Tachyarrhythmia Lecture. Doctor/ Jane Nader

Tachyarrhythmia different types for medical students

1. Tachyarrhythmia diagnosis & management Jane Nader, MD Lecturer of cardiology

2. Ca r d i ac arr h ythmias D e finition : A c a r diac ar r h y thmia i s d e fined as a d i s turbance of the elec t r i c al r h y thm of the h e ar t .  A h e art r a t e of mo r e th a n 100/min i s c al l ed a t ac h y c a r dia . E tiol o gy : s t r uc t u r al h e art dise a se ab n ormal c ond u c t i on or d e pola ri z a t i on i n a h e al t h y heart

3. AGENDA Definition Causes Clinical manifestation Management Types

4. Normal conduction pathway Normal ECG

5.  Physio l og i cal  Path o log i cal: V a lvu l ar he a rt d i s ea s e . Electrolyte di s turbances. Structur a l heart di s e a se. Ische m ic heart di s e a se. Hy p er t ensive heart dise a ses. C o ngenital heart di s e a se. Cardiomyo p athies. Carditi s . Drug rel a t ed. Per i card i tis. Pu l m o nary di s e a ses. O t hers.

6.  Palpit a tion.  Diz z in e ss.  Che s t Pa i n .  Dyspn e a.  Synco p e.  F a int i n g .  He m odyn a mic collap s e .  Sudden cardiac d e a t h .

7.  E C G  2 4 h Holter monitor  E c hocardiogr a m  Stress test  Coronary a n g iogr a phy  Electrophys i ology st u dy

8. Classification of tachyarrhythmia

9.  ■ Sinus tachycardia - mostly a physiologic response ■ Supraventricular- narrow-QRS complex Atrial fibrillation Atrial flutter SVT ■ Ventricular - broad-QRS complex

10. - An i nc r ea s e i n s ympa t h e t i c ac ti vi t y , HR > 100 bpm - Sig n s & s ym p t oms : palpi t a t i on, SO B , Ch e s t pain, L i gh t -h e ad e dne s s - E tiology: - - - - - - - - Normal r e s pon s e t o e m ot i ons s u c h a s f ea r , pain and A n x i e ty E x e r ci se H yp e r t h y r o i dism St r uc t u r al h e art dise a s e s, H F and MI P ulmona r y em b o li sm Anemia H yp ov o l emia salbutamol , d e c on g e s t a n ts, and s u b s t ance w i thd r a w al.

11. E C G findings • • • • • R egu l a r it y : R egu l ar H R : > 10 bpm P w a v e: P r es e n t Q R S c omp l e x: < 0.12 PR i n t e r v a l : N o r m al Mana g eme n t : - T r e a t the u n d er l y i ng c au s e, fluid. B blo c k er CCB s uc h as w i th o x y g en , a n ti b i o t ic s, pai n -k ill e r s or - -

12. - A t ri al flu tt er i s c au s ed b y a “ r e -e n t r y ” i n either a t ri um. This is wh e r e the elec t r i c al sign a l r ec i r c ul a t es i n a s el f -p e rp e tu a t i ng l oop due t o an e x t r a e l e c tri c al p a t h w a y in side the a tria . The sign a l g oes r ound and r ound the a t ri um w i thout i n t erru p t i on. This s t i mul a t es a t ri al c o n t r ac ti on a t 300 bpm . The signal ma k es i ts w a y i n t o the v e n t r icl es ev e r y s e c ond lap due t o the l ong r e f r a c t ory p e r i od of the A V node . - - E C G fi n d i ngs • • • • s a w - t ooth wa v es R eg u lar r h y thm nar r o w Q R S c omp l e x S a w - t ooth flu tt er w a v es a r e be s t seen in t h e i n f er i or l e ads (II, III, aV F )

13. Signs a n d s ym p t o ms : 1. 2. 3. 4. 5. Can b e a s y m p t om a tic P alpi t a tion d y spnea F a tigue S y s t e m ic e m bol i z a tion: a tr i a a r e not pumping p r ope r ly so the b lood s t a y s t ag n a n t in the a tr i a and the t h r ombus is f or m ed  O n ce th r ombus f or m ed c an s end e m boli t o di f f e r e n t ar t er i es in the b ody. T r e a tme n t • R a t e/r h y thm c o n t r ol w i th b e t a bloc k e r s or c a r di o v e r s i on • T r e a t the r e v e r s i ble u n der l ying c on d it i on (e . g. h y p er t ens i on or t h y r o t o x i c os i s) • Ra d iof r eque n cy abl a tion • D iscuss A n ti c oagul a ti o n. • • • • As s oci at ed Conditio n s : H yp e r t e n sion I s c ha e mic h e art dis e a s e Ca r dio m y op a t h y T h y r o t o x i c osis

14. Atrial fibrillation

15. - Atrial fibrillation is where the contraction of the atria is uncoordinated, rapid and irregular. This is due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node . - RISK FACTORS

16. E C G findin g s • • • • • • • R egula r ity: Ir r egular i r r eg u lar A tr i al r at e: >40 bpm V ar i able v e n tr i c u lar r at e P w a v e: ab s e n t Fibri l l a tion w a v es p r es e n t PR i nt e r v a l : ca n ’ t be me a su r ed Q R S c ompl e x: Nar r o w E tio l o g y Mo s t c om m on c auses of AF ( r e m e m ber th a t A F a f f ects SMI T H ) • S ep s is • M it r al v al v e p a thology ( st enos i s or r eg u r gi t a tio n ) • I s chaem i c heart di s ea s e • T h y r o t o x i c os i s • H y p er t ens i on

17. Compli c a tion s : 1. 2. 3. 4. Hemo dyn amic In st a b i l ity Ca r d io m y o p a t h y HF S t r o k e or embol i sm S y m p t o m s

18. treatment

19. FAVORING RATE CONTROL FAVORING RHYTHM CONTROL Persistent AF Paroxysmal AF or newly detected AF Less symptomatic More symptomatic Age ≥ 65 y Age < 65 y Hypertension No hypertension No history of HF HF clearly exacerbated by AF Previous failure of rhythm control No previous failure of antiarrhythmic drug Patient preference Patient preference

20. Goals of Rhythm Control Improve symptoms: Palpitations, dyspnea, fatigue. Prevent tachycardia-induced cardiomyopathy. May reduce stroke risk in some patients. Strategies for Rhythm Control a . Electrical Cardioversion: - Involves synchronized electrical shock to restore sinus rhythm. b. Antiarrhythmic medications: (amiodarone , flecainide ) to maintain normal rhythm. c . Surgical ablation: Maze procedure Anticoagulation Anticoagulation is often necessary even with rhythm control. Challenges and Risks Antiarrhythmic medications may have proarrhythmic effects. Electrical cardioversion may not maintain normal rhythm long-term. 26 RHYTHM CONTROL

21. Goals of Rate Control Manage symptoms: Reduce palpitations, dyspnea, and fatigue. Prevent tachycardia-induced cardiomyopathy. Improve quality of life . Target resting heart rate: < 80 bpm . Medications Beta-Blockers (e.g., Metoprolol, Atenolol): First-line for most patients. Calcium Channel Blockers (e.g., Diltiazem, Verapamil) Digoxin : Reserved for specific cases (e.g., heart failure ). Amiodarone NON-PHARMACOLGICAL : AV node ablation and pacemaker implantation in cases refractory to medical treatment Anticoagulation Anticoagulation is often required in addition to rate control . RATE CONTROL

22. Anticoagulation in atrial fibrillation

23. Importance of Anticoagulation Reduces the risk of stroke and systemic embolism. Essential for most AF patients to mitigate thromboembolic complications . Stroke Risk Assessment CHA2DS2-VASc Score: Determines the risk of stroke. Factors assessed: Age, sex, comorbidities (e.g., heart failure, hypertension, diabetes), prior stroke history . Monitoring Regular follow-up and adherence checks. INR monitoring for warfarin; not required for DOACs . Patient Education Emphasize the importance of adherence to therapy. Discuss bleeding risk and symptom recognition . Bleeding Risk Assessment Assess risk factors such as age, renal function, and concomitant medications . Assess the risk according to HAS BLED score Balance stroke prevention with bleeding risk in treatment decisions.

24. Types of anticoagulants 1 . Direct Oral Anticoagulants (DOACs) Apixaban , dabigatran, rivaroxaban , edoxaban . Advantages: Predictable anticoagulant effect. No need for routine INR monitoring. Lower bleeding risk compared to warfarin . 2. Warfarin (Vitamin K Antagonist ) Established anticoagulant therapy. Requires INR monitoring to maintain therapeutic levels. Interactions with diet and medications can be challenging . Target INR: Atrial Fibrillation: 2.0 to 3.0 Mechanical Heart Valves : 2.5 to 3.5

25. - - Ext r a e l e ctr i c al p a t h w a y c o nne ct i n g the a tr i a a n d v e n tr i c l es . Norma ll y the r e is o n l y one p a t h w a y c onn e c t i ng the a t ri a a n d v e n t ricl es ( A V) n o de . Th e e xt r a p a t h w a y th a t i s p r e s e n t i n W o lf f - P ar k i nso n - W hi t e s ynd r ome i s of t en c a ll ed the Bun d le of K e n t. B ypa s s e s A V nod e . Congeni t al dise a se oc c ur due t o f ai l u r e of ma t u r a t i on of the in s ul a t i ng a r ound A V r i n g . Au t osom a l domina n t - - - - Si g ns & s y mptoms: P a l p itati o ns, s y nc o p e , su d d e n car d i a c dead

26. ECG cha r a c te r istic s , D e lta w a ve  r ep r e s en ts the e a rly pea k cit a ti o n o f the ve n tric l e m u sc l e S h ort PR  the imp u lse by p a ssi n g the n o rmal A V -n o de p a th w a y , th u s co n d u ct to ve n tricl e s very fast. Wide QRS  the imp u lse trav e l l i n g thr o u g h acc e ssory p a th w a y a n d e x cit a ti o n o f v en tric le s th a t c au s e d b y i mpu lse trav e l thr o ug h A V - node p a th w a y .

27. T h e r ap y ; • T he b e st i n iti a l th e ra p y to co n trol tac h y arr h y th m ia in W PW i s o n e of the f o l l o w ing:  Proc a i n am i de  Ib u til i de  Flec a i n i d e  Ami o d a ro n e (no lo n ger g i ven b e ca u se it h a s a B -b l ock e r e f fect th u s bl o ck A V -n o d e , i n cre a se risk to pr o gr e ss to V . F i b )

28. - D e fined as r apid and r ep e tit i v e fi r ing of th r ee or m o r e ventricular ectopic beats in a r o w , a t a r at e of b e t w e e n 100 - 25 bpm * T w o typ e s up on du r a t io n : - N o n -s u s t ai ne d  l a s ts < 30 s e c - S u s t ai n e d  l a s ts > 30 s e c [mo r e d ange r ou s - a li f e th r e a t e n i n g ] • T w o typ e s u p on morph o l o gy of Q R S c omp l e x es : - mo n omo r p h i c  un i f orm Q R S c ompl e x es - p olym o r p h i c  v a r y i ng Q R S c ompl e x es - I f s u s t ai ne d the p a ti e n t p r e s e n ts with ;      P alp i t a t i on Che s t pa i n H ypo t e n sion S yn c ope Can p r og r e s s t o v e n t ric ular fibr i ll a t i on th a t l ead t o d e a th - E tio l ogy : - MI is the mo s t c ommon c au s e - - - St r uc t u r al h e art dise a s e s e . g. H F , L V H , MI Long Q T s yn d r ome T CA d rugs ov er l oad

29. D iagn o s i s: 1) 2) E C G; w i de and bi z ar r e Q R S c ompl e x - i f n orm a l pe r f orm e x e r c i s e s t r es s t e s t. E c ho c a r di o g r am; t o l ook f or a n y s t r uc t u r al heart d i s e as e . Ma n aging:  If the p a t i e n t has HF -> fi r s t o p t i mi z e the th e r a p y f or H F f o ll o w i ng the g u i de li ne d e t ec t ed me d i c al the r a p y (GD M L) Im p l a n t ICD ( i mpla n t able c a r di o v o l t er d e fibr i ll a t or) -> i n p a t i e n ts w i th s u s t ained v e n t ric ular t ac h y c a r dia and s t r uc t u r al h e art dis e a s e. If the p a t i e n t had ICD and on β -blo c k er and s t i l l h a v e signs and s ym p t oms -> add a n t i -ar r h y thmic dru g s as Amioda r on e .  

30. Bid i r ec ti onal VT

31. - A type of r apid polymo r ph i c v e n t ric ular t ac h y c a r dia i n the se t t i ng of Q T p r o l on g a t i on. - Cha r ac t e ri z e d b y: - H R ( 160-250)b p m - Con g eni t al or acqu i r ed l ong Q T - s ynd r omes - Ir r e g ular R-R in t e r v al -S t ar t s s u dde n l y and s t o p s s u dde n l y - > c an l ead t o V F and s u dden c a r diac d e a th. - - E tio l ogy : mo s t c ommon a r e Hy p o k al e m i a, A V b lo c k, Se v e r e IHD T r e a t w i th MgS O 4 (magn e sium s u l ph a t e); ev en if p a t i e n t has normal Mg.

32. R isk f ac t o r s of T o r sa de s d e p oin t e s

33. V e n t ric ular fibr i ll a t i on i s a r apid d i so r g ani z ed r h y thm; v e n t ricl es do n ’ t c o n t r act p r op e r l y and c a n t pu s h b l ood out of h e ar t , so the r e i s no c a r diac output and no d e t ec t able B P . E t i o l ogy : s t r uc t u r al h e art dise a se li k e i sche m i c h e art dis e a s es and T CA ov e r do s e P a t i e n t w i l l p r e s e n t w i th s u dden s yn c ope of s udd e n c a r diac ar r e s t. E C G f e a t u r es: • • • • V e n t ric ular r a t e b e tw 150-599 bpm Ir r e g ular r h y thm Bi z ar r e, i r r e g ula r , r an d om w a ve f orms NO i d e n t i fiable P w a v es or Q R S c ompl e x es or T w a v e s .

34. THANK YOU