Instrumental methods of examination of cardiovascular system

Department of Internal Medicine Propedeutics and Tuberculosis

Normal ECG

The scheme of ECG interpretation

1. Is heart rrhythm sinus or ectopic, regular or irregular.

2. Heart rate = 60/R-R (when paper speed is 50 mm/sec R-R=N×0,02).

3. Amplitude of ECG voltage (amplitude of R in standard leads ≥5 mm or their summation in I,II and III leads ≥15 mm.

4. Electrical axis deviation. 5. Assessment of all components of ECG.

Normal ECG

Components of ECG

Determination of inner deviation of etriums and ventricles

ECG in standard leads

ECG in amplified leads

Chest leads in norm

Causes of electrical axis deviation

causes of right axis deviation normal finding in children and tall thin adults right ventricular hypertrophy chronic lung disease even without pulmonary hypertension anterolateral myocardial infarction left posterior hemiblock pulmonary embolus Wolff-Parkinson-White syndrome - left sided accessory pathway atrial septal defect ventricular septal defect causes of left axis deviation left anterior hemiblock Q waves of inferior myocardial infarction artificial cardiac pacing emphysema hyperkalaemia Wolff-Parkinson-White syndrome - right sided accessory pathway tricuspid atresia ostium primum ASD injection of contrast into left coronary artery

Hypertrophies of heart chambers

Right atrial hypertrophy:

- high acute P in III, AVF, V1

Left atrial hypertrophy: - broad biphasic P in I,

AVL, V5-V6

Right ventricular hypertrophy:

- high R in III, AVF, V1 Discordant

displacement of ST segment opposite to the lagest wave in QRS complex

Left ventricular hypertrophy:

- high R in I, AVL, V5-V6

Discordant displacement of ST segment opposite to the lagest wave in QRS complex

Broad QRS (more than 0,1 sec)

Right atrial hypertrophy

Left atrial hypertrophy

Left ventricular hypertrophy

Hyperthrophy of the left ventricle

Hyperthrophy of the right ventricle

Disorders of heart rrhythm: I. Disorders of excitation (arrhythmias): 1. Sinus arrhythmia

sinus tachycardia, sinus bradycardia sinus arrhythmia

2. Ectopic arrhythmias: extrasystole (sinus, atrial, atrioventricular,

ventricular) Paroxismal tachycardia (atrial, ventricular).

II. Disorders of heart conduction: sinus, atrial,atrioventricular and ventricular blocks, III. Combined disorders of excitation and conduction: flutter (atrial and ventricular) fibrillation (atrial and ventricular)

SINUS ARRHYTHMIA

Sinus arrhythmia is a cyclic increase in normal heart rate with inspiration and decrease with expiration. It results from reflex changes in vagal influence on the normal pacemaker and disappears with breath-holding or increase of heart rate due to any cause. The arrhythmia has no significance except in older persons, when it may be associated with coronary artery disease.

SINUS TACHYCARDIA

Sinus tachycardia is a heart rate faster than 90 beats/min that is caused by rapid impulse

formation by the normal pacemaker secondary to fever, exercise, emotion, anemia, shock, thyrotoxicosis, or drug effect. The rate may reach 180/min in young persons but rarely exceeds 160/min.

In quick heart rate the patient feels palpitation.

SINUS BRADYCARDIA

Sinus bradycardia is a heart rate slower than 60/min due to increased vagal influence on the normal pacemaker. The rate increases after exercise or administration of atropine. Slight degrees have no significance, especially in youth, unless there is underlying heart disease, especially coronary heart disease or acute myocardial infarction.

Elderly patients may develop weakness, confusion, or even syncope with slow heart rates. Arrhythmia disappears to use ephedrine or atropine in some patients to speed the heart rate. Rarely, artificial pacemakers are necсessary.

а-normal sinus rrhythm б- sinus tachycardia в- sinus bradycardia г- sinus arrhythmia

The most common mechanisms of ectopic arrhythmia are:

1) reentry mechanism. The depolarization wave front proceeds antegradely through the fiber whose conduction is slowed and returns retrogradely in a nearly fiber that had unidirectional antegrade block.When this returning echo reaches the site of its origin, it may then reexcite the fiber, which is now no longer refractory.

Alternative mechanisms are: 2) abnormal automaticity, 3) triggered activity (more rarely). Repetitive reentry may result paroxysmal

tachycardia, if the atrial premature beat is appropriately timed. Similarly, a single atrial premature beat may terminate atrial tachycardia by making the reentry pathway refractory. Recent evidence indicates that about one-third of patients have aberrant pathways to the ventricles.

Ectopic arrhythmias

I. Extrasystole - atrial - atrioventricular - ventricular. II. Paroxismal tachycardia - atrial - ventricular.

ATRIAL PREMATURE BEATS(Atrial Extrasystoles)

Atrial premature beats occur when an ectopic focus in the atria fires off before the next expected impulse from the sinus node. Ventricular systole occurs prematurely, and the compensatory pause following this is only slightly longer than the normal interval between beats. P wave is byphasic.

ECG signs: 1) premature appearance of cardiac complex of ECG,

2) non-complete compensatory pause,

3) P wave is biphasic or negative, 4) P is always recorded before QRS.

Atrial extrasystole

Atrial extrasystoly

Atrial bigeminy

ATRIO-VENTRICULAR PREMATURE BEATS(AV extrasystoles)

ECG signs: 1) premature appearance of cardiac complex on

ECG, 2) non-complete compensatory pause, 3) Depending on the location of focus of

excitation P wave occurs before or after QRS complex or can be superimposed on the last one.

VENTRICULAR PREMATURE BEATS

Ventricular premature beats are similar to atrial premature beats in mechanism and manifestations but are much more common. Together, they are the commonest causes of a grossly irregular rhythm with anormal heart rate. Ectopic impulse formation causes ventricular contraction to occur sooner than then extexpected beat. The sound of this contraction is audible. The pause between the ectopic ventricular beat and the next normally occurring ventricular beat is longer than the usual interval between 2 regular beats. When this pause, combined with the coupling interval (the interval between the preceding regular ventricular beat and the ectopic beat), equals twice the cycle length of regularly occurring ventricular beats, the pause is compensatory, whereas the pause is not compensatory in atrial premature beats because the sinus node is depolarized and must start a new basic rhythm. Single premature beats that occur after every normal beat produce bigeminy. Exercise generally abolishes premature beats in normal hearts, and the rhythm becomes regular.

Premature beats have no definite significance in the absence of coronary disease, hypertrophic cardiomyopathy, or prolapse of the mitral valve unless they arise early in diastole, are frequent, occur from multiple foci, occur with rapid ventricular rates or inruns, interrupt the T wave (R-on-T phenomenon), or are due to digitalis toxicity. The importance of the R-on-T phenomenon in predicting the likelihood of ventricular fibrillation is still being debated. Sudden death occurs more frequently (presumably as a result of ventricular fibrillation) when ventricular premature beats occur in the presence of known coronary disease, hypertension, cardiomyopathy, and possibly prolapsed mitral valve, but not in individuals with no known cardiac disease even in themiddle-aged normal population.

а- extrasystole from the left ventricle б- extrasystole from the right ventricle

Ventricular Extrasystoles

Main features: premature appearance of heart complex; P wave is abcent; QRS complex is disfigured depending on the location of

pathological focus (right or left His bundlebranch) and broadened; Discordant displacement of ST segment opposite to the largest

wave in the QRS complex; complete compensatory pause.

Ventricular extrasystole

Ventricular bigeminy and quadrigeminy

Dangerous extrasystoles by Lawn

Paroxismal tachycardia

This is a group of 4 and more extrasystoles from one focus of excitation.

ECG signs: 1) Acceleration of heart rate more than

150 per min; 2) The same shape of all cardiac

complexes; 3) Sudden start and stop; 4) Equal R-R intervals.

PAROXYSMAL ATRIAL TACHYCARDIA

It occurs more often in young patients with normal hearts. Attacks begin and end abruptly and usually last several hours. The heart rate may be 140-240/min(usually 170-220/min) and is perfectly regular, therate will not vary more than 1-2 beats per minute.Exercise, change of position, breath-holding, carotid sinus massage, or induced gagging or vomiting either has no effect or promptly abolishes the attack. Patient sare asymptomatic except for awareness of rapid heart action unless there is underlying heart disease, especially mitral stenosis and coronary heart disease. Inprolonged attacks with rapid rates, dyspnea or tight-ness in the chest may be felt as palpitation, discomfort in heart region, dizziness.

а- atrial paroxismal tachycardia б- atrioventricular (nodal) tachycardia with premature

excitation of ventricles в- atrioventricular (nodal) tachycardia with

simultaneous excitation of ventricles and atriums

Atrial PT

Ventricular paroxismal tachycardia

Ventricular PT

ATRIAL FIBRILLATION

Atrial fibrillation is the commonest chronic arrhythmia. It occurs most frequently in rheumatic heart disease, especially mitral stenosis, and arteriosclerotic heart disease. It may appear paroxysmally before becoming the established rhythm in thyrotoxicosis and other disorders. Infection, trauma, surgery, poisoning, or excessive alcohol intake may cause attacks of atrial fibrillation in patients with normal hearts. It is the only common arrhythmia in which the ventricular rate is rapid and the rhythm irregular. An ectopic atrial pacemaker fires 400-600 times per minute.

The impulses pass through the atria at varying speeds and are mostly blocked at the atrioventricular node. The ventricular response is completely irregular, ranging from80 to 160/min in the untreated state. Because of the varying stroke volumes induced by the varying periods of diastolic filling, not all ventricular beats result in apalpable peripheral pulse. The difference between the apical rate and pulse rate is the "pulse deficit"; this deficit is greater when the ventricular rate is high. Exercise intensifies the irregularity when the heart rate is slow. Carotid sinus massage usually slows the ventricular response but does not terminate the arrhythmia.

Atrial fibrillation

ATRIAL FLUTTER Atrial flutter is uncommon and usually occurs inpatients with

rheumatic or coronary heart disease, cor pulmonale, or atrial septal defect or as a result of quinidine effect on atrial fibrillation. Ectopic impulse formation occurs at rates of 250-350, with transmission of every second, third, or fourth impulse through the atrioventricular node to the ventricles. The ventricular rate is usually one-half the atrial rate (2:1conduction), or 150/min. Carotid sinus massage causes sudden slowing or standstill, with rapid return of the rate to the original level on release of pressure.When the ventricular rate is 75 (4:1 block), exercise may cause sudden doubling of the rate to 150 (2:1block). The first heart sound varies slightly in intensity from beat to beat (but not when the patient is in aconstant 2:1 flutter).

Atrial flutter

Ventricular flutter and fibrillation

Ventricular fibrillation

а- ventricular flutter б- ventricular fibrillation

Disorders of heart conduction:

Atrial block Atrioventricular block:

I degree II degree (Mobitz I, II and III) III degreeHiss bundlebranch block (right, left).

Atrial block

ECG signs: broad P wave

Intraatrial block

AV block

I degree: Prolongation of PQ II degree: Prolongation of PQ and periodical

missing of QRS, - Mobitz I: Venkebach’s periods (gradual

PQ prolongation) - Mobitz II: PQ il longer but equal in all

complexes, periodical missing of QRS Mobitz III: long PQ, many missed QRS (more P

waves on ECG than QRS complexes but P is recorded before QRS)

III degree or complete AV block: more P waves on ECG than QRS complexes and P is recorded independently of QRS

AV block I degree

Permanent prologation of PQ more than 0,20с а- atrial form б- nodal form в- distal (trifascicular) form

I degree AV block

II degree AV block

III degree AV block

Left bundle branch block (LBBB)

Left HBBB

Right HBBB

LBBB

Right bundle branch block (RBBB)

Holter ECG monitoring

Heart sonohraphy (B-mode)

B- and M-mode ultrasound of a heart

X-ray of a heart. Aortic heart configuration

Mitral heart configuration