Arrhytmias

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Prepared by MD, PhD., Associate Professor, Marta R. Gerasymchyk, pathophysiology department of Ivano-Frankivsk National Medical University, Ukraine.
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Arrhytmias

  1. 1. Plan of the lecture 1. Organization of the circulatory system. 2. Cardiac cycle. 3. Conductive system of the heart. 4. Mechanisms of compensation 5. Arhytmias of the heart. Deffinition. Classification. Pathogenesis. 6. Ischaemic heart disease. 6. Heart failure.
  2. 2. 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 occuring spasmes. Arrythmia can be result in development of cardiac insufficiency.
  3. 3. FUNCTIONAL ORGANIZATION 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 wastes occurs. ■ 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 circulation.
  4. 4. 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).).
  5. 5. Electrocardiogram (ECG)Electrocardiogram (ECG)
  6. 6. (Frank-) Starling Law(Frank-) Starling Law • Within limits, the greater the stretching of the muscle fibers (preloadpreload), the greater the force of contraction. • The extra force of contraction is necessary to pump the increased volume of blood from the ventricle. • 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.
  7. 7. Cardiac ConductionCardiac Conduction SystemSystem
  8. 8. Origin and SpreadOrigin and Spread of Excitation in theof Excitation in the HeartHeart c
  9. 9. 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 % patientspatients..  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..
  10. 10. 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 myocardiummyocardium;;  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 concentration);concentration);  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 trauma).trauma).
  11. 11. • 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 3)3) conductivity.conductivity. • 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 conductivity.conductivity. IV. Arrhythmias, related with violations of excitabilityIV. Arrhythmias, related with violations of excitability and conductivity.and conductivity.
  12. 12. Normal Rhythms
  13. 13. 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 reductions;reductions;  b)b) sinus bradycardiasinus bradycardia is diminishing of frequency of cardiacis diminishing of frequency of cardiac reductions;reductions;  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]).
  14. 14. Arrhythmias, related withArrhythmias, related with violation of automatismviolation of automatism
  15. 15. 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 minuteminute ;;  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..
  16. 16. 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.
  17. 17. 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.  Opposite,Opposite, 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
  18. 18. 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 extrasystole: a)a) sinussinus (or nomotopic),(or nomotopic), b)b) atrialatrial,, 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 an electrocardiogram.
  19. 19. ExtrasystolesExtrasystoles ((ESES)) • 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)
  20. 20. 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.
  21. 21. Atrial extrasystolesAtrial extrasystoles • Atrial extrasystolesAtrial extrasystoles are observed at presence of heart beat of ectopic excitation in the different areas of atrium and are characterized: 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).
  22. 22. Atrio-Atrio- ventricularventricular extrasystoleextrasystole • 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 ventricles. • 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 complex QRS.
  23. 23. Ventricular extrasystoleVentricular extrasystole • Ventricular extrasystoleVentricular extrasystole are characterized presence of a completecomplete compensate pausecompensate pause after premature heartbeat and deformation complex QRS. • 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.
  24. 24. • 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 necessary. • 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.
  25. 25. 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 physiology rhythm. • 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 normal rhythm. Paroxysmal supraventrical tachycardia Paroxysmal supraventricular tachycardia: note accelerated rate and narrow QRS complexes.
  26. 26. 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.  ReasonsReasons:: 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: 1)1) intraatrialintraatrial;; 2)2) atrio-ventricular;atrio-ventricular; 3)3) intraventricularintraventricular..
  27. 27. SA BLOCKSA BLOCK Rate normal or bradycardia P wave those present are normal QRS normal Conduction normal Rhythm basic rhythm is regular*
  28. 28. Atrio-ventricularAtrio-ventricular blockblock  Four typesFour types of atrio-of atrio- ventricular (AV)-ventricular (AV)- block. From aboveblock. From above downwards:downwards:  First-degree AV-First-degree AV- block,block,  Second-degreeSecond-degree Mobitz I blockMobitz I block (Wenchebach),(Wenchebach),  Second-degreeSecond-degree Mobitz II block,Mobitz II block, andand  Complete AV-Complete AV- block.block.
  29. 29. First-Degree  Long PR interval (>200 msec; one big box)  Slowed conduction through the AV node  Characteristics: rate and rhythm are typically normal Heart Blocks Second-Degree 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. Two types:  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.
  30. 30. Third-Degree (Complete) 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 (usually); no consistent PR interval because impulses are not transmitted through the AV node; 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.).
  31. 31. Increase conductingIncrease conducting of impulsesof impulses • WPW-syndrome – characterized the speed-up conducting of impulses from atriums to the ventricles, as a result there is premature excitation of the last, tachycardia develops, the interval of PQ diminishes on an electrocardiogram.
  32. 32. Accessory pathway (Bundle of Kent) between atria and ventricles Characteristics: PR interval; steady rhythm and normal rate (usually); Slurred upstroke of the R wave (delta wave); widened QRS complex The cardiac impulse can travel in retrograde fashion to the atria over the accessory pathway and initiate a reentrant tachycardia. Wolff-Parkinson-White Syndrome
  33. 33. 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 disconnected;disconnected; 2 – some conductive way is2 – some conductive way is blocked;blocked; 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.
  34. 34. Potassium  Hyperkalemia: Increases rate of repolarization, resulting in sharp-spiked T waves  Shortened QT interval.  Hypokalemia: Decreases rate of repolarization, resulting in U waves  Prolonged QT interval. Calcium  Hypercalcemia: Decreases the QT interval  Hypocalcemia: Increases the QT interval
  35. 35. Excitation in Electrolyte Disturbances Hyperkalemia (> 6.5 mmol/L): Hypokalemia (< 2.5 mmol/L): Hypercalcemia (> 2.75 mmol/L total calcium) Hypocalcemia (< 2.25 mmol/L total calcium)
  36. 36. 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 // min).min). 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- 300300/m)./m). 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:
  37. 37. 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).
  38. 38. ECGs (lead II) showing abnormal rhythms A:Respiratory sinus arrhythmia. B:Sinus arrest with vagal escape. C:Atrial fibrillation. D:Premature ventricular complex. E:Complete atrioventricular block.
  39. 39. 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 beforebefore looking up thelooking up the answersanswers
  40. 40. 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.

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