ELECTROPHYSIOLOGY 2 (Abnormal Rhythms & Conduction Defects) PDF

ELECTROPHYSIOLOGY 2 (Abnormal rhythms & Doctor explanation Key information If you have any questions or concerns regarding Conduction defects)...

ELECTROPHYSIOLOGY 2 (Abnormal rhythms & Doctor explanation Key information If you have any questions or concerns regarding Conduction defects) Abbreviation Explanation this document. 219-220 notes Writer / Reviser: Ayat Aleid Mnemonic Writer / Reviser : Ali Aldandan Book DR. SHAHZEENFATIMA HUSSAINI Deleted BLOCK 1.3 chapter 13 Guyton 14th edition References  Doctor explanation Key information If you have any Abbreviation questions or concerns regarding Explanation this document. 219-220 notes Mnemonic Book Deleted References  Don’t rely on the doctor explanation during the lecture. It’s probably have some mistakes, read about it from the book. We have added some of the relative information from the book. A 20 year old patients suffering from high grade fever, 104Fº with episodes of nausea and vomiting. He was - Feeling of heart sound = Palpitation later diagnosed to be suffering from malaria. During - The patient is suffering from sinus tachycardia fever he had (feeling of heart sounds) palpitation due to which his ECG was taken. Lead II reading TACHYCARDIA The term “tachycardia” means fast heart rate, which We call it tachycardia because normal heart rate is around 70 – 80 beats per minute. usually is defined as faster than 100 beats/min in an When it is above 100 beats per minute this condition called tachycardia. adult. ECG is normal, all the waves ( P, T, QRS The ECG is normal except the time intervals between complex) are normal. However, the time interval between 2 QRS complexes or 2 R QRS complexes, is about 150 beats per minute instead waves decreased during tachycardia and is 150 beats per minute instead of 72 beats per of the normal 72 beats per minute. minute. That means, the number of small squares (between each 2 R waves) have been reduced. When you divide 1500 on the number of the small boxes (1500/10) = 150 beats / min which is above the normal. In normal ECG, the Around 10 squares number of squares Around 20 squares between each 2 R waves are more. It’s around 20 small squares, so 1500 / 20 = 75 beats per min which is within the normal range CAUSES OF TACHYCARDIA INCLUDE Increased body temperature (10 beats/min each F) 1. Each 1 Fahrenheit temperature Stimulation by the sympathetic nerves increases, it results in increasing the the heart rate around 10 Toxic conditions of the heart. beats. 2. The sympathetic nervous system would cause increasing the heart rate by the stimulation of beta receptors of heart. 3. Some toxic conditions of the heart ( doctor said we are not going into detail at your level you must understand the first two causes.)  A 40 year old lady who is house wife and suffers from - One of the antihypertensive drugs are beta blockers, so doctors prescribe this medicine hypertension was prescribed beta blockers by general (beta blocker) for hypertensive patients. - Letharginess = tiredness practioner to control her blood pressure. She - Dyspnea = difficulty in breathing. observed that now she felt letharginess and dyspnea - This patient is suffering from bradycardia. and sweats a lot during routine household work. An ECG was taken to assess her cardiac functions. Lead III  - From her ECG, we are going to count the heart rate. We BRADYCARDIA can see the beats QRS are normal which means a sinus rhythm, but the interval increase. Therefore, when you count the number of the small squares between 2 R waves, number of small squares increase as compare to The term “bradycardia” means a slow heart rate, the normal. When you calculate 1500 / the number of usually defined as fewer than 60 beats/min. small squares (1500/ 26 ≈ 57.6 beats / min -> less than normal) so she has bradycardia which means slow heart rate. Can occur in Always remember: - Around 60 beats / min we would consider it bradycardia. - It occurs: Atheletes Sympathetic nervous system increase the heart rate and 1. In athletes, they have dominant end vagal stimulation that means parasympathetic nervous system becomes parasympathetic nervous more dominant. Beta blocker system after the help of the 2. Beta blockers when we use them to treat hypertensive vagal nerve decrease the patients, they (beta blockers) could lead to bradycardia. Vagal stimulation heart rate. 3. Vagal stimulation. It’s a parasympathetic nerve which is then decreases the heart rate. In normal ECG, the Around 26 squares number of squares Around 20 squares between each 2 R waves are more. It’s around 20 small squares, so 1500 / 20 = 75 beats per min which is within the normal range  During the practical of ECG the students observed that whenever the subject takes deep inspiration the ECG shows increase in heart rate. Why? Sinus Arrhythmia  SINUS ARRHYTHMIA We can consider it normal during deep breathing. It occurs due to the discharge through the heart associated with respiratory cycle. - Sinus arrhythmia means the impulse is generated The heart rate increased and decreased 5 % during from the normal SA node. That means, there is no problem with the SA node and the pacemaker is quiet respiration - normal, but there is arrhythmia. Arrhythmia means abnormal rhythm of the heart. (more in Inspiration, then during deep expiration) The heart rate increased and decreased 5% during arrhythmia. - During inspiration the heart rate becomes more as compare to expiration. - It results from spillover which means out flow of Results mainly from “spillover” of signals from the the signals. There is fluctuation of the heart rate due to respiratory cycle out flow of the signals medullary respiratory center into the adjacent from the brain to the heart takes sometime. The respiration is controlled from the medullary vasomotor center during inspiratory and expiratory respiratory center from the brain. From here when the impulse reaches to the vasomotor cycles of respiration. center to the heart, it takes sometime that’s why heart rate increase during inspiration and Here are 2 YouTube videos that are short and helpful in understanding Sinus arrhythmia: decrease during expiration due to fluctuation in https://youtu.be/M1e53cYKp9I the out flow of the signal from the medullary https://youtu.be/Izt9FjAOzWQ respiratory center.  expiration inspiration ECG from the lecture Picture from google to help understanding CONDUCTION DEFECTS AV NODAL BLOCK It occurs when the impulses from Sino-atrial Now we are moving to conduction defect of the heart, to Atrio-Ventricular node does not occur. e.g. First is the AV nodal block. You know the impulses from the atria to the ventricle enter there is an AV node. It occurs when the impulses from the SA node to The reasons could be due to the AV node doesn’t occur. Or when there is a delay in the entry of the impulse from SA node to the AV node. 1. Inflammation The reason is: 2. Ischemia 1. Inflammation in the heart; may be there is inflammation. 2. Ischemia in the heart; which means reduce blood 3. Scarring or compression supply. 3. Scarring (thickening) or compression of the heart. 4. Extreme Vagus nerve stimulation 4. Extreme vagus nerve stimulation; which reduces the impulse generation. Here is a helpful YouTube video that is important in understanding AV node block types (the types would be discussed in the next slides): https://youtu.be/OgCB2_rMZ_w  A 16 year old student from Bangladesh had history of Now, you have to keep in the mind this is a frequent episodes of fever/month for 10 years. He is streptococcal throat infection. Rheumatic fever it occurs when there is a streptococcal lean thin and has migratory painfull joints swelling throat infection. (migratory arthritis)with past history of throat (At least to the problem in the joints and infections. swelling and pain this type of fever is known as rheumatic fever you can see which finding in the ECG.) unmake sense things that the He was treated as a case of rheumatic fever and ECG doctor have said. was advised. Lead II finding TYPE 1 OR INCOMPLETE A-V NODE HEART BLOCK - This is known as type 1 or incomplete AV node heart block. We are talking about type 1. However, we have type 1, type 2, and type 3 heart block. There is decrease in transfer of impulses from Sino- - This is the first, there is a decrease in transfer in impulses from SA node to AV node. Atrial to Atrio-Ventricular node. - What happened? P-R interval; you can see P-R interval increases from normal range. Normally, The PR interval increases from its normal range to P-R interval is very less. After P wave there is a Q wave RS. Here P-R interval is increased, it’s most more than 2.0 seconds it is called First degree heart common in rheumatic fever. So if anyone ask you what is the finding you can find in the ECG if the block In the book it’s written more than 0.20 second. Page 158 chapter 13 person is suffering from Rheumatic fever or type 1 AV heart block what’s finding you will find? It is most common in Rheumatic fever. The P-R interval becomes prolonged. Space between P wave and R wave increase. So, if the patient is suffering from rheumatic fever, ECG represent type 1 incomplete heart block and it’s represented as increase in the P-R interval. Prolonged P-R interval caused by 1st degree AV block. Duration is increased. As I told you, its normal duration was 0.16 second, but it can be increase around 0.2 seconds. INCOMPLETE ATRIOVENTRICULAR BLOCK First- Degree Block—Prolonged P- R Interval. The usual lapse of time between the beginning of the P wave and the beginning of the QRS complex is about 0.16 second when the heart is beating at a normal rate. This so- called P- R interval usually decreases in length with a faster heartbeat and increases with a slower heartbeat. In general, when the P- R interval increases to more than 0.20 second, the P- R interval is said to be prolonged, and the patient is said to have first- degree incomplete heart block. Figure 13-5 shows an ECG with a prolonged P- R interval; the interval in this case is about 0.30 second instead of the normal 0.20 second or less. Thus is defined as a delay of conduction from the atria to the ventricle but not actual blockage of conduction. The P- R interval seldom increases above 0.35 to 0.45 second because, by the time, conduction through the A-V bundle is depressed so much that conduction stops entirely. One means for determining the severity of some heart diseases, such as acute rheumatic heart disease, for example, is to measure the P- R interval.  A 60 year old patient who had previous history of myocardial infarction came to the cardiologist with complaints of palpitations , letharginess and chest pain during exertion. The cardiologist order ECG 1 2 3 4 - Palpitation means he can hear his heart sound. - Letharginess = tiredness - You can see P, Q, R, S (4 times), but here is (the arrow) you can find P wave this is type 2 AV block. Here the problem is a one dropped beat. There is no QRS complex here (the arrow on the picture). Lead II  TYPE 2 AV NODAL OR INCOMPLETE HEART BLOCK Few of the impulses from Sino-atrial node reaches - Now, we are going to talk about type 2 AV nodal or to Atrio-ventricular node. The PR interval is - incomplete heart block. Few of the impulses from SA node reaches to the prolonges 0.25 to 0.45 besides missing of QRS AV node and PR interval prolonged again. Again PR interval becomes prolonged and the duration it can beats. be prolonged from 0.25 to 0.45 seconds with a missing QRS beats. There are two types of second There are two types of second degree heart block degree heart block (type 2 block as two types again) Mobitz type 1 and Mobitz type 2. Mobitz Type 1: Prolongation of PR interval with drop of type 1 is prolongation of PR interval with one drop beat and there is no specific treatment is required. ventricular beat QRS wave on ECG. No specific treatment is required. Second-Degree Block. When conduction through the A-V bundle is slowed enough to increase the P-R interval to 0.25 to 0.45 second, the action potential is sometimes strong enough to pass through the bundle into the ventricles and sometimes not strong enough to do so. In this case, there will be an atrial P wave but no QRS-T wave, and it is said that there are "dropped beats" of the ventricles. This condition is called second-degree heart block. There are two types of second-degree A-V block block— Mobitz type I (also known as Wenckebach periodicity) and Mobitz type II. Type I block is characterized by progressive prolongation of the P-R interval until a ventricular beat is dropped and is then followed by resetting of the P-R interval and repeating of the abnormal cycle. A type I block is almost always caused by abnormality of the A-V node. In most cases, this type of block is benign, and no specific treatment is needed.  TYPE 2 HEART BLOCK - Again, let me explain to you. In type 2 block there is a fixed number of non-conducted P In type II block there is usually a fixed number of non- waves for every QRS complex. For example, conducted P waves for every QRS complex. For example, a 2 : there is a delay of impulse from SA node to AV node, so what happened? There are 2 P 1 block implies that there are two P waves for every QRS waves and 1 QRS complex or 3 P waves and 1 complex. QRS complex. - Type II block is generally caused by an At other times, rhythms of 3 : 2 or 3 : 1 may develop. abnormality of the bundle of His-Purkinje system. Type II block is generally caused by an abnormality of the - Require implantation that means second type bundle of His-Purkinje system Mobitz type 2 of 2nd degree heart block it needs the pacemaker. Require implantation of a pacemaker to prevent - What happen? P-R intervals increase as well as one drop ventricular beat as a result of progression to complete heart block and cardiac arrest. failure of conduction from the atria to the ventricles. P-R intervals of 0.30 second, as well as one dropped ventricular beat as a result of failure of conduction from the atria to the ventricles. These patients are treated with pacemakers.  Ok let me again explain to you, look at this picture (no.1). We are talking about the second degree heart block. The 2nd degree heart block has 2 types Mobitz type 1 and Mobitz type 2. In Mobitz type 1 you can see there is a progressive increase in the P-R interval and ultimately there is one drop beat. What is the difference between No.1 type 1 and type 2? In type 2 you can see 2 or 3 P waves and 1 QRS complex. But second degree Mobitz type 1, it doesn’t require any specific treatment but Mobitz type 2 where is 3 ratio or 2 ratio of 1 block then the patient require the pacemaker (artificial pacemaker Here you can find May be here you’ll find different different heart rate heart rate implantation). Now, we are not talking about the rhythm or artery. Now, we are talking about the blocks. These are the blocks because if you are going to count the heart rate, you will not find the equal. Heart rate and rhythm No.2 are variable. - Now, let me ask you, we discussed type 1 which is first degree heart block, in which what happen? There was only prolonged P-R interval. Here you can find different heart rate - In second degree heart block type 1 there was a progressive increase in the P-R interval which means here you can see progressively P-R interval is increasing with one drop beat. - Second degree type 2 heart block here you can see This is what the doctor said during the lecture and probably it has some there is 2 P waves 3 P waves and 1 QRS complex that mistakes, don’t rely on it, read about it from the book. I have added some means there is many dropping of QRS complex. (2 P information from the book. P159 waves 1 QRS complex.) In type Il block, there is usually a fixed number of non-conducted P waves for every QRS complex. For example, a 2:1 block implies that there are two P waves for every QRS complex. At other times, rhythms of 3:2 or 3:1 may develop. In contrast to type I block, with type Il block the P-R interval does not change before the dropped beat; it remains fixed. Type Il block is generally caused by an abnormality of the bundle of His-Purkinje system and may require implantation of a pacemaker to prevent progression to complete heart block and cardiac arrest. Figure 13-6 shows progressive P-R interval prolongation typical of type I (Wenckebach) block. Note prolongation of the P-R interval preceding the dropped beat, followed by a shortened P- R interval after the dropped beat.  A 65 years old patient suddenly collapsed while buying groceries from the market. His wife told the doctor that he has these episodes now more frequent. He was taken to the cardiac clinic for ECG Lead II  TYPE 3 HEART BLOCK When there is complete blockage of impulses reaching from sinoatrial node to atrio ventricular node. No coordination between atrial and ventricular rhythm Ventricles establish their own rhythm with the pacemaker in AV node or Purkinje fibers with 40 beats/min. The atria continue to beat with their own rhythm of 100 beats/min. Treatment with pacemaker.  TYPE 3 HEART BLOCK In the case of complete block of the impulse from the atria into the ventricles: - Ventricles establish their own signals (originating in the AV node) - Now AV is independent from the SN (each one beats by its own pacemaker) - leading to an incoordinate rhythm between the two (P waves become dissociated with QRS-T complexes). COMPLETE HEART BLOCK Non of P waves are conducted P-P are fixed QRS-QRS are fixed P-R independent PR interval is different in each rhythm  Next slide STOKES ADAM SYNDROME In some patients with complete AV block the ventricles after getting free from influence of SA node take some time before they start their own rhythm. During this period where there is no pacemaker the ventricles are in state of stand still. The blood supply to brain is decreased for few seconds leading to loss of consciousness (stokes Adam) before the new pacemaker from Av node or Purkinje fibers takes over from SA node with a rate of 15-40 beats/min. (sec, minutes, hrs, days, weeks) This period of time where ventricles find their new pacemaker and then again start their rhythm is called Ventricular escape.  - Ventricular escape = when ventricles use their own pacemaker (Purkinje system in the AV node) in case of complete blockage - Why is it called escape? Because ventricles are no longer associated with the atria (it escaped from it) In some patients with A-V block, the total block comes and goes; that is, impulses are conducted from the atria into the ventricles for a period of time and then, suddenly, impulses are not conducted. The duration of block may be a few seconds, a few minutes, a few hours, or even weeks or longer before conduction returns. This condition occurs in hearts with borderline ischemia of the conductive system. Each time A-V conduction ceases, the ventricles often do not start their own beating until after a delay of 5 to 30 seconds. However, after a few seconds, some part of the Purkinje system beyond the block, usually the distal part of the A-V node beyond the blocked point in the node, or in the A-V bundle, begins discharging rhythmically at a rate of 15 to 40 times/min, acting as the pacemaker of the ventricles. This phenomenon is called ventricular escape. Because the brain cannot remain active for more than 4 to 7 seconds without blood supply, most people faint a few seconds after complete block occurs because the heart does not pump any blood for 5 to 30 seconds, until the ventricles “escape.” After escape, however, the slowly beating ventricles (typically beating less than 40 beats/min) usually pump enough blood to allow rapid recovery from the faint and then to sustain the person.  STOKES ADAM SYNDROME :‫ﺑﺎﺧﺗﺻﺎر‬ When a sudden complete blockage happens: - ventricles need 5-30sc to generate their own beats (ventricular escape). - As a result, the heart does not pump any blood for 5-30sc. - patient will faint because the brain cannot be active for more than 4-7sc without blood supply. - When ventricular escape occurs, the patient will recover from the faint.  PHENOMENON OF RE-ENTRY “CIRCUS MOVEMENTS” Normally the cardiac impulse after passing all the way to ventricle subsides as all the ventricles muscle is in refractory period. The impulse dies in the end Under some circumstances, this sequence is broken and can initiate re-entry and lead to circus movements which cause ventricular fibrillation. - In ventricle muscles whenever an impulse goes in the ventricle, no other impulse can enter until the 1st one ends its circle dies. REASONS FOR RE-ENTRY 1. longer than normal pathway (atrial dilation) 2. Decrease in Velocity of conduction (blockade of Purkinje system, ischemia of muscle, high potassium levels 3. Shortened Refractory period (epinephrine, electrical stimulation). Division of impulses: It means single impulse breaks into two. VENTRICULAR FIBRILLATION Ventricular fibrillation is The most serious of all cardiac arrhythmias There is no typical waves seen on ECG. In ventricular fibrillation There is no clear waves pattern Coarse, irregular contractions of ventricles. The ventricles contract as many as 30 to 50 small patches. As no pumping of blood is occurring in ventricular fibrillation it is lethal unless stopped by some heroic therapy Defibrillation. Patients presents with dizziness, lethargicness and palpitations with sometimes chest pain. ELECTROSHOCK DEFIBRILLATION A strong high voltage current is applied 1000 volts of direct current for few thousand of seconds. The current passed through the ventricles for a fraction of second and causes all parts of ventricle muscle to be refractory. All action potential stops, and heart remain quiescent for 3 to 5 seconds. Electroshock defibrillation ATRIAL FIBRILLATION ECG shows no P waves. The atrial muscle is separated from ventricle muscle by a fibrous tissue. Therefore, atrial fibrillation occurs without ventricular fibrillation. The process occurs only in atrial muscle. Frequent cause of atrial fibrillation is atrial enlargement. ECG shows no P wave or only a high frequency, very low voltage wavy record. The QRST complex are normal. The ventricle is driven at 125 to 150 beats/min.  ATRIAL FIBRILLATION - The mechanism of atrial fibrillation is identical to that of ventricular fibrillation, except that the process occurs only in the atrial muscle mass instead of the ventricular mass. - For the same reasons that the ventricles will not pump blood during ventricular fibrillation, neither do the atria pump blood in atrial fibrillation. Therefore, the atria become useless as primer pumps for the ventricles. Even so, blood flows passively through the atria into the ventricles, and the efficiency of ventricular pumping is decreased by only 20% to 30%. Therefore, in contrast to the lethality of ventricular fibrillation, a person can live for years with atrial fibrillation, although at reduced efficiency of overall heart pumping. ATRIAL FLUTTER Atrial Flutter caused by circus movement of atria. The electrical signal travels a single large layer in one direction around atria muscle. Atrial flutter causes a rapid rate of contraction of atria, usually between 200 to 350 beats per minute. 150-200 will pass to the ventricles In comparison few impulses pass through AV node to ventricles. There are two to three atrial contractions for each ventricle contraction. P waves can be seen with a ratio of 2:1 or 3:1 rhythm. Next slide ATRIAL FLUTTER refractory periods: the period between two repeated action (passage of signals in our case) the signals reach the A-V node are too rapid for all of them to be passed into the ventricles because the refractory periods of the A-V node and A-V bundle are too long to pass more than a fraction of the atrial signals. Therefore, there are usually two to three beats of the atria for every single beat of the ventricles. For every two or three P waves (atria contraction), there is a one QRS-T (ventricles contraction. 2:1 or 3:1 rhythm  A 30 years old bus driver came to the doctor with complaints of chest pain, he describe the pain as someone has put a weight on his heart. The pain aggravates as tries to move and radiates to his left shoulder. He smokes two packs of cigarette daily and drink alcohol off and on. His ECG shows ANGINA PECTORIS Angina is a chest pain occurs due to decreased blood supply to the myocardium. It’s usually mild (short duration) ST segment elevations on the leads ST segment is elevated in angina  MYOCARDIAL INFARCTION Myocardial infraction (heart attack) happens due to ischemia. Prominent Q waves With ST segment elevation Sometime ST segments depression are also found in myocardial infraction, but most of the time it is elevated This picture might be helpful PREMATURE CONTRACTIONS Contraction of heart before time, is also called Extrasystole, Premature beat or Ectopic Beat. Ectopic Foci which emit abnormal impulses can occur due to: 1. Ischemia 2. Calcified plaque causing fiber irritation 3. Toxic Irritation of AV node, Purkinje fiber, or Myocardium caused by infection, drugs, nicotine, caffeine. 4. Cardiac Catheterization. PREMATURE CONTRACTIONS premature contraction is a contraction of the heart before the time that normal contraction would have been expected. Most premature contractions result from ectopic foci in the heart, which emit abnormal impulses at odd times during the cardiac rhythm. - Ectopic foci: when any other part of the conducting system starts to discharge impulses spontaneously, other than the SA node. - It can be AV node or any other one. Conducting system Causes in previous slide Premature Atrial Contractions The P wave occurred too soon, the PR interval is shortened. It means ectopic foci is close to AV node. The interval between the premature contraction and next succeeding contraction is slightly prolonged. Can occur in normal persons due to smoking, lack of sleep, ingestion of excessive coffee. PreMature Ventricular Contractions Series of Premature ventricular contraction (PVCs) with alternating normal ventricular contraction. It can result from ischemia - Ventricle diseases are lethal if not treated - Atrial diseases are easier to treat Q1) The following ECG is representing: Q2) what’s the most serious type of arrhythmia? A. Ventricular fibrillation B. Premature atrial beats A. Bradycardia C. Premature ventricular beats B. Sinus arrhythmia D. Atrial fibrillation C. Tachycardia Slide 30 Slide 27 D. Complete heart block Slide 8 1) B 2)- A Answers: 02/04/2022 26