arrhthmias (1).pptx......dr kamran .......

Physiology

1. CARDIAC ARRYTHMIAS KAMRAN

2. Definitions ARRHYTHMIA: Refers to irregular heart beat or disturbance in the rhythm of heart which may be fast or slow or there may be an extra beat or a missed beat; occurs in physiological and pathological conditions Tachycardia: M eans fast heart rate, usually defined in an adult person as faster than 100 beats/min Bradycardia : M eans a slow heart rate, usually defined as fewer than 60 beats/min

3. ECTOPIC ARRHYTHMIA: Ectopic arrhythmia is the abnormal heartbeat, in which one of the structures of heart other than SA node becomes the pacemaker; impulses produced by these structures are called ectopic foci EXTRASYSTOLE OR PREMATURE CONTRACTIONS: A premature contraction is a contraction of the heart before the time that normal contraction would have been expected; this condition is also called extrasystole, premature beat, or ectopic beat PAROXYSMAL TACHYCARDIA Paroxysmal tachycardia is the sudden attack of increased heart rate due to ectopic foci arising from atria, AV node or ventricle; also called Bouveret Hoffmann syndrome

4. SUPRAVENTRICULAR TACHYCARDIA (SVT): Increase in heart rate due to ectopic foci arising from either atria or AV node is called SVT; differs from ventricular tachycardia, which does not depend upon atria or AV node Fibrillation: T he heart muscle fibers contract in a totally irregular and ineffective way because of the very rapid discharge of multiple ectopic foci or a circus movement Flutter: T he heart muscle fibers contract in a regular but ineffective way as the electrical signal travels as a single large wave always in one direction around and around the muscle mass

5. CLINICAL APPLICATIONS: CARDIAC ARRHYTHMIAS NORMOTOPIC ARRHYTHMIA : Normotopic arrhythmia is the irregular heartbeat, in which SA node is the pacemaker Normal human heart beats (normal sinus rhythm, NSR) about 70 times a minute at rest The rate is slowed (sinus bradycardia ) during sleep and accelerated (sinus tachycardia) by emotion, exercise, fever, and many other stimuli The heart rate varies with the phases of respiration In healthy young individuals breathing at a normal rate and accelerates during inspiration but decelerates during expiration; this is called Resp . sinus arrhythmia

6. Respiratory sinus arrhythmia (RSA) Sinus tachycardia (lead I) Sinus bradycardia (lead III)

7. Sick Sinus Syndrome : Sick sinus syndrome ( bradycardia -tachycardia syndrome; sinus node dysfunction) is a collection of heart rhythm disorders that include sinus bradycardias , tachycardias and bradycardia -tachycardia (alternating slow and fast heart rhythms) Uncommon and is usually found in people older than 50, in whom the cause is often a nonspecific, scar-like degeneration of the heart’s conduction system When found in younger people, especially in children, a common cause of sick sinus syndrome is heart surgery, especially on the upper chambers

8. ABNORMAL PACEMAKERS Normal pacemaker of the heart is SA node and its discharge rate is more rapid than that of the other parts of the conduction system This is the reason that the SA node normally controls the heart rate The AV node and other portions of the conduction system can, in abnormal situations, become the cardiac pacemaker In addition, diseased atrial and ventricular muscle fibers can have their membrane potentials reduced and discharge repetitively

9. Heart Block: Heart block is the blockage of impulses generated by SA node in the conductive system and this results in improper or no impulse delivered to heart muscles, resulting in ectopic arrhythmia Two types: 1. Sinoatrial block 2. Atrioventricular block 1. Sinoatrial Block – AV Nodal Rhythm : In rare instances, the impulse from the sinus node is blocked before it enters the atrial muscle In ECG, it appears as sudden cessation of P waves, with resultant standstill of the atria

10. However, the ventricles pick up a new rhythm from the impulse usually originating from the A-V node which takes over the pacemaker function In ECG, the rate of the ventricular QRS-T complex is slowed but not otherwise altered SA block is due to the defect in internodal fibers and it occurs suddenly Any part of the AV node can starts beating with decreased rate of 40 to 60/ minute,ie ., upper, middle or lower part of AV node

11. Upper nodal rhythm of AV node: the appearance of inverted ‘P’ wave in ECG; The middle nodal rhythm: all chambers of the heart contract simultaneously, thus, no appearance of ‘P’ wave or its merging with QRS complex; In lower nodal rhythm, QRS complex appears prior to P wave and R-P interval is obtained instead of P-R interval; called reversed heart block Atrioventricular Block : The only way by which impulses ordinarily can pass from the atria into the ventricles is through the A-V bundle, also known as the bundle of His

12. Defect in the bundle or its branches either lead to delay of impulses from atria to ventricles (incomplete heart block) or no delivery of impulses (complete heart block) In case of incomplete heart block, Impulses reach ventricles late but in case of complete heart block, the ventricles beat in their own rhythm, independent of atrial beat Incomplete heart block is of four types: i. First degree heart block ii. Second degree heart block iii. Wenckebach phenomenon iv. Bundle branch block

13. i. First degree heart block : When the conduction of impulses through AV node is very slow, i.e. the AV nodal delay is longer, it is called 1 st degree heart block; common in young adults and atheletes ; rheumatic fever & some drugs In ECG, the P-R interval appears to be longer more than 0.2 second (normal 0.16 seconds); no other symptoms ii. Second degree heart block : Some of the impulses produced by SA node fail to reach the ventricles; also called the partial heart block The ventricular contraction occurs for every 2, 3 or 4 atrial contractions, i.e. 2 : 1, 3 : 1 or 4 In ECG, the QRST complex is missing accordingly

14. Prolonged P-R interval caused by first degree A-V heart block (lead II) Second degree A-V block, showing occasional failure of the ventricles to receive the excitatory signals (lead V3)

15. iii. Wenckebach phenomenon or syndrome : In this form of heart block, there are repeated sequences of beats in which the PR interval lengthens progressively until a ventricular beat is dropped (Wenckebach phenomenon) The PR interval of the cardiac cycle that follows each dropped beat is usually normal or only slightly prolonged

16. iv. Bundle branch block (BBB): Sometimes one branch of the bundle of His is inter- - rupted , causing right or left bundle branch block In BBB, excitation passes normally down the bundle on the intact side and then sweeps back through the muscle to activate the ventricle on the blocked side ECG shows normal ventricular rate, but the QRS complex is prolonged or deformed Two V leads in left bundle branch block

17. Block can also occur in the anterior or posterior fascicle of the left bundle branch, producing the condition called hemiblock or fascicular block Left anterior hemiblock produces abnormal left axis deviation in the ECG, whereas left posterior hemi- -block produces abnormal right axis deviation 2. Complete Heart block 3 rd degree HB: Also called complete AV block or third degree heart block In this case, conduction from the atria to the ventricles is completely interrupted and the ventricles beat at a low rate (idioventricular rhythm) independently of the atria

18. The block may be due to disease in the AV node (AV nodal block) or in the conducting system below the node (infranodal block) In AV nodal block, the unaffected tissue becomes the pacemaker and the rate of the idioventricular rhythm is approximately 45 beats/min In infranodal block due to disease in the bundle of His, the ventricular pacemaker is located more peripherally in the conduction system and the ventricular rate is lower averaging 35 beats/min, (may low as 15 beats/min in individual cases)

19. The resultant cerebral ischemia causes dizziness and fainting (Stokes–Adams syndrome)

20. ECTOPIC FOCI OF EXCITATION Normal rhythmicity of heart is controlled by SAnode The tendency of conducting system to discharge impulses spontaneously is low However, in abnormal conditions, the His–Purkinje fibers or the myocardial fibers may discharge spontaneously This results in increased automaticity of the heart Ectopic focus formation result in a beat that occurs before the expected next normal beat and transie - - ntly interrupts the cardiac rhythm (atrial, nodal, or ventricular extrasystole or premature beat )

21. If the focus discharges repetitively at a rate higher than that of the SA node, it produces rapid, regular tachycardia (atrial, ventricular, or nodal paroxysmal tachycardia or atrial flutter ) Atrial premature beat (lead I) A-V nodal premature contraction (lead III) Premature ventricular contractions (PVCs) demonstrated by the large abnormal QRS-T complexes (leads II and III) Vectorial analysis & Axis of PVC

22. REENTRY PHENOMENON: A more common cause of paroxysmal arrhythmias is a defect in conduction that permits a wave of excitation to propagate continuously within a closed circuit (circus movement) A transient block on one side of a portion of the conducting system cause the impulse to go down the other side If the block then wears off, the impulse may conduct in a retrograde direction in the previously blocked side back to the origin and then descend again, establishing a circus movement

23. ATRIAL ARRHYTHMIAS Excitation spreading from ectopic focus in the atria stimulates the AV node prematurely and is conducted to the ventricles The P waves of atrial extrasystoles are abnormal, but the QRST configurations are usually normal The excitation may depolarize the SA node, which must repolarize and then depolarize to the firing level before it can initiate the next normal beat This results a pause between the extrasystole and the next normal beat The length of this pause is usually equal to the interval between the normal beats preceding the extrasystole, and the rhythm is “reset”

24. Atrial tachycardia occurs when an atrial focus discharges regularly or there is reentrant activity producing atrial rates up to 220/min P wave in ECG is inverted, with normal QRST in paroxysmal atrial tachycardia The atrial rate is 200–350/min in atrial flutter Max. number of impulses conducted by AV node is about 230 to 240 /minute and there is large counter clockwise circus movement in the right atrium So, during atrial flutter, the second degree of heart block occurs This produces a characteristic sawtooth pattern of flutter waves due to atrial contractions It is always associated with 2:1 or greater AV block

25. Prolonged atrial flutter may lead to AF or HF In atrial fibrillation (AF), the atria beat very rapidly (300– 500/min) in a completely irregular and disorganized fashion Because the AV node discharges at irregular intervals, the ventricles also beat at a completely irregular rate, usually 80–160/min The condition can be paroxysmal or chronic, and in some cases may be genetic predisposition Most of the cases are due to multiple concurrently circulating reentrant excitation waves in both atria Some cases seem to be produced by discharge of one or more ectopic foci Many of these foci appear to be located in the pulmonary veins as much as 4 cm from the heart

26. VENTRICULAR ARRHYTHMIAS Premature beats originating from ventricular ectopic focus slowly spread to the rest of ventricles and usually have bizarrely shaped prolonged QRS They are usually incapable of exciting the bundle of His, and retrograde conduction to the atria therefore does not occur In the meantime, the next succeeding normal SA nodal impulse depolarizes the atria The P wave is usually buried in the QRS of the extrasystole If the normal impulse reaches the ventricles, they are still in the refractory period following depolarization from the ectopic focus

27. However, the second succeeding impulse from the SA node produces a normal beat Thus, ventricular premature beats are followed by a compensatory pause that is often longer than the pause after an atrial extrasystole Furthermore, ventricular premature beats do not interrupt the regular discharge of the SA node, whereas atrial premature beats often interrupt and “reset” the normal rhythm Atrial and ventricular premature beats are not strong enough to produce a pulse at the wrist if they occur early in diastole; improper diastole filling

28. Paroxysmal VT arise as a result of a series of rapid, regular ventricular depolarizations usually due to a circus movement involving the ventricles Torsade de pointes is a form of VT in which the QRS morphology varies SV tachycardias (paroxysmal nodal tachycardia) can be distinguished from paroxysmal VT by use of the HBE; in SVT, a His bundle H deflection is present, whereas in VT, there is none Ventricular premature beats, in the absence of ischemic heart disease, are usually benign

29. In VF, the ventricular muscle contract in a totally irregular and ineffective way due to very rapid discharge of multiple ventricular ectopic foci or a circus movement VF can be produced by an electric shock or an extra-systole during a critical interval, the vulnerable period This period coincides in time with the midportion of the T wave, i.e., the time when some of the ventri - - cular muscles are depolarized, some in the state of repolarizing, and some completely repolarized The fibrillating ventricles cannot pump blood effectively, and circulation of the blood stops

30. ACCELERATED AV CONDUCTION Normally, the only conducting pathway between the atria and the ventricles is the AV node However in some individuals, who are prone to attacks of paroxysmal atrial arrhythmias, have an additional aberrant muscular or nodal tissue connection (bundle of Kent) between the atria and ventricles This conducts impulses more rapidly than the slowly conducting AV node, and the ventricles are excited early resulting in VT VT is more serious because cardiac output is ↓, and VF is an occasional complication of VT

31. On ECG, it appears as a short PR interval and a prolonged QRS deflection slurred on the upstroke, with a normal interval between the start of the P wave and the end of the QRS complex (“PJ interval”) This represents accelerated AV conduction and the syndrome is called Wolf–Parkinson White syndrome The paroxysmal atrial tachycardias seen in this syndrome often follow an atrial premature beat This beat conducts normally down the AV node but spreads to the ventricular end of the aberrant bundle, and the impulse is transmitted retrograde to the atrium

32. Accelerated AV conduction Normal sinus beat Short PR interval; wide, slurred QRS complex normal PJ interval (Wolf –Parkinson–White syndrome) Short PR interval, short PJ interval, normal QRS complex ( Ganong –Levine syndrome)

33. A circus movement is thus established Less commonly, an atrial premature beat finds the AV node refractory but reaches the ventricles via the bundle of Kent, setting up a circus movement in which the impulse passes from the ventricles to the atria via the AV node Attacks of paroxysml SVT, usually nodal tachycardia, are seen in individuals with short PR intervals and normal QRS complexes ( Lown – Ganong –Levine syndrome) In this condition, depolarization presumably passes from the atria to the ventricles via bundle of Kent that bypasses the AV node but enters the intraventricular conducting system distal to the node

34. CURRENT OF INJURY Current of injury means flow of current from an injured region of heart to the unaffected part When ischemia occurs in any part of the ventricular musculature due to coronary occlusion, that part of ventricle becomes depolarized either partially or completely and the repolarization does not occur It causes flow of current from affected (depolarized) part to unaffected part of the ventricular muscle Current of injury in myocardial infarction affects the ECG pattern and cardiac vector In ECG, the J point and ST segments are displaced

35. Cardiac Axis : In the infarction of anterior wall of the ventricle, the cardiac axis (vector) is deviated to right up to +150° due to current of injury and in the posterior wall infarction, there is left axis deviation up to –95°

36. Shaded areas of the ventricles are depolarized (−); nonshaded areas are still polarized (+)

37. EFFECTS OF CHANGES IN THE IONIC COMPOSITION OF THE BLOOD Changes in ECL Na+ & K+ affect the potential and the electric activity of the heart Clinically, a fall in the plasma level of Na+ may be associated with low-voltage electrocardiographic complexes, but changes in the plasma K+ level produce severe cardiac abnormalities Hyperkalemia is a very dangerous and potentially lethal condition because of its effects on the heart Rise in plasma K + (7meq)(8.5 qrs becomes broadened)cause the appearance of tall peaked T waves in ECG as a manifestation of altered repolarization

38. Paralysis of the atria and prolongation of the QRS complexes occur at even higher conc. Ventricular arrhythmias may develop The fibers eventually become unexcitable, and the heart stops in diastole Conversely, a ↓ in the plasma K+ level causes prolong- - ation of the PR interval, prominent U wave, & occasio - - nally , late T wave inversion in the precardial leads ↑ in extracellular Ca2+ conc. ↑ myocardial contractility When large amounts of Ca2+ are infused into experimental animals, the heart relaxes less during diastole and eventually stops in systole (calcium rigor) Hypocalcemia causes prolongation of the ST segment and consequently of the QT interval