Type to enter text CardiacCardiovascular PhysiologyC as a Physiology Country Doc

EpisodeEpisode 2:2: The EKG Electrocardiography I

Patrick Eggena, M.D. Novateur Medmedia Type EPISODEto enter text 2

Type to enter text

THE EKG

by Patrick Eggena, M.D.

i Copyright

This Episode is derived from:

Course in Cardiovascular Physiology by Patrick Eggena, M.D. © Copyright Novateur Medmedia, LLC. April 13, 2012 The United States Copyright Registration Number: PAu3-662-048

Ordering Information via iBooks: ISBN 978-0-9905771-1-9 Cardiac Physiology as a Country Doc, Episode 2: The EKG.

Contact Information: Novateur Medmedia, LLC 39 Terry Hill Road, Carmel, NY 10512 email: [email protected]

Credits: Oil Paintings by Bonnie Eggena, PsD. Music by Alan Goodman from his CD Under the Bed, Cancoll Music, copyright 2005 (with permission). Illustrations, movies, text, and lectures by Patrick Eggena, M.D.

Note: Knowledge in the basic and clinical sciences is constantly changing. The reader is advised to carefully consult the instruc- tions and informational material included in the package inserts of each drug or therapeutic agent before administration. The Country Doctor Series illustrates Physiological Principles and is not intended as a guide to Medical Therapeutics. Care has been taken to present correct information in this book, however, the author and publisher are not responsible for errors or omissions or for any consequence from application of the information in this work and make no warranty, expressed or implied, with re- spect to the contents of this publication or that its operation will be uninterrupted and error free on any particular recording de- vice. Novateur Medmedia, LLC shall not be held liable for any punitive damages resulting from the use or inability to use this work. This work is copyrighted by Novateur Medmedia, LLC. Except to store and retrieve one copy of the work, you may not reproduce, decompile, reverse engineer, modify or create derivative works without prior written permission by Novateur Medme- dia, LLC.

ii iii This Episode is dedicated to Bonnie and

to our children Kendra and Brandon and

to our grandchildren Basia, Anika, and August.

iv Foreword

This is the second of seven episodes in the Cardiac Physiology Series. Each episode starts with a case where the student finds himself or herself in the imaginary world of a Country Doctor who is called upon to manage a clinical problem related to a 50-minute lec- ture given by the author to First Year Medical Students. Video tapes of these lectures are divided into short segments which are interwoven with relevant chapters of the author’s text, “The Physiological Basis of Primary Care.”

v About the Author

The author was born in London in 1938. His parents had fled from Germany in 1933 after his fa- ther was wrongly accused of burning down the Reichstag in Berlin as Hitler was rising to power. When War broke out, the author’s family was interned on the Isle of Man and, after the War ended, transported back to Germany. There the author grew up on a farm, attended Gymna- sium, and emigrated to America at the age of 18.

Shortly after arriving in the US he was drafted into the Army and sent overseas where he served as a Medic. Upon returning to the US he attended Kenyon College and then Medical School at the University of Cincinnati. After serving as a house officer at the Cincinnati General Hospital he started a career in Medical Research, first as an NIH post-doctoral fellow at the Brookhaven National Laboratories and the University of Copenhagen and then as an Established Investigator of the American Heart Association at the Mount Sinai School of Medicine. There he rose through the academic ranks to Professor of Physiology & Biophysics and served for 5 years as Acting Chairman of the Department.

He chaired the Physiology Course for more than 20 years, taught all aspects of Physiology, and participated in the Art and Science of Medicine courses for First and Second Year Medical Students.

After retiring from teaching and research, the author returned to living on a farm with his wife and horses. Once a week he functions as an Emergency Physician in a nearby hospital --alone for the 16-hour night shift -- where he applies his understanding of Physiology to every- day patient care at the bedside.

Students at The Mount Sinai Medical School showed their appreciation for his teaching by awarding him The Excellence in Teaching Award on twelve occasions. Student comments and evaluations relating to the episodes published here are given on the next page.

vi Student Evaluations

People Comments Report Printed: 4/5/2010 Patrick Eggena Comments about Educator: Please provide any constructive feedback about this educator.

Dr. Eggena is the best teacher I have ever had. I always felt secure that he would explain things thoroughly and logically and address our questions effectively. He is so familiar with the material, and its application to clinical practice, that I think he knows how to anticipate students' questions and confusion, and that makes him an excellent teacher. I also thought his text book and the sup- plemental practice programs online were invaluable resources. I feel that Eggena has given me a very firm grasp of the basics of cardiopulmonary physiology, and I'm very grateful to have had him as a teacher.

I thought Dr. Eggena was great. It was really helpful to have both his book and his computer pro- gram to supplement lectures - with 3 ways to learn the same information (and in the same order!) it is hard not to eventually understand each concept. The computer program with quizzes was espe- cially useful. Lectures were clear and well organized.

Dr. Eggena is one of the finest teachers I've yet experienced. His patience and thorough explana- tions allowed me a deep understanding of the material, while his focus on the practical aspects of each topic left me with a sense of competency that I will remember in the coming years. I enjoyed each of his lectures and have a deep respect for his dedication to providing study materials for stu- dents beyond the lectures and his wonderful text book. This has been an exciting and memorable learning experience.

Great lecturer, very clear.

Very clear lectures. Keep up the good work!

Great professor, very knowledgeable, patient, clear, concise.

Dr. Eggena was very thorough and clear in his explanations of cardiovascular and pulmonary physi- ology. His handouts were very helpful, as were his multimedia programs.

Very clear and concise. Very engaging.

Dr. Eggena is a very dedicated professor and a superb lecturer. His presence is a boon to educa- tion at Mount Sinai.

I love Dr. Eggena. I love his vignettes. I love his multimedia programs. I love that he has been teaching this subject for years and that we have a bond with all the other classes of students that have taken his course.

vii People Comments Report Printed: 9/28/2011 Patrick Eggena Comments about Educator: Please provide any constructive feedback about this educator.

Oh my goodness, where to begin? Dr. Eggena is PHENOMENAL. He is so old-school using his projector and sharpie, drawing schematics and graphs he's obviously done a million times, and has such a story-teller's voice. But that's what makes him GREAT. More professors shoiuld real- ize that maybe the powerpoint isn't the best format to teach, that maybe a less recently available form of technology would be a better teaching aide. More professors should give up trying to find a working dry erase board marker and switch to projectors and sharpies. On top of that, to have created a multimedia program and quizes that reinforce the material in such an entertaining way! Really I can't think of anything negative to say except that Dr. Eggena's lectures didn't extend to the whole of physiology and that his multimedia program did not have anything on kidneys, endo- crine, GI, etc. I found some of his lectures to be a little too fast paced, and unclear in some points. But he has a definite great rapport with the students, seems to really care about teaching, and his multimedia programs and multitude of practice questions were invaluable.

One of the best professors I have had yet. Very clear explinations, always happy to answer ques- tions. A kind and approachable professor with clear clinical applications.

A truly masterful educator. And physician. excellent

Great instructor!

Eggena is the best. So clear! good

Fantastic teacher.

Once I got the hang of it, his outlines were helpful and it was a change to draw along during class rather than just typing away on a computer. His multimedia programs were also immensely help- ful and the only reason I passed.

Dr. Eggena was a phenomenal educator and lecturer. I truly learned a lot from him regarding car- dio and respiratory physiology. His online material was very helpful in studying for quizzes and ex- ams. Thanks for a great semester!

Dr. Eggena was great. He went quickly but clearly through the material, and he always presented concepts in terms of actual patient care, which made it all seem real.

The best--great teaching style and great textbook

viii Performance Analysis Report Printed: 9/28/2011 Report Notes: School of Medicine Evaluation System Subject: Patrick Eggena Activity Group: Physiology Starting Request Date: 12/01/2010 Ending Request Date: 09/28/2011 Location: Mt. Sinai

1 Clarity of presentation Using the lecture/educator list above to link this instructor with the lecture (s)he gave, please rate their clarity of presentation. Average: Minimum: Maximum: Non-Zero Count: Scale: Standard Dev: 4.35 2 5 138 1 to 5 0.74 Answer Value: Answer Choices: Choice Count: Percentage: 0 Unable to Evaluate 1 1% 1 Unacceptable 0 0% 2 Below Average 3 2% 3 Average 13 9% 4 Very Good 55 40% 5 Superior 67 48%

2 Rapport with students Please rate this educator's rapport with students. Average: Minimum: Maximum: Non-Zero Count: Scale: Standard Dev: 4.62 3 5 138 1 to 5 0.52 Answer Value: Answer Choices: Choice Count: Percentage: 0 Unable to Evaluate 1 1% 1 Unacceptable 0 0% 2 Below Average 0 0% 3 Average 2 1% 4 Very Good 48 35% 5 Superior 88 63%

3 Quality of Tracking Please rate this educator's overall quality of teaching. Average: Minimum: Maximum: Non-Zero Count: Scale: Standard Dev: 4.51 2 5 138 1 to 5 0.63 Answer Value: Answer Choices: Choice Count: Percentage: 0 Unable to Evaluate 1 1% 1 Unacceptable 0 0% 2 Below Average 1 1% 3 Average 7 5% 4 Very Good 50 36% 5 Superior 80 58%

Page 1 of 1 Performance Analysis Report Printed: 4/5/2010 Report Notes: School of Medicine Evaluation System Subject: Patrick Eggena Activity Group: Physiology Time Frame Start Date between: 01/11/2010 and 04/05/2010

1 Clarity of presentation Please rate this educator's clarity of presentation. Average: Minimum: Maximum: Non-Zero Count: Scale: Standard Dev: 4.38 3 5 136 1 to 5 0.62 Answer Value: Answer Choices: Choice Count: Percentage: 0 Unable to Evaluate 0 0% 1 Unacceptable 0 0% 2 Below Average 0 0% 3 Average 10 7% 4 Very Good 65 48% 5 Superior 61 45%

2 Rapport with students Please rate this educator's rapport with students. Average: Minimum: Maximum: Non-Zero Count: Scale: Standard Dev: 4.68 3 5 136 1 to 5 0.50 Answer Value: Answer Choices: Choice Count: Percentage: 0 Unable to Evaluate 0 0% 1 Unacceptable 0 0% 2 Below Average 0 0% 3 Average 2 1% 4 Very Good 40 29% 5 Superior 94 69%

3 Quality of Tracking Please rate this educator's overall quality of teaching. Average: Minimum: Maximum: Non-Zero Count: Scale: Standard Dev: 4.57 3 5 136 1 to 5 0.58 Answer Value: Answer Choices: Choice Count: Percentage: 0 Unable to Evaluate 0 0% 1 Unacceptable 0 0% 2 Below Average 0 0% 3 Average 6 4% 4 Very Good 47 35% 5 Superior 83 61%

Page 1 of 1 The Country Doctor The Situation

Movie 1.1

Introduction to Case Time: 1:43 minutes

12 James is 23. He is well groomed. His tack,” he insists. His right hand is voice is pressured and uncertain --does clenched into a fist. Crusts have formed not look into your eyes --- his hands trem- over abrasions on his knuckles. He is anx- bling as you asked him why he has come. ious, irritable, possibly delusional, para- noid and assaultive. Not a good time to in- “Are you a psychiatrist?” sist on protocol.

“No - a medical doctor.” “Good idea. Take off your shirt and lay down over here,” you say in a calming “Good! My heart is broken. I’m having a voice as best as you can muster. heart attack. It hurts right here,” he says pointing to his left chest. “I want you to As you are putting the precordial leads on take my EKG --see if I’m having a heart at- his chest, he asks:

13 “What will the EKG show ---that is, if I’m Figure 1b James’ EKG having a heart attack?”

“It will show so-called elevation of ST seg- ments. Unlikely, though, for a young man in good physical condition --but you never know. Now be quiet and lay there still, so we get a good tracing that we can inter- pret.”

James seems to calm down. Is less con- frontational, less demanding, more re- laxed. You look at the tracing as it is ejected from the machine. You examine

“Is something wrong, Doc?” He says at- tempting to jump off the examining table with lead wires still attached.

“No, no --it’s fine, just relax, calm down. Lay back down.”

“How can I. What are the --STs? Tell me, Doc! Are they elevated? Let me see!” He reaches for the ECG tracing in your hands. the tracing with some care, which takes time. More time than James is willing to “Tell me, Doc. Show me!” wait. He is becoming more and more anx- ious and irritable. “James, you have to calm down and relax if you want me to explain your EKG trac- ing. “

14 You point to the elevated ST-segments in blood pressure cuff from his arm, and lead II of the EKG print-out. walks nervously around the room.

“See here. See this segment of the trace “How do I know that you are not making in lead II? ---It is clearly elevated above this up?” the baseline. Can you see it?” “You don’t, but I can do another test that “Oh, yes, Doc --but now you’re scaring me!”

“Well, I didn’t tell you before that there are two kinds of ST-segment elevations --the bad kind which we see in people with a heart attack and the good kind in athletic people with strong, healthy hearts like yours.

“Doc. please tell me the truth.” He is be- coming agitated. His hands are shaking, pearls of sweat are appearing on his fore- head. will convince you with that machine over “In athletic hearts, such as yours, we see a there.” You point to the Cardiac Enzyme special kind of ST-segment elevation --a Analyzer. scooped out (convex) appearance instead of the downward sloping (concave) pattern “What is that?” of a heart attack. It’s called early repolari- zation. “It’s a blood test for cardiac enzymes, so- called troponins. These troponins are Perfectly normal. And you have a large used by heart muscle cells to make them heart --probably from exercising.” contract and keep your heart beating. When these cells are injured during a heart He takes a deep breath in and lets it out attack, these enzymes leak out into the with a sigh of relief. But his peace of mind blood stream where they can be meas- soon vanishes as he stands up, rips the

15 ured. I have a machine here that will do it. chest pain. It should go away in a day or It takes about 20 minutes. Do you want two. Don’t worry about it, but we’ll see this test?” what the troponins show.

“Yes, Doc.” Let me listen to your lungs. Take a deep breath --in --and --out.” You remove the “Alright, we will keep you on the cardiac stethoscope from your ears after listening. monitor above your head until we see the results from your blood test.” “Yes --diminished breath sounds on the left where you had part of your left lung re- You take a blood sample from his right moved, but breath sounds are alright on ante-cubital vein. the right side. Now let me listen to your heart. Deep breath in and hold it please.” “While your blood is being analyzed, I would like to listen to your heart and lungs You listen at the base and apex of his and ask you some more questions. heart and then remove the stethoscope from your ears. First of all is it possible that you have strained your chest muscles or hurt your “Your heart is fine -- no need to worry ribs, which seems to me a more likely about it.” cause for your chest pain?” “I’m still anxious Doc. Can you give me “I’ve been helping my Dad on the farm. something for my nerves?” Used a chain saw yesterday to cut up a tree. Didn’t hurt my ribs, but I left part of “Are you driving?” my left lung in Afghanistan.” He says point- ing to a long scar on his left back. “No my Mom brought me.”

“What happened?” “Alright, I’ll get you an Ativan.” You give him a 1 mg tablet from the medicine cabi- “Don’t remember. Was in a coma. ---Three- net. days. Humvee ----IED.” “Are you being followed by the Veterans “Well, sore chest muscles from using a Hospital?” chain saw are a more likely cause for your

16 “Yes, I have an appointment for the VA He hesitates. Wipes his face with his right clinic here in town next week with a psy- arm. “My girl friend left me. Can’t find chiatrist.” work. Don’t know where to go. I’m think- ing about signing up for another tour in Af- “Have you been taking any medicines?” ghanistan. Am ashamed being helpless. Can’t sleep. Get into fights over nothing.” “Not lately. They make me feel different. Not like myself. Embarrassing. Couldn’t “James, have you had thoughts of hurting have sex. So I stopped.” yourself or anyone else?” He looks down at his shoes. “What medicines were you on?” “Sort of.” “Don’t remember.” “What do you mean?” “Was this for PTSD?” “Sometimes think it best to end it all.” “I guess so.” “How would you do that?” “Do you have flash-backs to Afghanistan?” “Drive my motorbike into a tree.” “Yes, but I don’t want to talk about it.” “Have you tried to kill yourself before?” “That’s Okay. Do they keep you from sleeping?” “Yes, once --tried to hang myself in the barn -- but the rope broke.” “Yes --haven’t slept for days. And then I wake up --- soaked in swet.” “I see. --You know, I want you to be safe --that is why we are checking your heart “Are you hearing any voices?” on the monitor above your head.” “Sometimes.” “Are you feeling better after the Ativan?” “What do they say.” “Yes, Doc.” “Don’t know --they whisper in Arabic.” “Your heart is beating at a normal rate --ac- “Have you been feeling depressed?” tually a little slower, as is typical for some-

17 to call the doctor on duty over there at the hospital and see if they will accept you?”

“Well --I don’t know --- my Mom is waiting for me outside in the car --and who will feed my dog?”

“I’ll talk to her and see how she feels about it.”

You walk with him out to the car where you find his Mom sitting behind the wheel cry- one with an athletic heart. And your lungs ing. are working just fine --putting enough oxy- gen into your blood -- as you can see by “Are you alright?” the 97% oxygen saturation on the monitor up there. You ask as she rolls down her window. She wipes the tears from her face--. I’m going to check on the troponins. They should be done by now.” “We need to transport your son by ambu- lance to the VA hospital tonight.” You walk over to the analyzer and look at the print-out: Troponins < 0.05 ng/ml “Oh my --did he have a heart attack?” --negative. “No --his heart is fine, but I am concerned You show him the slip. that he may try to hurt himself with his PTSD and all. He will be safer in the hospi- “See, the blood test for a heart attack is tal where psychiatrists can care for him negative. Your heart is just fine. But we --possibly get him into a special PTSD pro- now need to take care of this problem you gram for veterans. have with PTSD. You need to be in a safe place -- in a VA hospital with psychiatrists And --(looking at James) can you feed his who specialize in helping veterans return- dog while he is there?” ing from Afghanistan. Would you like me

18 “Yes, of course --please make the arrange- having a heart attack because his girl ments. I have been worried about this my- friend “broke his heart.” His PTSD is symp- self. “ tomatic with depression, anxiety, irritability and sleep disturbances. He has auditory “Do you want to come inside --coffee --wa- hallucinations and suicidal ideations with a ter --?” concrete plan and a past history of an at- tempt. He may be assaultive if he does She waves the Kleenex and shakes her not get his way, so be careful. He has head ---blows her nose. stopped taking his meds --don’t know ”Oh Doc, what did they do to him over what he was taking.“ there in Afghanistan? What did they do to “I’m not a psychiatrist, but I can put him him --to my boy?” on a psychiatric ward on close (1:1) obser- “Are you sure I can’t get anything for you?” vation for suicidal ideation and he will be seen by the psychiatrist in the morning. “No thanks --I’ll be alright. I’m sorry.” What do you recommend for tonight?” You walk over to the front lawn where you cannot be heard by James and his mother “I’ve given him Ativan 1 mg PO here for as you call the VA Hospital on your cell anxiety, but you may have to be repeat a 1 phone. or 2 mg dose of Ativan every four hours for anxiety later on tonight. A 2 mg dose of “Hi, Prazosin along with 200 mg of Trazodone may help with his nightmares and insom- I’m calling about a 23-year old veteran nia. with PTSD, depression, and suicidal idea- tion who I would like to transfer to you for “Anything for his depression?” evaluation by a psychiatrist. “Trazodone should help. You could also “Please tell me a little bit about him.” start him on Bupropion in the morning. It’s supposed to interfere less with sexual func- “He is alert and oriented, well groomed, tions than some of the other serotonin up- but minimally cooperative, confrontational take inhibitors. This is one of the reasons and irritable. His speech is pressured with he stopped taking his meds. But the psy- minimal eye contact. He has delusions of

19 chiatric team in the morning can decide what’s best for him. Perhaps he can get into the long-term PTSD program at your hospital.”

“OK, thanks. About when do you think he’ll get here?”

“He’s coming by BLS ambulance. Should be there in about an hour. Good luck!”

20 The Discussion

A General Practitioner --a Nurse Practitio- ner.”

“How long will that take?”

“A few more years. Depending on whether I pass my exams --and whether or not you teach me enough,”she says with a ques- tioning smile.

“You want me to teach you stuff?”

“Yes --that would help.”

“Well, I’ll be glad to try --but you have to ask questions.”

“Alright, let’s start right now.”

“Right now? What do you want to know?”

“We are studying EKGs right now in class. “Kay, you look tired.” You know ---the basics. How to hook up

“I am Doc, was up late studying.” the leads and so forth. But it’s so confus- ing. So many details. How does it all fit to- “Studying what?” gether? For example --you just looked at James’ EKG for a minute or so and knew “Advanced nurse’s courses --at night.” that it was normal. How did you do that?”

“Why? Do you want to be a Physician’s As- “Well, to start with James. Any com- sistant?” plaint of chest pain must be taken seri- “No Doc --don’t want to be anyone’s assis- ously until the possibility of a heart at- tant. I want to be my own boss --like you. tack has been ruled out, even though in

21 Figure 1e. James’ EKG

this case his heart was obviously “bro- sive R-waves are equal (look at the ken” from other causes. After a careful rhythm strip for V1.) history and physical examination this in- 2. What is his rate? It’s about 60 bpm, volves taking an EKG and a blood sam- i.e. there are 5 large boxes between ple for cardiac enzymes. That is why I R-waves --300 bpm/5 = 60 bpm. took my time looking at his EKG. That is alright --you can’t just glance at it. 3. Where is his pacemaker? In the SA You have to check in a systematic way node, because there is a P-wave be- whether the tracing is normal or not. fore each QRS complex. Here are the questions I asked myself in looking at his EKG tracing: 4. Any conduction delays? (1) His P- R interval is normal, i.e. the distance 1. What is his rhythm? It is regular, be- from the starting point of the P-wave cause the intervals between succes- to the starting point of the QRS com-

22 plex fits into one large box (it is less “That seems important to me!” than 0.20 seconds). Thus conduction “Well, the problem is that you usually do to (and through) the AV-node is nor- not have an earlier ECG when the pa- mal. (2)The duration of his QRS com- tient was healthy for comparison.” plex is normal, i.e., fits into three small boxes (it is less than 0.12 seconds). “I see.” Thus conduction along the right and left bundle branches and through ven- “But you still need to know how to deter- tricular muscle is normal. mine the axis to learn if it has changed.

5. What is his mean QRS axis? It is in Alright --so much for the mean QRS the normal range, because R-waves axis. Next I want to know: are taller than S-waves are deep in 6. Are his atria hypertrophied? No. leads I and aVF. The mean QRS axis The P-wave in V1 does not show an is about +60 degrees.” enlarged upward (right atrium) or “Oh --Doc, we spent a lot of time in downward (left atrium) component. class talking about the axis. Why is this 7. Are his ventricles hypertrophied? so important?” (1) Right ventricle. No, because the S- “It actually is not very important --only if wave in V1 is much deeper than the there is a sudden change in the axis of a R-wave in V1. (2) Left ventricle. patient complaining of chest pain.” Yes, because the S-wave in V1 (19 mm) plus the R-wave in V5 (17 mm) is “Why?” greater than 35 mm. Thus, he meets the minimal voltage criteria for left ven- “Because an infarct can block conduc- tricular hypertrophy, which may be a tion along one of the two bundle normal variant. branches (or fascicles of the left bundle) resulting in a sudden change in the axis 8. Is there any evidence for myocar- to the right or the left.” diac ischemia? No, because his T-

23 waves are not inverted, except in V1 You will develop your own way of look- where the T-wave may normally be up- ing at EKGs. right or inverted. “Doc, this stuff is so complicated. I stay 9. Is there any evidence for myocar- up late and read and read before the dial injury? Perhaps. The ST- test and it doesn’t sink in.” segments are clearly elevated above “Probably more than you think.” baseline in the limb leads (e.g., Lead II) and precordial leads (e.g., V3). “You think that you go back over things However, the elevation is concave you’ve learned during the day at night (bulging inward) rather than convex when you sleep?” (bulging outward). This suggests that he has a vigorous, healthy heart that “If something had an impact on you dur- repolarizes early. ing the day --like James --some of it re- mains with you.” 10.Any evidence for myocardial infarc- tion? No. There are no significant “Well, he was still dreaming about what (wider than 1 small box or deeper happened years ago to him back in Af- than one-fourth of the R wave) Q- ghanistan.” waves. “How much time do you think you actu-

11.Summary. James has a normal si- ally spend dreaming, Doc?”

nus rhythm at 60 beats/min with early “Not much, I think about 20% or so repolarization and minimal criteria for --most of the time is spent in light sleep. LVH. (Fig.1f).”

“Okay, thanks Doc. I’ll try to remember “Okay Doc, it’s time for me to go. all of this.” Thanks for the lesson on EKGs. I’ll see you tomorrow. Sleep well.” “Don’t remember the sequence which I followed here. It’s just the way I do it. “Good night, Kay.”

24 25 Reflections

Movie 1.2

Reflections Time: 1:18 minutes

26 2

Depolarizing and Repolarizing the Heart 1. Depolarization and Repolarization of the Ven- tricles

Movie 2.1

Lecture 2-1: Depolarization and Repolarization of the Ventricle. Time: 3:44 minutes Learning Objectives: 1. Understand the vectors of depolarization and repolarization of the ventricles. 2. Appreciate why depolarization start at the endocardium but repolarization at the epicar- dium. 3. Know the vectors of depolarization for the interventricular septum.

28 Figure 2.0 Depolarization and Repolarization of the Ventricle

A B Endocardial cell

Repolari- zation 0 3 Depolari- Depolari- Repolari- zation zation zation

Epicardium Epicardial cell Endocardium Time

(A) Depolarization of the left ventricle from endocardium to epicardium and repolarization from epicardium to endocardium. (B) Action potentials of typical ventricular muscle cells at the endocar- dial and epicardial surfaces of the ventricle. Depolarization of these cells occurs during phase 0 of their action potentials, while repolarization occurs during phase 3. Note that, even though endocar- dial cells depolarize first, they are last to repolarize because they have the longest action potentials.

As an impulse spreads from the SA (see Fig.2-0, B). Thus, although phase 0 node over the atria, through the AV node (related to depolarization) of endocardial and down the Purkinje fibers the ven- cells precedes phase 0 of epicardial tricular muscle cells on the endocardial cells, phase 3 (related to repolarization) (inside) surface of the ventricles are first of epicardial cells precedes phase 3 of to depolarize. The wave of depolariza- endocardial cells. As a result, depolariza- tion then spreads through the ventricular tion proceeds from endocardium to wall to myocardial cells at the epicardial epicardium, but repolarization proceeds (outside) surface. Although the epicar- from epicardium to endocardium. dial cells are last to depolarize, they are first to repolarize. So the wave of repo- larization proceeds from the epicardium to the endocardium (see Fig. 2-0, A). This apparent paradox is due to the fact that the epicardial cells have shorter ac- tion potentials than the endocardial cells

29 Depolarization of a Ventricular Muscle Strip

Movie 2-2

Lecture 2-2: Depolarization of a Ventricular Muscle Strip Time: 5:53 minutes Learning Objectives:

1.Understand why the ECG machine records an upright wave, i.e., an R-wave, when a wave of depolarization is moving along a ventricular muscle strip toward the positive pole of a lead wire. 2. Appreciate why an isoelectric line is recorded before and after depolarization of the ventricu- lar muscle strip.

30 Depolarization and Repolarization of and a recording device (a strip chart re- Ventricular Muscle corder). As we shall see shortly, the EKG machine has 12 leads with which the volt- As the ventricle depolarizes (and then con- age across the heart is measured from 12 tracts), positively charged sodium ions different angles. However, let us start our move from the surfaces to the interior of all discussion with only one pair of electrodes the individual cells that make up the ventri- and let's consider a hypothetical experi- cle. When the ventricle then repolarizes ment in which we follow the voltage (and relaxes), positively charged potassium changes across a section of left ventricular ions move from the interior to the exterior wall as it first depolarizes and then repolar- surface of cell membranes. Depolarization izes. does not occur at precisely the same in- stant in all cells, so that cells near the endo- In the experiment shown in Figure 2-1, one cardial surface of the ventricles are depo- electrode has been placed on the endocar- larized before those at the epicardial sur- dial side of a strip of ventricular muscle faces. Similarly, repolarization does not oc- and the other electrode on the epicardial cur simultaneously in all cells, so that cells side, with a sensitive voltmeter (EKG ma- toward the epicardial surface of the ventri- chine) connecting the two electrodes. Let cles are repolarized before others at the en- us make the electrode on the epicardial docardial side. As a consequence, dipoles side positive relative to the other, and let (regions with opposite electric charges, us set the polarity on the EKG machine so like the positive and negative poles of a that it records a positive voltage (and in- battery) are generated across the ventricu- scribes an upward deflection on the record- lar wall during depolarization and repolari- ing paper) when the epicardial surface is zation. These dipoles can be measured positive relative to the endocardial surface. with a sensitive voltmeter connected to Before starting with the experiment, let us electrodes placed around the heart at the calibrate the EKG machine so that a 1 mV surface of the chest. A recording of the pulse gives an upward deflection equal to changes in dipoles across the atrial and 1 cm (or 10 mm), and let us set the speed ventricular walls during the cardiac cycle is at which the paper moves past the record- called the electrocardiogram (ECG or EKG ing pen at 25 mm/second. In this way we for short). The EKG apparatus contains a will obtain a precise record of the magni- voltmeter, a series of electrodes (its leads), tude of the voltage generated by the

31 muscle strip and the time it takes. To facili- Figure 2.1 Voltmeter tate precise timing we will use special EKG - + Electrode A + + + + + + Na Na Na Na Na Na chart paper on which distances are 25 mm/second ECG - + machine

m V marked by thin lines that are 1 mm apart + + + + + + 1 Na Na Na Na Na Na Endocardial Epicardial 0.2 sec cell cell - + and by thicker lines that are 5 mm apart. Gap Depolarization B junction + + + Na Na Na + + + ECG Na Na Na Thus, the distance between two thin lines machine - + + + Na Na Na+ + + + (or within one small box) equals 0.04 sec- Na Na Na - +

C onds (1 mm/25 mm/second), and the dis- + + + + + + Na Na Na Na Na Na ECG - + machine + + + + + tance between two thick lines (or within Na Na Na+ Na Na Na - + one large box) equals 0.2 seconds (5 mm/ D + + + Repolarization K K K + + + Na Na Na ECG - + machine 25 mm/second). + + + Na Na Na + + + K K K - + E + + + + + + Let us start the experiment by observing K K K K K K R T ECG - + machine the muscle strip at rest (Fig.2-1,A). When + + + + + + K K K K K K all the individual muscle cells in the strip of Voltmeter muscle are at rest (in phase 4 of their indi- Intracellular Recording Endocardial cell F vidual action potentials), sodium ions will mV Voltage Recorder -90 Time be evenly distributed over the surface of Endocardial Epicardial Epicardial cell cell cell the muscle strip and the voltmeter will re- cord zero mV (the needle of the recorder Fig.2-1. Depolarization and repolariza- tion of a strip of ventricular muscle. will draw a flat line on graph paper). As Voltage across a strip of ventricular mus- muscle cells at the endocardial surface of cle is recorded with surface electrodes the strip are stimulated (phase 0 of their ac- placed at its endocardial and epicardial surfaces. A recorder (an ECG apparatus) tion potentials), sodium ions rush into the plots voltage as a function of time. In (A) cells, causing a (relative) deficit in positive the muscle is at rest, the voltmeter re- surface charges at the endocardial side. cords 0 mV, and the recorder pen draws a flat (isoelectric) line on the graph paper. The resulting voltage change across the In (B) the muscle strip is stimulated at its muscle strip is recorded as an upward (or endocardial side, the voltmeter records a positive) deflection on the graph paper. positive voltage, and the pen draws a positive (upright) deflection on the paper. This positive deflection reaches a maxi- In (C) the entire muscle strip has been de- mum when the endocardial half of all the polarized, the voltmeter records 0 mV, cells in the muscle strip has been depolar- and the recording pen draws a flat, isoe- lectric line. In (D) the muscle strip is repo- ized (Fig.2-1,B). As the other (epicardial)

32 half of the cells becomes depolarized, the same, i.e., they are both upright, because voltage across the strip returns to zero. depolarization of the muscle strip occurs These voltage changes, recorded as a func- from endocardium to epicardium; whereas, tion of time as ventricular muscle cells are repolarization occurs from epicardium to progressively depolarized, are called the R endocardium. Why does repolarization oc- wave. Just after the R wave, all cells in the cur in a direction opposite to depolariza- muscle strip remain depolarized (these tion? The reason is that the action poten- cells are in phase 2 of their action poten- tials in epicardial cells are shorter than tials), so that the voltmeter again records they are in endocardial cells (Fig.2-1,F). Be- zero mV (a flat line on the graph paper), cause epicardial cells have a shorter pla- (Fig.2-1,C). teau phase (phase 2), repolarization (phase 3) occurs in epicardial cells before it does After muscle cells have been depolarized in endocardial cells. for a while (leaving time for the cells to con- tract ), they start to repolarize (so they can relax). Repolarization of the muscle strip is initiated by cells at the epicardial side. Po- tassium ions move out onto the surface of these cells during phase 3 of their action potentials, which results in a relative ex- cess in surface charges at the epicardial side and causes a voltage change that is recorded as an upward deflection. Again, voltage is maximal when one-half the cells has repolarized (Fig.2-1,D). The voltage then returns to zero mV as the other (endo- cardial) half of cells is repolarized (Fig.2-1,E). These voltage changes during repolarization of ventricular muscle are called the T wave. The T wave is wider than the R wave, because repolarization takes longer than depolarization. The polar- ity of the T and R waves is normally the

33 Repolarization of a Muscle Strip

Movie 2-3

Lecture 2-3: Repolarization of a Muscle Strip Time: 2:55 minutes. Learning Objective: 1. Understand why the ECG machine records an upright wave, i.e., a T-wave, when a wave of repolarization is moving along a ventricular muscle strip toward the negative pole of a lead wire. 2. Appreciate the origin and significance of an abnormal, i.e., inverted, T-wave an ECG record- ing.

34 um, which results in inversion of the T Figure 2.2 - + A wave (Fig.2-2,A). + + + K K K + + + Na Na Na ECG - + machine + + + The reason for this is complex, but the clini- Na Na Na + + + K K K T-wave inversion cal implications are important. First, when in ischemia Voltmeter the coronary blood supply to ventricular

Intracellular muscle is diminished, endocardial cells be- microelectrode Intracellular Recording B Endocardial cell come ischemic before epicardial cells be-

Voltage cause blood vessels in the subendocar- Recorder -90 mV Endocardial Epicardial Time dium (area toward the inside of the ven- cell swollen cell (normal) Epicardial cell due to ischemia tricular wall) are more compressed during Fig.2-2. Repolarization in an ischemic ventricu- systole than are vessels on the outside of lar muscle strip. (A) Repolarization in a strip of the heart. Second, when endocardial cells ventricular muscle, which is ischemic on its endo- cardial side, starts at the endocardium (by diffu- become ischemic, rapid depolarization sion of potassium ions out of cells). This results in (phase 0) occurs more slowly than in nor- inversion of the T wave on the ECG tracing. (B) mal cells (compare the ischemic endocar- Intracellular recordings of action potentials from dial cell with normal epicardial cell in Fig- ischemic endocardial and normal epicardial cells. The ischemic endocardial cells show more posi- ure 2-2,B). Because the speed at which im- tive resting potentials (phase 4), diastolic depolari- pulses are conducted decreases as the zation during phase 4, and shortened plateau slope of phase 0 depolarization dimin- (phase 2). These changes in ischemic endocardial cells cause the normal epicardial cells to repolar- ishes, the wave of depolarization from en- ize later than endocardial cells, which reverses docardium to epicardium is slowed. In the normal process and results in T wave inver- part, because of this delay in epicardial sion. cell depolarization, the ischemic endocar- dial cell starts to repolarize (phase 3) be- 2. Repolarization of a Strip of Ischemic fore the epicardial cell. Another reason for Ventricular Muscle (Genesis of Inverted early repolarization of the ischemic endo- T Waves) cardial cell, is that the plateau (phase 2) is shortened so that repolarization (phase 3) When ventricular muscle becomes starts earlier than usual. Because ischemic ischemic (lacks adequate oxygen), repolari- endocardial cells repolarize before normal zation occurs in a direction opposite from epicardial cells do, the direction of repolari- normal, i.e., from endocardium to epicardi- zation is reversed, and the T wave on the

35 EKG becomes inverted. For these reasons, sudden inversion of T waves in a subject who has been asked to exercise during a stress test is a sign of coronary artery insuf- ficiency.

36 3

Cardiac Vectors, Waves and Intervals 2. Cardiac Vectors, Waves, and Intervals

Movie 2-4

Lecture 2-4: Cardiac Vectors and EKG Waves Time: 9:17 minutes Learning Objectives: 1.Appreciate the origins of the P-wave, the QRS complex, and the T-wave on an EKG record- ing. 2. Know when is a P-R interval too long and what this implies. 3. Know which interval on an EKG tracing corresponds to systole. 4. Understand what the R-R interval of an EKG tracing represent.

38 A. Vectors Figure 2-3

Let us now apply the lesson learned from A. Cardiac Vectors the isolated muscle strip to interpreting the P S waves seen on an EKG, recorded with two T Q ECG electrodes on the chest wall across the R + heart (Fig. 2-3,A). Let us make the elec- trode on the left chest, overlying the left B. Waves c ventricle, positive with respect to the elec- +1 a e f trode on the right chest. As the left ventri- mV 0 b cle depolarizes from endocardium to -1 epicardium, the wave of depolarization d C. Intervals moves toward the positive electrode (or k g j lead) on the chest and, accordingly, in- +1 scribes an upright (or positive) deflection mV 0 h on the EKG paper. Let us pretend that we -1 i could depolarize the right ventricle inde- pendent of the left. Now the wave of depo- 0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 larization moves away from the positive Seconds electrode, and a downward (or negative) deflection is made on the EKG tracing. Fig.2-3. The waves and intervals of the ECG. In (A) a lead on the chest over the left heart explores The upward deflection by left ventricular vectors coming toward or moving away from it. Posi- depolarization would be greater than the tive vectors (moving toward the lead) result from atrial depolarization (P), left ventricular depolarization downward deflection by right ventricular (R), and left ventricular repolarization (T). Negative depolarization, because the ventricular vectors (moving away from the lead) result from depo- muscle mass is considerably greater on larization of the interventricular septum (Q), and depo- larization of the most lateral/superior part of the left the left than it is on the right. The peak volt- ventricle (S). All of these vectors occur sequentially ages of these upward or downward deflec- and, therefore, produce characteristic waves, as is tions could be measured (in mV or mm) shown in the ECG tracing in (B). In (C), the various intervals and segments of the normal ECG along with and expressed as vectors (arrows with the J-point are illustrated for a heart rate of 60 beats/ lengths proportional to their magnitudes) min. directed toward or away from the position

39 where the lead was placed on the left because depolarization of the two ventri- chest wall. Now, if the right and left ventri- cles in sequence takes longer than usual, cles depolarize simultaneously (as they nor- PVCs characteristically have much wider R mally do), the opposing vectors would and S waves than normal. tend to cancel one another. Accordingly, the upright deflection in a lead overlying the left ventricle is normally less than it B. Waves would be if the right ventricle were not de- polarizing at the same time as the left. During the cardiac cycle different parts of the heart depolarize and repolarize - some Now let us assume that the two ventricles parts simultaneously, others not. As a con- do not depolarize simultaneously, but se- sequence some vectors are hidden (e.g., quentially, first the left ventricle and then the right ventricle) and others are blunted the right. One sees this with premature ven- (e.g. the left ventricle). Vectors that occur tricular contractions (PVCs), If an irritable sequentially can be identified as upward or focus discharges in the left ventricle, the downward deflections on the EKG tracing; left ventricle will depolarize before the these deflections are called waves and are right, because the impulse is now con- identified by letter names (Fig.2-3). When- ducted much more slowly than usual to ever the net (or averaged) vector is di- the right ventricle (conduction occurs via rected toward an EKG lead (always the gap junctions of muscle cells rather than positive pole of an electrode), an upward along the specialized Purkinje system). or positive wave will appear on the EKG re- Now the upward deflection caused by the cord. Whenever the net vector is directed wave of depolarization across the left ven- away from an EKG lead, a downward or tricular wall will be unopposed, giving rise negative wave will be seen. to a much larger positive deflection, and the wave of depolarization in the opposite The cardiac cycle starts with depolariza- direction across the right ventricular wall tion of the SA node. As the impulse will no longer be hidden and will show it- spreads from the SA node over specialized self as a large negative deflection. For this conductive pathways to the right and left reason, PVCs show much taller upright atria, the muscle depolarizes toward the waves (R waves) and much deeper in- lead, which causes an upright deflection to verted waves (S waves) than normal, and, be inscribed on the EKG tracing, called the

40 P wave (Fig.2-3). The P-wave is followed depolarization is toward the left (because by a short delay (a flat line at zero mV) as the muscle mass is considerably greater the impulse is slowly conducted through on the left than the right), causing an up- the AV node (the mass of these conducting ward deflection, the R-wave. As the wave fibers is too small to register a depolariza- of depolarization reaches the furthest and tion on the surface EKG). The delay at the most lateral parts of the thick left ventricle, AV node allows the atria to contract and to the vector is once again directed away pump blood into the ventricles. (Keep in from the lead, causing a downward deflec- mind that the P wave represents the electri- tion, called an S-wave. (Unlike a Q-wave, cal activity of atrial muscle and not the me- an S-wave must always follow an R-wave. chanical event,i.e., contraction). If there is no R-wave, i.e. no upward deflec- tion, the downward deflection is not called The impulse emerges from the AV node an S wave, but rather a QS complex. A QS and enters the ventricular septum via the complex is abnormal and signifies myocar- right and left bundle branches. The ven- dial infarction. tricular septum is the first part of the ventri- cles to be depolarized. Because the left Following the QRS complex is a delay (a ventricle contributes more muscle to the flat line at zero mV), as the ventricles con- septum than does the right ventricle, the tract and blood is pumped to the lungs net vector during depolarization (from en- and the peripheral organs. (Keep in mind docardium to epicardium) is from left to that the QRS complex represents the elec- right, i.e., it is directed away from the left trical activity of the ventricles just before chest lead. Therefore, this vector is re- the mV 0 mechanical event, i.e., ventricular corded as a downward deflection, called a systole.) Q-wave. Small Q-waves are normal; large ones are not. (They indicate myocardial in- As the ventricles repolarize from epicar- farction.) Small, normal Q-waves are some- dium to endocardium and relax, the vector times referred to as septal Q-waves. of ventricular repolarization is directed to- ward the lead on the left chest wall, which The impulse spreads rapidly and almost si- causes an upright deflection, the T-wave. multaneously from the interventricular sep- (One might expect a similar, albeit smaller, tum via the Purkinje network to the right wave for atrial repolarization. However, and left ventricles where the net vector for atrial repolarization occurs during ventricu-

41 lar depolarization and is, presumably, ob- of the R wave. It represents the time re- scured by the much larger QRS complex.) quired for the atria to depolarize and for Immediately following the T wave a small the impulse to be conducted through the upright deflection is sometimes seen (e.g., AV node and along the His-Purkinje net- with hypokalemia. This is a U wave. Its ori- work. The PR interval is primarily affected gin is uncertain. It may represent delayed by changes in conduction at the AV node. after-depolarizations of ventricular muscle When conduction is abnormally slowed or delayed repolarization of Purkinje (i.e., in first degree AV block), the PR inter- fibers with electrolyte imbalance. val is prolonged to more than 0.20 sec- onds (more than 1 large box). When con- C. Intervals duction is abnormally fast (e.g., in Wolff- Parkinson-White and Lown-Ganong-Levine syndromes), the PR interval is shortened to Table 2-1.Normal Values for ECG Waves less than 0.12 seconds. and Intervals The QRS interval is the time interval from Duration (seconds) Comment beginning of the Q-wave (or more often the PR 0.12 - 0.20 <1 large box R wave because there is no Q-wave) to the end of the S-wave. It represents the time Q < 0.04 <1 small box required for the ventricles to depolarize. QRS 0.05 - 0.10 <2.5 small boxes This interval is normally less than 0.10 sec- onds, so the QRS complex fits into 2.5 QT 0.40 2 large boxes (Only if heart rate = 60 /min.) small boxes. This interval is prolonged to more than 0.12 seconds in bundle branch QTc 0.40 blocks. Wide QRS complexes are also seen in the Wolff-Parkinson-White syn- Table 2-1 gives normal values for the dura- drome. tion of EKG waves and intervals expressed The QT interval is the time interval from the both in seconds and in number of boxes beginning of the Q-wave (or R-wave) to the on the EKG graph paper. end of the T-wave. It reflects the duration The PR interval is the time interval from the of cardiac systole and varies with age and beginning of the P-wave to the beginning heart rate. At a heart rate of 60 beats per

42 minute, the QT interval is 0.40 seconds or that digitalis increases myocardial contrac- the width of 2 large boxes. The QT interval tility by raising the level of intracellular cal- is usually less than one-half of the RR inter- cium. val at normal heart rates, reflecting the fact that systole is normally shorter than dias- The ST segment extends from the end of tole. At a heart rate of 60 beats/min, for in- the S-wave (the J-point) to the beginning stance, the RR interval equals one second of the T-wave. This segment is normally (i.e., 5 large boxes between R-waves), and flat and has the same voltage as the base- the heart spends 40% of the time in sys- line just before the QRS complex (i.e., this tole and 60% in diastole. As heart rate in- segment is isoelectric). Depression or ele- creases, the RR interval (and the cardiac vation of this segment is often associated cycle) is shortened, but diastole is short- with myocardial ischemia, but nonspecific ened more than is systole. The following changes are also seen quite commonly. ST equation corrects the observed QT interval segments are raised in pericarditis, for in- for heart rate: stance, and depressed in patients on digi- talis. QTc = QT divided by the square root of RR where QTc is the observed QT interval cor- rected for heart rate. At a heart rate of 60 beats/min, for example, the QTc interval equals the QT interval (0.40 seconds di- vided by the square root of 1 equals 0.40 seconds). The QT interval defines the dura- tion of systole and, as such, reflects the ve- locity of ventricular contraction and relaxa- tion. In patients with hypercalcemia, for in- stance, the QT interval is shortened, while it is longer than normal with hypocalcemia. The QT interval is also longer than normal in patients with congestive heart failure; fol- lowing treatment with digitalis the QT inter- val shortens again. It is interesting to note

43 4

EKG Leads Einthoven’s Standard Leads

Movie 3-5

Lecture 2-5: Einthoven’s Triangle Time: 3:19 minutes Learning Objective: Know how to attach the standard leads I, II, and III to the limbs, and appreciate which end of each lead is positive and which is negative.

45 Figure 2-4

Fig.2-4. Einthoven's standard limb leads. The attachment of electrodes to various limbs and their polarities are shown. The positive poles of these standard limb leads sense de- polarization of atria and ventricles directed toward 0 degrees (lead I), +60 degrees (lead II), or +120 degrees (lead III) (in the frontal plane).

46 The Limb Leads Einthoven used three sets of electrodes (or leads) to record voltage changes across the heart during the cardiac cycle (Fig.2-4). With lead I he compared the voltage be- tween the right arm (negative pole) and the left arm (positive pole), with lead II the volt- age between the right arm (negative pole) and left leg (positive pole), and with lead III the voltage between the left arm (negative pole) and left leg (positive pole). The di- poles measured by these three sets of leads are approximately 60 degrees apart in the frontal plane, forming a triangle around the heart (Einthoven's triangle). Thus, the dipole (or vector) measured in lead II is 60 degrees removed from the di- pole in lead I (which is directed toward 0 degrees); whereas, the dipole in lead III is 120 degrees removed from the dipole in lead I. These three leads are referred to as the standard limb leads. Although the elec- trodes are usually strapped to the limbs (close to the wrists and ankles), identical records would be obtained if electrodes were attached to the corners of a triangle formed by the two shoulders and the pu- bis. This is because body fluids readily con- duct electrical currents, not only from the heart to the surfaces of the chest, but also along the limbs.

47 The Augmented Leads

Movie 2-6

Lecture 2-6: Augmented Leads Time: 2:02 minutes Learning Objective: 1. Know the angles of the standard and augmented limb leads. 2. Understand the relative sizes of the R- and S-waves when the mean cardiac vector is pointing (a) toward or (b) away from a given lead.

48 Figure 2.5 aVR aVL o -150 o -30

o 0

I

+120 o o +90 o +60 Mean QRS Axis

III II aVF

Fig. 2-5. The standard and augmented limb leads. The relative positions from which the standard and augmented limb leads record cardiac vectors are shown with typical ECG patterns for each for a normal heart with a mean QRS axis of +60 degrees. Note that a vector directed toward a lead will result in an upward deflection (R wave) and a vector directed away from a lead in a downward deflection (S wave).

The three standard leads probe cardiac the standard limb leads. The augmented vectors only at 60 degree intervals. Wilson leads did not require placement of addi- developed three additional leads, the aug- tional electrodes but simply involved elec- mented limb leads, to sample cardiac vec- trical manipulations of the three standard tors at 30 degree intervals. They were leads already present on arms and leg. In called augmented leads, because he had aVR (augmented voltage right arm) the to augment their voltages to equal those of right arm (now positive) was compared to

49 both other limb leads, in aVL (augmented coming toward us nor would it be moving voltage left arm) the left arm (positive) was away. In other words, the vector would be compared with the other limb leads, and in exactly 90 degrees removed from our point aVF (augmented voltage left foot) the left of view, so that the average vector would foot (positive) was compared with both equal zero. A mean QRS vector of zero im- other leads. Lead aVR views cardiac vec- plies that the R-wave is equal in magni- tors from the perspective of the right shoul- tude (i.e., in mV or mm) to the S-wave in der (-150 degrees), aVL from the left shoul- aVL (the septal Q-wave is too small to mat- der (-30 degrees) and aVF from the feet ter) as is illustrated in Figure 2-5. (+90 degrees) (see Fig. 2-5 for a summary of all the limb leads). Leads I and aVL view the electrical activity of the heart (in the frontal plane) from its lat- The average, normal heart is situated in eral aspect. They are the lateral limb leads. the chest in such a way that the average Leads II, III, and aVF examine the electrical vector during ventricular depolarization activity of the heart (in the frontal plane) (the mean QRS axis in the frontal plane) is from its inferior aspect. They are the infe- toward +60 degrees. In such a heart the rior limb leads. Lead aVR does not fit ei- major vector during ventricular depolariza- ther of these classifications. Situated at tion will be toward lead II. Accordingly, one the right shoulder, this lead sees similar in- would expect to see the tallest R-wave in formation to lead II, except it is all in re- lead II (recall that depolarization of the ven- verse. (Thus, the apparent Q-wave in aVR tricle toward a lead gives an upward deflec- is really an inverted R-wave and does not tion on the EKG tracing). This is illustrated signify infarction as large Q-waves do in in Figure 2-5. other leads.)

Each of the other leads views the very same QRS vector, but simply from a differ- ent angle or from a different point of view. For instance, let us pretend to be viewing this mean QRS vector that is directed at +60 degrees from the point of view of aVL (-30 degrees) which is at the left shoulder. The mean QRS vector would be neither

50 The Precordial Leads

Movie 2-7

Lecture 2-7: The Precordial Leads Time: 6:26 minutes Learning Objectives: 1. Know where to place the precordial leads on a patient’s chest. 2. Why does the R-wave get taller (and the S-wave smaller) in progressing from lead V1 to V5? 3. What is the R-wave in V1 and the S-wave in V6 due to? 4. What is the significance of a missing R-wave in V1?

51 Figure 2.6

Between V2 and V4 4th intercostal space, 5th intercostal space, left of sternum mid-clavicular line 4th intercostal space, right of sternum 5th intercostal space, anterior axillary line V1 V 2 V 3 5th intercostal space, V4 V5 V 6 midaxillary line

Back

Chest wall Cross-sectional view of heart and chest wall

V 6

V5 Sternum V4 V3 V1 V 2 Front

Fig.2-6. The precordial leads. Placement of the precordial leads on the chest is shown with typical ECG complexes for these leads in a normal heart (top). The relationship of the precordial leads to the underlying structures of the heart are depicted in a cross-sectional (or horizontal) view of the chest (bottom).

52 The Precordial Leads vector directed away from a lead will cause a downward deflection. It would seem that the six limb leads should suffice to detect any abnormalities The small R-wave normally seen in V1 and since they all show the same electrical V2 (Fig.2-6) is caused by septal depolariza- events merely from different angles. In- tion in an anterior direction. The same vec- deed, a single lead - as is used on cardiac tor is seen in V5 and V6 as a small (septal) monitors - is adequate for diagnosing ab- Q-wave. (A missing R-wave in V1 and V2 normalities in cardiac rhythm. However, if suggests a myocardial infarction of the sep- one wants to localize a myocardial infarct tum). As the main muscle mass of the ven- or hypertrophy of a heart chamber, six pre- tricle depolarizes, the main vector is away cordial leads are needed to view cardiac from V1 and V2 and toward V5 and V6, vectors from a horizontal plane in addition which results in deep S-waves in V1 and to the six limb leads that view cardiac vec- V2 and tall R-waves in V5 and V6. Thus, in tors only from the frontal plane. a normal ECG one expects to find a smooth progression of increasingly tall R- Unlike the limb leads, which may be waves as one moves from the right toward placed anywhere along an arm or leg (or the left precordial leads (i.e., from V1 to even in a triangular arrangement on the V5). Lead V6 is a little further from the left chest and abdomen around the heart), the ventricle than V5, so that the R-wave is precordial leads must be placed in special usually a little smaller in V6 than it is in V5. positions over the heart on the chest wall (see Fig. 2-6). The right anterior chest leads, V1 and V2, are close to the right atrium and the right ventricle; whereas, the left anterior chest leads, V5 and V6, are close to the left ventricle (Fig.2-6). Leads V3 and V4 are in between, i.e., they are situated over the interventricular septum. All precordial leads represent the positive pole of unipolar electrodes, so that a wave of depolarization toward any one lead will cause an upward deflection; whereas, a

53 5

Review Multiple Choice Questions

55 Review 2-1.Please select the one best answer.

Question 1 of 10 The first ventricular muscle cell to repolarize is the

A. endocardial cell

B. purkinje cell

C. epicardial cell

D. first cell to depolarize

Check Answer Drag to Target Questions

57 Review 2-2 .Please drag labels to appropriate targets.

Question 1 of 10 In a STEMI (ST-segment elevation MI) involving the septum, anterior or lateral aspects of the myocardium the following leads are affected.

Lateral Septal Anterior

Septal Anterior Lateral

Check Answer Interactive Questions

59 Interactive 2.1 Depolarization and Repolarization of the Left Ventricle Voltmeter - + Electrode A + + + + + + Na Na Na Na Na Na 25 mm/second ECG - + machine m V + + + + + + 1 Na Na Na Na Na Na Endocardial Epicardial 0.2 sec cell cell - + Gap Depolarization B junction + + + Na Na Na + + + ECG Na Na Na machine - + + + Na Na Na+ + + + Na Na Na - +

C + + + + + + Na Na Na Na Na Na What does the R-wave on ECG - + machine + + + + + Na Na Nathe+ Na EKGNa Na represent? - + What does the T-wave on D + + + Repolarization the EKG represent? K K K + + + Na Na Na ECG - + machine + + + Na Na Na + + + K K K - + E + + + + + + K K K K K K R T ECG - + machine

+ + + + + + K K K K K K

Voltmeter

Intracellular Recording Endocardial cell F mV Voltage Recorder -90 Time Endocardial Epicardial Epicardial cell cell cell Interactive 2.2: Depolarization and Repolarization of the ventricle.

Why is the last cell to depolarize the first to repolarize ?

A B Endocardial cell

Repolari- zation 0 3 Depolari- Depolari- Repolari- zation zation zation

Epicardium Epicardial cell Endocardium Time

Explain how an impulse arrives at epicardial cells of the left ventricle starting at the SA node. Interactive 2.3

- + A + + + K K K + + + Na Na Na ECG - + machine + + + Na Na Na + + + K K K T-wave inversion in ischemia VoltmeterYour patient is complaining of chest pain while running on a treadmill dur- ing a stress test. This is his EKG. Ex- Intracellularplain. microelectrode Intracellular Recording B Endocardial cell

Voltage Recorder -90 mV Endocardial Epicardial Time cell swollen cell (normal) Epicardial cell due to ischemia Interactive 2.4 Waves and Intervals of the EKG

A. Cardiac Vectors

P S

T Q ECG R +

B. Waves If this wave were wider than 0.04 sec- R onds and deeper +1 If this interval were P T than 1/4th of the R- U wave, your patient --- longer than shownmV here,0 your patient --- Q -1 S C. Intervals RR interval

+1 PR interval ST interval

mV 0 J-point -1 QT interval

0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 Seconds Interactive 2.5 Standard Leads of the EKG

You see a tall R-wave in this lead. There- fore the main vector of ventricular depo- larization is pointing ---

You see a tall R-wave in this lead. There- fore the main vector of ventricular depo- larization is pointing --- Interactive 2.6 Standard and Augmented Leads

You see a tall R-wave in this lead. There- fore the main vector of ventricular depo- larization is pointing --- aVR aVL o -150 o -30

o 0

I

You see a tall oR-wave in this lead.+120 There- You see a deep S- o fore, the main vector o wave in this lead. +90 +60 of ventricular depo- MeanTherefore QRS Axis the main larization is pointing vector of ventricular --- III depolarization is II pointing --- aVF Interactive 2.7

This wave is due to

This wave is due to

V1 V 2 V3

V4 V5 Essay or Small Group Questions

67 A. Essay/Small Group Discussion Ques- lar muscle strip toward the negative pole tions. of a lead wire?

Depolarization and Repolarization of Cardiac Vectors and Waves Ventricles 6. Explain how a P-wave, a QRS com- 1. Why does a wave of depolarization plex, and a T-wave is generated on an sweeps over the left ventricle from right to ECG tracing. left and over the right ventricle from left to ECG Intervals right? 7. When is a P-R interval too long and 2. What are the vectors of depolarization what does this observation imply? for the inter-ventricular septum? 8. Which interval of an ECG tracing corre- Depolarization of a Ventricular Muscle sponds to systole? Strip 7. What does the R-R interval of an ECG 3. Why does the ECG machine records an tracing represent? upright wave, i.e., an R-wave, when a wave of depolarization is moving along a Standard Limb Leads ventricular muscle strip toward the positive pole of a lead wire? 8. How are the standard leads I, II, and III attached to your patient? Also indicate 4. Why is an isoelectric line recorded both which end of each lead is positive and before and after depolarization of a ven- which is negative. tricular muscle strip, and where are these lines on an ECG tracing? Standard and Augmented Leads

Repolarization of a Ventricular Muscle 9. What are the angles of the standard Strip and augmented limb leads relative to lead I? 5. Why does the ECG machine record an upright wave, i.e., a T-wave, when a wave 10. What are the relative sizes of the R- of repolarization is moving along a ventricu- and S-waves when the mean cardiac

68 vector is pointing (a) toward and (b) away from a given lead?

Precordial Leads

11. Where do you place the precordial leads on a patient’s chest?

12. Why does the R-wave get taller (and the S-wave smaller) in progressing from lead V1 to V5?

13. What does the R-wave in lead V1 and a Q-wave in V5 represent in a normal heart?

14. Please explain the origin of a biphasic P- wave which is often seen in V1.

69 6

EKG Pre-Test True/False Pre-test Questions

71 EKG Pre-Test: The EKG shown below is normal.

Question 1 of 10

A. true

B. false

Check Answer

7 More Episodes in iBooks

Physiology as a Country Doc

Series 1. Cardiac Physiology as a Country Doc

by Patrick Eggena, M.D.

Episode 1. Electrophysiology

Episode 2. The EKG

Episode 3. Heart Attack

Episode 4. Irregular Beats

Episode 5. Excitation-Contraction

Episode 6. The Heart as a Pump

Episode 7. Murmurs and Gallops

73