visceral and parietal pericardial layers in which fibrin is deposited (in pericarditis), cancer nodes develop, etc. The mechanism by which pericardial friction sounds are generated is similar to that of the pleural friction sounds, except that they depend not onthe respiratory movements but on the movements of the heart during systole and diastole. Pericardial friction murmurs vary. Sometimes they resemble pleural friction or the crisping sounds of snow, and sometimes they are very soft, as if produced by rattling of paper or scratching.
The following signs can be used for differentiation between pericardial friction sounds and intracardiac sounds:
(1)there is no complete synchronism of pericardial friction sounds with systole and diastole; friction sounds are often continuous, their intensity increasing during systole or diastole;
(2)friction sounds can be heard for short periods during various phases of the heart work, either during systole or during diastole;
(3)pericardial friction sounds are not permanent and can reappear at
intervals;
(4)friction sounds are heard at sites other than the best auscultative points; they are best heard in the areas of absolute cardiac dullness, at the heart base, at the left edge of the sternum in the 3rd and 4th intercostal spaces; their localization is inconstant and migrates even during the course of one day;
(5)friction sounds are very poorly transmitted from the site of their generation;
(6)the sounds are heard nearer the examiner's ear than endocardial
murmurs;
(7)friction sounds are intensified if the stethoscope is pressed tighter to the chest and when the patient leans forward, because the pericardium layers come in closer contact with one another.
Pleuropericardial friction murmurs arise in inflammation of the pleura
adjacent to the heart and are the result of friction of the pleural layers (synchronous with the heart work). As distinct from pericardial friction sounds, pleuropericardial friction is always heard at the left side of relative cardiac dullness. It usually combines with pleural friction sound and changes its intensity during the respiratory phases: the sound increases during deep inspiration when the lung edge comes in a closer contact with the heart and decreases markedly during expiration, when the lung edge collapses.
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Electrocardiography examination:
Algorithm of interpreting ECG. ECG signs of hypertrophy of heart chambers. ECG in IHD (ischemic heart disease)
Electrophysiological bases of ECG (electrocardiography)
Electrocardiography is a method of graphic recording of electric currents generated in the working heart. Contractions of the heart are preceded by its excitation during which physicochemical properties of cell membranes change along with changes in the ionic composition of the intercellular and intracellular fluid, which is accompanied by generation of electric current.
Electrophysiological functions of heart:
-Automaticity – function of pacemaker cells to produce spontaneously the action potential (transient depolarization);
-Conduction - capability to impulse propagation through cardiac tissues; -Excitability – capability to become excited under the influence of impulses; -Refractoriness is a property of cardiac cells that defines the period of recovery that cells require before they can be reexcited by a stimulus; -Contractility – capability of myocardium to contract in response to excitement.
Cardiac conduction system
The depolarization stimulus for the normal heartbeat originates in the sinoatrial (SA) node or sinus node, a collection of pacemaker cells. These cells fire spontaneously; that is, they exhibit automaticity. Pacemaker cells exhibit automaticity in all departments of conduction system: I- sinus node (SA), II - AV junction (and atrial fibres) and AV node and His-bundle), III- His-bundle branches, Purkinje fibers.
The first phase of cardiac electrical activation is the spread of the depolarization wave through the right and left atria, followed by atrial contraction. Next, the impulse stimulates pacemaker and specialized conduction tissues in the atrioventricular (AV) nodal and His-bundle areas; together, these two regions constitute the AV junction. The bundle of His bifurcates into two main branches, the right and left bundles, which rapidly transmit depolarization wavefronts to the right and left ventricular myocardium by way of Purkinje fibers. The main left bundle bifurcates into two primary subdivisions, a left anterior fascicle and a left posterior fascicle. The depolarization wave fronts then spread through the ventricular wall, from endocardium to epicardium, triggering ventricular contraction. Ventricular depolarization can be divided into two major phases, each represented by a vector. The first phase denotes depolarization of the ventricular septum, beginning on the left side and spreading to the right. Simultaneous
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depolarization of the left and right ventricles (LV and RV) constitutes the second phase.
Recording ECG
Twelve-lead ECG recording has gained wide use: three standard leads (classical), six chest, and three augmented unipolar limb leads (Table 7). Special leads are also used in some cases.
The six frontal plane and six horizontal plane leads provide a threedimensional representation of cardiac electrical activity. The frontal plane leads - standard and augmented leads. The horizontal plane leads – chest leads.
|
|
Table 7 |
|
Basic leads of ECG |
|
Leads |
Position of an electrode |
Projection of heart chambers |
|
|
|
Standard leads |
Right arm - left arm |
Anterior wall of left ventricle |
I |
|
|
II |
Right arm - left foot |
- |
|
|
|
III |
Left foot - left arm |
Posterior wall of left ventricle |
|
|
and right ventricle |
Augmented |
|
|
leads |
Left arm |
Anterior wall of left ventricle |
aVL |
|
|
aVR |
Right arm |
- |
|
|
|
aVF |
Left foot |
Posterior wall of left ventricle |
|
|
and right ventricle |
Chest leads |
|
|
V1 |
right sternal borderthe 4th |
Anterior wall of right and left |
|
intercostal space |
ventricle |
|
|
|
V2 |
left sternal borderthe 4th |
Anterior part of interventricular |
|
interspace |
septum |
V3 |
between V2 and V4 |
Anterior wall of left ventricle |
|
|
to apex |
V4 |
left midclavicular line – the |
Apex of left ventricle |
|
5th interspace |
|
V5 |
left anterior axillary line – the |
Side wall of left ventricle |
|
5th interspace |
|
V6 |
left midaxillary line – the 5th |
Side wall of left ventricle |
|
interspace |
|
|
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|
Normal ECG
Basic ECG waves and intervals
During diastole the heart does not generate current and an electrocardiograph records a straight line which is called isoelectrical. Action current is represented by a specific curve. An ECG of a healthy subject has the following elements: (1) positive waves P, R, and T, negative waves Q and S; the positive wave U is accidental; (2) P-Q, S-T, T-P, and R-R intervals; (3) QRS and QRST complexes (Table 8, Fig. Suppl. 2-3). Each of these elements characterizes the time and sequence of excitation of various parts of the myocardium.
Generation of ECG waves and intervals: P – depolarization of atriums, QRS - depolarization of ventricles, ST,Т,U - repolarization of ventricles. The QRS-T cycle corresponds to different phases of the ventricular action potential.
Table 8
Waves and intervals of normal ECG
Waves |
Width |
Height |
Other characteristics |
Intervals |
(s) |
(mm) |
|
P |
≤0.10 |
≤2-2.5 |
(+) I, II, aVF, (-) aVR |
|
|
|
may be (±) III, aVL, V1-2 |
PQ |
0.12—0.20 |
- |
isoline |
|
|
|
|
QRS |
0.06—0.10 |
≥5 all leads; |
Q(<0.04 s, ≤2 mm) except aVR, |
|
|
≥ 10 chest |
V1-2 ; transition zone (R wave = S |
|
|
leads |
wave) between V2 –V4 |
ST |
- |
- |
isoline (as rule); may be - (+)1 or |
|
|
|
(-) 0.5 mm in aVL, aVF. aVR; |
|
|
|
oblique (+) 3 mm in V1-6 |
T |
- |
≤1/4-1/2 R |
(+) I, II, V3—V6; (-) aVR, V1; |
|
|
|
may be(±) III, aVL, aVF, V1-2 |
QT |
0.30—0.46 |
- |
QT = K/√RR (<0.46-0.47 s, |
|
correlates |
|
K=0.37 for men and 0.39 for |
|
HR |
|
women) |
In normal conditions, the cardiac cycle begins with excitation of the atria (P wave on an ECG). The ascending portion of the P wave is mainly due to excitation of the right atrium, while the descending one of the left atrium. The wave is small, and its normal amplitude does not exceed 1-2 mm; the length is 0.08-0.1 s. The P wave is followed by a straight line lasting to Q wave; if this wave is small, the line extends to the R wave. This is the P-Q interval. It extends from the beginning of the P wave to the beginning of the Q (or R) wave and corresponds to the time from the beginning of atrial excitation to the beginning of ventricular excitation, i.e. includes the time of
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pulse propagation in the atria and its physiological delay in the atrioventricular node. The normal length of the P-Q interval is 0.12-0.18 s (to 0.20 s).
Excitation of the ventricles corresponds to the QRS complex. Its waves vary in size and are different in various leads. The length of the QRS complex (measured from the beginning of the Q wave to the end of the 5 wave) is 0.06—0.1 s. This is the time of intraventricular conduction. The first wave of this complex is the negative Q wave. It corresponds to excitation of the interventricular septum. Its amplitude is small and does not normally exceed 1A amplitude of the R wave; the length of the Q wave does not exceed 0.03 s. The Q wave may be absent on an ECG. The R wave corresponds to almost complete excitation of both ventricles. It is the highest wave of the ventricular complex; its amplitude varies from 5 to 15 mm. The negative 5 wave is recorded in full excitation of the ventricles; usually it is not high, actually not exceeding 6 mm (2.5 mm on the average). Sometimes the 5 wave is very small. At the moment of complete depolarization of the myocardium, the potential difference is absent and the ECG is therefore a straight line (the S-T interval.) The length of this interval varies greatly depending on the cardiac rhythm; the S-T interval may be displaced from the isoelectric line to not more than 1 mm.
The T wave corresponds to the repolarization of the ventricular myocardium. The T wave is normally asymmetrical: the gradual ascent converts into a rounded summit, which is followed by an abrupt descent. Its amplitude varies from 2.5 to 6 mm, the length from 0.12 to 0.16 s. A small positive U wave sometimes follows the T wave in 0.02—0.04 s. Its amplitude exceeds 1 mm in rare cases: the length is 0.09—0.16 s. The origin of the U wave is disputed.
The Q-T interval (QRST complex) shows the time of excitation and recovery of the ventricular myocardium i.e. it corresponds to their electrical system. It extends from the beginning of the Q wave (or the R wave, if the Q wave is absent) to the end of the T wave. Its length depends on the rate of cardiac contractions: in accelerated heart rhythm the Q-T interval shortens. The Q-T interval in women is longer than in men (at the same heart rate). For example, at the rate of 60-80 beats per minute, the length of the Q-T interval in men is 0.32-0.37 s and in women—0.35-0.40 s.
The T-P interval (from the end of the T to the beginning of the P wave) corresponds to the electrical diastole of the heart. It is located on the isoelectric line because all action currents are absent at this moment. Its length depends on the cardiac rhythm: the faster the heart rate the shorter the T-P interval.
The R-R interval is a distance between the summits of two neighbouring R waves. It corresponds to the time of one cardiac cycle, whose length depends on the cardiac rhythm as well.
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