ECG – signs of disorders of heart rhythm and conduction.

ECG -signs of combine disorders of automatism and conductivity of myocardium.

Instrumental methods of examination of cardiovascular system

It is difficult to overestimate the clinical importance of electrocardiography. It is used to reveal disorders of heart activity, and to diagnose coronary circulatory disorders. Electrocardiography helps reveal dystrophic and sclerotic changes in the myocardium. ECG changes also in abnormalities of electrolyte metabolism, due to various toxic substances or certain medicines (e.g. quinidine, digitalis, etc).

An arrhythmia is an abnormal heart rhythm resulting from any change, deviation or malfunction in the heart’s conduction system –the system through which normal electrical impulses are generated and travel through the heart. An arrhythmia may result in a heartbeat that is unusually fast (tachycardia), unusually slow (bradycardia), regular or irregular. Some arrhythmias are signs of more serious heart problems while others are not. An arrhythmia may be brief and unnoticeable, or it may be startling, obvious or even fatal. Skips, pauses and palpitations (strong, fast, “galloping” heartbeats) may commonly occur in the general population. In the majority of cases, a skipped beat is not medically significant. The most serious arrhythmias, however, contribute to approximately 500,000 deaths in the United States each year according to the American Heart Association. One type of arrhythmia (ventricular fibrillation) causes most of the 330,000 sudden cardiac deaths (SCD) that occur each year. SCD occurs when a patient dies following an episode of cardiac arrest, in which the heart suddenly stops beating. It is fatal unless the patient receives immediate and urgent medical attention.

In general, the probable outcome of an arrhythmia is largely dependent on any structural heart abnormalities. Outcomes tend to be worse among patients with poor heart function such as those with large heart attacks or cardiomyopathy. Arrhythmias are classified and treated based upon where in the heart they originate, how they manifest themselves and what cardiac functions they affect. For example, sinus arrhythmia is a type of heart rhythm that originates in the heart’s natural pacemaker (sinus node) but is characterized by changing heart rates often associated with breathing. For instance, heart rate may increase when inhaling and decrease when exhaling. It is almost always harmless.  More dangerous is sudden arrhythmia death syndrome (SADS), which is any disorder of the conduction system (e.g., long QT syndrome) that increases the risk of sudden cardiac death.

Diagnosing an arrhythmia is very important, because the longer an arrhythmia lasts without detection or treatment, the greater the chances of permanent damage and additional heart dysfunction. If someone experiences what feels like a flutter, skipped beat or any other unusual beat activity, a medical opinion and diagnosis should be obtained as soon as possible.

Diagnosis may be done through noninvasive tests such as an EKG (electrocardiogram) or an event monitor, or it may be done through a more invasive test such as an electrophysiology study.  Most nonsustained (temporary) arrhythmias need no treatment (other than lifestyle changes, perhaps). When arrhythmias do require treatment, it may include medications, cardioversion, a catheter ablation, and/or surgery to implant either a pacemaker or an implantable defibrillator (ICD).

There are a number of tests that physicians may use to diagnose an arrhythmia. The type of test(s) used will depend on a number of factors, including the specific symptoms of a patient as well as his or her personal and family medical history. These include:

·         An electrocardiogram (EKG), often considered the best diagnostic tool when an arrhythmia is suspected. It measures the heart’s electrical activity either at rest or under stress (a stress test). EKGs can be done by a physician in an office or hospital setting, or they can be portable and measured over time by a Holter Monitor or event recorder. An EKG that’s performed as the patient is lightly exercising is known as a stress test.  

• An echocardiogram of the heart uses sound waves to track the structure and function of the heart. A moving image of the patient’s beating heart is played on a video screen, where a physician can study the heart’s thickness, size and function.

• Cardiac catheterization procedures may be used to help a physician learn more about a patient’s specific arrhythmia. One such test is an electrophysiology study (EPS), which uses controlled electrical stimuli to locate the exact origin and nature of an arrhythmia. Once the electrical malfunction is pinpointed, catheter ablation may be used to treat it. An implantable cardioverter defibrillator (ICD) may be recommended based on the results of EPS testing. 

• A tilt table test may be used to evaluate causes of fainting spells (syncope) that are unrelated to arrhythmias. In the test, the patient is strapped onto a table. Then the table is tilted upright and the heart rate and blood pressure are monitored. This is not a direct test for arrhythmias. However, symptoms common with arrhythmia may also be caused by other medical problems. Tilt table tests may be used to rule out these other causes.

 

 

An electrocardiogram is the gold standard for the diagnosis of cardiac arrhythmias

Entering acqaintance with tthythm disorders it is necessary to repeate some data aboun ECG graph ans its decoding:

• Tachycardia (a heart rate of over 100 beats per minute)

• It guides therapy and risk stratification for patients with suspected acute myocardial infarction

• It helps detect electrolyte disturbances (e.g. hyperkalemia and hypokalemia)

• It allows for the detection of conduction abnormalities (e.g. right and left bundle branch block)

• It is used as a screening tool for ischemic heart disease during a cardiac stress test

• It is occasionally helpful with non-cardiac diseases (e.g. pulmonary embolism or hypothermia)

The electrocardiogram does not directly assess the contractility of the heart. However, it can give a rough indication of increased or decreased contractility.

 

Leads V1, V2, and V3 are referred to as the right precordial leads and V4, V5, and V6 are referred to as the left precordial leads.

The QRS complex should be negative in lead V1 and positive in lead V6. The QRS complex should show a gradual transition from negative to positive between leads V2 and V4. The equiphasic lead is referred to as the transition lead. When the transition occurs earlier than lead V3, it is referred to as an early transition. When it occurs later than lead V3, it is referred to as a late transition. There should also be a gradual increase in the amplitude of the R wave between leads V1 and V4. This is known as R wave progression. Poor R wave progression is a nonspecific finding. It can be caused by conduction abnormalities, myocardial infarction, cardiomyopathy, and other pathological conditions.

Two leads that look at the same anatomical area of the heart are said to be contiguous.

• The inferior leads (leads II, III and aVF) look at electrical activity from the vantage point of the inferior or diaphragmatic wall of the left ventricle.

• The lateral leads (I, aVL, V₅ and V₆) look at the electrical activity from the vantage point of the lateral wall of left ventricle. Because the positive electrode for leads I and aVL are located on the left shoulder, leads I and aVL are sometimes referred to as the high lateral leads. Because the positive electrodes for leads V5 and V6 are on the patient’s chest, they are sometimes referred to as the low lateral leads.

• The septal leads, V₁ and V₂ look at electrical activity from the vantage point of the septal wall of the left ventricle. They are often grouped together with the anterior leads.

• The anterior leads, V₃ and V₄ look at electrical activity from the vantage point of the anterior wall of the left ventricle.

• In addition, any two precordial leads that are next to one another are considered to be contiguous. In other words, even though V4 is an anterior lead and V5 is a lateral lead, they are contiguous because they are next to one another.

• Lead aVR offers no specific view of the left ventricle. Rather, it views the endocardial wall from its perspective on the right shoulder.

Normal atrial activation is over in about 0.10s, starting in the right atrium. A good place to look at P waves is in II, where the P shouldn’t be more than 2.5mm tall, and 0.11 seconds in duration.

A tall P wave (3 blocks or more) signifies right atrial enlargement, a widened bifid one, left atrial enlargement:

In V1, another good place to look, depolarisation of the right atrium results in an initial positive deflection, followed by a vector away from V1 into the left atrium, causing a negative deflection. The normal P wave in V1 is thus biphasic. It’s easy to work out the corresponding abnormalities with left or right atrial enlargement:

There are a few other tips:

·         A qR in V1 suggests right atrial enlargement, often due to tricuspid regurgitation.

·         If the overall QRS amplitude in V1 is under a third of the overall QRS amplitude in V2, there is probably RA enlargement.

A P wave originating in the left atrium often has a `dome and dart’ configuration.

 

The heart’s electrical axis refers to the general direction of the heart’s depolarization wavefront (or mean electrical vector) in the frontal plane. It is usually oriented in a right shoulder to left leg direction, which corresponds to the left inferior quadrant of the hexaxial reference system, although -30^o to +90^o is considered to be normal.

• Left axis deviation (-30^o to -90^o) may indicate left anterior fascicular block or hypertrophy of the left ventricle.

• Right axis deviation (+90^o to +180^o) may indicate left posterior fascicular block,  or a right ventricular strain pattern.

• In the setting of right bundle branch block, right or left axis deviation may indicate bifascicular block.

The baseline voltage of the electrocardiogram is known as the isoelectric line.

The P wave on the EKG is upright in II, III, and aVF (since the general electrical activity is going toward the positive electrode in those leads), and inverted in aVR (since it is going away from the positive electrode for that lead). A P wave must be upright in leads II and aVF and inverted in lead aVR to designate a cardiac rhythm as Sinus Rhythm.

• The relationship between P waves and QRS complexes helps distinguish various cardiac arrhythmias.

• The shape and duration of the P waves may indicate atrial enlargement.

The PR interval is usually 0.12 to 0.20 sec (120 to 200 ms). On an ECG tracing this is defined as 3 to 5 small boxes.

• A prolonged PR interval may indicate a first degree heart block.

• A short PR interval may indicate a pre-excitation syndrome via an accessory pathway that leads to early activation of the ventricles, such as seen in Wolff-Parkinson-White syndrome.

• A variable PR interval may indicate other types of heart block.

• PR segment depression may indicate atrial injury or pericarditis.

• Variable morphologies of P waves in a single ECG lead is suggestive of an ectopic pacemaker rhythm such as wandering pacemaker or multifocal atrial tachycardia

A normal QRS complex is 0.06 to 0.10 sec (60 to 100 ms) in duration.

Not every QRS complex contains a Q wave, an R wave, and an S wave. By convention, any combination of these waves can be referred to as a QRS complex. However, correct interpretation of difficult ECGs requires exact labeling of the various waves. Some authors use lowercase and capital letters, depending on the relative size of each wave. For example, an Rs complex would be positively deflected, while a rS complex would be negatively deflected. If both complexes were labeled RS, it would be impossible to appeciate this distinction without viewing the actual ECG.

• The duration, amplitude, and morphology of the QRS complex is useful in diagnosing cardiac arrhythmias, conduction abnormalities, ventricular hypertrophy.

The ST segment connects the QRS complex and the T wave and has a duration of 0.08 to 0.12 sec (80 to 120 ms). The relationship between the ST segment and T wave should be examined together. It should be essentially level with the PR and TP segment.

• The normal ST segment has a slight upward concavity.

• Flat, downsloping, or depressed ST segments may indicate coronary ischemia.

• Inverted (or negative) T waves can be a sign of left ventricular hypertrophy.

• When a conduction abnormality (e.g., bundle branch block, paced rhythm) is present, the T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T wave discordance.

There are some basic rules that can be followed to identify a patient’s heart rhythm. What is the rate? Is it regular or irregular? Are P waves present? Are QRS complexes present? Is there a 1:1 relationship between P waves and QRS complexes? Is the PR interval constant?

As the atria contract, the blood pressure in each atrium increases, forcing additional blood into the ventricles. The additional flow of blood is called atrial kick. Atrial kick is absent if there is loss of normal electrical conduction in the heart, such as during atrial fibrillation, atrial flutter, and complete heart block.

Regulation of the cardiac cycle

Cardiac muscle is myogenic, which means that it is self-exciting. This is in contrast with skeletal muscle, which requires either conscious or reflex nervous stimuli for excitation. The heart’s rhythmic contractions occur spontaneously, although the frequency or heart rate can be changed by nervous or hormonal influences such as exercise or the perception of danger. For example, the phrenic nerve accelerates heart rate and the vagus nerve decelerates heart rate.                                                                                                         

 

 

Heart conductive system

 

The rhythmic sequence of contractions is coordinated by the sinoatrial (SA) and atrioventricular (AV) nodes. The sinoatrial node, often known as the cardiac pacemaker, is located in the upper wall of the right atrium and is responsible for the wave of electrical stimulation that initiates atrial contraction. Once the wave reaches the AV node, situated in the lower right atrium, it is delayed there before being conducted through the bundles of His and back up the Purkinje fibers, leading to a contraction of the ventricles. The delay at the AV node allows enough time for all of the blood in the atria to fill their respective ventricles. In the event of severe pathology, the AV node can also act as a pacemaker; this is usually not the case because their rate of spontaneous firing is considerably lower than that of the pacemaker cells in the SA node and hence is overridden.

An Approach

ECGs can be very confusing, and there are dozens of different methods of interpretation. It’s perhaps best if everyone works out their own individual approach, but here’s just one approach you can build upon:

Of the above steps, the fourth seems counter-intuitive and unnecessary. In fact, it’s the most important. As in all medicine, complacence is dangerous. Avoid it!

Now, let’s sketch out a systematic approach. Ours is:

1.     Check the patient details – is the ECG correctly labelled?

2.     What is the rate?

3.     Is this sinus rhythm? If not, what is going on?

4.     What is the mean frontal plane QRS axis (You may wish at this stage to glance at the P and T wave axes too)

5.     Are the P waves normal (Good places to look are II and V1)

6.     What is the PR interval?

7.     Are the QRS complexes normal? Specifically, are there:

o    significant Q waves?

o    voltage criteria for LV hypertrophy?

o    predominant R waves in V1?

o    widened QRS complexes?

8.     Are the ST segments normal, depressed or elevated? Quantify abnormalities.

9.     Are the T waves normal? What is the QT interval?

10.           Are there abnormal U waves?

Knowing the paper speed, it’s easy to work out heart rate. It’s also very convenient to have a quick way of eyeballing the rate, and one method is as follows:

1.     Remember the sequence: 300, 150, 100, 75, 60, 50

2.     Identify an R wave that falls on the marker of a `big block’

3.     Count the number of big blocks to the next R wave.

If the number of big blocks is 1, the rate is 300, if it’s two, then the rate is 150, and so on. Rates in between these numbers are easy to `interpolate.

But always remember that in the heart, because we have two electrically `isolated’ chambers, the atria and ventricles, that we are really looking at two rates — the atrial and ventricular rates! It just so happens that in the normal heart, the two are linked in a convenient 1:1 ratio, via normal conduction down the AV node. In disease states, this may not be the case.

Conventionally, a normal heart rate has been regarded as being between 60 and 100, but it’s probably more appropriate to re-adjust these limits to 50 — 90/min. A sinus tachycardia then becomes any heart rate over 90, and bradycardia, less than 50. Note that you have to look at the clinical context — a rate of 85 in a highly trained athlete may represent a substantial tachycardia, especially if their resting rate is 52/minute! One should also beware of agressively trying to manage low rates in the presence of good perfusion and excellent organ function.

 

Normally, the septum depolarises before other parts of the left ventricle. This is seen as a small initial vector, which in the `septal leads’ (V1 and V2) is a positive deflection, and in lateral leads (e.g. V6) is seen as a small q. This observation is of relevance, as in conditions such as left bundle branch block, where the septum cannot depolarise normally, the lateral (septal) q is conspicuously missing.

Something of some importance is the time it takes the ventricle to depolarise, often termed the ventricular activation time. We can estimate this from the surface ECG by looking at the time from the onset of the QRS to the sudden downstroke of the QRS. (The fancy name for this sudden downstroke is the `intrinsicoid deflection’). In right orientated leads, a normal VAT is 0.02s, and on the left (e.g. V6) the duration should not exceed 0.04s.

 

Electrocardiography in diagnostics of  hypertrophy and arrhythmias

 

The ECG of healthy persons depends on their age and constitution, on the posture at the moment of taking an ECG (sitting, lying), on the preceding exercise, etc. ECG may change during deep breathing (the position of the heart in the chest is changed during deep inspiration and expiration), in increased tone of the sympathetic and parasympathetic nervous systems and in some other conditions.

 

ECG in standard leads with normal position of the heart’s electrical axis.

 

ECG in standard leads with the vertical position of the heart axis

 

ECG in standard leads with the horizontal position of the heart axis

 

Hypertrophy of heart chambers

If the atrium is enlarged and its myocardium is hypertrophied, the P wave changes. Since an enlarged atrium is slower excited, the length of the P wave becomes longer than 0.1 s. The amplitude of the P wave increases because a higher potential is generated to excite the large mass of the myocardium. If dystrophic or sclerotic changes occur in the myocardium, the shape of the P wave changes: it becomes serrated and split (with two phases). Enlargement of the left atrium changes the P wave in standard leads I and II. Enlargement of the right atrium changes the P wave in standard leads II and III.

Hypertrophy of the left atrium

Hypertrophy of right left atrium

 

Ventricular hypertrophy causes the following changes in ECG: (1) the position of the electrical axis is changed: in left-ventricular hypertrophy it deviates to the left, and in right-ventricular hypertrophy to the right; (2) the amplitude of the ventricular complex and its length increase, i.e. the time of excitation of the ventricles increases; (3) the recovery of the myocardium is upset and this shows itself in the changed terminal part of the ventricular complex of the ECG, namely, the S-T segment is displaced and the T wave changes; (4) in left-ventricular hypertrophy, the amplitude of the S wave in the right chest leads increases: the amplitude of the R wave in the left chest leads increases too. In right-ventricular hypertrophy the changes in the S and R waves are the reverse, i.e. a high R wave appears in the right chest leads, and a deeper S wave in the left leads.

Hypertrophy and chamber enlargement

Because of the thin-walled nature of the atria, from an ECG point of view, one cannot talk about “atrial hypertrophy” but only about enlargement. Conversely, thickening of the ventricle may result in increased voltages seen on the surface ECG, and we can then discuss “ventricular hypertrophy”.

Left ventricular systolic overload/hypertrophy (LVH)

The absence of LVH on ECG means nothing, as the features are insensitive. If however they are present, LVH is very likely. Because the criteria were formulated on white males, they are very insensitive in e.g. black women.

Systolic overload results in increased QRS deflections, with the sum of the S in V1 and the R in V5 or V6 over 35mm indicating hypertrophy. (In the above picture, also note the predominantly negative deflection of the P wave in V1, suggesting left atrial enlargement). A host of other criteria have been proposed. Useful are:

·                     R in I over 15mm

·                     R in AVL over 11mm

·                     Sum of all QRS voltages under 175mm (!)

T wave axis changes can be predicted knowing Schamroth’s rule .

LV   hypertrophy

LV diastolic overload

Features of LVH may be present (as above). Enormous R waves may be seen in left-sided leads, especially with aortic or mitral regurgitation. In contrast to systolic overload, where septal q waves in the lateral leads are often diminished or absent, in diastolic overload, prominent lateral Qs are noted. Unlike systolic overload (where the T waves are often inverted), T waves are usually upright, very symmetrical, and somewhat pointed.

Inverted U waves in V4-6 suggest either systolic or diastolic LV overload.

RV hypertrophy

A number of ECG abnormalities have been associated with right ventricular hypertrophy. These include:

·         right axis deviation;

·         A tall R wave (bigger than the S) in V1;

·         A `little something’ in V1 (an initial slur of the QRS, a small r, or a tiny q).

·         Increased VAT in V1

·         left-sided RS or rS complexes, partial or complete RBBB, or RS complexes in the mid-precordial leads.

Whenever you see a tall R in V1, consider the following differential:

·         posterior myocardial infarction

·         RV hypertrophy

·         Right bundle branch block

·         Wolff-Parkinson-White syndrome (with an appropriately placed accessory pathway)

·         Other rare causes such as dextrocardia, Duchenne muscular dystrophy, and so on

·         and, of course, incorrect lead placement

 

RV hypertrophy. High R vaves in right ECG leads

 

 

 

 

Hypertrophy

Hypertrophy criteria are fairly straightforward; we will be looking for enlargement of any of the four chambers.

 

Arrhythmias

Any deviations from the normal rhythm of the heart are called arrhythmias. These imply alterations in the heart rate, in succession or force of heart contractions, and also changes in the sequence of excitation and contraction of the atria and ventricles. Most arrhythmias are connected with functional changes or anatomical affections of the heart’s conduction system.

Under normal conditions, the sino-atrial node has the highest automaticity . therefore it is the pacemaker of the cardiac rhythm. Impulses are generated in the sino-atrial node at regular intervals (from 60 to 70 beats per min). The impulses are transmitted from sinus node (Wenckebach, Bachman, Thorel bundles) to the atrioventricular node at 0.8-1 m/s. This rate sharply decreases in the region of the atrioventricular node and the atrial systole therefore ends earlier than the excitation spreads over onto the miocardium of the ventricles to cause their contraction. Impulses are trasmitted from the aitrioventricular node through the His bundle at a higher rate (1—1.5 m/s), while the rate of its propagation in Purkinje’s fibres is as high as 3-4 m/s. Excitation is the triggering mechanism for the heart contraction. During the heart contraction, and immediately after systole, its discharges and is absolutely refractory; then its excitability gradually restores.

Automaticity is characteristic of the entire conduction system of the heart, but iormal conditions it is inhibited by the high activity of the sino-atrial node, which is the automaticity centre of the first order. If the sino-atrial node is affected, or the transmission of excitation is impared, the atrioventricular node becomes the pacemaker of the second-order i.e. automaticity centre. Impulses are generated here at a rate of 40 to 50 per the His bundle is affected, the impulses causing contraction of the heart may be genn the Purkinje fibres (automaticity centre of the third order), but the rate of the cardiac then slows down to 20-30 beats per min.

The normal cardiac rhythm may change (1) in affected automaticity of  the sino-atrial node, when the rate or sequence of impulses is altered; (2) in development of a focus of increased activity in the myocardium, which generates impulses to initiate heart contractions apart from their generation in the sino-atrial node (ectopic arrhythmia); (3) in disordered conduction of the impulses from the atria to the ventricles or inside the venitricules themselves. Abnormal rhythm can also be due to impaired contractility of the myocardium. Arrhythmia can sometimes depend on changes in such functions of the heart such as automaticity, excitability, conduct i contractility.

Arrhythmias associated with altered automaticity of the sino-atrial node (sinus arrhythmia). When automaticity of the sino-atrial node is upset, the rate of impulse generation may either accelerate (sinus tachycardia) or slow down (sinus bradycardia), or the sequence of impulses may be changed with their generation at irregular intervals (sinus arrhythnia).

Sinus tachycardia is directly connected with effects of biologically active substances which increase excitability of the sino-atrial node. This phenomenon may also depend on the change in the tone of the vegitative nervous system. It develops with intensified effect of the sympathetic nervous system. The rate of cardiac contractions in sinus tachycardia  varies from 90 to 120 and sometimes to 150—160 per min. Sinus tachvcardia develops during meals, physical exertion and emotional stress, elevated body temperature, the heart rate increases by 8—10 per each degree over 37 °C. Sinus tachycardia is a frequent symptom of myocarditis, heart defects, and other diseases. It develops in heart failure and in response to the increased pressure in the Hues of venae cavae. Tachycardia often develops ieurosis, anaemia  and in many infectious diseases and toxicosis; it can be proved by some pharmacological preparations (adrenaline, caffeine, lupine sulphate, etc.), and in thyrotoxicosis.

The clinical signs of sinus tachycardia is heart palpitation. The T-P interval on ECG shortens and the P wave may superimpose on the T wave.

Always consider pain as a possible cause of tachycardia.

There’s a long list, however:

·         Any cause of adrenergic stimulation (including pain);

·         thyrotoxicosis;

·         hypovolaemia;

·         vagolytic drugs (e.g. atropine)

·         anaemia, pregnancy;

·         vasodilator drugs, including many hypotensive agents;

·         fever

·         myocarditis

If the rate is almost exactly 150, always make sure that you are not mistaking atrial flutter with a 2:1 block for sinus tachycardia. A common error.

Sinus bradycardia is connected with slowed excitation of the sino-atrial node, which in turn depends mostly on the increased influence of the  asympathetic nervous system on the heart (or decreased influence of the sympathetic nervous system). Automaticity of the sino-atrial node increases in sclerotic affections of the myocardium and in the cold. The heart rate in sinus bradycardia decreases to 50—40 (in rare cases to 30) per min. Bradycardia may occur in well-trained athletes. It is not permanent and the heart rhythm is accelerated during exercise as distinct from pathological bradycardia in atrioventricular block when bradycardia persists during and after exercise. If automaticity of the sino-atrial node sharply decreases (sick-sinus syndrome), the second- or third-order centres may function as the pacemaker, i.e. ectopic arrhythmias develop.

Sinus bradycardia  may accur in increased intracranial pressure (tumour or oedema of the brain, meningitis, cerebral haemorrhage), in myxoedema, typhoid fever, jaundice, starvation, lead and nicotine poisoning, and due to effect of quinine and digitalis preparations. It may develop by reflex during stimulation of baroreceptors of the carotid sinus and the aortic arch in essential hypertension, and can be provoked by pressure on the eye-ball (Dagnini-Aschner reflex), or by irritation of receptors of the peritoneum and the internal organs.

Mild bradycardia is not attended by any subjective disorders, nor does it produce any effect on the circulation. Marked bradycardia (under 40 beats per min) may cause nausea and loss of consciousness due to cerebral anaemia. Objective examination reveals slow pulse. The ECG in sinus bradycardia reveals the unchanged atrial or ventricular complexes; the T-P interval only increases to show protraction of electrical diastole of the heart; the P-Q interval sometimes increases insignificantly (to 0.20-0.21 s).

Apart from fit, but otherwise normal individuals, there’s a long list of situations where sinus bradycardia occurs, including:

·         hypothermia;

·         increased vagal tone (due to vagal stimulation or e.g. drugs);

·         hypothyroidism;

·         beta blockade;

·         marked intracranial hypertension;

·         obstructive jaundice, and even in uraemia;

·         structural SA node disease, or ischaemia.

Sinus arrhythmia. Sinus arrhythmia and heart rate variability

There is normally a slight degree of chaotic variation in heart rate, called sinus arrhythmia. Sinus arrhythmia is generally a good thing, and loss of this chaotic variation is of ominous prognostic significance. Post myocardial infarction, a metronome-like regularity of the heartbeat is associated with an increased likelihood of sudden death, and just before the onset of ventricular tachycardia (or fibrillation), variability is lost! Absence of any sinus arrhythmia suggests an autonomic neuropathy.

Sinus arrhythmia characterized by irregular generation of impulses  due to variations in the tone of the vagus. It would commonly be associated with respiratory phases {respiratory arrhythmia): the cardiac rhythm accelerates during inspiration and slows down during expiration. Sinus arrhythmia is observed in children and adolescents (juvenile arrhythmia), in patients convalescing from infectious diseases, and in certain diseases of the central nervous system. It can be a sign of pathology in rare cases when arrhythmia is not connected with respiration or when it develops in the aged during normal respiration.

Clinically sinus arrhythmia is not attended by any subjective disorders. The cardiac rhythm and pulse rate only change with respiratory phases, and the intervals between the heart complexes (R-R intervals) vary in length on the ECG.

 

Ectopic arrhythmias. Additional (heterotopic or ectopic) foci of excitation can arise at any site of the conduction system (in the atria, ventricles, atrioventricular region). They can cause premature contraction of the heart before termination of the normal diastolic pause. This premature contraction is called extrasystole, and the disorder of the cardiac rhythm is called extrasystolic arrhythmia. If the activity of the ectopic focus is very high, it can become a temporary pacemaker, and all impulses governing the heart will during this time be emitted from this focus. The cardiac rhythm is then markedly accelerated. The condition is known as paroxysmal tachycardia.-Ectopic arrhythmias are often due to increased excitability of the myocardium. The phenomenon known as re-entry can be another mechanism of ectopic arrhythmia.

Extrasystolic arrhythmia. Extrasystole usually develops during normal contractions of the heart governed by the sino-atrial node (nomotopic contractions). Ectopic foci of excitation can arise at any site of the conduction system. Usually excitations arise in the ventricles, less frequently in the atria, the atrioventricular node, and in the sino-atrial node (sinus extrasystole). A nomotopic contraction of the heart that follows extrasystole occurs in a longer (thaormal) lapse of time. This can be explained as follows. During the atrial extrasystole, excitation from the ectopic focus is transmitted to the sino-atrial node to “discharge” it, as it were. The next impulse arises in the sino-atrial node only in a lapse of time that is required to “discharge” the node and to form a new impulse.

 

 

Extrasystole is premature appearance of cardiac complex

 

Atrial extrasystole. These arise from ectopic atrial foci. Commonly, the ectopic beat always arises at about the same time after the sinus beat.

The ectopic beat usually discharges the SA node, so subsequent beats of SA origin are not in synchrony with the previous sinus rhythm.

If the extrasystole occurs early on, it may find the His-Purkinje system not quite ready to receive an impulse, and a degree of block may be seen. This is termed `aberration’.

 

 

Atrial extrasystole

 

In ventricular extrasystole, the time between the extrasystolic contraction and subsequent nomotopic contraction is even longer. The impulse from the heterotopic focus, located in the ventricles, propagates only over the ventricular myocardium; it would not be usually propagated to the atria via Aschoff-Tawara node. The impulse occurs iormal time in the sino-atrial node but it is not transmitted to the ventricles because they are refractory after the extrasystolic excitation. The next impulse from the sino-atrial node will only excite and contract the atria and the ventricles. A long “compensatory” pause therefore follows the ventricular extrasystole which lasts till the next nomotopic contraction.

Extrasystolic arrhythmia is quite common. It may occur in practically healthy individuals as a result of overexcitation of certain sites of the conduction system due to the action of the extracardiac nervous system in heavy smokers and in persons abusing strong tea or coffee; it can occur by reflex in diseases of the abdominal organs. Extrasystole often attends various cardiovascular pathological conditions due to inflammatory or dystrophic affections of the myocardium or its deficient blood supply; or it may be due to hormonal disorders (thyrotoxicosis, menopause), various intoxications, disorders of electrolyte metabolism, etc.

Patients with extrasystole can feel their heart missing a beat (escape beat) and a subsequent strong stroke. Auscultation of the heart reveals its premature contraction with a specific loud first sound (due to a small diastolic filling of the ventricles). Extrasystole can be easily revealed by feeling the pulse: a premature weaker pulse wave and a subsequent long pause are characteristic. If extrasystole follows immediately a regular contraction, the left ventricle may be filled with blood very poorly and the pressure inside it may be so small that the aortic valve would not open during the extrasystolic contraction and the blood will not be ejected into the aorta. The pulse wave on the radial artery will not be then detectable (missing pulse). The ECG of all extrasystoles are characterized by: (1) premature appearance of the cardiac complex; (2) elongated pause between the extrasystolic and subsequent normal contraction. According to the origin, extrasystoles are classified as atrial and atrioventricular (which are given a commoame of supraventricular), and also ventricular (left- and right-ventricular) extrasystoles.

Excitation of the atria only changes in atrial extrasystole because the impulse is generated not in the sino-atrial node, and the ventricles are excited by the usual way. The ECG of atrial extrasystole is characterized by the following signs: (1) premature appearance of the cardiac complex; (2) preservation of the atrial P wave which may be slightly, disfigured and superimposed on the preceding T wave; this depends on abnormal atrial excitation from a heterotopic focus; (3) normal shape the ventricular complex; (4) slight elongation of the diastolic pause interval following the extrasystolic contraction.

In atrioventricular (nodal) extrasystole the Aschoff-Tawara node impulse is transmitted to the atria retrogradely, from boil to top. The ventricles are excited iodal extrasystole in the usual way. The following signs are characteristic of the ECG iodal extrasystolr (1) premature appearance of the cardiac complex; (2) changes in the P wave which becomes negative to show the retrograde atrial excitation (in some cases the P wave is absent on the ECG); (3) the position of the P wave is differ respect to the ventricular complex changes, which depends on the ranning  of the excitation wave onto the atria and the ventricles. If excitation of the atria is followed by excitation of the ventricles, the negative P wave is recorded before the ORS complex; if the ventricles are excited first the negative P wave follows the QRS complex. If the atria and ventricle are excited synchronously, the P wave is not recorded separately but superimposes the QRS complex to alter its configuration. In other cases, the configuration of the ventricular complex in

 

Ventricular extrasystole. Excitation order changes sharply in ventricular extrasystole. The ventricular impulse is not usually transmitted retrogradelly through the Aschoff-Tawara node and the atria are not therefore excited. As the focus of excitation is located in one ventricle, the ventricles are not excited synchronously (as iormal cases), .but each after another, i.e. that ventncle is excited first where the ectopic is located The time of excitation of the ventricles is therefore longer and ORS complex is wider. The ECG is characterized by the following: (1) premature appearance of the ventricular complex (2) absence of P wave; (3) deformation of the QRS complex; (4) since the sequence of relaxation in the ventricles is not synchronous the shape and the height of the T wave changes as well. As a rule, it is enlarged and its direction is opposite to that of the maximum wave of the  complex (the T wave is negative if  R wave is high and positive if S wave is deep). (5) The ventricular extrasystole is followed by a complete compensatiry pause (except in interpolated extrasystoles): the ventricles are excited by the sinus impulse that follows the extrasystole but the  ventricle are in refractory at this moment.

Configuration of the ventricular complex in various ECG leads depends on the location of ectopic focus. Left-ventricular extrasystole is characterized by a high R wave in the third standard lead and the deep S wave in the first lead. In right-ventricular extrasystole there will be opposite changes.

Chest leads are very important for the topic diagnosis of ventricular extratrasystole. Left-ventricular extrasystoles are characterized by the presence of the extrasystolic complex with a high R wave in the right  leads and a broad or deep S wave in the left chest leads. In right-ventricular extrasystole, on the contrary, the deep S wave is recorded in the right  leads, and a high R wave in the left chest leads. If excitability of myocardium is high, several (rather than one) ectopic foci may exist, extrasystoles are generated in various heart chambers and having different figuration then appear on the ECG {polytopic extrasystole).

 

 

Ventricular extrasystole

Wherever an ectopic focus may arise, its impulses may alternate in the certain order with the normal impulses of the sino-atrial node, phenomenon is known as allorhythmia. Extrasystole may alternate each sinus impulse (bigeminy), or it may follow two normal  pulses (trigeminy), or three normal impulses (quadrigeminy). If the heterotopic focus is even more active, a normal contraction may be followed by several extrasystoles at a run (group extrasystole) which sometimes precedes an attack of paroxysmal tachycardia.

Because ventricular extrasystoles arise within an ectopic focus within the ventricular muscle, the QRS complex is wide, bizarre, and unrelated to a preceding P wave. There is usually a constant relationship (timing) between the preceding sinus beat and a subsequent ventricular beat, because the preceding beat influences the ectopic focus.

The ventricular beat is not usually conducted back into the atria. What happens to the atrial beat that occurred, or was about to occur when the VE happened? Usually, this is blocked, but the subsequent atrial beat will occur on time, and be conducted normally.

Rarely, the ventricular beat may be conducted retrogradely and capture the atrium (resulting in a P wave after the QRS, with an abnormal morphology as conduction through the atrium is retrograde). The atrial pacemaker is now reset! In the following rather complex tracing, we have a ventricular rhythm (a bit faster than one might expect, perhaps an accelerated idioventricular rhythm) with retrograde P waves, and something else — some of the P waves are followed by a normal looking `echo’ beat as the impulse is conducted down back in Because the intrinsic rate of an ectopic focus often tends to be slow-ish, extrasystoles will tend to arise more commonly with slower rates. In addition, if the rate is varying, extrasystoles will tend to `squeeze in’ during long RR intervals. Some have called this the “rule of bigeminy”.

Couplet

Two VE’s are termed a couplet.

Fusion beat

Occasionally, a VE occurs just after a sinus beat has started to propagate into the His-Purkinje system. This results in a `fusion beat’, which combines the morphology of a normal sinus beat and that of the extrasystole.

Paroxysmal tachycardia. This is a sudden acceleration of the cardiac rhythm (to 180—240 beats per min). At attack of paroxysmal tachycardia exist from several seconds to a few days and terminate just as unexpectivelly as it begins. During an attack, all impulses arise from a monotopic focus because its high activity inhibits the activity of the sino-atrial node. Paroxysmal tachycardia (like extrasystole) may occur in increased nervous excitability, in the absence of pronounced affections of the heart muscle, but it arises more likely in the presence of heart disease (e.g. myocardial infarction, heart defects or cardiosclecrosis).

•During an attack of paroxysmal tachycardia, the patient feels strong palpitaition, discomfort in the chest, and weakness. The skin turns pale, when attack persists, cyanosis develops. Paroxysmal tachycardia is followed by swelling and pulsation of the neck veins, because during accelerated pulse (to 180-200 per min) the atria begin contracting before ventricular systole ends to increase venous pressure.  Auscultation of the heart during the attack of paroxysmal tachycardia reveals decreased diastolic pause, the heart rhythm becomes pendulum. The first sound increases due to insufficient ventricular filling. The pulse is rhythmic, very fast, and small. Arterial pressure may fall. If an attack persists (especially if it develops in a heart disease) symptoms of cardiac insufficiency develop.

Like in extrasystole, the heterotopic focus in paroxysmal tachycardia i be located in the atria, the atrioventricular node, and the ventricles. It pos\sible to locate the focus only by electrocardiography: a series of ex-stoles follow on an ECG at regular intervals and at a very fast rate. In supraventricular PT the P wave cannot be seen because of accelerated herat rhythm and the shape of the ventricular complex is not changed; in ventricular PT series of altered and broadened ventricular complexes are recorded).

Supraventricular tachyarrhythmias (SVT)

Irregular SVT

By far the commonest cause of irregular SVT is atrial fibrillation, where the atrial rate is in the region of 450 to 600/min, and the atria really do not contract rhythmically at all. The atrium “fibrillates”, writhing like a bag of worms. The conventional view of the pathogenesis of AF is that there are multiple re-entrant `wavelets’ moving through the atrial muscle, but recent evidence suggests that much AF actually arises from ectopic activity in the muscular cuff surrounding the pulmonary veins where they enter the left atrium. AF is thought to beget further AF through “electrical remodelling” — electrophysiological changes that are induced in atrial myocytes due to fast rates and the consequent calcium loading.

Regular SVT

Atrial flutter is common. The atrial rate is commonly 300/min, and there is usually a 2:1 block, resulting in a ventricular response rate of 150/min. Other ratios are possible, and sometimes the ratio varies. This rhythm is often unstable, and the heart may flip in and out of sinus rhythm, or there may be runs of atrial fibrillation.

Distinguishing causes of SVT

A few pointers are in order. The important thing to look for is the P wave.

 

Supraventricular paroxysmal tachycardia

Ventricular tachycardia

Three or more ventricular extrasystoles are a bad sign, and are termed ventricular tachycardia (VT). There is usually severe underlying myocardial disease. Sustained VT (more than about 30 beats) often degenerates into ventricular fibrillation, resulting in death.

Ventricular paroxysmal tachycardia

 

Arrhythmias due to disordered myocardial conduction. Transmission of the impulse may be blocked at any part of the heart’s conduction system. The following types of heart blocks are distinguished: (1) sinoatrial block, in which beats are sometimes missing in the sino-atrial node and the impulse is not transmitted to the atria; (2) intra-atrial block, in which transmission of excitation through the atrial myocardium is impaired; (3) atrioventricular block, in which conduction of impulses from the atria to the ventricles is impaired; (4) intraventricular block, in which conduction of impulses through the His bundle and its branches is impaired.

Block may develop in inflammatory, dystrophic, and sclerotic affections of the myocardium (e.g. rheumatic and diphtheritic myocarditis, cardiosclerosis). The conduction system may be affected by granulous  cicatrices, toxins, etc. Conduction is often impaired in disordered coronary circulation, especially in myocardial infarction (the interventricular septum is involved). Block may be persistent and intermittent. Persistent block usually connected with anatomic changes in the conduction system whereas intermittent block depends largely on the functional condition in the atrioventricular node and the His bundle and is often connected with increased influence of the parasympathetic nervous system; atropine sulphate is an effective means that restores conduction.

Sino-atrial block is characterized by periodic missing of the heart beat and pulse beat. -r, in the presence of  a regular sinus rhythm (neither P wave nor the QRST complexes are recorded); the length of diastole doubles.

SA node block. Intra-atrial block can only be detected electrocardiographically because clinical signs are absent. since the time of atrial excitation increases, the length of the P waves is increased too.

This is a diagnosis of deduction, as no electrical activity is seen. An impulse that was expected to arise in the SA node is delayed in its exit from the node, or blocked completely. A second degree SA block can be `diagnosed’ if the heart rate suddenly doubles in response to, say, administration of atropine. If the SA node is blocked, a subsidiary pacemaker will (we hope) take over, in the atrium, AV node, or ventricle. Intraatrial block is characterised by prolongation of P wave.

AV nodal blocks

There are three “degrees” of AV nodal block:

1.     First degree block:

simply slowed conduction. This is manifest by a prolonged PR interval;

Conduction intermittently fails completely. This may be in a constant ratio (more ominous, Type II second degree block), or progressive (The Wenckebach phenomenon, characterised by progressively increasing PR interval culminating in a dropped beat — this The QRS complex

2.     Second degree block:

–         Mobitz Type I second degree heart block;

–          Mobitz Type II second degree heart block;

–         Mobitz Type III second degree heart block;

 

 

 

3. Third degree (complete) block.

 

Atrioventricular block is most important clinically. It is classified into three degrees by gravity. The first degree can only be revealed electrocar-diographically by the increased P-Q interval (to 0.3-0.4 s and more). This block cannot be detected clinically, except that splitting of the first sound may sometimes be detected by auscultation (splitting of the atrial component).

The second-degree atrioventricular block is characterized by dualism of its signs.

Mobitz I. Conduction of the Aschoff-Tawara node and His bundle is impaired: each impulse transmitted from the atria to the ventricles increases and the P-Q interval on the ECG becomes longer with each successive beat. A moment arrives at which one impulse does not reach the ventricles and they do not contract, hence the missing QRS complex on an ECG. During a long diastole, which now follows, the conduction power of the atrioventricular system is restored, and next impulses will again be transmitted, but their gradual slowing down will be noted again; the length of the P-Q interval will again increase in each successive complex. Period which follows the P wave is called the Samoilov- Wenckebach period.

Mobitz II. This type of block is characterized by periodically missing ventricular contractions, and hence missing beats, which correspond to the Samoilov-Wenckebach period.

Mobitz III type of the second-degree atrioventricular block can be characterised by a worse conduction. The P-Q interval remains constant, but only i second, third, or (less frequently) fourth impulse is transmitted to the’ tricles. The number of P waves on the ECG is therefore larger than ventricular complexes. This is known as incomplete heart block with a 2:1, 3:1, etc. ratio. Considerable deceleration of the ventricular rhythm and slow pulse are characteristic, especially in 2:1 block. If each third or fourth beat is missing, the pulse is irregular and resembles trigeminy or quadrigeminy with early extrasystoles and pulse deficit. The heart rhythm slows down significantly, the patient may complain of giddiness, everything going black before his eyes, and transient loss of consciousness due to anaemia of the brain.

The third-degree atrioventricular block is called complete heart block. Atrial impulses do not reach the ventricles and the sino-atrial node becomes the only pacemaker for the ventricles. The ventricles contract by their own automaticity in the centres of the second or third order. The number of their contractions in complete he block is about 30-40 per min, and ventricular rhythm slows down with  lower position of the pacemaker in the conduction system.

The ECG in complete heart block is characterized by the following signs: (1) atrial P waves and ventricular complexes are recorded dependently of each other, and part of the P waves may superimpose  on ventricular complex and become invisible on the ECG; (2) the number of ventricular (complexes is usually much smaller than the number of atrial waves; the pacemaker arises from the Aschoff-Tawara node or His bundle. The heart rate in persistent complete heart block may be sufficiently decreased  (40 50 beats/rnin) but the patient may be unaware of the disease for a time. Examination of such patients reveals slow, rhythmic, and full pulse. Tie heart sounds are dulled but a loud first sound (“pistol-shot” according to Strazhesko) may be heard periodically. It occurs due to simultaneous contractions of the atriums and ventricles. If the ventricular nun slows down significantly (to 20 beats/min and less), or when incomplete heart block converts into a complete one patients condition significantly worthens. When the impulses from the atria are not conducted to the ventricles, Their automaticity has not yet developed, attacks (the Morgagni-Stokes syndrome) may occur due to disordered blood supply in the central nervous system. During an attack the patient loses consciousness, falls, general epileptiform convulsions develop, the respiration becomes deep, the skin is pallid, the pulse is very slow or even impalpable.

Bundle branch blocks

Involves the left and/or right bundle branches, which transmit the heart signal to the ventricles.Left bundle branch block (LBBB) is further classified as complete or partial (anterior fascicular block or posterior fascicular block). Right bundle branch block (RBBB) is also classified as complete or partial. Other types of bundle branch block include bifascicular block and trifascicular block.

A broadened QRS complex suggests a bundle branch block, although there are other causes:

RBBB

Diagnostic criteria for right bundle branch block are somewhat empiric, but useful. Here they are:

1.     Tall R’ in V1;

2.     QRS duration 0.12s or greater (some would say, >= 0.14);

In addition, there is usually a prominent S in the lateral leads (I, V5, V6).

RBBB is sometimes seen in normal people, or may reflect congenital heart disease (e.g. atrial septal defect), ischaemic heart disease, cardiomyopathy, or even acute right heart strain.

 

 

RBBB.

LBBB

Diagnose this as follows:

1.     No RBBB can be present;

2.     QRS duration is 0.12s or more;

3.     There must be evidence of abnormal septal depolarization. The tiny q waves normally seen in the left-sided leads are absent. (And likewise for the normal tiny r in V1).

In addition, the VAT is prolonged, and tall, notched R waves are seen in the lateral leads (RR’ waves). There is usually a notched QS complex in V1 and V2.

 

 

LBBB

Left anterior hemiblock (LAHB) is interruption of the thin anterosuperior division of the left bundle. Suspect it if there is left axis deviation (past -45^o) without another cause (such as inferior myocardial infarction, or some types of congenital heart disease or accessory pathways).

Other features of LAHB include an initial QRS vector which is down and to the right, a long VAT, and several other minor changes.

LAHB may indicate underlying heart disease, but is much more worrying when associated with other abnormalities (such as PR interval prolongation or RBBB).

The diagnosis of left posterior hemiblock is mentioned only to be avoided!

Bundle-branch block can only be detected electrocardiographically. On ECG  deformed QRS complexes will be recorded cccording to the location of block. Besides QRS complex is wide due to prolongation of the period of inner deviation, ST segment is displaced opposite to the direction of the maximum wave of the QRS complex. If the right branch of the bundle is affected, the shape of the ventricular complexes resembles that of left-ventricular extrasystoles and  vice versum. It has no subjective signs.

Atrial and ventricular flutter and fibrillation

 Fibrillation is otherwise known as complete or absolute arrhythmia. It arises in cases with suddenly increased excitation of the myocardium and simultaneous conduction disorders. The sino-atrial node fails to function as the pacemaker and many ectopic excitation foci (to 600-800 per min) arise in the atrial myocardium, which becomes only possible with a marked shortening of the refractory period. Since conduction of these impulses is difficult, each of them only excites and causes contraction of separate muscular fibers rather than the entire atrium. As a result, minor contractions develop in the atrium (atrial fibrillation) instead of adequate atrial systole. The mechanism of fibrillation is not fully understood. It is believed that permanent circulation of the circular excitation wave in the atria can account for the development of this disorder. Only part of the impulses are transmitted to the ventricles through the Aschoff-Tawara node. Since conduction of atrial impulses is irregular, the ventricles contract at irregular intervals to cause complete arrhythmia of the pulse. Depending on the conductability of the Aschoff-Tawara node, three forms of atrial fibrillation are distinguished: tachyarrhythmic, in which ventricles contract at a rate from 120 to 160 per min, bradyarrhythmic, in which the heart rate does not exceed 60 per min, and normosystolic, in which the ventricles contract at a rate of 60-80 per min.

Fibrillation is characteristic of mitral heart diseases (especially of mitral stenosis), coronary atherosclerosis, thyrotoxicosis, etc. Fibrillation may occur as a permanent symptom or in attacks of tachyarrhythmia. Clinically fibrillation (bradyarrhythmia) may cause no subjective symptoms. Tachyarrhythmia is usually characterized by palpitation. Examination of the heart reveals complete irregularity of the heart contractions. Variations in the length of diastole account for variations in ventricular filling and hence in the intensity of the heart sounds. The pulse is also arrhythmic; pulse waves vary in height (irregular pulse), and pulse deficit often develops in frequent heart contractions. The ECG of a patient with fibrillation shows the following changes: (1) the P wave disappears; (2) multiple small waves appear which are designated by the letter T; (3) ventricular complexes follow at irregular intervals, their shape does not change substantially.

Atrial fibrillation (cilliary arrhythmia) arises during sharp increasing of myocardium excitability,and also simultaneous conductivity violation . Sinus node loses  function of a pacemaker. One can observe multifocal excitation of atriums, generating 600-800 impulses per minute, that it is possible only during sharp shortening of refractory period. Conduction of these impulses is aggravated, they are not spread on atrium at all, each of them couse excitation and contraction of separate muscular fibres; as a result smallest fibrilar contraction (twinkling of atriums) are appeared instead of full value systola. Ventricles receive part of impulses which are conducted through atrioventricular node . There is no conformity in conduction of atrial impulses, the ventricles are contracted in irregular time intervals, which cause completelly arrhythmic pulse.

Ciliary arrhythmia can exist permanently or like attacks of tachyarrhythmia. There are three forms of ciliar arrhythmia: tachyairhythrnic (the ventricles are contracted with the rate 120-160/ min); bradyarrhythmic (with rate less then 60/ min); normosystolic (60-80/ min.).

Bradyarrhythmic form of ciliar arrhythmia may not couse any feelings in the patient. Tachyarrhythmia is followed by feeling of palpitation. During examination of the heart  full irregularity in sequence of cardiac contraction is observed. During auscultation there is loud I sound at the apex.

Pulse is    arhythmic, unequal,  pulse deficiene is observed quite often.

 On ECG:  1. Disappearance of P wave;

2. appearance of many small waves (waves f);

3.Ventricular complexes are recorded in irregular time intervals, their form is not changed.

 

Atrial fibrillation

Flutter of atriums is violation of cardiac rhythm, in which number of impulses, appeared in atrium, does not exceed 250-300 per min. and are conducted throught atrio-ventricular node rhythmically. Each second, third, fourth impulse is conducted to ventricles. It depends from AV block degree. Sometimes its conductivity can change, and then contraction of ventricles are arhythmic.

During frequent cardiac contraction the patient complains of palpitation. On ECG there are high waves f (instead of P wave),  number of which before ventricular complex depends on conductivity coefficient of AV node.

Flutter and fibrillation ventricles are threatening disorders of cardiac rhythm, when a full value ventricles systole is absent, contraction of separate muscular areas is followed by sharp violation of haemodynamics and rapidly caused death. During these arrhythmias a patient loses consciousness, sharply turns pale,  pulse and blood preasure are not determined. On ECG disorderly deformed complexes are recorded, it is difficult to distinguish the separate waves on the  ECG  curve.

 

 

 

Atrial flutter

Ventricular flutter

Ventricular ‘flutter’ is a bizarre sine-wave like rhythm, and usually degerates into ventricular fibrillation. You won’t see it often (or for long).

 

 

Ventricular flutter

Ventricular fibrillation

This is a chaotic ventricular rhythm that rapidly results in death. It is often precipitated by a critically timed extrasystole, that occurs during the relative refractory period of the myocardial fibres. Conventional wisdom has it that this results in chaotic, uncoordinated wavelets of depolarisation moving through the ventricular mass.

VF is a dire emergency. If unsynchronised DC counter shock is applied within 30s of the onset of VF, there is an approximately 97% chance that sinus rhythm will be restored, and the person will survive. Survival decreases exponentially thereafter, with every minute of delay.

 

Ventricular fibrillation

 

Diagnosis methods for arrhythmias

The ECG criteria for diagnosing right or left ventricular hypertrophy are very insensitive (i.e., sensitivity ~50%, which means that ~50% of patients with ventricular hypertrophy cannot be recognized by ECG criteria). However, the criteria are very specific (i.e., specificity >90%, which means if the criteria are met, it is very likely that ventricular hypertrophy is present).

 

2. Left Ventricular Hypertrophy (LVH)

 General ECG features include:

 > QRS amplitude (voltage criteria; i.e., tall R-waves in LV leads, deep S-waves in RV leads)

 Delayed intrinsicoid deflection in V6 (i.e., time from QRS onset to peak R is >0.05 sec)   Widened QRS/T angle (i.e., left ventricular strain pattern, or ST-T oriented opposite to QRS direction)   

 Leftward shift in frontal plane QRS axis

 Evidence for left atrial enlargement (LAE) (lessonVII)

 ESTES Criteria for LVH (“diagnostic”, >5 points; “probable”, 4 points)

 

 CORNELL Voltage Criteria for LVH (sensitivity = 22%, specificity = 95%)

 S in V3 + R in aVL > 24 mm (men)  

 S in V3 + R in aVL > 20 mm (women)

 

 Other Voltage Criteria for LVH

 Limb-lead voltage criteria:

 R in aVL >11 mm or, if left axis deviation, R in aVL >13 mm plus S in III >15 mm 

 R in I + S in III >25 mm

 

 Chest-lead voltage criteria:

 S in V1 + R in V5 or V6 > 35 mm

Symptoms of arrhythmias vary from person to person, and depend on the source of the abnormality. Some people have no symptoms at all. If symptoms are experienced, these may include any of the following:

• Palpitations (strong or “galloping” heartbeat)

• Skipped heartbeat

·         Dizziness, fatigue or fainting (syncope) as a result of the braiot getting enough oxygen-rich blood

 

 

 

Abnormal heartbeats & conduction defects

If the electric or muscular function of the heart is disturbed for some reason, it will affect how the electric signals spread through the heart muscle. One example is Arrythmia, a condition where the heart beats irregularly due to a defect in the electric conduction system. A left or right Bundle Branch Block delays the electric wave from spreading to the left or right part of the heart. Sometimes these conditions affect the heart’s ability to pump blood.       Left Bundle Branch Block

 

 

 

Treatment of cardiac arrhythmia includes the following measures: (1) (jidgement of the diseases which caused arrhythmia (myocarditis, dimcmic heart disease, neurosis, hyperthyroidism, etc.); (2) using means Ito restore ionic equilibrium in the myocardium and improve metabolism of potassium salts, vitamins, ATP, etc.); (3) in cases with increased excitability of the myocardium and in ectopic arrhythmias the following preparations are recommended: quinidine, novocainamide, aimaline, beta-blocking agents, etc.; (4) progressive ventricular fibrillation is managed by electric defibrillation, i.e. short (0.01 s) single discharge of 5000—7000 V, which causes instantaneous excitatio all parts of the myocardium and restores the normal cardiac rhythm.

Fibrillation is managed by an apparatus known as a defibrillator. Its two electrodes are attached to the chest (one below the left scapula and the apex on the heart, or one below the right clavicle and the other over the in .heart apex). Electric impulses are also given to treat permanent fibrillation (in paroxysmal tachycardia if medicamentous therapy proves inefficient); (3) electric stimulation of the heart (artificial pacemaker) is also indicated In stoppage of the heart, in pronounced bradycardia, in complete atrioventricular block.

 

 

 

 

Electrostimulation

Emergency care in ventricular flutter and fibrillation:

Stroke on the sternum;

 

Artificial breathing (upper airways should be free by fixation of low jaw)

 

 

 

 

 

Artificial pacemaker (appearance)

 

 

 

 

Artificial pacemaker on the X-ray

 

COMMON CARDIAC INVESTIGATIONS

 

 

Ambulatory ECG monitoring

Ambulatory recording can be made using cassette tape recorders or solid-state devices with digital memory. These make a continuous ECG recording that can be analysed by computer and checked by a cardiac technician. A typical recording lasts 24-48 hours. Patient-activated recorders are useful for capturing occasional arrhythmias and are activated only when symptoms occur.

 

Exercise ECG

Patients with stable angina often have a normal ECG at rest and an abnormal ECG during stress. An exercise ECG is a form of controlled physiological stress that may unmask evidence of coronary heart disease. Severe ECG abnormalities, or changes that occur during minor exertion, are of prognostic  significance and may prompt invasive investigation with cardiac catheterization.

Exercise testing is commonly used. The patient is placed in the lying position and a 12-lead ECG taken at rest. The patient is then asked to perform exercise, e.g. change his posi­tion (sit up), squat, ascend and descend stairs, etc. A special two-step exercise test is used: the patient is allowed to walk up and down a special pair of 22.5-cm-high steps for 1.5-3 minutes, ap.d ECG are then taken immediately after the exercise, and in 3 and 6 min. The test is used to reveal latent coronary insufficiency, the signs of which can be detected on the ECG after ex­ercise. A bicycle ergometer is now also used. The patient is asked to rotate pedals, like in riding a bicycle, the resistance to pedalling being controlled. Treadmills are also used for the purpose. Similar examinations of patients can be done with hypoxaemic tests, in which air containing only 10 per cent of oxygen is inhaled for 10-20 minutes with subsequently record­ed ECG, which also reveals latent coronary insufficiency.

Pharmacological tests are used to differentiate between functional and organic disfunction in coronary circulation. Curantin (dipiridamole) and Isadrin (Isoproterenole) are used for the purpose. The i ECG is compared with ECG taken before and after intake of these agents which provoke ischemic changes on ECG in ill persons.

Propranolole test. Disappearnce of  signs of myocardial ischaemia after taking vasodilatory preparations indicates the ischemic I character of coronary disorders.

 

Tests by which the tone of the vagus nerve is modified are used to assess some  changes of the cardiac rhythm.

Aschner’s test. Pressure on the eyeball for 6-10 s increases the tone of the vagus, -which increase its effect on the heart: the heart slows down and the time of the atrioventricular transmission increases.

Atropine test. The subject is given 1 ml of a 0.1 per cent atropine solution b; cutaneous injection, and ECG are then taken in 5, 15, and 30 minutes. Atropine blocU vagus and thus provides conditions for a better interpretation of disorders in the rhythm and transmission. If, for example, the P-Q interval on the pre-injection EO elongated but normalized after administration of atropine, the disorder in the atriover.; I transmission was due to the increased vagus tone and not due to an organic myocari¹‘ tion.

Telecardiography (radioelectrocardiography) is now also used to study the effects of physiological stress imposed on the heart. The electrjc currents of the heart are tnuuriiiti a radio device attached to the examinee and the ECG is thus recorded at a distance fcoi patient. This method is very useful for taking ECG during exercise, (sportsmen, asc; pilots).

 

Chest X-ray

The chest X-ray is important in the investigation of heart disease. An enlarged heart, as judged by the cardiothoracic ratio , is a common feature of valvular heart disease and heart failure. In heart failure this is often accompanied by distension of the upper lobe pulmonary veins, diffuse shadowing within the lungs due to pulmonary oedema and the finding of Kerley B lines (horizontal engorged lymphatics at the periphery of the lower lobes).

Roentgenoscopy is a very important instrumental method for the study of the cardiovascular system. Routine X-ray studies include roentgenoscopy and roentgenography. In direct projection, the patient faces the screen with the X-ray tube being behind the patient’s back. In oblique projection, the patient is positioned at an angle of 45° to the screen: first with i tight and then with the left shoulder forward. Direct projection outlines silhouettes of the heart and the great vessels: they appear as convex arches. The upper flattened arch is formed by the aorta and the superior vena cava, while the lower arch by the right atrium. The next arch is formed on the left by the aorta; the next arch is the pulmonary trunk and the left pulmonary artery; the lower part -is formed by the auricle of the left atrium and still inferiorly by the left ventricle. The silhouette of the heart with the vessels depends on the body fiuild of the patient and position of his heart in the chest. In hypersthenic individuals and in subjects with hight diaphragm, the heart assumes a more horizontal position than it does in normosthenic subjects. The position of heart in asthenic individuals and in subjects with low diaphragm is more central and vertical, and its silhouette is therefore smaller since the heart has a contact with the diaphragm over a small area. It looks as if dunging from the vascular bundle (drop heart). The heart position may change in pleurisy, pleuropericardial adhesion, in the presence ill mediastinal tumours, etc.

When examining the silhouette of the heart and the great vessels in direct projection, it is necessary to pay attention to the magnitude of the angle formed by the bundle of the great vessels and the heart silhouette on the left. The angle becomes more significant when the left ventricle is heart silhouette is displaced in the lateral rather than in the medial direction during systole, pulsation is assessed as paradoxical, which is characteristic of cardiac aneurysm.

 

 

Position of the heart’s chambers in (a) direct projection; (b) first oblique and (c) se­cond oblique projection. 1—aorta; 2—pulmonic artery; 3—right atrium; 4—right ventricle 1—left ventricle; 6—left atrium

 

The heart in frontal projection

 

 

 

Angiocardiography is the method of X-ray examination by which pictures of various heart chambers or the great vessels can be taken after administration of special contrast substances into them. Venous angiocardiography and selective angiocardiography are distinguished. In the former case a contrast substance (cardiotrast, diotrast, etc.) is injected into a peripheral vein and X-ray pictures are taken to record the entry of the substance into the right chambers of the heart and the vessels of the lesser circulation. The left chambers are poorly contrasted because the contrast substance is highly diluted in the blood flowing in the left chambers and the vessels of the lesser circulation. In selective angiography contrast substance is administered through a catheter directly into the right or left chambers of the heart (see “Cardiac Catheterization”). A better contrast is thus obtained in the studied part of the heart or vessel with a small amount of the administered substance.

Angiocardiography is very useful in diagnosing congenital heart defects. It reveals pathological communications between the heart chambers and the great vessels, determines the direction and amount of blood ejected from one chamber of the heart to another, locates stenosed portions of the vessels, and determines the degree of stenosis. Moreover, angiocar­diography helps diagnose complicated acquired heart defects and evaluate indications for surgical treatment in cases where clinical findings are insufficiently informative. Selective angiography of the aorta and its branches (aortography) is used to study the condition of the vessels. This method is” widely used to determine the condition of the coronary arteries (coronography).

 

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Computer angiography

 

 

Echocardiography is a method of examination of a heart, based  on the using of impulse reflection of the ultrasound  waves from  heart structures. Echocardiograph has a data appliance which beams the supersound-impulse and grasps echoreflections. Reflected signals are registered on the  echocardiogram which tells us about the dimension of the heart,  its conditions and functions.

Echocardiography was originally devised to evaluate valve abnormalities, but is now most commonly used to assess left ventricular function. In addition to imaging cardiac structure, blood flow can be displayed (Doppler echocardiography), and analysed to quantitate valve stenosis and regurgitation. Most scans are performed through the anterior wall of the chest (transthoracic) but when high-resolution images of posterior structures (e.g. left atrium or descending aorta) are required transoesophageal imaging is employed. This can be carried out safely in outpatients using topical anaesthesia and intravenous sedation

Echocardiography is used to study the heart by detecting ultrasound • hoes from its various structures, such as the valves, ventricular myocardium, interventricular septum, etc. The instrument used for the purpose is mi as the echocardiograph. It emits ultrasound impulses which are icturned from the organ under examination and received as echoes to be hcprcsnited graphically on a moving paper chart, the echocardiograms.

The device emitting ultrasound impulses (the probe) is placed in the region of absolute dullness where the heart is not covered by the lungs, i.e. to the left of the sternum at the 2nd or 3rd intercostal space in hypersthenics  4th or 5th interspace in asthenics.

Echocardiography is very useful for the diagnosis of various heart diseases since it determines the condition of the heart valves and reveals indices characterizing contractility of the left ventricular myocar­dium.

Radionuclide studies

Radionuclides are injected intravenously and detected using a gamma camera. Technetium-99 is used to label the circulating blood and provide an accurate assessment of left ventricular function. Thallium and sesta-MIBI are taken up by myocardial cells and provide an indication of myocardial perfusion, both at rest and during exercise.

Circulation time can be determined by injecting isotopes (^2<Na, ^13II, ⁸⁵Kr) intravenously and detecting them by a special counter at any given point of the vascular system.

Oxyhaemography. This method can also be used for determining blood circulation time. The sensitive unit of an oxyhaemograph includes a photocell which detects changes in the col­our of the blood depending on its oxygen content. The pick-up is attached to the lobe of the ear, where it records blood oxygen saturation. The respiratory movements are recorded syn­chronously. After the initial blood oxygen content has been determined, the patient is asked to keep breath for 10—15 s, which reduces the oxygen concentration in the blood. The patient then makes a deep inspiration and the recording device of the oxyhaemograph records the in­crease in the oxyhaemoglobin content of the blood. The records of the respiratory movements are then compared with the oxygen curse, and the time from the beginning of the deep inspira­tion to the increase in oxyhaemoglobin content is calculated. This is the ear-to-lung circulation time.

 

Cardiac catheterization

This invasive procedure involves introducing fine catheters, approximately 2 mm in diameter, into the femoral (or radial) artery and/or vein, and advancing them to the left or right side of the heart respectively. Originally these techniques were developed to measure pressures in the different cardiac chambers in patients with valve disease. However, patients are now fully evaluated by echocardiography. Coronary angiography is performed using catheters designed to select the left and right coronary arteries and inject X-ray contrast medium into them. The findings are used to determine the need for, and mode of, revascularization in patients with coronary artery disease.

Cardiac catheterization is used to measure blood pressure and study the gas composition i blood in various chambers of the heart and the main vessels, to reveal abnormal comnm tions between them in congenital heart defects, to record ECG and PCG directly in thr I chambers, and to carry out angiography.

Cardiac catheterization is carried out in specially equipped operating rooms chambers of the heart and the pulmonary trunk are usually catheterized. To that end i the peripheral veins (usually the basilic vein of the left arm) is opened and a catheter inn ed. The progress of the catheter is controlled by X-rays. The catheter is introduced ml right atrium, right ventricle, the pulmonary artery and further into one of its bi.n Pressure of blood is measured and its specimens are taken from all heart chambers

Left chambers of the heart are usually catheterized by a septal puncture of ill atrium, i.e. the catheter is passed from the right atrium to the left one through the inn-septum. The left chambers of the heart can also be examined by passing the catheter thri peripheral artery (e.g. femoral artery) and further through the aorta and the aortic v.ii -the left ventricle; the left atrium is inaccessible through the mitral orifice.

Pressure in the heart chambers and the great vessels can vary in cardiovascular clli In stenosis of the left venous orifice, for example, the blood flow from the left atrium left ventricle during diastole becomes difficult and diastolic pressure therefore increase left atrium and decreases in the ventricle. This difference in diastolic pressure incrc.i-.. the degree of stenosis. In stenosis of the pulmonary artery, systolic pressure in the right cle increases, while systolic pressure in the pulmonary artery remains normal.

The gas composition of blood taken from various chambers of the heart is of hi^, portance for diagnosis of congenital heart diseases and for detection of pathologu al munications between the heart chambers and the great vessels. In the presence of mi< tricular communication, blood passes from the left ventricle to the right one, and i saturation of blood in the right ventricle will be higher than in the right atrium. If tlici difference between oxygen saturation of blood in the right atrium and right ventn. li the oxygen content of blood taken from the pulmonary artery is increased, it suggests »tt ( arterial communication through which arterial blood passes from the aorta li pulmonary trunk.

 

CT and MR scanning

Computerized tomography (CT) and magnetic resonance imaging can be used to identify structural defects of the heart and great vessels. MR imaging is helpful in congenital heart defects and infiltrative disorders, e.g. cardiac sarcoidosis. Recently electron beam CT has been used to screen for coronary arterial calcification, an early marker of coronary atherosclerosis.

 

 

Phonocardiography is the method of registration of  sounds which arise during heart beating. A phonocardiograph consist from microphone, amplifier of eletrical signals, system of frequency filter, register appliance. Microphone grasps vibrations and convert them into electrical signals, which become stronger and get to system of frequency filter, then to the register appliance where they are recorded in a form of  a  curve (phonocardiogram).

The normal phonocardiogram consists of vibrations which reflect the first and second heart sounds. Between them there is the straight horisontal   line, which coincides with systolic and diastolic pauses. The first sound is vibrations after point Q in electrocardiogram (ECG). The main central part of the first sound is represented by 2-3 vibrations of a high amplitude, which appear on the level of point S. The amplitude of the first sound is the highest at the heart apex, where it is 1,5-2 times more high than the amplitude of the second sound. Normally the pause Q-to-first sound is not more than 0.07-0.06 seconds.  The second sound is the group of vibrations which appear at the ending of point T wave  of synchronous ECG. The group  of  first more high vibrations coincides with the closure  of   aortal valve. The next are of the smallest amplitude. The amplitude of the second sound is highest on the base of a  heart, it becomes higher than the amplitude of the first sound  here.

On the phonocardiogram besides the 1 and 2 heart sounds. there is the third one, which looks as 2-3 vibrations of low frequency and not high amplitude. They follow the second sound in a time 0,12-0,18 seconds, they coincide with P  wave   on  ECG. The fourth sound is 1-2 vibrations of low frequency which appear after P  wave..

 Phonocardiogram defines type of heart murmurs: time when murmurs appear, the place where it is most intensive,  duration and characteristic of frequency. The frequency of systolic murmurs is between 50-600 cycles per second:, diastolic murmurs is between 120-800 cycles per second.  Systolic murmurs may be located between 1 and 2 heart sounds or coincides with them. When we study diastolic murmurs, first of all is necessary note at what moment of  diastole it appears. Theote the changes of strength of  murmur (increasing or decreasing) and frequency characteristics.

Phonocardiography is an essential supplement to heart auscultation because it can record sounds otherwise inaudible to the human ear, such as the third and fourth heart sounds, low-frequency components of the first and the second heart sounds, and low-frequency murmurs.

Sounds generated in the heart are recorded on a phonogram as a curve (PCG) by an apparatus known as a phonocardiograph. It consists of a microphone, an amplifier, a system of sound filters, and a recording device. The microphone picks up sounds and converts them into electrical signals. These are amplified and transmitted into the system of sound filters where the sounds are separated by their frequencies Gow, medium-and high-frequency sounds) for their separate recording. Oscillations of a certain frequency are transmitted to the recording device which draws a curve. A phonogram can be recorded by ink on a chart paper, or by a beam of light (on a photosensitive paper). Phonocardiograms are taken in com­plete silence with the patient in the lying position; the breath should be kept at the expiration phase. The microphone is placed successively on those sites of the chest where heart sounds are audible during auscultation, and also on those areas where the sounds can be heard best. Phonocardiograms should be analysed and diagnosis established only by interpreting the phonocardiogram together with the auscultation findings. For a better in­terpretation of phonocardiograms, an electrocardiogram should be taken synchronously.

A normal phonocardiogram gives a graphic picture of vibrations caus­ed by the first and second heart sounds, with a straight line in between, cor­responding to the systolic and diastolic pauses. The first sound is represented as several vibrations arising after the Q wave syn­chronously with the ECG (70-150 Hz). The initial vibrations of the first sound have a low amplitude; these are connected with atrial systole. The main or central part of the first sound is shown in the form of 2—3 vibra­tions of high amplitude, which are found at the level of the S wave and correspond to vibrations of closed atrioventricular valves. The main portion of the first sound is followed by additional vibrations of lower amplitude which are caused by vibrations of the myocardium and by the vascular component.

The amplitude of sound waves on a PCG depends not only on the work of the heart but also on the conditions of sound conduction (for example, the amplitude decreases in patients with obesity or lung emphysema).

The amplitude of the first sound is the highest at the heart apex, where it exceeds 1.5-2 times the amplitude of the second sound. The amplitude of the first sound at the heart base can be very small. While interpreting this sound at the heart apex, it is necessary to determine the lag of its cen­tral portion from the Q wave on a synchronously recorded ECG. The nor­mal Q-l sound  interval does not exceed 0.04-0.06 s. It corresponds to the time lasting from the beginning of ventricular excitation to the closure of the mitral valve.

 

 

Normal PCG. a—at the heart apex; b—at the heart base

 

 

 

In mitral  stenosis the mitral valve closes with a delay and the Q-l sound interval increases.

The second sound is composed of several vibrations which appear at the end of the T wave synchronous with ECG. Its frequency varies from 70 ill 150 Hz. Higher amplitude corresponds to the closure of the aortic valve while subsequent lower amplitude corresponds to the closure of the valve of the pulmonary trunk. The amplitude of the second sound is the highter at the base of the heart, where it exceeds the amplitude of the first sound.

In addition to the first and second sounds, a phonocardiogram has the third heart sound which is recorded as two or three low-frequem J waves of small amplitude. They follow the second sound in 0.12—0.1H m and appear before the P wave of a synchronous ECG. The fourth heart sound is recorded less frequently. It has the form of one or two low frequency low-amplitude waves appearing after the P wave.

Phonocardiography helps diagnose many cardiovascular diseases, he;ni defects in the first instance. It verifies and supplements auscultative fiiui ings. This is especially important in tachycardia or arrhythmias, i.e. cases where it is difficult to establish by auscultation alone during the phase of the cardiac cycle the sounds appeared. PCG helps reveal change in the heart sounds, their duplication, splitting, and ensures a more cornmon interpretation of additional sounds, such as physiological third and fotrh heart sounds, the sound of the opening of the mitral valve, and the gallop rhythm. Phonocardiograms show graphically the changes in the sounds that were first revealed by auscultation. For example, in stenosis«[ the left venous orifice the amplitude of the first sound at the apex markedly increases, and in mitral valve incompetence it decreases. The amplitude of the second sound over the aorta in patients with essential hypertension higher than over the pulmonary trunk.

The sound of the opening of the mitral valve, usually designated opening snap, is very important in diagnosis of mitral stenosis, distinct from the third heart sound, it is recorded in the high-frequem v channel, 0.04—0.12 s after the second heart sound. This II sound-OS into val (like the Q-l sound interval) depends on the pressure in the left atrium the higher the pressure, the earlier opens the mitral valve during diastcli, and the shorter the II sound-OS interval will be.

Phonocardiography is very helpful in interpreting the character of hean murmurs; PCG determines the time of appearance of murmur, site of in maximum intensity, length, and frequency (which is determined mainly lf the sound intensity as recorded in the high- or low-frequency channel).

 

Doplerechocardiography – method which uses a famous  physical Doppler’s effect. The essence of this effect is that the frequency of waves alters when is reflected from the moving object. If object is moving e towards source of signal, the ultrasound frequency rises up. When the object  is moving from source of signal, the ultrasound frequency     is decreased. With the help of doplerocardiography one can find abnormal movement to the blood during the working of a heart.

Apexcardiography-method notes  moving of the of the left ventricle during heart   contractions. It is used for making analysis of diastole.