other criteria also suggest it).
  • High R wave:
    • left ventricular enlargement.
  • Broad QRS complex:
    • chamber enlargement,
    • intraventricular conduction disorders.
  • Small QRS complex:
    • normal volatility,
    • pericardial effusion,
    • pleural effusion,
    • pneumothorax,
    • Hypothyroidism,
    • obesity.
  • Deep S wave:
    • normal volatility,
    • right ventricular enlargement,
    • left ventricular hypertrophy.

ST segment

It connects the S wave with the T wave.

It can be below or above the isoelectric line.

  • ST segment elevation> 0.15 mV:
    • severe myocardial ischemia,
    • myocardial hypoxia,
    • pericardial effusion,
    • pericarditis,
    • digoxin toxicity,
    • transmural myocardial infarction.
  • ST lowering> 0.2 mV:
    • myocardial hypoxia,
    • digoxin toxicity,
    • potassium imbalance,
    • subendocardial myocardial infarction.

QT interval

The main factors that can influence the QT interval are heart rate and factors that influence the speed of chemical processes (e.g. body temperature, electrolyte levels, acid-base balance, hypoxia).

The QT interval is inversely related to the heart rate.

  • QT Extension:
    • hypokalemia,
    • hypocalcemia,
    • hypothermia,
    • bradycardia,
    • quinidine therapy,
    • conduction disturbances,
    • ethylene glycol poisoning.
  • QT Shortening:
    • hyperkalemia,
    • hypercalcemia,
    • digoxin,
    • atropine,
    • β-blockers and calcium channel antagonists.

T wave

It can be positive or negative, it can also be two-phase.

It is assessed in relation to the R wave, and its amplitude should not exceed 1/4 of the height of the R wave.

  • High (amplitude> 1 / 4R):
    • hypoxia and ischemia of the heart muscle,
    • interventricular conduction disturbances,
    • bradycardia,
    • chamber enlargement,
    • hyperkalemia.
  • Short:
    • pleural and / or pericardial effusion,
    • Hypothyroidism,
    • pneumothorax,
    • obesity,
    • the norm in cats.

Other changes visible in the ECG test:

Left ventricular enlargement

Electrocardiographic examination is not a method used to assess the size of the heart and should not be used as a basis for determining the enlargement of the cardiac silhouette.

However, in some situations it may lead to a suspicion of ventricular or atrial hypertrophy, which should lead to more extensive diagnostics (chest X-ray, heart echo).

Left ventricular enlargement is suspected when ECGs are visible on the examination high R waves.

If the R wave is higher in lead I than in lead II or aVF, this may indicate a hypertrophy.

If the R wave is high in all three leads (I, II, and III), it may be due to an expansion of the ventricle.

Left ventricular enlargement may also be indicated by:

  • increase in the duration of the QRS complex,
  • lowering the S-T section,
  • shifting the mean electrical axis of the heart (MEA) to the left.

Clinically, left ventricular enlargement (dilation) may be related to:

  • mitral valve regurgitation,
  • dilated cardiomyopathy,
  • aortic valve regurgitation,
  • patent ductus arteriosus,
  • cavities in the interventricular septum,
  • subvalvular aortic stenosis.

Right ventricular enlargement

They are suggested by deep S waves, as well as an increase in the duration of the QRS complex and a shift in the mean electrical axis of the heart (MEA) to the right.

Right ventricular enlargement (hypertrophy) occurs due to m.in.:

  • hypertrophic cardiomyopathy,
  • subvalvular aortic stenosis.

Left atrial enlargement

The enlargement (or expansion) of the left atrium may result in an elongation of the P wave (sometimes also its ribbing).

Since left atrial enlargement is often associated with mitral valve insufficiency, such an elongated P wave is called P-mitral.

The dent (notch) on the wave is the result of a lack of synchronization in the depolarization of both atria (because the left atrium is enlarged, it takes longer to activate than normal).

Giant breed dogs may have a physiological prolongation of the P wave.

Left atrial enlargement may be due to:

  • mitral valve regurgitation,
  • cardiomyopathy,
  • patent ductus arteriosus,
  • subvalvular aortic stenosis,
  • cavities in the interventricular septum.

Right atrium enlargement

With the enlargement (or expansion) of the right atrium, the amplitude of the P wave (i.e. its "height ") may increase.

Since the enlargement of the right atrium may be related to the so-called. heart, the high amplitude P wave is referred to as P-pulmonale. P-pulmonals can occur in animals with chronic respiratory diseases.

Right atrium enlargement may occur as a result of:

  • tricuspid valve regurgitation,
  • chronic respiratory diseases,
  • cavities in the interventricular septum,
  • subvalvular aortic stenosis.

Low voltage qrs

Low QRS amplitudes may be present:

  • in obese animals,
  • in patients with effusion into body cavities (e.g. ascites, hydrocardium, pleural fluid),
  • in hypothyroidism,
  • hyperkalemia,
  • pneumothorax,
  • certain respiratory diseases,
  • hypovolemia,
  • sometimes as an individual trait.

The ECG examination shows a low amplitude of the QRS complexes in the leads of the limbs (in dogs below 0.5 mV).

In cats, low QRS complexes are normal.

Electrical variability

It consists in the occurrence of a variable amplitude of the QRS complexes, occurring approximately every second beat.

Such electrical variability accompanies the presence of exudate fluid in the pericardial sac (during its work, the heart is as if "bounced" from side to side in the pericardial sac filled with fluid).

This movement causes alternating changes in the axis of the heart, shown by the variable amplitude of the QRS complex.

Presence of a notch (notch) on the arm of qrs

The presence of an indentation can occur with:

  • microscopic intramural infarction,
  • the presence of areas of fibrosis in the heart muscle,
  • intraventricular conduction abnormalities,
  • like an artifact (e.g. muscle tremors).

Hyperkalemia (elevated serum potassium)

Too high level of potassium in the serum quite often results in changes in the ECG record, however, the lack of these changes does not exclude hyperkalemia.

This condition may be accompanied by:

  • severe renal failure,
  • Addison's disease,
  • ketoacidosis (in the course of diabetes),
  • severe damage to skeletal muscles.

With the increasing level of potassium in the blood there are changes in the ECG record:

  • progressive bradycardia,
  • increased amplitude of the T wave (narrow and pointed),
  • progressive decrease in R-wave amplitude,
  • P-wave atrophy, atrial stop with slow nodal rhythm,
  • eventually ventricular fibrillation or asystole.


When analyzing the electrocardiogram, you can come across various artifacts, i.e. falsifications of the record.

Their identification during the ECG assessment is extremely important - incorrect interpretation of the record may result in incorrect diagnosis and implementation of inappropriate drugs, or abandonment of treatment.

The most common causes of artifacts are:

  1. Lack of proper contact between the patient's skin and the electrode.
    Most often it is caused by the electrode sticking to the hair or by using too little alcohol or test gel.
  2. Electrical interference, which may be caused by the patient not being isolated from the table, by the person holding the animal touching the electrodes, or by contacting electrodes on adjacent limbs.
    Such interference may also occur when testing is performed near high voltage sources.
  3. Movement of the animal during the examination is the most common source of artifacts.
    In addition to the usual movements of the limbs or head (with which the animal tries to free itself), restless breathing or panting or even purring can cause incorrect ECG recording.

Long-term recording of the heart rate


In addition to the standard - ambulatory ECG examination, it is also possible to use long-term heart rate recording in animals.

Then the so-called. cardiomonitoring, which is based on observing the ECG recording on the monitor screen.

In such a situation, the doctor assesses the current heart rhythm without fully analyzing the record.

It pays attention to the fact whether the heart rhythm is normal or whether it is disturbed.

Examples of the use of cardiomonitoring are:

  • monitoring the work of the heart during surgery,
  • monitoring the heart rate during exercise,
  • monitoring of the heart rhythm after the introduction of drugs (checking the effectiveness of therapy).

Holter test for ECG

Many heart rhythm abnormalities are not detected during outpatient ECG examination.

This is due to the fact that some arrhythmias are transient in nature and manifest at different times.

They may depend on e.g. on the patient's activity, current stressful situations, etc.

An animal showing disturbing symptoms that may suggest arrhythmias (e.g. fainting), during a short examination, the ECG may not show any disturbing changes in the record.

Therefore, in order to detect them, an animal's 24-hour ECG record during its normal activity is most often used.

During this time, the patient stays at home, leading a typical lifestyle.

If the distressing symptoms occurred in the dog or cat under certain circumstances (e.g. during intense exercise), the caregiver should recreate similar situations, in a way provoking the arrhythmia.

During this time, the tutor runs the so-called. diary of events, in which he notes the time and specific activity of his student / ward.

Holter examination is a more sensitive method than ambulatory ECG recording, because it is performed around the clock in conditions conducive to the recurrence of arrhythmias.

In the office, during a short recording during which the patient remains immobilized, as well as in unusual conditions, many arrhythmias remain undetected (especially those related to a slow heart rate).

Holter examination apparatus it is a small set, placed on a dog's or cat's chest.

Before wearing the recorder, it is necessary to shave the hair on both sides of the chest.

In these places, self-adhesive, disposable electrodes are glued, which are connected with the recorder by means of wires.

The recorder, in turn, is placed on the animal's back (between the shoulder blades) and secured with a bandage or placed in a special jacket with a pocket.

For 24 hours, the device records the ECG record and saves it on an audio cassette or on a digital medium.

This data is then analyzed after the recording is completed.

Correct 24/7 ECG record in dogs it is usually characterized by fairly wide variability in heart rate:

it may even be 30-40 beats per minute during sleep, and during extreme exercise, it can be very high (up to 250 beats per minute).

Periods of sinus depression, episodes of single ventricular premature syndromes, and second degree AV blocks are possible during sleep.

It is common sinus arrhythmia.

Particular attention is paid to presence premature ventricular syndromes.

In cats, during the 24-hour ECG recording, the heart rate varies approximately between 110 - 200 beats per minute.

In many cats, it is noticeable during sleep sinus arrhythmia.

Indications for an ECG Holter test

  1. Assessment of the severity of arrhythmias detected during the clinical examination and / or during the resting ECG test.
  2. Determining the effectiveness of the introduced antiarrhythmic therapy.
    This test is extremely useful in the treatment of cardiac arrhythmias.
    Due to the significant variability in the appearance of ventricular arrhythmias, a short study conducted in office conditions may underestimate the effectiveness of the introduced drugs.
  3. Assessment of syncope for arrhythmias.
    Holter examination in many cases of syncope allows to confirm the cardiogenic cause of syncope.
  4. Detection (with echocardiography) of subclinical cardiomyopathy.
    This is a study important in dobermans, in whom the presence of additional ventricular contractions may precede the overt clinical symptoms of cardiomyopathy, thus providing a reliable indicator of the developing disease.
    Seemingly healthy dogs that have more than 50 ventricular extras within 24 hours may develop an overt disease or may develop sudden cardiac death.
    So if a Doberman has more than 100 ventricular beats or tachycardias, the latent form of the disease is very strongly suspected.
  5. Implanted functioning assessment pacemaker.

How much does an ECG test cost?

The cost of an electrocardiogram it is not high - as a rule, it is within the limits PLN 30-50.

If it is necessary to carry out subsequent, control records - their price may be even lower.

On the other hand Holter examination is an expense of the order 250-300 PLN.


Electrocardiographic examination is an important diagnostic method in recognizing arrhythmias in animals.

Interpretation of the record is not easy and often causes great problems for veterinarians.

Hence, when finding any abnormalities - whether it is during auscultation of the heart during a clinical examination or during the assessment of an electrocardiogram - it is worth consulting your suspicions about a specialist dealing with veterinary cardiology on a daily basis.

It should be remembered that the ECG test can only show us certain heart rhythm disturbances.

Even if, during the analysis of the cardiogram curve, obvious features that may indicate enlargement of individual chambers of the heart become visible, it is not a conclusive study.

Additional examinations, such as X-ray examination, if echo of the heart.

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