The main function of the circulatory system, which consists of the heart and blood vessels, is transport. The circulatory system delivers oxygen and nutrients needed for metabolic processes to the tissues, carries waste products from cellular metabolism to the kidneys and other excretory organs for elimination, and circulates electrolytes and hormones needed to regulate body function. This process of nutrient delivery is carried out with exquisite precision so that the blood flow to each tissue of the body is exactly matched to tissue need.
CIRCULATION (starting with return of blood to the heart from the peripheral circulation) • Deoxygenated blood returns to the right side of the heart from venae cavae during diastole (relaxation) • It enters the right atrium at a pressure of 0–10 mmHg • Right atrial contraction increases pressure until the tricuspid valve opens • Blood flows through the tricuspid valve into the right ventricle during diastole, partially assisted by atrial contraction (the ‘atrial kick’) • As right atrial pressure rises, the tricuspid valve closes and the pulmonary valve opens • Right ventricular systole (contraction) sends blood via pulmonary arteries to the lungs at a pressure of about 30 mmHg • Blood is oxygenated in the lungs and returns to the left atrium via the pulmonary veins • Left atrial systole increases pressure until the mitral valve opens • Blood flows through the mitral valve into the left ventricle during diastole • Left ventricular contraction during systole • As pressure rises, the mitral valve closes (‘lub’) and the aortic valve opens • Left ventricular contraction during systole sends blood via the aorta to the body at a maximum pressure of about 120 mmHg • Ventricular pressure falls and the aortic valve closes (‘dup’) • Blood perfuses the periphery and oxygenates tissues • Mean pressure falls to 30 mmHg at the arterial end of capillaries and 15 mmHg at the venous end • Deoxygenated blood returns to the heart via the veins; flow is facilitated by the peripheral muscle pump, and back flow is prevented by one-way venous valves
CARDIAC CYCLE (starting at end of diastole) • Impulses originate in the sino-atrial node, which controls rhythm and causes atrial systole • Impulses spread across the atrium to the atrioventricular node • Impulses traverse the bundle of His and bundle branches in the septum (between Left and Right heart) • Ventricular systole starts from the apex of the ventricles • Intraventricular pressure rises, initially without change of size because the aortic and pulmonary valves are closed (isovolumic phase) • Impulse spreads towards the base of the ventricles (valves) via Purkinje fibres • Mitral and tricuspid valves close as pressure rises • Aortic and pulmonary valves open as pressure exceeds systemic or pulmonary • Blood propelled towards the aortic and pulmonary valves by contractile wave spreading from the apex and twisting deformation of the ventricles due to asymmetric myocardial muscle sheets (ejection phase) • Blood flows to the lungs from the right ventricle, and to the rest of body from the left ventricle • Pressure in the ventricles falls and the aortic and pulmonary valves close • Blood flows from the aorta into the coronary arteries as the ventricles relax; ventricular diastole
Cardiac Output: SV (ml/beat) X HR (beats/min) = CO(ml/min.) 70 ml X 80 = 5600 ml /min. or 5.6 liters L/min Factors affecting cardiac performance Preload: pressure generated at the end of diastole; depends on both heart and vascular system –the amount of filling of the ventricle during relaxation Afterload: resistance to ejection during systole; depends on both heart and vascular system - the force that opposes ejection of blood from the heart; for the LV, this is the aortic systolic pressure Heart rate: a intrinsic characteristic of the heart tissue that is influenced by nervous and endocrine systems Myocardial contractility: the ability of the heart muscle to contract, the force of contraction - another cardiac tissue characteristic that is influenced by nervous and endocrine systems
Regulation of Heart Rate Sympathetic N.S. increases heart rate and force of contraction – secrete norepinephrine –accelerator nerves Parasympathetic N.S. decrease heart rate and force of contraction through the vagus nerve. Sends continuous impulses. Secretes acetylcholine
Electrocardiogram An ECG reveals to the trained eye both qualitative and quantitative information about the heart’s activity and electrical conduction system. The multiplicity of leads enables localization of certain lesions; e.g. where an infarction has occurred. Exercise provocation and 24-h recording may be useful modifications. The trace as it most commonly appears in generic ECG illustrations (similar to lead II) is shown in Pictures on slide, together with an account of the origin of each component. A number of basic ECG traces will be used in the relevant sections below to illustrate some typical abnormalities. THE SHAPE OF THE ECG The muscle mass of the atria is small compared with that of the ventricles, and the electrical change accompanying the contraction of the atria is therefore small. Contraction of the atria is associated with the ECG wave called ‘P’. The ventricular mass is large, and so there is a large deflection of the ECG when the ventricles are depolarized. This is called the ‘QRS’ complex. The ‘T’ wave of the ECG is associated with the return of the ventricular mass to its resting electrical state (‘repolarization’). The basic shape of the normal ECG is shown in Picture. The letters P, Q, R, S and T were selected in the early days of ECG history, and were chosen arbitrarily. The P, Q, R, S and T deflections are all called waves; the Q, R and S waves together make up a complex; and the interval between the S wave and the T wave is called the ST ‘segment’. The different parts of the QRS complex are labelled as shown in Picture. If the first deflection is downward, it is called a Q wave (Fig. 1.3a). An upward deflection is called an R wave – whether it is preceded by a Q wave or not. Any deflection below the baseline following an R wave is called an S wave – whether there has been a preceding Q wave or not (picture). Times and speeds ECG machines record changes in electrical activity by drawing a trace on a moving paper strip. All ECG machines run at a standard rate and use paper with standard-sized squares. Each large square (5 mm) represents 0.2 seconds (s), or 200 milliseconds (ms), so there are five large squares per second, and 300 per minute (min). So an ECG event, such as a QRS complex, occurring once per large square is occurring at a rate of 300/min (Picture). The heart rate can be calculated rapidly by remembering the sequence in Table 1.1. Table 1.1 Relationship between the number of large squares covered by the R–R interval and the heart rate R–R interval (large squares) Heart rate (beats/min) 1 300 2 150 3 100 4 75 5 60 6 50 Just as the length of paper between R waves gives the heart rate, so the distance between the different parts of the P–QRS–T complex shows the time taken for conduction of the electrical discharge to spread through the different parts of the heart. The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex, and is the time taken for excitation to spread from the SA node, through the atrial muscle and the AV node, down the bundle of His and into ventricular muscle. The normal PR interval is 0.12–0.2 s (120–200 ms), represented by three to five small squares. Most of the time is taken up by delay in the AV node (next slide). If the PR interval is very short, either the atria have been depolarized from close to the AV node, or there is abnormally fast conduction from the atria to the ventricles. The duration of the QRS complex shows how long excitation takes to spread through the ventricles. The QRS duration is normally 0.12 s (120 ms) (represented by three small squares) or less, but any abnormality of conduction takes longer, and causes widened QRS complexes.
RECORDING AN ECG The word ‘lead’ sometimes causes confusion. Sometimes it is used to mean the pieces of wire that connect the patient to the ECG recorder. Properly, a lead is an electrical picture of the heart. The electrical signal from the heart is detected at the surface of the body through five electrodes, which are joined to the ECG recorder by wires. One electrode is attached to each limb, and one is held by suction to the front of the chest and moved to different positions. Good electrical contact between the electrodes and skin is essential. It may be necessary to shave the chest. The ECG recorder compares the electrical activity detected in the different electrodes, and the electrical picture so obtained is called a ‘lead’. The different comparisons ‘look at’ the heart from different directions. For example, when the recorder is set to ‘lead I’ it is comparing the electrical events detected by the electrodes attached to the right and left arms. Each lead gives a different view of the electrical activity of the heart, and so a different ECG pattern. Strictly, each ECG pattern should be called ‘lead ...’, but often the word ‘lead’ is omitted. It is not necessary to remember which electrodes are involved in which leads, but it is essential that the electrodes are properly attached, with the wires labelled ‘LA’ and ‘RA’ connected to the left and right arms, respectively, and those labelled ‘LL’ and ‘RL’ to the left and right legs, respectively. As we shall see, the ECG is made up of characteristic pictures, and the record as a whole is almost uninterpretable if the electrodes are wrongly attached. The 12-lead ECG ECG interpretation is easy if you remember the directions from which the various leads look at the heart. The six ‘standard’ leads, which are recorded from the electrodes attached to the limbs, can be thought of as looking at the heart in a vertical plane (i.e. from the sides or the feet). Leads I, II and VL look at the left lateral surface of the heart, leads III and VF at the inferior surface, and lead VR looks at the right atrium. The V leads are attached to the chest wall by means of a suction electrode, and recordings are made from six positions, overlying the fourth and fifth rib spaces as shown in Picture. The six numbered V leads look at the heart in a horizontal plane, from the front and the left side. Thus, leads V1 and V2 look at the right ventricle, V3 and V4 look at the septum between the ventricles and the anterior wall of the left ventricle, and V5 and V6 look at the anterior and lateral walls of the left ventricle. As with the limb leads, the chest leads each show a different ECG pattern. In each lead the pattern is characteristic, being similar in different individuals who have normal hearts. Calibration A limited amount of information is provided by the height of the P waves, QRS complexes and T waves, provided the machine is properly calibrated. For example, small complexes may indicate a pericardial effusion, and tall R waves may indicate left ventricular hypertrophy. A standard signal of 1 millivolt (mV) should move the stylus vertically 1 cm (two large squares), and this ‘calibration’ signal should be included with every record. Making a recording When making a recording: 1. The patient must lie down and relax (to prevent muscle tremor) 2. Connect up the limb electrodes, making certain that they are applied to the correct limb 3. Calibrate the record with the 1 mV signal 4. Record the six standard leads – three or four complexes are sufficient for each 5. Record the six V leads. THE SHAPE OF THE QRS COMPLEX We now need to consider why the ECG has a characteristic appearance in each lead. The QRS complex in the limb leads The ECG machine is arranged so that when a depolarization wave spreads towards a lead the stylus moves upwards, and when it spreads away from the lead the stylus moves downwards. Depolarization spreads through the heart in many directions at once, but the shape of the QRS complex shows the average direction in which the wave of depolarization is spreading through the ventricles. If the QRS complex is predominantly upward, or positive (i.e. the R wave is greater than the S wave), the depolarization is moving towards that lead. If predominantly downward, or negative (S wave greater than R wave), the depolarization is moving away from that lead. When the depolarization wave is moving at right angles to the lead, the R and S waves are of equal size. Q waves have a special significance, which we shall discuss later. The cardiac axis Leads VR and II look at the heart from opposite directions. Seen from the front, the depolarization wave normally spreads through the ventricles from 11 o’clock to 5 o’clock, so the deflections in lead VR are normally mainly downward (negative) and in lead II mainly upward (positive). The average direction of spread of the depolarization wave through the ventricles as seen from the front is called the ‘cardiac axis’. It is useful to decide whether this axis is in a normal direction or not. The direction of the axis can be derived most easily from the QRS complex in leads I, II and III. A normal 11 o’clock–5 o’clock axis means that the depolarizing wave is spreading towards leads I, II and III and is therefore associated with a predominantly upward deflection in all these leads; the deflection will be greater in lead II than in I or III. If the right ventricle becomes hypertrophied, the axis will swing towards the right: the deflection in lead I becomes negative (predominantly downward) and the deflection in lead III will become more positive (predominantly upward). This is called ‘right axis deviation’. It is associated mainly with pulmonary conditions that put a strain on the right side of the heart, and with congenital heart disorders. When the left ventricle becomes hypertrophied, the axis may swing to the left, so that the QRS complex becomes predominantly negative in lead III. ‘Left axis deviation’ is not significant until the QRS deflection is also predominantly negative in lead II, and the problem is usually due to a conduction defect rather than to increased bulk of the left ventricular muscle. An alternative explanation of the cardiac axis Some people find the cardiac axis a difficult concept, and an alternative approach to working it out may be helpful. The cardiac axis is at right angles (90°) to the lead in which the R and S waves are of equal size. It is, of course, likely that the axis will not be precisely at right angles to any of the leads, but will be somewhere between two of them. The axis points towards any lead where the R wave is larger than the S wave. It points away from any lead where the S wave is larger than the R wave. The cardiac axis is sometimes measured in degrees, though this is not clinically particularly useful. Lead I is taken as looking at the heart from 0°; lead II from +60°; lead VF from +90°; and lead III from +120°. Leads VL and VR are said to look from –30° and –150°, respectively. The normal cardiac axis is in the range –30° to +90°. For example, if in lead II the size of the R wave equals that of the S wave, the axis is at right angles to lead II. In theory, the axis could be at either –30° or +150°. If lead I shows an R wave greater than the S wave, the axis must point towards lead I rather than lead III. Therefore the true axis is at –30° – this is the limit of normality towards what is called the ‘left’. If in lead II the S wave is greater than the R wave, the axis is at an angle of greater than –30°, and left axis deviation is present. Similarly, if the size of the R wave equals that of the S wave in lead I, the axis is at right angles to lead I or at +90°. This is the limit of normality towards the ‘right’. If the S wave is greater than the R wave in lead I, the axis is at an angle of greater than +90°, and right axis deviation is present. Why worry about the cardiac axis? Right and left axis deviation in themselves are seldom significant – minor degrees occur in long, thin individuals and in short, fat individuals, respectively. However, the presence of axis deviation should alert you to look for other signs of right and left ventricular hypertrophy (see Ch. 4). A change in axis to the right may suggest a pulmonary embolus, and a change to the left indicates a conduction defect. The QRS complex in the V leads The shape of the QRS complex in the chest (V) leads is determined by two things: The septum between the ventricles is depolarized before the walls of the ventricles, and the depolarization wave spreads across the septum from left to right. In the normal heart there is more muscle in the wall of the left ventricle than in that of the right ventricle, and so the left ventricle exerts more influence on the ECG pattern than does the right ventricle. Leads V1 and V2 look at the right ventricle; leads V3 and V4 look at the septum; and leads V5 and V6 at the left ventricle. In a right ventricular lead the deflection is first upwards (R wave) as the septum is depolarized. In a left ventricular lead the opposite pattern is seen: there is a small downward deflection (‘septal’ Q wave). In a right ventricular lead (V1 and V2) there is then a downward deflection (S wave) as the main muscle mass is depolarized (Fig. 1.20) – the electrical effects in the bigger left ventricle (in which depolarization is spreading away from a right ventricular lead) outweighing those in the smaller right ventricle (in which depolarization is moving towards a right ventricular lead). In a left ventricular lead there is an upward deflection (R wave) as the ventricular muscle is depolarized. When the whole of the myocardium is depolarized the ECG returns to baseline. The QRS complex in the chest leads shows a progression from lead V1, where it is predominantly downward, to lead V6, where it is predominantly upward. The ‘transition point’, where the R and S waves are equal, indicates the position of the interventricular septum. Why worry about the transition point? If the right ventricle is enlarged, and occupies more of the precordium than is normal, the transition point will move from its normal position of leads V3/V4 to leads V4/V5 or sometimes leads V5/V6. Seen from below, the heart can be thought of as having rotated in a clockwise direction. ‘Clockwise rotation’ in the ECG is characteristic of chronic lung disease. HOW TO REPORT AN ECG You now know enough about the ECG to understand the basis of a report. This should take the form of a description, followed by an interpretation. The description should always be given in the same sequence: 1. Rhythm 2. Conduction intervals 3. Cardiac axis 4. A description of the QRS complexes 5. A description of the ST segments and T waves. Reporting a series of totally normal findings is possibly pedantic, and in real life is frequently not done. However, you must think about all the findings every time you interpret an ECG. THINGS TO REMEMBER 1. The ECG results from electrical changes associated with activation first of the atria and then of the ventricles. 2. Atrial activation causes the P wave. 3. Ventricular activation causes the QRS complex. If the first deflection is downward it is a Q wave. Any upward deflection is an R wave. A downward deflection after an R wave is an S wave. 4. When the depolarization wave spreads towards a lead, the deflection is predominantly upward. When the wave spreads away from a lead, the deflection is predominantly downward. 5. The six limb leads (I, II, III, VR, VL and VF) look at the heart from the sides and the feet in a vertical plane. 6. The cardiac axis is the average direction of spread of depolarization as seen from the front, and is estimated from leads I, II and III. 7. The chest or V leads look at the heart from the front and the left side in a horizontal plane. Lead V1 is positioned over the right ventricle, and lead V6 over the left ventricle. 8. The septum is depolarized from the left side to the right. 9. In a normal heart the left ventricle exerts more influence on the ECG than the right ventricle.
Measures electrical activity of the heart P wave – represents atrial contraction (depolarization) QRS complex – represents ventricular contraction (depolarization) T wave – represents ventricular relaxation (repolarization)
PROPRTIES OF CARDIAC MUSCLE 1- EXCITABILITY 2- CONTRACTILITY 3- RHYTHMICITY 4- CONDUCTIVITY 1- EXCITABILITY Definition: Excitability is the ability of the cardiac muscle to respond to a stimulus by generating an action potential followed by a contraction. Cardiac muscle resting membrane potential and action potential differ in different parts of the heart. IONIC BASIS OF VENTRICULAR ACTION POTENTIAL Phase 0: Initial rapid depolarization: due to Na+ inflow due to opening of fast Na+ channels. Phase 1: Brief initial repolarization: due to opening of transient K+ channels. Phase 2: Prolonged plateau: due to opening of slow Ca++ - Na+ channels.( A balance is created between influx of Na+ and Ca+ and outflux of K+) Phase 3: Late rapid repolarization: due to delayed opening of K+ channels. Phase 4: Resting membrane potential ( -100 mv) LONG REFRACTORY PERIOD - Cardiac muscle action potential differs from skeletal muscle action potential. - Cardiac action potential is characterized by A LONG REFRACTORY PERIOD due to the plateau phase, during which the heart cannot be restimulated. - The action potential results in a mechanical response: contraction (systole) followed by relaxation (diastole). NON TETANIZING PROPERTY - The cardiac muscle has a long refractory period (due to plateau phase), which coincides with the whole period of systole. - Thus the heart remains non excitable for the entire contraction phase. - This ensures that the heart cannot go into a sustained state of contraction (tetanus) which could lead to stopping of circulation. 2- CONTRACTILITY Definition: It is the ability of the cardiac muscle to contract to pump blood. The heart is a strong muscular pump that contracts and relaxes all the time day and night, and its cessation means death. There are two types of muscle contraction: a- Isometric contraction: increase muscle tension without shortening (e.g. during early systole) b- Isotonic contraction: Tension is constant but muscle shortens and work is done (e.g. during late systole when blood is ejected) The cardiac contractility obeys two laws: ALL OR NONE LAW: If other conditions are constant, the cardiac muscle either contracts maximally ( if the stimulus is adequate) or does not contract at all ( if the stimulus is inadequate) STARLING’s LAW: [LENGTH-TENSION RELATIONSHIP] The ability of the cardiac muscle to generate force, is dependent on the initial length of the muscle prior to contraction, i.e. end diastolic volume (EDV). The greater the initial length of the muscle fibers, the greater the force of contraction (within limits). Application of STARLING LAW If the amount of blood returning to the heart increases (i.e.↑venous return) this will stretch the cardiac muscle fibers, i.e. increase its length at end of diastole (↑↑EDV: end diastolic volume ) increase the force of contraction at systole increase stroke volume. [ Thus, the heart will pump out whatever volume is delivered to it]
3- RHYTHMICITY Definition: It is the ability of the cardiac muscle to initiate its own regular impulses (rhythm), independent of any nerve supply. Cause: The cardiac muscle has a specialized excitatory conductive system, which have the property of auto rhythmicity. Rate of autorhythmicity: SA Node: 70-80 beats/min AV Node: 40-60 beats/min Bundle of His: 30 beats /min Purkinje fibers: 15 beats/min (incompatible with life) PACEMAKER OF THE HEART The area which determines the pace or rhythm of the heart is called the pacemaker of the heart. The SA Node is the pacemaker of the heart because: 1- it has the highest rhythm 2- and the whole heart obeys it. If the SA Node is destroyed, the AV Node will be pacemaker. VAGAL TONE: It is the continuous impulses in the vagus nerve which decrease the inherent high rhythm of the SA Node from 90-100/min to 70-80/min (the normal heart rate) PACEMAKER POTENTIALPacemaker cells have unique electric properties: Prepotential: Unstable membrane potential due to slow continuous leakage of Na+ ions into the myocardium leads to: spontaneous diastolic depolarization. After reaching firing level, the next action potential follows automatically. No plateau is seen.
Origin and Spread of Excitation in the Heart The heart contains muscle cells (fibers) that produce and distribute excitation impulses (conducting system), as well as working myocardium, which responds to the excitation by contracting. Contrary to the situation in skeletal muscle, excitation originates within the organ (autorhythmicity or autonomy of the heart). Atrial and ventricular myocardium each consists functionally of a syncytium, i.e., the cells are not insulated from one another but connected through gap junctions. A stimulus that originates somewhere within the atria or ventricles thus always leads to complete contraction of both atria or of both ventricles, respectively (all-or-nothing contraction). Normal excitation of the heart originates within the sinus node, the heart’s pacemaker. Excitation (Picture A) spreads from there through both atria to the atrioventricular node (AV node) and from there, via the His bundle and its two (Tawara) branches, reaches the Purkinje fibers, which transmit the excitation to the ventricular myocardium. Within the myocardium the excitation spreads from inside to outside (endocardium toward epicardium) and from apex toward the base, a process that can be followed—even in the intact organism— by means of the ECG (Picture C). The potential in the cells of the sinus node is a pacemaker potential (Picture A, bottom). It has no constant resting potential, but rises after each repolarization. The most negative value of the latter is called maximal diastolic potential ([MDP] ca. – 70 mV). It rises steadily until the threshold potential ([TP] ca. – 40 mV) is reached once more and an action potential (AP) is again triggered. The following changes in ionic conductance (g) of the plasma membrane and thus of ionic currents (I) cause these potentials: Beginning with the MDP, nonselective conductance is increased and influx (If; f = funny) of cations into the cell leads to slow depolarization (prepotential = PP). Once the TP has been reached, gCa now rises relatively rapidly, the potential rising more steeply so that an increased influx of Ca2+ (ICa) produces the upstroke of the AP. While the potential overshoots to positive values, leading to an outward K+ flux IK, the pacemaker cell is again repolarized to the MDP. Each AP in the sinus node normally results in a heart beat, i.e., the impulse frequency of the pacemaker determines the rate of the heart beat. The rate is lower if – the rise of the slow depolarization becomes less steep, – the TP becomes less negative, – the MDP becomes more negative so that spontaneous depolarization begins at a lower level, or – repolarization in an AP starts later or is slower. What the first three processes have in common is that the threshold is reached later than before. All parts of the excitation/conduction system have the capacity of spontaneous depolarization, but the sinus node plays the leading role in normal cardiac excitation (sinus rhythm is ca. 70–80 beats per minute). The reason for this is that the other parts of the conduction system have a lower intrinsic frequency than the sinus node (in B, C; causes are that slow depolarization and repolarization are flatter; see above). Excitation starting from the sinus node will thus arrive at more distal parts of the conducting system, before their spontaneous depolarization has reached the TP. However, if conduction of the sinus impulse is interrupted, the intrinsic frequency of more distal parts of the conduction system take over and the heart then beats in AV rhythm (40–60 beats per minute) or, in certain circumstances, at the even lower rate of the so-called tertiary (ventricular) pacemakers (20–40 beats per minute). In contrast to the sinus and AV nodes with their relatively slowly rising AP, due largely to an influx of Ca2+ (!C), there are in the working myocardium so-called rapid, voltage-gated Na+ channels that at the beginning of the AP briefly cause a high Na+ influx and therefore, compared with the pacemaker potential, a relatively rapid rise in the upstroke of the AP (!C). The relatively long duration (compared 180 with skeletal muscle) of myocardial AP, giving it the shape of a plateau, has an important function in that it prevents circles of myocardial excitation (reentry). This also holds true for very high and low heart rates, because the duration of AP adapts to the heart rate (!A). The AP results in Ca2+ being taken up from the extracellular space via voltage-gated Ca2+ channels that are sensitive to dihydropyridine. In consequence, the cytosolic Ca2+ concentration rises locally (Ca2+ “spark”), whereupon the ligand-gated and ryanodine-sensitive Ca2+ channels of the sarcoplasmic reticulum, acting as Ca2+ store, open up (so-called trigger effect). Ca2+, which enters from there into the cytosol, finally triggers the electromechanical coupling of cardiac contraction. The cytosolic concentration of Ca2+ is also determined by the Ca2+ uptake into the Ca2+ stores (via Ca2+-ATPase) as well as by Ca2+ transport into the extracellular space. The latter is brought about both by a Ca2+-ATPase (exchanges 1 Ca2+ for 2 H+) and by a 3 Na+/Ca2+ exchange carrier that is driven by the electrochemical Na+ gradient, thus indirectly by Na+-K+-ATPase, across the cell membrane. Although the heart beats autonomously, adaptation of cardiac activity to changing demands is mostly effected through efferent cardiac nerves. The following qualitites of cardiac activity can be modified by nerves: – Rate of impulse formation of the pacemaker and thus of the heart beat (chronotropism); – Velocity of impulse conduction, especially in the AV node (dromotropism); – The force ofmyocardial contraction at a given distension, i.e., the heart’s contractility (inotropism); – Excitability of the heart in the sense of changing its excitability threshold (bathmotropism). These changes in cardiac activity are caused by parasympathetic fibers of the vagus nerve and by sympathetic fibers. Heart rate is increased by the activity of sympathetic fibers to the sinus node (positive inotropic effect via &quot;1-receptors) and decreased by parasympathetic, muscarinic fibers (negative chronotropic effect). This is due to changes in the slow depolarization rise and altered MDP in the sinus node (respectively). Flattening of the slow depolarization and the more negative MDP under vagus action are based on an increased gk, while the increased steepness of slow depolarization under sympathetic action or adrenalin influence is based on an increase in gCa and, in certain circumstances, a decrease in gK. The more subordinate (more peripheral) parts of the conduction system are acted on chronotropically only by sympathetic fibers, which gives the latter a decisive influence in any possible takeover of pacemaker function by the AV node or tertiary pacemakers (see above). The parasympathetic fibers of the left vagus low down while the sympathetic fibers accelerate impulse transmission in the AV node (negative or positive dromotropic action, respectively). The main influence is on the MDP and the steepness of the AP upstroke. Changes in gK and gCa play an important role here as well. In contrast to chronotropism and dromotropism, the sympathetic nervous system, by being positively inotropic, has a direct effect on the working myocardium. The increased contractility is due to an increase in Ca2+ influx, mediated by &quot;1-adrenergic-receptors, from outside the cell that allows an increase in the Ca2+ concentration in the cytosol of the myocardial cells. This Ca2+ influx can be inhibited pharmacologically by blocking the Ca2+ channels (so-called Ca2+ antagonists). Contractility is also increased by prolonging the AP (and as a result lengthening Ca2+ influx), as well as inhibiting Na+-K+-ATPase, for example, bymeans of the cardiac glycosides digoxin and digitoxin (smaller Na+ gradient across the cell membrane ! lower efficiency of 3 Na+/Ca2+ exchange !decreased Ca2+ extrusion !increased cytosolic Ca2+ concentration). At a lower heart rate the Ca2+ influx over time is low (few APs), so that there is a relatively long period in which Ca2+ outflux can take place between APs. Thus, the mean cytosolic concentration of Ca2+ becomes lower and contractility is held low as a result. The vagus nerve can also act via this mechanism; however, it does so indirectly through negative inotropy (frequency inotropism). The converse is true for sympathetic stimulation.
Definitions · An electrocardiogram (ECG) is a curve showing the potential variations against time in the whole body stemming from the heart, which is an electrochemical generator suspended in a conductive medium. · Asystolia refers to cardiac arrest. · Atrial fibrillation is a continuous atrial activation with 400 or more contractions per min. Contractions spread through the atrial tissue almost without mechanical effect and only few electrical signals are conducted to the ventricles. Atrial flutter is an atrial contraction rate around 300 per min, often with every second contraction conducted to the ventricles. Sawtooth-like flutter waves characterise the ECG. · Bradycardia is an unduly slow heart rate. Sinus bradycardia is a sinus rhythm at rest below 60 beats per min during the day or less than 50 at night. · Calcium concentration in plasma (total): Normal range is 2-2.5 mM. · Heart block is a blockage somewhere along the pathway for impulse conduction in the heart. · Mean QRS- axis of the ventricles or the mean cardiac vector is the net force in the frontal plane during ventricular depolarisation and repolarisation. Many electrical potentials are propagated in different directions and most of these cancel each other out. The main direction of the mean cardiac vector is from the base of the ventricles towards the apex. · Left-sided axis deviation is characterised by a positive RI and a negative RIII (Fig. 11-7). Cardiologists use the net area of the QRS-complex for precise diagnosis. · Pacemaker cells are small pale cells located in the sinus node of the heart. The sinus node is the primary determinator of the cardiac rhythm, because its cells have the highest spontaneous frequency. · Potassium concentration in plasma: Normal range is 3.5-5 mM. · Right-sided axis deviation is characterised by a negative RI and a positive RIII (Fig. 11-7). Cardiologists use the net area of the QRS-complex for precise diagnosis. · Sinus rhythm refers to the normal cardiac pacemaker rhythm from the sinus node. The spontaneous discharge at rest is usually 100 beats per min, but the parasympathetic inhibitory tone predominates in healthy individuals resulting in a resting heart rate around 75 beats per min. · Tachycardia refers to a cardiac rate above 100 beats per min. Sinus tachycardia is a sinus rhythm above 100, which can be caused by anaemia, cardiac failure, catecholamines, emotion, exercise, fever, pregnancy, pulmonary embolism or thyrotoxicosis. · Ventricular tachycardia is defined as three or more ventricular beats occurring at a rate of 120 beats per min or more. · Ventricular fibrillation is an extremely rapid ventricular activation without pumping effect. Electrical defibrillation is the only effective therapy. · Vulnerable period is a dangerous period in cardiac cycle just at the end of the contraction (simultaneous with the T-wave in the ECG). Electrical conversion (an electrical shock) given during this period may in itself initiate ventricular fibrillation. Refractory areas of cardiac muscle are spread among non-refractory areas.
Ability to automatic impulses formation depends on pacemaker cells activity of the sinoatrial node, in which spontaneous slow depolarization of cells membrane takes place during diastole. As the result, action membrane potential arises after achievement of some critical level (threshold level critical potential). Impulses generation depends on maximum diastolic potential of these cells, on maximum diastolic potential measure, after which action membrane potential arises, and on speed of slow diastolic depolarization. The decrease of the threshold level maximum diastolic potential SA node p-cells or/and slow diastolic depolarization speed increase stimulates of the sinus tachycardia appearance at body temperature increase, in the result of sympathetic stimulation or withdrawal of vagal tone. On the contrary, decrease of speed slow spontaneous diastolic depolarization or/and increase threshold level critical potential and hyperpolarization in diastole causes the sinus bradycardia. Tone oscillations of n. Vagus at breathing time can induce the sinus respiratory arrhythmia (increase of hear beats during the inspiration). Respiratory arrhythmia in norm is in children, but now very often can be observed in adult. Action potential formation in the sinus node occurs at a rate of 60–100 per minute (usually 70–80 per minute at rest). During sleep and in trained athletes at rest (vagotonia) and also in hypothyroidism, the rate can drop below 60 perminute (sinus bradycardia), while during physical exercise, excitement, fever, or hyperthyroidism it may rise to well above 100 per minute (sinus tachycardia). In both cases the rhythm is regular, while the rate varies in sinus arrhythmia. This arrhythmia is normal in juveniles and varies with respiration, the rate accelerating in inspiration, slowing in expiration.
Nomotopic (sinus node) rhythms. 1. Sinus tachycardia refers to a rapid heart rate (&gt; 100 to 180 beats per minute) that has the origin in the SA node. The main reasons are physical or emotional stress, myocardial ischemia or infarction, myocardial dystrophy, congestive heart failure, fever, hyperthyroidism, pharmacological agents (atropine, isoproterenol, adrenalin), compensatory response to decreased cardiac output. ECG sings: all waves have normal configuration and priority, P wave and PR interval (0.12 to 0.20 second) precedes each QRS complex (sinus rhythm), all R-R are shortened.
2. Sinus bradycardia describes a slow heart rate (&lt; 60 to 40 beats per minute) that has the origin in the SA node. It may be normal in trained athletes who maintain a large stroke volume, during sleep; in pathological condition after influenza or typhoid, intracranium pressure rise, irritation of the n. Vagus nucleases, may be an indicator of poor prognosis in patient with acute myocardial infarction that is associated with hypotension. ECG sings: all waves have normal configuration and priority, normal P wave and PR interval precedes each QRS complex (sinus rhythm), all R-R are lengthened. This arrhythmia may cause heart output decrease and leads to cerebral or coronary blood flow insufficiency, in that condition ectopic pacemaker could be activated.
3. Sinus (respiratory) arrhythmia is characterized by gradually lengthening (at expiration) and shortening (at inspiration) R-R intervals and is the result of intrathoracic pressure changes during respiration. It is the normal for the children and can occur in adult after influenza, at neurocirculative dystone, hypertension, congestive heart failure, diabetes mellitus. ECG sings: sinus rhythm, difference of all R-R is more than 0.15 second (at norm difference of all R-R is less than 0,15 sec).
Heterotopic rhythms. They are the result of ectopic automatism driver activation that is localized out SA node (for example, in atrium, in AV-node or in ventricle) because SA node failure (reasons - digitalis toxicity, myocardial infarction, acute myocarditis, excessive vagal tone, hyper- or hypokalemia). 1.Tardy ectopic rhythm (vicarious, passive) arises at the SA node arrest. ECG sings: heart beats not more 60 per minute. If ectopic pacemaker is localized in atrium on ECG inverted P wave is observed before QRS. If ectopic pacemaker is localized in AV node on ECG inverted P wave is observed after normal QRS, or hidden in QRS (atrial-ventricular rhythm). If ectopic pacemaker is localized in ventricle heart rate is less then 40 per minute, QRS is deformed (wide, distorted), it is so called idioventricular rhythm. 2. Unparoxismal tachycardia begins and ends gradually, heart rate is 90 –130/min. Ectopic driver may be localized in atrium, in AV node or in ventricle. So, complex PQRST has sings of nonsinus rhythm (alteration of configuration, duration and succession waves). 3. Migration of supraventricular rhythm driver is characterized by the gradual removal of rhythm driver from SA node to AV one. ECG sings: violation of P wave configuration and lasting, dysrtythmia.
Change of level: a) maximal diastolic potential, b) critical potential or c) speeds of slow diastolic depolarization lead to change of frequency of generation of impulses or to appearance of other sources of impulses.
Sinus tachycardia Reasons: physical load, emotional stress, heart failure, myocardium ischemia or infarction, myocardium dystrophy ECG: sinus rhythm, HR 90-180 /min, R-R duration&lt;0,60 sec Sinus bradycardia Reasons: n. Vagus high activity (sportsmen, flu, typhoid), intracranial pressure increase (results from irritation of n.Vagus nucleas) ECG: sinus rhythm, HR 59-40 /min, R-R duration&gt;1,0 sec Sinus (respiratory) arrhythmia Reasons: breathing (in children), after fly (ifluenza), neurocirculative dystone ECG: sinus rhythm, difference between the shortest R-R and longest R-R &gt;0,15 sec
Own automatism of lower part conductive heart system can appear in pathological conditions (arises so-called heterotopic or ectopic rhythm driver). That condition is the result of the automatism sinoatrial node ability decrement, so generation of the impulses arises in another myocardium conductive parts, new ectopic automatism driver appears. Beginning such automatism driver is the result damage of the different part conductive system, or electrical heterogeneous of myocardiocytes, or electrical unstable of myocardiocytes (especially in fourth phase action potential during formation of the resting membrane potential). In that cases extraordinary heart contractive or only ventricles arises (extrasystole). There are three mechanisms of the new ectopic rhythm driver appearance. By other mechanism which results in appearance of ectopic hotbed of excitation, there can be an origin of difference of potentials between located alongside myocytes. That observed as a result of unsimultaneous completion of repolarization in them, which can cause excitations in fibres, which already went out from the phase of adiphoria. Such phenomenon is observed: a) at the local ischemia of myocardium and b) at poisoning digitalis glycoside. Extrasystoles (ES). When an action potential from a supraventricular ectopic focus is transmitted to the ventricles (atrial or nodal extrasystole), it can disturb their regular (sinus) rhythm (supraventricular arrhythmia). An atrial ES can be identified in the ECG by a distorted (and premature) P wave followed by a normal QRS complex. If the action potential originates in the AV node (nodal ES), the atria are depolarized retrogradely, the P wave therefore being negative in some leads and hidden within the QRS complex or following it. Because the sinus node is also often depolarized by a supraventricular ES, the interval between the R wave of the ES (= RES) and the next normal R wave is frequently prolonged by the time of transmission from ectopic focus to the sinus node (postextrasystolic pause). The intervals between R waves are thus: RES–R &gt; R–R and (R–RES + RES–R) &lt; 2 R–R. An ectopic stimulus may also occur in a ventricle (ventricular extrasystole). In this case the QRS of the ES is distorted. If the sinus rate is low, the next sinus impulse may be normally transmitted to the ventricles (interposed ES). At a higher sinus rate the next (normal) sinus node action potential may arrive when the myocardium is still refractory, so that only the next but one sinus node impulse becomes effective (compensatory pause). The R–R intervals are: R–RES +RES–R = 2 R–R.
So, the descriptives paroxysmal tachycardia, flutter, and fibrillation refer to the &quot;rates&quot; of the arrhythmia, e.g. - it could be atrial fibrillation (wavy baseline refers to the atria going &gt;350 bpm.), or ventricular fibrillation (with the ventricle not contracting in a coordinated fashion resulting in only an erratic line that isn&apos;t possible to count).
*In a type I SA block, the P-P interval shortens until one P wave is dropped. *In a type II SA block, the P-P intervals are an exact multiple of the sinus cycle, and are regular before and after the dropped P wave. This usually occurs transiently and produces no symptoms. It may occur in healthy patients with increased vagal tone. It may also be found with CAD, inferior MI, and digitalis toxicity.
Atrio-ventricular (transversal) block of heart can be: a) complete and b) incomplete. In an incomplete block hearts distinguish 3-e degrees: AV block of I of degree is characterized multiplying time of conducting of impulse from atriums to the ventricles, that is accompanied lengthening [elongation] the PQ-interval (0,2-0,5 sec). AV block of the II degree (Wenckebach phenomenon) is characterized the making progress increase of PQ-interval until one of excitations, usually eighth-tenth, not conducted. After the fall of beat of ventricle the interval of P-Q recommences, gradually prolonged with every reduction of heart. AV block of the III degree is observed fall each second or third beat, how vice versa, every second, third or fourth excitation of atrium is conducted only. Complete AV-block. Impulses do not conduct through atrio-ventricular node. Everyone has own rhythm: atriums with frequency about 70, ventricles are about 35 beats per 1 min (idioventricular rhythm). The Adams-Stokes syndrome (Adam–Stokes attack or syncope) is a clinical disorder caused by partial [incomplete] AV block suddenly become a total [complete]. Dysplays: unconsciousness and cramps caused by brain hypoxia. (Ventricular atopic pacemakers then take over (ventricular bradycardia with normal atrial excitation rate), resulting in partial or total disjunction of QRS complexes and P waves. Ventricles cannot pump enough blood → brain ischemia → syncope (fainting) ETIOLOGY The AV node is supplied by the parasympathetic and sympathetic nervous systems and is sensitive to variations in autonomic tone. Chronic slowing of AV nodal conduction may be seen in highly trained athletes who have hypervagotonia at rest. A variety of diseases and drugs can also influence AV nodal conduction. These include acute processes such as myocardial infarction (particularly inferior); coronary spasm (usually of the right coronary artery); digitalis intoxication; excesses of beta and/or calcium blockers; acute infections such as viral myocarditis, acute rheumatic fever, infectious mononucleosis; and miscellaneous disorders such as Lyme disease, sarcoidosis, amyloidosis, and neoplasms, particularly cardiac mesotheliomas. AVnodal block may also be congenital. Two degenerative diseases are commonly responsible for damage to the specialized conducting system and produce AV block usually associated with bundle branch block (Chap. 210). In Lev’s disease, there are calcification and sclerosis of the fibrous cardiac skeleton, which frequently involve the aortic and mitral valves, the central fibrous body, and the summit of the ventricular septum. Lenegre’s disease appears to be a primary sclerodegenerative disease of the conducting system with no involvement of the myocardium or the fibrous skeleton of the heart. These two diseases are probably the most common causes of isolated chronic heart block in adults. Hypertension and aortic and/or mitral stenosis are specific disorders that either accelerate the degeneration of the conducting system or have a direct effect by calcification and fibrosis involving the conducting system. First-degree AV block, more properly termed prolonged AV conduction, is classically characterized by a PR interval 0.20 s, but use of this value may be misleading in terms of clinical significance. Since the PR interval is determined by atrial, AV nodal, and His-Purkinje activation, delay in any one or more of these structures can contribute to a prolonged PR interval. In the presence of a QRS complex of normal duration, a PR interval 0.24 s almost invariably is due to a delay within the AV node. If the QRS is prolonged, delays may be present at any of the levels mentioned above. Delay within the His-Purkinje system is always accompanied by a prolonged QRS duration but can occur with a relatively normal PR interval. However, as indicated below, it is only with intracardiac recordings that the exact site of delay can be determined. Second-degree heart block (intermittent AV block) is present when some atrial impulses fail to conduct to the ventricles. Mobitz type I second-degree AV block (AV Wenckebach block) is characterized by progressive PR interval prolongation prior to block of an atrial impulse. The pause that follows is less than fully compensatory (i.e., is less than two normal sinus intervals), and the PR interval of the first conducted impulse is shorter than the last conducted atrial impulse prior to the blocked P wave. Usually the difference between the longest and shortest PR intervals exceeds 100 ms. This type of block is almost always localized to the AV node and associated with a normal QRS duration, although bundle branch block may be present. It is seen most often as a transient abnormality with inferior wall infarction or with drug intoxication, particularly digitalis, beta blockers, and occasionally calcium channel antagonists. This type of block can also be observed in normal individuals with heightened vagal tone. Although Mobitz type I block can progress to complete heart block, this is uncommon, except in the setting of acute inferior wall myocardial infarction. Even when it does, however, the heart block is usually well tolerated because the escape pacemaker usually arises in the proximal His bundle and provides a stable rhythm. As a result, the presence of Mobitz type I second-degree AV block rarely mandates aggressive therapy. Therapeutic decisions depend on the ventricular response and the symptoms of the patient. If the ventricular rate is adequate and the patient is asymptomatic, observation is sufficient. In Mobitz type II second-degree AV block, conduction fails suddenly and unexpectedly without a preceding change in PR intervals. It is generally due to disease of the His-Purkinje system and is most often associated with a prolonged QRS duration. When Mobitz type II block occurs with a normal QRS duration, an intra-His site of block should be expected. It is important to recognize this type of block because it has a high incidence of progression to complete heart block with an unstable, slow, lower escape pacemaker. Therefore, pacemaker implantation is necessary in this condition. Mobitz type II block may occur in the setting of anteroseptal infarction or in the primary or secondary sclerodegenerative or calcific disorders of the fibrous skeleton of the heart. In so-called high-degree AV block there are periods of two or more consecutively blocked P waves, but intermittent conduction can be demonstrated. Block is usually in the His-Purkinje system, but simultaneous block in the AV node may also be present. Regardless of the site of origin of the escape rhythm, if it is slow and the patient is symptomatic, a cardiac pacemaker is mandatory. Third-degree AV block is present when no atrial impulse propagates to the ventricles. If the QRS complex of the escape rhythm is of normal duration, occurs at a rate of 40 to 55 beats/min, and increases with atropine or exercise, AV nodal block is probable. Congenital complete AV block is usually localized to the AV node. If the block is within the His bundle, the escape pacemaker is usually less responsive to these perturbations. If the escape rhythm of the QRS is wide and associated with rates 40 beats/min, block is usually localized in, or distal to, the His bundle and mandates a pacemaker, since the escape rhythm in this setting is unreliable. Some patients with infra-His bundle block are capable of retrograde conduction. In such patients, a “pacemaker syndrome” (see below) may develop if a simple ventricular pacemaker is used. Dual-chamber pacemakers eliminate this potential problem.
Bundle branch block is a block of the right or the left bundle branches. The signal is conducted first through the healthy branch and then it is distributed to the damaged side. This distribution takes more time than usual, so the QRS-complex is wider than normal (more than 0.12 s in Fig. 11-13). In right bundle branch block, the right ventricle is activated late, which is shown by a tall double R-wave in V1 (ie, the second late R-wave is from the right side), and a deep wide S-wave in leads I and V6 . The left bundle branch block is characterized by a late activation of the left ventricle from apex towards basis. This results in a solid R-wave in the left precardial leads (V5 andV6), whereas there is a deep broad S-wave in V1 and III
Appearing of this syndrome connect with additional bundles of conducting. To such ways belong: a) bundle of Paladino-Kenta - conduct impulses from atrium to the ventricles, passing a AV-node; b) bundle of Maheyma. Connects overhead part of His&apos; bundle with ventricles; c) bundle of James. Connect atrium with lower part of AV-node or with the His&apos; bundle. On additional ways impulses are conducted quickly and achieve ventricles more early than impulses which pass an ordinary way through a AV-node. It lead to the premature activating some part of ventricles. WPW-syndrome or Wolf-Parkinson-White block is not a direct block of the conduction through the Hiss bundle and branches, but is caused by a short cut through an extra conduction pathway from the atria to the ventricles. This abnormal conduction pathway is congenital and called the bundle of Kent . Due to this short-cut, the slow conduction through the AV-node is bypassed and the ventricles are depolarised faster than normal. The WPW-syndrome is recognized in most ECG leads as a short PQ (PR)-interval followed by a wide QRS-complex with a delta wave. The patients often have paroxysmal tachycardia or they may develop atrial fibrillation. Some patients are treated with ablation of the bundle of Kent. Other patients are asymptomatic and in good physical condition. The long QT-syndrome. This is frequently a genetic condition, where fast repolarised cells are restimulated by cells that have not repolarised. When acquired the condition is caused by myocardial ischaemia, by drugs or by a low serum [Ca2+] - below 2 mM. Normally, the QT-interval is less than 50% of the preceding RR-interval. The long QT-interval symbolises a long ventricular systole. Actually, the ST-interval is simultaneous with the phase 2 plateau of the ventricular membrane action potential. Here, the slow Ca2+ -Na+ - channels remain open for more than 300 ms as normally. The net influx of Ca2+ and Na+ is almost balanced by a net outflux of K+. Hereby, a long phase 2 plateau or isoelectric segment is formed. Cardiac pacemakers Implanted cardiac pacemakers are successful in keeping heart patients alive. This is often a beneficial treatment of Adam Stokes syndrome or ventricular tachycardia. An electrical pacemaker is a small stimulator with battery planted underneath the skin. The electrodes are connected to the right ventricular muscle tissue, whose contraction rate is controlled by the stimulator. Cardiopulmonary resuscitation Cardiac arrest is cessation of all spontaneous cardiac rhythmicity. Cardiac arrest is most often caused by anoxia. The cause of anoxia is inadequate respiration due to terminal lung disease, thoracic trauma, and shock or deep anaesthesia. Cardiopulmonary resuscitation is important in keeping the heart alive until electrical defibrillation can be performed with a large electrical shock. Alternating current is applied for 100 ms, or 1000 mV direct current is applied for a few ms.
Reentry in the myocardium. A decrease in dV/dt leads to slow propagation of excitation (υ), and a shortening of the AP means a shorter refractory period (tR). Both are important causes of reentry, i.e., of circular excitation. When the action potential spreads from the Purkinje fibers to the myocardium, excitation normally does not meet any myocardial or Purkinje fibers that can be reactivated, because they are still refractory. This means that the product of υ · tR is normally always greater than the length s of the largest excitation loop (!1). However, reentry can occur as a result if – the maximal length of the loop s has increased, for example, in ventricular hypertrophy, – the refractory time tR has shortened, and/or – the velocity of the spread of excitation υ is diminished (!2). A strong electrical stimulus (electric shock), for example, or an ectopic ES that falls into the vulnerable period can trigger APs with decreased upstroke slope (dV/dt) and duration, thus leading to circles of excitation and, in certain circumstances, to ventricular fibrillation. If diagnosed in time, the latter can often be terminated by a very short high-voltage current (defibrillator). The entire myocardium is completely depolarized by this counter shock so that the sinus node can again take over as pacemaker. Reentry in the AV node. While complete AV block causes a bradycardia (see above), partial conduction abnormality in the AV node can lead to a tachycardia. Transmission of conduction within the AV node normally takes place along parallel pathways of relatively loose cells of the AV node that are connected with one another through only a few gap junctions. If, for example, because of hypoxia or scarring (possibly made worse by an increased vagal tone with its negative dromotropic effect), the already relatively slow conduction in the AV node decreases even further, the orthograde conduction may come to a standstill in one of the parallel pathways (block). Reentry can only occur if excitation (also slowed) along another pathway can circumvent the block by retrograde transmission so that excitation can reenter proximal to the block (reentry). There are two therapeutic ways of interrupting the tachycardia: by further lowering the conduction velocity &quot; so that retrograde excitation cannot take place; or 2) by increasing &quot; to a level where the orthograde conduction block is overcome.
Excitation in Electrolyte Disturbances Hyperkalemia. Sodium levels: Na does not alter the electrical activity of the heart severely. Low level of Na in the body: reduces the electrical activity of cardiac muscle & ECG shows low voltage waves. Mild hyperkalemia causes: Elevation of the MDP in the SA node. It can sometimes have positive chronotropic effects. In severe hyperkalemia: the more +ve MDP leads to the inactivation of Na+ channels and to a reduction in the slope and amplitude of APs in the AV node (negative dromotropic effect). The (gK) rises, and the PP slope becomes flatter due to a negative chronotropic effect. Faster myocardial repolarization decreases the cytosolic Ca2+ conc. In extreme cases, the heart stops in diastole (cardiac paralysis). Hypokalemia (moderate) has positive chronotropic and inotropic effects. It reduces the sensitivity of the heart. Hypocalcemia: effects the heart more than hypercalcemia. Hypercalcemia is thought to raise the gK and thereby shortens the duration of the myocardial AP continuous contraction of the heart heart stops in systole. Calcium rigor: Stoppage of heart in systole due to hypercalcemia. ECG. Changes in serum K+ and Ca2+ induce characteristic changes in myocardial excitation. Hyperkalemia (&gt; 6.5 mmol/L): Tall, peaked T waves (C), an increased PR interval (D) and a widened QRS (E). In severe hyperkalemia: P wave is absent (E) as the atrial muscle is unexcitable. QRS complex merges with T wave & Cardiac arrest can occur stopping the heart in diastole. Hypokalemia (&lt; 2.5 mmol/L): P waves may become peaked (D), ST depression below isoelectric line (E), T waves becomes flattened (F) & U wave becomes more prominent. Hypercalcemia (&gt; 2.75 mmol/L total calcium): Shortened QT interval due to a shortened ST segment. Hypocalcemia (&lt; 2.25 mmol/L total calcium): Prolonged QT interval due to a prolonged ST segment.
Fibrillation At presence of numerous ectopic hotbed of excitation plus change of conducting of impulse at which speed of it conducting is violated on the different areas of myocardium or there is distribution of impulse only in one direction, terms are created for the protracted circulation of wave of excitation in the certain department of heart, there are disorders of rhythm - fibrillation arrhythmia which shows up flutter and fibrillation of atriums. At flutter atriums frequency of their reductions achieves 250-400 per min. Thus a relative cardiac blockade develops as a result of inability of ventricles to reproduce the high rhythm of atriums; ventricles answer reduction on every second, third or fourth reduction of atriums, as other waves of excitation get in the phase of refractory. At this case, reduction of ventricles can arise up before, than sufficient filling will come by their blood which causes heavy violations of circulation of blood. If the amount of impulses in atriums achieves 400-600 per min, it is fibrillation of atriums. Separate muscular fibres are thus abbreviated only, and all atriums is in a state of incomplete reduction, it participating in pumping over of blood is halted. Impulses which helter-skelter come to the atrium-ventricular node on the separate muscular fibres of atrium are mostly uncapable to cause its excitation, because find a node in the state of refractive or does not achieve a maximum level. Those a atrio-ventricular node is excited irregularly, and reductions of ventricles take casual character. As a rule, the number of reductions of ventricles per minute exceeds normal. Often reductions of ventricles take place to their filling blood and not accompanied a pulse wave. That is why frequency of pulse appears less frequency of reductions of heart (deficit of pulse). More frequent in all reason of development of fibrillation arrhythmia are: mitral stenosis; b) thyrotoxicosis; c) atherosclerotic cardiosclerosis. Most acknowledged presently there is a theory of the repeated entrance of impulses (re-entry), which explains the mechanism of development of fibrillation arrhythmia. In accordance with this theory, flutter and fibrillation is conclusion of violations of conductivity, at which: distribution of impulses is halted anterograde direction and b) saved in reverse (to retrograde). Terms are created for permanent circular motion of impulses on myocardium. In normal terms the wave of excitation, arising up in one place, spreads in both sides of cardiac chamber. Under reaching an opposite wall, she goes out, meeting with other wave which leaves after itself the area of refractivity. If as a result of origin of temporal block or delay of arrival of impulses on some fibres of myocardium, they comes to the place which already went out from the state of refractivity, terms are created for the protracted circulation one time of arising up excitation. Fibrillation of ventricles Reasons of origin of such phenomenon are: a) passing of electric current through a heart, b) anesthesia by a chloroform or cyclopropane, c) obstruction of coronal arteries or other cases of acute hypoxia, d) trauma of heart, e) action of toxic doses of digitalis and calcium. Thus: a) as a result of chaotic reduction of separate muscular fibres normal force of reductions is practically absent, b) circulation of blood is halted and c) the loss of consciousness and death comes quickly. Diminishing of concentration of intracellular potassium promote appear of fibrillation. It connect with decline of diaphragm potential of cardiomyocytes that led to more easy origin in them of depolarization and excitation, and also change of maintenance of nervous mediators, especially catecholamines. At treatment of fibrillation of ventricles most effective is admission through the heart of a short strong be single electric impulse, which results in simultaneous depolarization of all fibres of myocardium and is reason of stopping of asynchronous excitation of muscular fibres.
Tachycardia of ectopic origin. Even when the stimulus formation in the sinus node is normal, abnormal ectopic excitations can start from a focus in an atrium (atrial), the AV node (nodal), or a ventricle (ventricular). High-frequency ectopic atrial depolarizations (saw-toothed base line instead of regular P waves in the ECG) cause atrial tachycardia, to which the human ventricles can respond to up to a rate of ca. 200 per minute. At higher rates, only every second or third excitation may be transmitted, as the intervening impulses fall into the refractory period of the more distal conduction system, the conduction component with the longest AP being the determining factor. This is usually the Purkinje fibers, which act as frequency filters, because their long action potential stays refractory the longest, so that at a certain rate further transmission of the stimulus is blocked (between 212 and 229 per minute; recorded in a dog). At higher rates of discharge of the atrial focus (up to 350 per minute = atrial flutter; up to 500 per minute = atrial fibrillation), the action potential is transmitted only intermittently. Ventricular excitation is therefore completely irregular (absolutely arrhythmic). Ventricular tachycardia is characterized by a rapid succession of ventricular depolarizations. It usually has its onset with an extrasystole. Ventricular filling and ejection are reduced and ventricular fibrillation occur (high-frequency and uncoordinated twitchings of the myocardium;). If no countermeasures are taken, this condition is just as fatal as cardiac arrest, because of the lack of blood flow.
1) Atrial fibrillation is a condition in which the sinus node no longer controls the rhythm and the atrial muscle fibres undergo a tumultuous rapid twitching. A total irregularity of ventricular contractions characterise the fibrillation. An excitation wave with 400-600 cycles per min, courses continuously through the atrial wall over a circular pathway about the origin of the great veins (the circus motion theory). There is a continuous activation with more than 400 P-waves per min, where regular atrial contraction is impossible. It is difficult to see and count the P-waves of the ECG. Because of the refractoriness of the AV-bundle, only some of the excitation waves result in ventricular beats. The pulse of the patient is therefore irregular as the occurrence of QRS-complexes in the ECG. The many P-waves (also called f-waves for fluctuations) are characteristic for atrial fibrillation. Untreated atrial fibrillation has a QRS-frequency of 150-180 bpm. Old patients with chronic heart disease often show the so-called slow atrial fibrillation with a QRS-frequency below 60 bpm. Most cardiac disorders can lead to atrial fibrillation or flutter. Atrial flutter is related to atrial fibrillation, but the atrial frequency - counted from the P-waves - is much lower than 400 bpm - usually around 300 bpm and the AV-conduction is more regular. The consequences to the patient depend upon the number of impulses conducted from the atria through the AV-node to the ventricles (recorded as QRS-complexes). Often every second impulse reaches the ventricles, so the ratio of AV-blocks is 2:1, but the ratio can also be 3:1, 4:1 etc. Atrial flutter is recognized in the ECG as sawtooth-like P-waves. 2) Ventricular fibrillation is a tumultuous twitching of ventricular muscle fibres, which are ineffectual in expelling blood. The condition is lethal without effective resuscitation. The irregular ventricular rate is 200-600 twitches/min. Without contractile co-ordination the force is used frustraneous. Actually, the heart does not pump blood, so within 5 s unconsciousness occurs, because of lack of blood to the brain. In patients with coronary artery disease, ventricular fibrillation is a cause of sudden death. The trigger is anoxia (with an ineffective Na+-K+-pump) and the impulses arise from several foci in the ventricular tissue. There is no regular pattern in the ECG. Ventricular fibrillation is initiated when a premature signal arrives during the downslope of the T-wave (vulnerable period). Electrical shock (electrocution) also triggers ventricular fibrillation. Ventricular fibrillation is the most serious cardiac arrhythmia. It must be converted to sinus rhythm at once by the application of a large electrical shock to the heart (ventricular defibrillation) or the patient will die. Alternating current is applied for 100 ms or 1000 volts direct current is applied for a few milliseconds. The vulnerable period (VP is actually phase 3 and represented in the ECG as the T-wave) is dangerous, because an electrical shock, when given during this period, will cause in itself ventricular fibrillation. Here is shown sinus rhythm and one ectopic beat followed by ventricular fibrillation. The only effective treatment is rapid institution of electrical defibrillation. Shifting pacemaker is a condition where the impulse originates in shifting locations inside the SN, or the pacemaker shifts from the SN to the AV-node. In the first case the P-wave change size from beat to beat, and in the second case the P-wave is found either in front of the QRS-complex or behind.
Multiple Choice Questions I. Answers A, B, and D are true statements, whereas C and E are false. II. Answers C, D. and E are true statements, whereas A and B are false. III. Answers A and D are true statements, whereas B, C, and E are false.
Plan of the lecture
1. Organization of the circulatory
2. Cardiac cycle.
3. Conductive system of the heart.
4. Mechanisms of compensation
5. Arhytmias of the heart. Deffinition.
6. Ischaemic heart disease.
6. Heart failure.
Actuality of the lectureActuality of the lecture
The disorders of cardiac rhythm concern to complex manifestations of
pathology of heart. Its can arise in rather small damage of the conducting
system, and in some cases in structural changes. More often arrythmia
arise with infectious illnesses and intoxications as consequence of
miocarditis or dystrophy processes in cardiac muscle, and also in heart
ishemic disease, cardiosclerosis.
The disorders of cardiac rhythm arise also owing to reflex influences from
various interreceptors areas (disease of liver, intestinal tract, uterus), and
also in hemodynamic disorders (arterial hypertension). Not infrequently
аrrythmia is a result of disturbance of functions central and vegetative
parts of nervous system. For example, the increase of activity
parasymphatic nervous system lead to delay of conductivity. Similar is
observed also by overdose of some medicin drugs (digitalis, quinidine,
morphine). If bradycardia is accompanied complete atrioventricular
blockade, can occur ischemia of brain with loss consciousness and
Arrythmia can be result in development of cardiac insufficiency.
OF THE CIRCULATORY SYSTEM
■ The circulatory system consists of the heartheart,
which pumps blood; the arterial systemarterial system,
which distributes oxygenated blood to the
tissues; the venous systemvenous system, which collects
deoxygenated blood from the tissues and
returns it to the heart; and the capillariescapillaries,
where exchange of gases, nutrients, and
■ The circulatory system is divided into two
parts: the low-pressure pulmonarylow-pressure pulmonary
circulationcirculation, linking the transport function of
the circulation with the gas exchange
function of the lungs; and the high-pressurehigh-pressure
systemic circulationsystemic circulation, providing oxygen and
nutrients to the tissues.
■ The circulation is a closed system, so the
output of the right and left heart must be
equal over time for effective functioning of
THE HEARTTHE HEART■■ TheThe heart is a four-chamberedheart is a four-chambered pumppump
consisting ofconsisting of two atriatwo atria (the right atrium,(the right atrium,
which receives blood returning to the heartwhich receives blood returning to the heart
from the systemic circulation, and the leftfrom the systemic circulation, and the left
atrium, which receives oxygenated bloodatrium, which receives oxygenated blood
from the lungs) andfrom the lungs) and two ventriclestwo ventricles (a right(a right
ventricle, which pumps blood to the lungs,ventricle, which pumps blood to the lungs,
and a left ventricle, which pumps bloodand a left ventricle, which pumps blood
into the systemic circulation).into the systemic circulation).
■■ Heart valvesHeart valves control the direction ofcontrol the direction of
blood flow from the atria to the ventriclesblood flow from the atria to the ventricles
(the(the atrioventricular valvesatrioventricular valves), from the right), from the right
side of the heart to the lungs (side of the heart to the lungs (pulmonicpulmonic
valvevalve), and from the left side of the heart), and from the left side of the heart
to the systemic circulation (to the systemic circulation (aortic valveaortic valve).).
■■ TheThe cardiac cyclecardiac cycle is divided into twois divided into two
major periods:major periods: systolsystole, when the ventriclese, when the ventricles
are contracting, andare contracting, and diastolediastole, when the, when the
ventricles are relaxed and filling.ventricles are relaxed and filling.
■■ TheThe work and efficiency of the heartwork and efficiency of the heart
is determined by the volume of blood itis determined by the volume of blood it
pumps out (pumps out (preloadpreload), the pressure that it), the pressure that it
must generate to pump the blood out ofmust generate to pump the blood out of
the heart (the heart (afterloadafterload), and the rate at which), and the rate at which
it performs these functions (it performs these functions (heart rateheart rate).).
(Frank-) Starling Law(Frank-) Starling Law
• Within limits, the greater the stretching of the
muscle fibers (preloadpreload), the greater the force of
• The extra force of contraction is necessary to
pump the increased volume of blood from the
• Cardiac output increases
Neural reflexesNeural reflexes
• Bainbridge reflex – increased heart rate due
to increased right atrial pressure
• Increased pressure in arteries stimulates a
baroreceptor reflex that decreases heart rate.
Origin and SpreadOrigin and Spread
of Excitation in theof Excitation in the
ARRHYTHMIAS OFARRHYTHMIAS OF
HEARTHEART Violation of rhythm of heartViolation of rhythm of heart accompanies aaccompanies a
number of diseases of the cardio-vascular system.number of diseases of the cardio-vascular system.
Most often they are observed at coronaryMost often they are observed at coronary
insufficiency.insufficiency. Arrhythmia registeredArrhythmia registered inin the acutethe acute
period of heart attack of myocardium in 95-100 %period of heart attack of myocardium in 95-100 %
In most world countriesIn most world countries sudden cardiac death issudden cardiac death is
about 15 %about 15 % from all cases of «natural» death. Thefrom all cases of «natural» death. The
main reason of sudden death at cardiac pathologymain reason of sudden death at cardiac pathology
in 93 % is arrhythmias.in 93 % is arrhythmias.
Arrhytmias are violation of frequency, rhythm,Arrhytmias are violation of frequency, rhythm,
co-ordination and sequence of heartbeatco-ordination and sequence of heartbeat..
Etiology of heart rhythm disorderEtiology of heart rhythm disorder
The rhythm violations arise under the influence of different pathologicalThe rhythm violations arise under the influence of different pathological
agents, which can be divided on such groups:agents, which can be divided on such groups:
Functional violationsFunctional violations andand influencesinfluences, for example:, for example: violation ofviolation of
vegetative nerves systemvegetative nerves system condition (sympathetic or parasympatheticcondition (sympathetic or parasympathetic
link hyperactivity),link hyperactivity), physical workphysical work,, physical overloadphysical overload,, body temperaturebody temperature
changeschanges,, the increase of intracranium pressurethe increase of intracranium pressure,, respirationrespiration (especially(especially
in children);in children);
Organic injury of myocardiumOrganic injury of myocardium , for example:, for example: inflammation ofinflammation of
myocardiummyocardium (as the result of infection), the(as the result of infection), the myocardium dystrophymyocardium dystrophy (in(in
the result of hypoxia, ischemia or amiloidosis),the result of hypoxia, ischemia or amiloidosis), necrosis ofnecrosis of
Influences of toxic substances on the myocardiumInfluences of toxic substances on the myocardium (alcohol,(alcohol,
drugs, big dose adrenalin and noradrenalin, glucocorticoids, bacterialdrugs, big dose adrenalin and noradrenalin, glucocorticoids, bacterial
toxins, phosphororganic substances);toxins, phosphororganic substances);
Hormone balance disorderHormone balance disorder (hyperthyroidism, hypothyroidism,(hyperthyroidism, hypothyroidism,
hyperfunction of supranephral glands);hyperfunction of supranephral glands);
Violation of intracellular or extracellular ions balanceViolation of intracellular or extracellular ions balance
(changes of sodium, potassium, calcium, magnesium and chlorine(changes of sodium, potassium, calcium, magnesium and chlorine
Mechanical influences on the heartMechanical influences on the heart (catheter using for the(catheter using for the
diagnosis and treatment heart diseases, operation on the heart, chestdiagnosis and treatment heart diseases, operation on the heart, chest
• Development of arrhythmiasDevelopment of arrhythmias can be related tocan be related to
violations of basic functions of the conductingviolations of basic functions of the conducting
system of heart:system of heart:
1) automatism1) automatism,,
2)2) excitabilityexcitability andand
• Classification of arrhythmias:Classification of arrhythmias:
I. Arrhythmias, related with violations of automatism.I. Arrhythmias, related with violations of automatism.
II. Arrhythmias, related with violations of excitability.II. Arrhythmias, related with violations of excitability.
III. Arrhythmias, related with violations ofIII. Arrhythmias, related with violations of
IV. Arrhythmias, related with violations of excitabilityIV. Arrhythmias, related with violations of excitability
and conductivity.and conductivity.
Arrhythmias, related with violationArrhythmias, related with violation
ofof automatismautomatism of heartof heart
Distinguish two groups of arrhythmiasDistinguish two groups of arrhythmias, related with, related with violationviolation
of automatism of heart.of automatism of heart.
1)1) Nomotopic arrhythmiasNomotopic arrhythmias -- the generation of impulsesthe generation of impulses, as well, as well
as in a norm,as in a norm, takes place bytakes place by pacemaker cells (P-cells) inpacemaker cells (P-cells) in
sinoatrial [sinus] node, [nodus sinuatrialis]sinoatrial [sinus] node, [nodus sinuatrialis]. To them belong:. To them belong:
a)a) sinus tachycardiasinus tachycardia is multiplying frequency of cardiacis multiplying frequency of cardiac
b)b) sinus bradycardiasinus bradycardia is diminishing of frequency of cardiacis diminishing of frequency of cardiac
c)c) sinus (respiratory) arrhythmiasinus (respiratory) arrhythmia is a change of frequency ofis a change of frequency of
heartbeat in the different phases of respiratory cycleheartbeat in the different phases of respiratory cycle
(become more frequent at inhalation [breath] and(become more frequent at inhalation [breath] and
diminishing is at exhalation [outward breath]).diminishing is at exhalation [outward breath]).
Arrhythmias, related withArrhythmias, related with
violation of automatismviolation of automatism
Heterotopic ArrhythmiasHeterotopic Arrhythmias
2)2) heterotopic arrhythmiasheterotopic arrhythmias areare a syndrome ofa syndrome of weakness of sinusweakness of sinus
nodenode.. The generation of impulses appears into other structures ofThe generation of impulses appears into other structures of
the conducting system. A syndrome develops as a result ofthe conducting system. A syndrome develops as a result of
diminishing of activity or stopping of activity of sinus node at thediminishing of activity or stopping of activity of sinus node at the
damage of it cells or primary functional violations. The followingsdamage of it cells or primary functional violations. The followings
types of pathological rhythms of heart can develop:types of pathological rhythms of heart can develop:
a)a) atrium slow rhythmatrium slow rhythm - a driver of rhythm is in the structures of- a driver of rhythm is in the structures of
left atrium, frequency of heartbeatleft atrium, frequency of heartbeat lesser than 70 per 1 minlesser than 70 per 1 min;;
b)b) atrio-ventricular rhythmatrio-ventricular rhythm - the source of impulses are drivers- the source of impulses are drivers
of rhythm of the II order (overhead, middle or lower part of atrio-of rhythm of the II order (overhead, middle or lower part of atrio-
ventricular node), frequency of heartbeat in dependence on theventricular node), frequency of heartbeat in dependence on the
place of generation of impulsesplace of generation of impulses diminishes from 70 to 40 perdiminishes from 70 to 40 per
c)c) idioventricular rhythmidioventricular rhythm - the generation of impulses appears in- the generation of impulses appears in
the drivers of rhythm of the III order (His' bundle, atrioventricularthe drivers of rhythm of the III order (His' bundle, atrioventricular
fascicle, fasciculus atrioventricularis and pedunculi of it),fascicle, fasciculus atrioventricularis and pedunculi of it),
frequency of heartbeatfrequency of heartbeat lesser than 40 per minutelesser than 40 per minute..
Reason and mechanisms of development ofReason and mechanisms of development of
sinus tachy- and bradycardiasinus tachy- and bradycardia
► Sinus tachycardia and bradycardiaSinus tachycardia and bradycardia relate to therelate to the
groupgroup of nomotopic arrhythmias, connect withof nomotopic arrhythmias, connect with
violations of function of automatismviolations of function of automatism..
► A capacity for automatic formation of impulsesA capacity for automatic formation of impulses
depends on cells, located in the conductingdepends on cells, located in the conducting
system of heart (system of heart (p-cellsp-cells) in which present) in which present
spontaneous slow depolarization of cellularspontaneous slow depolarization of cellular
membrane in the period of diastole.membrane in the period of diastole.
► Frequency of generation of impulses dependsFrequency of generation of impulses depends onon::
a)a) maximal diastolic potential of these cellsmaximal diastolic potential of these cells;;
b)b) level of critical potential on a membranelevel of critical potential on a membrane, after, after
which appearswhich appears potential of actionpotential of action; and; and
c)c) speeds of diastolic depolarization.speeds of diastolic depolarization.
Reason and mechanisms of development ofReason and mechanisms of development of
sinus tachy- and bradycardiasinus tachy- and bradycardia
Increase generating of impulsesIncrease generating of impulses .. Reasons:Reasons:
a) at diminishing of level of maximal diastolic potential of cells of sinus nodea) at diminishing of level of maximal diastolic potential of cells of sinus node
b) at approaching to it of maximum critical potential,b) at approaching to it of maximum critical potential,
c) at multiplying speed of slow diastolic depolarization.c) at multiplying speed of slow diastolic depolarization.
Such phenomenon is observed:Such phenomenon is observed:
a) under act of the promoted temperature of bodya) under act of the promoted temperature of body
b) stretching areas of sinus node,b) stretching areas of sinus node,
c) under act of mediators of sympathetic system.c) under act of mediators of sympathetic system.
a) diminishing of speed of slow diastolic depolarization,a) diminishing of speed of slow diastolic depolarization,
b) hyperpolarization in a diastole andb) hyperpolarization in a diastole and
c) the decreasing of critical maximum potential, as it is observed at annoying ac) the decreasing of critical maximum potential, as it is observed at annoying a
vagus nerve, are accompanied deceleration of generation of impulses, andvagus nerve, are accompanied deceleration of generation of impulses, and
consequently -consequently -
The instability [fluctuation, variation] of tone of vagus nerve during the act ofThe instability [fluctuation, variation] of tone of vagus nerve during the act of
breathing predetermine respiratory arrhythmia (become more frequentbreathing predetermine respiratory arrhythmia (become more frequent
palpitation at inhalation, deceleration - at exhalation).palpitation at inhalation, deceleration - at exhalation).
Children have respiratory arrhythmia in a normChildren have respiratory arrhythmia in a norm , sometimes it also, sometimes it also
observed for adults.observed for adults.
Tachycardia developsTachycardia develops
Bradycardia developsBradycardia develops
Arrhythmias, related to violations of excitabilityArrhythmias, related to violations of excitability
The main reason is appearance so-called ectopic hotbed of
excitations which generate premature impulsespremature impulses.
The most widespread arrhythmias of this group are:
a) extrasystole [beat]a) extrasystole [beat] andand
b) paroxysmal [recurrent, reentrant] tachycardia.b) paroxysmal [recurrent, reentrant] tachycardia.
Extrasystole is a type of arrhythmias, which are stipulated
violations of function of excitability which shows up the origin
of premature contraction of heart or only ventricles.
In dependence on localization of hotbed which an premature
impulse goes out from, distinguish the followings types of
a)a) sinussinus (or nomotopic),(or nomotopic),
c)c) atrio-ventricularatrio-ventricular andand
d)d) ventricular [ventricular premature beats].ventricular [ventricular premature beats].
As a wave of excitation, which arose up in an unusual place,
spreads in the changed direction, it is reflected on the
structure of the electric field of heart and finds a reflection on
• When an action potential from a
supraventricular ectopic focus is transmitted
to the ventricles (atrial or nodal extrasystole),
it can disturb their regular (sinus) rhythm
(supraventricular arrhythmia). An atrial ES
can be identified in the ECG by a distorted
(and premature) P wave followed by a normal
QRS complex. If the action potential
originates in the AV node (nodal ES), the
atria are depolarized retrogradely, the P wave
therefore being negative in some leads and
hidden within the QRS complex or following it
(1, blue frame). Because the sinus node is
also often depolarized by a supraventricular
ES, the interval between the R wave of the
ES (= RES) and the next normal R wave is
frequently prolonged by the time of
transmission from ectopic focus to the sinus
node (postextrasystolic pause). The intervals
between R waves are thus: RES–R > R–R
and (R–RES + RES–R) < 2 R–R ( 1 ). An
ectopic stimulus may also occur in a ventricle
(ventricular extrasystole → 2, 3). In this
case the QRS of the ES is distorted. If the
sinus rate is low, the next sinus impulse may
be normally transmitted to the ventricles
(interposed ES; 2). At a higher sinus rate the
next (normal) sinus node action potential may
arrive when the myocardium is still refractory,
so that only the next but one sinus node
impulse becomes effective (compensatory
pause). The R–R intervals are: R–RES
+RES–R = 2 R–R.
Ectopic Origin of Stimulus (1–5)
Abnormal Conduction (5)
Sinus extrasystoleSinus extrasystole
• Sinus extrasystole arises up
as a result of premature
excitation part of cells of
sinus node. On ECG:
shortening interval TP.
• As a result shortening of
diastole and diminishing of
filling of ventricles a pulse
wave is diminished too.
Atrial extrasystolesAtrial extrasystoles
• Atrial extrasystolesAtrial extrasystoles are
observed at presence of heart
beat of ectopic excitation in the
different areas of atrium and are
a) change the form P-waveform P-wave
(reduced, two-phase, negativereduced, two-phase, negative);
b) at the stored complex QRS and
c) some lengthening of diastolic
interval after extrasystole (an
incomplete compensate pauseincomplete compensate pause).
• Atrio-ventricular extrasystole is observed in case of occurring of
additional impulse in atrio-ventricular node.
• The wave of excitation, which goes out from overhead and middle
parts of node, spreads in two directions:
a) into ventricles - as normal
b) into atrium - retrograde direct. Thus:
a) the negativenegative P-waveP-wave can be present before or laybefore or lay on complex QRSon complex QRS;
b) diastole interval after a extrasystole is a little prolonged.
A extrasystole can be accompanied simultaneous beat of atrium and
• At a atrio-ventricular extrasystole which goes out from lower part of
node, there is a compensate pause, the same, as well as at a
ventricular extrasystole and P-wave is negative and situated after
Ventricular extrasystoleVentricular extrasystole
• Ventricular extrasystoleVentricular extrasystole are
characterized presence of a completecomplete
compensate pausecompensate pause after premature
heartbeat and deformation complex
• Next beat of ventricles arises up onlyNext beat of ventricles arises up only
after arrival to them of duty normalafter arrival to them of duty normal
impulseimpulse.. That is why duration of a
compensate pause equals duration of
two normal diastolic pauses. However if
reductions of heart are so rare that to the
moment of arrival of duty normal impulse
ventricles have time to go out from the
state of adiphoria, a compensate pause
is absent. Premature heartbeat gets in an
interval between two normal and in this
case called the inserted extrasystole.
• 1) Atrial ectopic beatsAtrial ectopic beats appear as early
(premature extrasystoles) and abnormal
P-waves in the ECG; they are usually
followed by normal QRS-complexes.
Following the premature beat there is
often a compensatory interval. A
premature beat in the left ventricle is weak
because of inadequate venous return, but
after the long compensatory interval, the
post-extrasystolic contraction (following a
long venous return period) is strong due
the Starling´s law of the heart. -
Adrenergic b-blockers are sometimes
• 2) Ventricular ectopic beatsVentricular ectopic beats
(extrasystoles) are recognized in the ECG
by their wide QRS-complex (above 0.12
s), since they originate in the ventricular
tissue and slowly spread throughout the
two ventricles without passing the Purkinje
system. The ventricular ectopic beat is
recognized by a double R-wave. The
classical tradition of simultaneous cardiac
auscultation and radial artery pulse
palpation eases the diagnosis. Now and
then a pulsation is not felt, and an early
frustraneous beat is heard together with a
prolonged interval. A beat initiated in the
vulnerable period may release lethal
ventricular tachycardia, since the tissue is
no longer refractory.
Paroxysmal tachycardiaParoxysmal tachycardia
• Paroxysmal tachycardiaParoxysmal tachycardia is arrhythmia, which is stipulated
violations of function of excitability, which shows up the
origin of group of extrasystoles which fully repress a
• At paroxysmal tachycardia the normal rhythm of heart isnormal rhythm of heart is
suddenly brokensuddenly broken by attack of beats with frequency from 140
to 250 shots per minute.
• Duration of attack can be different - from a few secondsfew seconds to a
few minutesfew minutes. It is suddenly stopped and recommences
Paroxysmal supraventricular tachycardia: note accelerated
rate and narrow QRS complexes.
Arrhythmias, related to violation ofArrhythmias, related to violation of
conductivity of impulsesconductivity of impulses
Select two groups of such arrhythmias:Select two groups of such arrhythmias:
1) Heart block.1) Heart block.
2) Increased conducting of impulses –2) Increased conducting of impulses – WPW-syndromeWPW-syndrome (Wolf-Parkinson-(Wolf-Parkinson-
White block)White block)
Heart blocksHeart blocks are arrhythmias, conditionedare arrhythmias, conditioned deceleration or completedeceleration or complete
stopped conducting of impulsesstopped conducting of impulses on the conducting system.on the conducting system.
a)a) the damage of conductive ways,the damage of conductive ways,
b)b) worsening of other functional descriptionsworsening of other functional descriptions, which is accompanied, which is accompanied
deceleration or complete stopped conducting of impulse.deceleration or complete stopped conducting of impulse.
Violations of conductivity canViolations of conductivity can arise up:arise up:
a)a) between a sinus node and atriumsbetween a sinus node and atriums
b)b) inwardly atriums,inwardly atriums,
c)c) between atriums and ventricles andbetween atriums and ventricles and
d)d) in one of legs of His' bundle.in one of legs of His' bundle.
Followings types of blockades select:Followings types of blockades select:
SA BLOCKSA BLOCK
Rate normal or bradycardia
P wave those present are normal
Rhythm basic rhythm is regular*
Four typesFour types of atrio-of atrio-
ventricular (AV)-ventricular (AV)-
block. From aboveblock. From above
First-degree AV-First-degree AV-
Mobitz I blockMobitz I block
Mobitz II block,Mobitz II block,
Complete AV-Complete AV-
Long PR interval (>200 msec; one big box)
Slowed conduction through the AV node
Characteristics: rate and rhythm are typically normal
Every QRS complex is preceded by a P wave, but not every P wave is
followed by a QRS complex.
Some impulses are not transmitted through the AV node.
Mobitz type I (Wenckebach) - Progressive prolongation of PR interval until
a ventricular beat is missed and then the cycle begins again. This arrhythmia
will have an unsteady rhythm.
Complete dissociation of P waves and QRS complexes
Impulses are not transmitted through the AV node.
Characteristics: steady rhythm (usually) and very slow ventricular HR
no consistent PR interval because impulses are not transmitted through the
rate for P waves is different than rate for R waves
Mobitz type II:
The PR interval is consistent, i.e.,
It doesn’t lengthen and this separates it from Wenckebach.
The rhythm can be steady or unsteady depending upon block ratio (P to QRS
ratio: 2:1, 3:1, 3:2, etc.).
Increase conductingIncrease conducting
of impulsesof impulses
• WPW-syndrome –
atriums to the
ventricles, as a
result there is
excitation of the
interval of PQ
diminishes on an
Accessory pathway (Bundle of Kent) between atria and
PR interval; steady rhythm and normal rate (usually);
Slurred upstroke of the R wave (delta wave); widened QRS
The cardiac impulse can travel in retrograde fashion to the
atria over the accessory pathway and initiate a reentrant
Re-entry mechanismRe-entry mechanism
Under normal conditions, anUnder normal conditions, an
electrical impulse is conductedelectrical impulse is conducted
through the heart in an orderly,through the heart in an orderly,
sequential manner. Thesequential manner. The electricalelectrical
impulse then dies out and does notimpulse then dies out and does not
reenter adjacent tissuereenter adjacent tissue becausebecause thatthat
tissue has already been depolarizedtissue has already been depolarized
and is refractory to immediateand is refractory to immediate
stimulationstimulation. However, under certain. However, under certain
abnormal conditions, an impulse canabnormal conditions, an impulse can
reenter an area of myocardium thatreenter an area of myocardium that
was previously depolarized andwas previously depolarized and
depolarize it again. There threedepolarize it again. There three
conditions are the necessary for thisconditions are the necessary for this
mechanism beginning:mechanism beginning:
1 – two conductive ways are the1 – two conductive ways are the
functionally or anatomicallyfunctionally or anatomically
2 – some conductive way is2 – some conductive way is
3 – the antegrade conductive way3 – the antegrade conductive way
is blocked, but the retrograde oneis blocked, but the retrograde one
is preserved.is preserved.
So, in that condition impulse (orSo, in that condition impulse (or
impulses) travels numerous throughimpulses) travels numerous through
some area of conductive system andsome area of conductive system and
returns through another pathway toreturns through another pathway to
the reactivated myocardiocytes.the reactivated myocardiocytes.
Increases rate of repolarization, resulting in
sharp-spiked T waves
Shortened QT interval.
Decreases rate of repolarization, resulting in
Prolonged QT interval.
Decreases the QT interval
Increases the QT interval
Excitation in Electrolyte
Hyperkalemia (> 6.5 mmol/L): Hypokalemia (< 2.5 mmol/L):
Hypercalcemia (> 2.75 mmol/L
Hypocalcemia (< 2.25 mmol/L
Arrhythmias with violation of functions ofArrhythmias with violation of functions of
excitability and conductivityexcitability and conductivity
1)1) atrial flutteratrial flutter (frequency of(frequency of
atrium beats -atrium beats - 250-400250-400 //
2)2) Atrial fibrillationAtrial fibrillation (frequency(frequency
of impulses which arise upof impulses which arise up
in atrium isin atrium is 400-600400-600 / min)./ min).
► Atrial flutterAtrial flutter andand
fibrillation have identicalfibrillation have identical
reasons of developmentreasons of development
and can pass one toand can pass one to
another. So, these twoanother. So, these two
types of violation of rhythmtypes of violation of rhythm
of heart combine into oneof heart combine into one
and called isand called is fibrillationfibrillation..
3)3) ventricle flutterventricle flutter (frequency(frequency
of ventricle beat isof ventricle beat is 150-150-
4)4) FibrillationFibrillation of ventriclesof ventricles
(frequency of impulses in(frequency of impulses in
ventricles isventricles is 300-500300-500 / min)./ min).
► ArrhythmiasArrhythmias which arise up as a result of simultaneous violation of functionswhich arise up as a result of simultaneous violation of functions
ofof excitabilityexcitability andand conductivityconductivity.. To them belong:To them belong:
Even when the stimulus
formation in the sinus
node is normal,
excitations can start
from a focus in an
atrium (atrial), the AV
node (nodal), or a
Self-AssessmentSelf-AssessmentMultiple Choice QuestionsMultiple Choice Questions
I. Each of the following five statements have True/False options:I. Each of the following five statements have True/False options:
Stem statement: The ventricular action potential isStem statement: The ventricular action potential is
A.A. initiated by rapid entry of Na+. initiated by rapid entry of Na+.
B.B. characterised by slow Ca2+ -Na+- channels. characterised by slow Ca2+ -Na+- channels.
C.C. characterised by closed K+- channels in phase 3. characterised by closed K+- channels in phase 3.
D.D. dependent upon Ca2+-influx. dependent upon Ca2+-influx.
E.E. independent of the Na+-K+ -pump in phase 4. independent of the Na+-K+ -pump in phase 4.
II. Each of the following five statements have True/False options:II. Each of the following five statements have True/False options:
A.A. In myocardial cells, as in nerve and skeletal muscle cells, K+ plays a minor role in determiningIn myocardial cells, as in nerve and skeletal muscle cells, K+ plays a minor role in determining
the resting membrane potential.the resting membrane potential.
BB. The impulse propagates from the sinus node via five bundles of internodal syncytial cells through. The impulse propagates from the sinus node via five bundles of internodal syncytial cells through
the left and right atrial wall to the atrioventricular node.the left and right atrial wall to the atrioventricular node.
C.C. The long absolute refractory period of the ventricular cells, covers the whole shortening phaseThe long absolute refractory period of the ventricular cells, covers the whole shortening phase
of the contraction, where all the fast Na+-channels are voltage-inactivated. As a consequence,of the contraction, where all the fast Na+-channels are voltage-inactivated. As a consequence,
no stimulus is sufficient regardless of size.no stimulus is sufficient regardless of size.
D.D. The fast Na+-influx causes phase 0 of atrial- , ventricular- , and Purkinje- action potentials. TheThe fast Na+-influx causes phase 0 of atrial- , ventricular- , and Purkinje- action potentials. The
fast Na+-channels are both voltage- and time-dependent.fast Na+-channels are both voltage- and time-dependent.
E.E. Noradrenaline activates a-adrenergic constrictor receptors in the coronary vessels, whereas Noradrenaline activates a-adrenergic constrictor receptors in the coronary vessels, whereas
adrenaline activates b-adrenergic vasodilatator receptors.adrenaline activates b-adrenergic vasodilatator receptors.
III.III. The following five statements have True/False options.The following five statements have True/False options.
A.A. WPW-syndrome or Wolf-Parkinson-White block is caused by a short cut through an extraWPW-syndrome or Wolf-Parkinson-White block is caused by a short cut through an extra
conduction pathway from the atria to the ventricles.conduction pathway from the atria to the ventricles.
BB. Atrial fibrillation is more malignant than ventricular fibrillation.. Atrial fibrillation is more malignant than ventricular fibrillation.
C.C. All pacemaker abnormalities arise in the sinus node.All pacemaker abnormalities arise in the sinus node.
DD. Premature beats are also called atrial ectopic beats.. Premature beats are also called atrial ectopic beats.
EE. Only few cardiac arrhythmias can lead to atrial fibrillation and flutter.. Only few cardiac arrhythmias can lead to atrial fibrillation and flutter.
Try to solveTry to solve
the problemsthe problems
looking up thelooking up the
LiteratureLiterature General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin –General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin –
Vinnytsia: Nova Knuha Publishers – 2011. – p.286–287, 322–333.Vinnytsia: Nova Knuha Publishers – 2011. – p.286–287, 322–333.
Handbook of general and Clinical Pathophysiology / Edited byHandbook of general and Clinical Pathophysiology / Edited by
prof.A.V.Kubyshkin. – CSMU. – 2005. – p.142–144.prof.A.V.Kubyshkin. – CSMU. – 2005. – p.142–144.
Pathophysiology / Edited by prof. Zaporozan. – OSMU. – 2005. – p.125–Pathophysiology / Edited by prof. Zaporozan. – OSMU. – 2005. – p.125–
133, 145–153.133, 145–153.
Essentials of Pathophysiology: Concepts of Altered Health StatesEssentials of Pathophysiology: Concepts of Altered Health States
(Lippincott Williams & Wilkins), Trade paperback (2003)(Lippincott Williams & Wilkins), Trade paperback (2003) // Carol MattsonCarol Mattson
Porth, Kathryn J. GaspardPorth, Kathryn J. Gaspard
Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicineSymeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine
Publishing. – 2010. – p. 348-351 .Publishing. – 2010. – p. 348-351 .
General and clinical pathophysiology. Workbook for medical students andGeneral and clinical pathophysiology. Workbook for medical students and
practitioners. – Odessa. – 2001.practitioners. – Odessa. – 2001.
J.B.Walter I.C.Talbot General pathology. Seventh edition. – 1996.J.B.Walter I.C.Talbot General pathology. Seventh edition. – 1996.
Stephen J. McPhee, William F. Ganong. Pathophysiology of Disease, 5Stephen J. McPhee, William F. Ganong. Pathophysiology of Disease, 5thth
edition. – 2006.edition. – 2006.
Robbins and Cotran Pathologic Basis of Disease 7Robbins and Cotran Pathologic Basis of Disease 7thth
edition./ Kumar, Abbas,edition./ Kumar, Abbas,
FautoFauto. –. – 2006.2006.
Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth,Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth,
Glenn Matfin. – New York, Milwaukee. – 2009. – p.584-606.Glenn Matfin. – New York, Milwaukee. – 2009. – p.584-606.