Cardiac Physiology as a Country Doc Episode 4: Irregular Beats

Patrick Eggena, M.D. Novateur Medmedia EPISODE 4

IRREGULAR BEATS

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 978-0-9905771-3-3 Cardiac Physiology as a Country Doc, Episode 4: Irregular Beats

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 fourth 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 lecture given by the author to First Year Medical Students. Video tapes of these lectures are di- vided 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 father 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 Gymnasium, 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 Asso- ciation 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 Chair- man 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 understand- ing of Physiology to everyday patient care at the bedside.

Students at The Mount Sinai Medical School showed their appreciation for his teach- ing 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 pages.

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 4-a The Situation

Introduction to the case Time: 1:29 minutes

12 Movie 4-b Cardiac Monitor

13 “Doc, come fast --Mr. Jones is not breath- Movie 4-c ing.”

You run into the treatment room.

“Mr. Jones --are you alright?” You ask shaking him by the shoulders.

No answer.

You look up at the monitor.

Kay is getting the defibrillator ready He’s in V-Fib. “Yes, Doc --got it.” “Kay, I’ll do CPR. “Now attach the two leads and bring them You get the defibrillator.” over here. “ “Alright, Doc --will do.” She moves the defibrillator into position You don’t bother with his breathing. next to Mr. Jones.

Start compressing his lower sternum --fast “Where on the chest do you want me to --about 100/min--- and deep --about 2 put the pads, Doc?” inches. “One up on the right chest just below the “Doc, are you going to use paddles or clavicle, the other over here on the left pads?” chest by the axilla --we want the current to flow across his heart.” “The machine is already hooked up for pads --just pull off the safety cap, take the “Right, Doc.” pads out off the bag. See here (Fig. 4-c)?” She sticks the pads onto Mr. Jones’ chest.

14 The jolt lifts Mr. Jones’ upper torso up off the stretcher as his muscles contract.

“It didn’t work, Kay --he’s still in V-fib.”

You immediately start compressing his chest again.

“Kay, please get 1 mg epinephrine from the crash cart.”

“Doc, it’s good that we already have an IV line in, isn’t it?”

“Good, now turn the green dial to 150 “Yes, it is. Please give it now with a 10 cc joules and push the charge button,” you flush of normal saline.” say while compressing his chest. “Doc, it’s in. What next?” “Like this, Doc?” “I’m going to give him two breaths --blow- “Yes, that’s good. Please don’t push the ing through the face mask --- and then I’m shock button -- I’ll do that.” going to shock him again. This time with 200 joules.” You stop with chest compressions.

“Stand clear, Kay. I’m going to shock him.”

You make sure Kay is not touching the stretcher.

You press the shock button --the one with the lightening.

“Okay --shock delivered !” “Doc, it’s charging --I’m clear.”

15 “Shock delivered!” tion and try again. Don’t worry --he’s get- ting some air from my chest compres- Another jolt -- sions.”

“Kay, please get the Ambu-bag so we can She tries again. Still can’t do it. give him some fresh air with oxygen. ---don’t want to keep on blowing through “Kay, would you please take over com- the mask every thirty compressions.” pressing his chest? I’m getting tired.”

“Sure, Doc --I know how.”

“And I’ll put in an airway that will keep his tongue from falling back into his throat.”

Kay takes over compressing his chest while you insert the airway -- first upside down into his mouth and then --with a twist --rotate it into position behind his tongue.

“Kay, stop compressing for a moment while I give him some oxygen.” His chest rises as you blow two breaths into his She attaches the oxygen line to the Ambu- lungs. bag, places the face mask over Mr. Jones’ mouth and nose and gives two breaths. “Kay--look here how I hold the mask firmly over his nose and mouth by forming a His chest does not rise in response. Air is clamp with my thumb and two fingers leaking around the face mask. Kay is start- ---shaped into a “C” configuration.” ing to get nervous. “Yes, Doc --looks easier than it is.” “Doc, it’s not working --can’t get the air in.” “You’ll get a chance in a little while, but first keep pushing down a little harder “You’re almost there, Kay. It’s difficult. --chest should cave in about 2 inches!” Move his chin up into the “sniffing” posi-

16 “I’m trying, Doc ---pushing as hard as I “Alright --I’m going to give him vaso- can, but the mattress is giving way --- it’s pressin instead of the second dose of epi- too soft. nephrine.”

Should we put him on the floor?” “Whatever, Doc.”

“No --he’s too heavy. Let’s take the front “40 units vasopressin going in.” panel off the crash-cart --it’s designed to function as a board for this purpose.” You flush with 20 cc normal saline and af- ter about 1 minute you charge the defibrilla- You remove the panel and slide it under his tor again to its maximum of 200 joules. back. “Kay, stand clear --here comes another “That’s much better now, Doc,” Kay says shock.” as she continues chest compressions. Kay stops compressing and stands back. “I’m going to inject Amiodarone now. Where is it?”

“It’s in the upper drawer of the crash cart. Do you want me to get it?”

“No, no Kay, I’ll find it. You keep on push- ing down -- hard and fast.”

“I’m trying, Doc.”

You look in the upper drawer.

“I found it --.” And shortly after: “200 joule shock delivered.”

“300 mg of Amiodarone going in.

Kay, has it been about 3 minutes since we gave the epinephrine?”

“Think so, Doc -- perhaps 4 or 5 minutes.”

17 “Keep up with the compressions. I’m go- ing to check his PETCO2.”

You attach the capno-meter to the endotra- cheal tube.

The meter shows a maximum reading of 20 mmHg PCO2 as Kay forces the last bit of air out of his lungs at the end of com- pressions.

“Kay --the meter here says that you are do- ing an excellent job with your compres- “Kay, he’s still in V-Fib. ---Can you keep on sions.” compressing his chest? --- I need to intu- bate him. Will you be alright?” “Really?”

“Yes, Doc --I’m hanging in there.” “Yes, that’s what the gadget here says. You are squeezing the heart well enough to You manage to slide a size 7 endotracheal move the blood all the way around to his tube past his vocal chords into his trachea lungs, where he is now exhaling a reason- with a laryngoscope, fill the balloon near able amount of CO2.” its tip with air to hold it in place, attach the Ambu-bag, and blow two breaths into the “What’s perfect, Doc.” tube while Kay is listening below over his stomach for gurgling sounds with a stetho- “About 40 mmHg --but you can’t get there scope. with external cardiac massage. We’ll have to wait until his heart starts pumping on its “Can’t hear a thing, Doc --certainly no gur- own.” gling sounds.” “When will that be, Doc? I’m getting pretty “That’s good, Kay ---means we are in the tired. right place--not blowing air into his stom- ach. --Oh, no --I think he’s going to throw up.”

18 Mr. Jones is retching and vomitus is com- “150 of Amiodarone going in, Doc.” ing up around the endotracheal tube onto your lap. “Great --charge the defibrillator.”

“Doc, he got you good. Do you want me to “200 joules again, Doc?” suction him?” “Yes, please.”

“Yes, please --I’ll take over now with com- “Stand clear ---200 joule shock delivered.” pressions. You can give him one breath with the Ambu-bag about every 6 seconds You look up at the screen. This is what or so. I won’t have to stop compressions you see (Fig.4-g). while you doing it --now that we have a tube in.” “We did it, Doc ---we did it. --- He has a rhythm.”

Kay takes the cover off the Gomco and “Yes, Kay --but does he have the beat --a suctions vomitus from Mr. Jones‘ mouth. pulse?”

“Kay, please give Mr. Jones an injection of “I’ll check.” 150 mg Amiodarone and follow it with a 10 Kay feels for his carotid --5, 6, 7, -- 8 sec- ml flush of normal saline.” onds --. She looks over to you. About a minute later: “No pulse yet, Doc --that I can feel.”

19 You double check. --She’s right. -- He has “Kay, can you hold off with the breathing no pulse! for a moment to give him another 1 mg of epinephrine? I’m going to keep on com- “Sorry, Kay --we’re not done yet --need to pressing his chest.” continue CPR.” Kay gives him the injection and then picks “What’s wrong?” up the Ambu-bag and gives him three big breaths one right after another. “He has PEA --Pulseless Electrical Activ- ity.” “Kay, that’s too much. Just squeeze the bag so it empties about half-way --and “What do we do for that?” only once every 6 seconds or so.” “We have to keep doing CPR and giving “Doc, I want to make sure he is not hypoxe- him epinephrine every 5 minutes or so mic.” --and, meanwhile, look for causes that we might be able to reverse. “ “He needs oxygen, but every time you push air in, you squeeze down on the ves- “Like what?” sels in the lung --- less blood runs into the “Hypoxemia or hypovolemia.” heart and it pumps less out.”

“He’s not hypoxemic, Doc, with all the oxy- “Got it Doc, I’ll slow down ---about 10 gen we are giving him. And I can see his breaths/minute?” chest expand as I blow air into his lungs. “Yes, that’s perfect.” And you said yourself with that capno- thing that we were doing fine with CPR.” “Doc, the IV bag is almost empty. Do you want me to check his pulse again?” “I agree. Let’s increase his preload. Let’s infuse --as a bolus -- what’s left of the 500 “Yes, please do.” cc of normal saline we already have hang- ing up there.” She slides 2 fingers into the grove along his trachea ---eyes fixed on her fingers as Kay fumbles with the IV line to increase the if she could see what she is feeling. flow rate.

20 “Doc, I can feel a pulse. It’s weak, but it’s sure. We’d like to get it above 90 before there.” we put him in the ambulance.”

“What is his blood pressure?” “Oh, Doc --I hope he makes it --hope he wakes up and every thing’s working.” She blows up the cuff around his arm and listens over his brachial artery with her “I hope so too, Kay.” stethoscope.

“ It’s about 70/40.”

You notice that he is now attempting to breathe on his own. His abdomen is mov- ing out as his diaphragm contracts --pull- ing oxygen enriched air into his lungs.

“He’s breathing on his own, Doc, --- but he’s not waking up.”

“Doc, I can hear the ambulance in the dis- tance. It will be here soon.”

“Do we have normal saline in the refrigera- tor?”

“Yes, I believe so. Do you want me to get it?”

“Yes please.“

She brings 1 liter of cold, normal saline.

“Kay, let’s run this in as a bolus --as fast as possible --it may protect his brain from fur- ther damage and also raise his blood pres-

21 3. Heron, Horses, Deer --and Ticks.

Movie 4-d. The Heron and the Horses.

Time: 1:08

22 The Discussion

“Oh, I got bitten by a deer tick. Just no- ticed a “bulls eye” on my leg.”

“Let me see (Fig 4g).”

“Yupp --that’s Lyme disease alright. I’ll get the Doxycycline.”

She finds the medicine and soon returns with a smile on her face, carrying a piece of bread, a 100 mg Doxycycline capsule, and a cup of water. “Kay --do we have Doxycycline?” “Here, take this now and one this evening “Yes, I believe so, what do you want it with food and keep doing this for two for?” weeks.”

23 “Kay, you’re already talking like a Nurse “But you already had the machine set up Practitioner.” for pads instead of paddles. Why?”

“I’m getting there. “First of all, they work just as well. Sec- ondly, you have your hands free to do Doc --you know -- we did good with Mr. other things. And thirdly, if you have to Jones.” switch the machine for synchronized car- dioversion or transcutaneous pacemaker, “Yes, Kay, we were lucky --so far -- I you can use the same pads for every- hope.” thing.” “Doc, I have a question about the defibrilla- “I see.” tor --it all happened so fast. “Now you first gave a shock of 150 joules On TV in ER they always use the paddles. and after that always the maximum of 200 Why didn’t we use them?” joules.” “Paddles make a bigger impression on TV, “I could have gone right away to the maxi- but I also use them on a patient with a mum that the machine will do. It differs hairy chest where the pads don’t stick well with different manufacturers. I wanted to to the skin --you know you have to make see if a smaller shock would do the trick electrical contact with the skin to defibril- and then increase the joules as needed.” late?” “But always from low to high?” “Makes sense. Mr. Jones doesn’t have a hairy chest.” “Yes --that’s right --not the other way.”

“Well --even if he did, we could shaved “Doc, you said I was doing good when him --which takes time --or we could still you looked at the capno-something. I use the pads --pretty good glue on them didn’t understand how this works.” --and then rip them right off with the hair.” “It’s a little complicated. “Ouch!” As you are sitting there resting, you are “Yes --and then put fresh pads on the consuming about 250 ml of oxygen every skin.”

24 minute and producing 200 ml/min of car- “The capno-meter measures the partial bon dioxide which has to be exhaled by pressure of CO2 in exhaled air --measured your lungs.” in mmHg ---rather than the amount -- measured in milliliters. “But you said 40 --not 200 --was perfect.”

25 You see, the CO2 in your blood is dis- of exhaling your tidal volume --that is --at solved and not in gas form. As these dis- the end of a normal breath-out.” solved molecules move about and bump into each other and other gas molecules, “Why only at the end?” they create pressure. It’s only “partial” be- “The first air you breathe out has no CO2 cause the other gas molecules, such as in it because it comes from your mouth, oxygen and nitrogen, make up the rest pharynx, larynx, trachea and large airways --raising the total to atmospheric pressure --the so-called anatomic dead space. It’s of 760 mmHg at sea level. Look here at the not involved in exchanging oxygen for picture (Fig. 4h). “ CO2.”

“That’s too complicated, Doc.” “Right, we learned that. Gas exchange

“It’s like the CO2 in a bottle of Coca Cola only happens down deep in alveoli.” --it’s in solution and only becomes a gas “Yes, that’s where the last part of what you when you open the bottle and it fizzles exhale comes from --the alveoli or respira- out.” tory zone --where gases in the lung and

“Okay, so the CO2 fizzles out of the blood blood equilibrate.” in the lung, but what’s the partial pressure “So you are saying that PETCO2 is the of CO2 in blood?” same as CO2 in arterial blood?”

“It’s about 40 mmHg in arterial blood and “A little lower, but almost the same.” 46 in venous blood. The difference being what the arterial blood picks up as it “So, if you have a low PETCO2 reading moves through the tissues-- and a little that means your arterial CO2 is low?” later gives off as gas as it moves through the lungs.” “Oh Kay, --not always.

“Alright, enough about the “P” part of PET- First of all, if your PETCO2 is zero, your en- CO2. What about the “ET” part?” dotracheal tube is probably in the esopha- gus rather than the trachea. That’s a real “ET stands for End Tidal --it means the problem. That is why we do the measure- measurement of CO2 is made at the end

26 ment in the first place --to make sure we Is that a possibility here? When I was venti- are in the trachea.” lating Mr. Jones too much and you were perhaps pressing too hard on his chest?” “--and also that’s why you had me listen over his stomach after you pushed air in.” “Good thinking. Yes, indeed, if you were to hyperventilate by breathing twice as “Right. --Now if the PETCO2 is less than much as you need to, your arterial blood 10 mmHg in our situation --that is during PCO2 would drop to 20 mmHg and you resuscitation and you are sure that you are would feel dizzy (from “normal” to point in the trachea -- it suggests that blood “A” in Fig.4i). This is what would happen flow to the lungs is so sluggish that only lit- if you had hyperventilated Mr. Jones with tle CO2 is being delivered to the lungs to the Ambu-bag. His PaCO2 would have be exhaled.” been low and his pH high, i.e., a respira-

“Makes sense, Doc.” Figure 4i “But if the PETCO2 value is 20 mmHg --as it was when you were doing cardiac mas- sage --it means that you were doing a very good job in generating cardiac output and making blood flow through the lungs.”

“So we learned in our Respiratory lectures that when you over-ventilate, you blow-off CO2 and lower your CO2 level in blood and get a respiratory alkalosis. And that makes you feel dizzy or even faint --and Generating a respiratory alkalosis by volun- you then have to breathe into a paper bag tary hyperventilating (normal to point A). and you’re alright again. Like in this figure The alkalosis is rapidly corrected by raising here (Fig. 4i) moving back from point A to PaCO2 from 20 mmHg back to 40 mmHg by breathing into a paper bag. With prolonged Normal. hyperventilation the kidney compensates (A to C) by excreting bicarbonate into urine.

27 tory alkalosis with an arterial blood pH “That’s alright, we can calculate it. The above 7.40.” oxygen concentration is always 21%.”

“Doc --but as is shown in the figure (Fig.4i “No matter how high up you are, Doc?” A to C), his kidneys would have returned his pH back to normal --would have com- “Yes --unless you are in a satellite in outer pensated?” space. So the partial pressure of oxygen you would be breathing on the mountain “Eventually --in a few days --yes, but not would be 21% of the atmospheric pres- acutely within minutes.” sure or 0.21x548 mmHg = 115 mmHg.”

“Are there actually patients who breathe “Doc, this is quite a bit lower than the PO2 too much all the time?” of 160 mmHg that we are breathing right now. That’s what it says in figure 4h. ” “Yes --patients with stiff lungs --like coal miners with Interstitial Fibrosis --or you on “Correct. Now as you breathe in the dry a trip to Peru high up in the Mountains at air up on the mountain, the partial pressure the Inca ruins in Machu Picchu.” of oxygen falls, because you have to make room for the vapor pressure which is 47 “I’d like that. A paid vacation from you, mmHg. Doc?” So in moist tracheal air your PO2 is now “Sorry, no --but look up on your i-Phone only 21% x (547-47) mmHg = 105 mmHg. what the partial pressure of oxygen would This air is drawn down into the alveoli be up there.” where oxygen is moving into blood and CO2 is being added. The CO2 in alveolar Kay takes out her phone and tries to look it gas (and in arterial blood) is regulated by up. chemoreceptors in the medulla. It’s value “Doc, it’s about 10,000 feet high or so is normally kept at 40 mmHg. Now a little --barometric pressure 547 mmHg --I think more oxygen is leaving alveolar gas than that’s today --no partial pressures or oxy- CO2 is entering, the exchange ratio (CO2/ gen concentrations that I can find.” O2) being 0.8 on the average American diet which you are eating. Right?”

28 “Guess so, Doc.” respiratory alkalosis with a pH somewhere above 7.5.” “So we have to subtract the 50 mmHg (40 mmHg/0.8 = 50 mmHg) of oxygen mole- “I see, Doc, but you said that my kidneys cules that are leaving alveolar gas from the would now start to compensate --trying to 105 mmHg --- which is 55 mmHg. This is get my blood pH back to the normal value what the oxygen tension (or PAO2) would of 7.4. So my question is: how do my kid- be in your alveolar gas up on the moun- neys know that I’m up there at Machu Pic- tain. chu hyperventilating on my vacation?”

Now there is normally a small --about 3 “Let’s look over here at this figure (Fig 4j.) mmHg --difference in oxygen tensions be- The blood from your lungs -- where you tween alveolar gas and arterial blood. have blown of CO2 -- reaches your kid- Thus -- finally -- we estimate that your neys and diffuses into cells. There CO2 is PaO2 up on the mountain would be hydrated with an enzyme (carbonic anhy- roughly 50 mmHg.” drase) to form carbonic acid which, in turn, dissociates to form hydrogen ions and bi- “And what would that do to me, Doc?” carbonate ions. Now because there is less CO2, fewer bicarbonate ions are made (or “It would stimulate your peripheral chemo- retrieved from forming urine) and returned receptors in the carotid bodies and make to blood. So the concentration of bicar- you hyperventilate.” bonate in blood slowly drops and with it “By how much?” the pH of blood declines in the direction of normal. That’s basically it --in a nut shell.” “I don’t know. And I think it varies consid- erably from one person to the next. But “Pretty complicated, Doc. But what’s so let’s assume it doubles your alveolar venti- bad about having a respiratory alkalosis lation. This would decrease your PaCO2 for a little while?” from 40 mmHg to 20 mmHg and, accord- “It predisposes to seizures and cardiac ar- ingly, your bicarbonate concentration in ar- rhythmias.” terial blood would drop from 24 to about 20 meq/L and you would have an acute “Oh --that’s important. Good thing we were careful in not over-ventilating Mr.

29 Figure 4j.

FIG. 4j. Renal compensation for a respiratory alkalosis at Machu Picchu (atmospheric pres- sure ~548 mmHg). Hypoxia stimulates peripheral chemoreceptors causing hyperventilation and a fall in PCO2 in arterial blood and in renal tubular cells from 40 to 20 mmHg. Fewer hydro- gen and bicarbonate ions form in tubular cells and are secreted into tubular fluid or blood, re- spectively. Diminished secretion of hydrogen ions into tubular fluid allows some of the filtered bicarbonate ions to escape into urine. The number of H-ATPases in type A intercalated cells is decreased by the high intracellular pH which facilitates removal of ATPases from the luminal membrane and (possibly) recycling into storage vesicles. In type B intercalated cells, the high intracellular pH causes a switch of H-ATPases from the luminal to the basolateral membrane and of Cl/HCO3 antiporters from the basolateral to the luminal membrane, which results in ac- tive HCO3 secretion into urine. As blood bicarbonate concentration decreases, blood pH re- turns toward normal (A to C in Fig 4h). 30 Jones! “But you didn’t even look at the monitor right after you gave the shock, but immedi- However, Doc, you really went overboard ately started compressions.” with the chest compressions.” “Even if the shock works --as it finally did “You’re right. Nothing more important ex- for Mr. Jones --it may take a little while for cept for shocking as soon as possible.” a pacemaker in the heart to pick up the beat. That’s valuable time for keeping “Even more important than breathing?” blood flowing with cardiac massage.” “Yes --remember --you only gave 2 “What does the shock actually do?” breaths at the end of 30 compressions. “It depolarizes all cells in the heart at once First of all, when the chest wall snaps back --and after a short pause --the hope is that after having been pushed in, air is auto- some focus in the atria or ventricles will matically sucked into the lungs. pick up the beat.” Too much time is often wasted attempting “Where did Mr. Jones’ beat eventually to blow air into a patient in cardiac arrest come from?” and meanwhile you’re not compressing the heart. So blood is not moving through the “From the SA node with frequent PVCs in lungs to pick it up the oxygen anyhow.“ a bigeminal rhythm (see Figure 1-g).”

“Doc, you even kept on pushing down on “Doc, he wasn’t breathing ---and I had his chest while I was charging the defibrilla- trouble ventilating him with the Ambu-bag. tor --lucky I didn’t push the wrong button.” Is that why you intubated him?”

“Kay, I would have let you know. “No, no Kay --you would have done fine once the airway was in and his tongue no You see, the only blood --and not much at longer fell backwards and obstructed his that --which was flowing to Mr. Jones’ airways. We really needed to have better heart and brain was during external car- control of his ventilation, especially during diac compression.” transport in the ambulance. --And he would need to be intubated when he ar-

31 rived at the hospital if they were going to “Doc, they really should invent an easier put him on a mechanical ventilator.” way to get that breathing tube in.”

“It was also good to have it when he vom- “They actually have.” ited on you --right Doc?” “Why don’t we have it?” “Yes, the endotracheal tube with the in- flated cuff near its end protects the lungs “It’s too expensive ---don’t have to intu- from inhaling gastric contents.” bate that often.”

“That’s important, isn’t it, to keep his lungs “What is the instrument?” clean.” “Oh --it is sort of an electric eye on the

“Yes, he could have gotten aspiration end of the laryngoscope with which you pneumonia which is very difficult to treat can more readily see the vocal chords and and often fatal.” know just where to push the tip of the en- dotracheal tube. It’s much easier to use “I noticed, Doc, that you were really sweat- --but expensive, as I mentioned. They ing trying to get the tube into his trachea.” have them now in Emergency Rooms and in the OR for anesthesiologists.” “Yes, Kay, I took a little longer than I should have. --- I’m not so good at it. --- “Doc, why does it take so long to invent Not experienced like anesthesiologists things that seem so simple. I have had an who do this sort of thing every day.” electric eye on the back of my car for years to keep me from bumping into things “But we didn’t have a choice, right Doc?” when I back up.”

“No, Kay, we did have a choice --I didn’t “You are right, Kay. I often wonder too. have to do it --- Could have just stuck with the mask and Ambu-bag. Works perfectly There is actually another easy-to-use de- well if you keep a tight fit, with chin up, vice for establishing an airway in emer- and airway to keep the tongue from falling gency situations. It is essentially a short backwards and obstructing airflow.” endotracheal tube which you just slide into a patient’s pharynx by hand --without the use of a laryngoscope. Once you are in,

32 you simply blow up two balloons to keep it “Yes, some tissues --the brain and the in place --and that’s all --it’s so simple.” heart --but not everything else -- like the GI tract, kidneys, muscle, etc.” “So why bother at all with an endotracheal tube?” “But how do you keep from clamping down on the coronaries and brain vessels “Well, you need it for patients who have to as well?” be put on a ventilator --patients with exac- erbation of COPD, for example --heavy “They have fewer alpha-1 adrenergic recep- smokers --many of them.” tors. Hardly any in brain vessels, and in the coronaries there are beta adrenergic re- “And, also --as in Mr. Jones’ situation -- ceptors that vasodilate and powerful keeps vomitus from seeping into the lungs. autoregulatory mechanisms working We were lucky --got the tube in, just in through adenosine that see to it that the time.” coronaries remain open.”

“Yes, Kay, luck is an important part of suc- “But not in Mr. Jones --with his heart at- cess.” tack?”

“Doc, I’m going to let you have a cup of “True --a mechanical obstruction --a throm- tea and then I have some more questions. bus --can’t be dilated with adenosine. No, Is that alright?” he needed stents for that -- which he got.”

------“What about vasopressin? You said that you can use it instead of epinephrine. “So Doc, why did we give Mr. Jones epi- Does it act the same way.” nephrine after the first shock didn’t work?” “Same thing --except that different recep- “It was a high dose --works on alpha-1 re- tors are involved --V1 instead of alpha 1 ceptors --causes constriction of arteri- --and particularly strong vasoconstrictor oles.” effects in the GI tract.” “But you want the blood to flow to the tis- “We learned that vasopressin is another sues --don’t you?” name for ADH, the antidiuretic hormone. Isn’t that so?”

33 “Yes, but a different story and different re- Do you remember where this effect of ceptors --V2 receptors. They are activated Amiodarone takes place on the ventricular at much lower concentrations of vaso- muscle membrane potential, Kay?” pressin than we are talking about in Mr. Jones’ case.” “Is it phase 2?”

“I understand the dose difference, but the “No --potassium moves out of heart mus- V2 receptors should also be activated in cle during phase 3 of the action potential.” the kidneys. Shouldn’t they?” “Oh, right --I remember now --and phase 0

“Yes, but this has no practical effect on has to do with sodium ion entry?” anything, because Mr. Jones’ kidneys are “Correct --and this phase is actually also already shut down from the constrictor ac- inhibited by Amiodarone.” tions of high concentrations of epinephrine and circulating angiotensin II. “Slows conduction?”

You see, if no plasma is being filtered in “Right.” the renal glomeruli, there is little or no wa- ter in the renal collecting ducts that could “So was it the Amiodarone that stopped be reabsorbed back into blood by an ac- the fibrillation?” tion of ADH.” “I don’t know. Probably a combination of “Okay, so that’s not important here. What the drug, your good CPR, my shocking about Amiodarone?” and a lot of luck.”

“It blocks potassium channels -- prolongs “Yes, but that was not the end, because he the effective refractory period of ventricular had a rhythm without a pulse. muscle cells --may interrupt circular cur- We learned in Physiology that calcium ions rents from flowing between cells. That’s are involved in Excitation-Contraction Cou- the problem in ventricular fibrillation.” pling. That is why I was thinking of phase 2 “So Amiodarone stops the heart from quiv- before. ering ineffectively ---like a bag of worms?” So Doc, why didn’t we give him calcium “Hopefully. ions?”

34 “It’s true what you say about calcium ions “We would not have used cold saline if he coupling excitation with contraction, but it had awakened and understood what he turns out that in practice it doesn’t help in was asked. But he was unconscious when reversing PEA (Pulseless Electrical Activity) we were getting ready to put him in the am- to normal.” bulance. We didn’t know if he had a stroke or brain injury from lack of blood “Why not?” flow during resuscitation.”

“It is likely that Mr. Jones actually had a “I saw on TV someone who was found pulse but that it was so weak that you dead --buried in snow-- only to wake up could not feel it.” and be alright once he was thawed out.”

“So excitation was coupled to contraction “Yes, it can happen. Same principle here in his case?” with Mr. Jones --lower metabolism by in- ducing hypothermia --- protect the brain “Yes--his heart was contracting, but be- from further damage.” cause it was almost empty, his stroke vol- umes were small and only little blood was “Doc, I can’t wait. I’m going to call the hos- ejected.” pital right now and find out how he’s do- ing.” “No preload?” She calls the hospital and soon returns re- “Seems that was the case, because when porting with a smile: ”Doc, you won’t be- we gave him a bolus of normal saline you lieve this.” could feel a pulse and measure a blood pressure.” “What did they say?”

“But not high enough --only 70 systolic.” “He’s awake and alert with no brain dam- age. They put three stents in his heart. “Yes, that is why we gave him the second He’s just fine.” bolus --hoping to get the pressure up to at least 90 mmHg systolic.” “Great!

“But why the cold saline?” It’s been a long day, Kay. Go home early.”

35 “Thanks, Doc --see you in the morning.”

36 2

Cardiac Rhythms Measuring Heart Rates

Movie 4-1. Heart Rates

4-1 Lecture: Determining Heart Rates Time: 1:59 Learning Objectives Appreciate how to estimate heart rates by glancing at an EKG tracing.

38 Figure 4-1. Heart Rates

0.2 sec Paper speed: ECG 25 mm/sec Machine

300 150 100 75 60 Beats/min

3 seconds Beats/min 50 30

Fig.4-1. Determining heart rates. When the paper speed of the ECG apparatus is 25 mm/second, the distance between two heavy lines is 0.2 seconds. For heart rates at least 50 beats/min., the heart rate is equal to 300 beats/min. divided by the number of large boxes between successive R waves. For lower heart rates count the R waves between two 3-second markers and multiply by 10.

III. Cardiac Rhythms illustrated in Figure 4-1. Choose a lead that shows tall R waves (e.g., lead II) or A. Measuring Heart Rates deep S waves (e.g. lead V1) and count the number of large boxes between any two R To determine the rate at which a person's (or S) waves. If only one box fits in be- heart is beating from an ECG record, you tween waves, the rate is 300/min (60 must know the speed at which the paper is sec/min/0.2 sec). moving past the recording pen of the ECG machine (Fig. 4-1). All ECG machines are If two boxes fit between waves, the rate is calibrated so that the distance of one large 150/min (300/2), for 3 boxes the rate is box on the paper equals 0.2 seconds. 100/min (300/3), for 4 boxes the rate is 75/ Each large box is subdivided into 5 seg- min (300/4), etc. For very slow rhythms it is ments of 0.04 seconds. With this informa- more convenient to use the 3-second mark- tion heart rates are readily calculated, as ers on the ECG paper. Count the number

39 of R waves for 6 seconds (two 3-second intervals) and multiply by 10 to give the beats per minute.

40 Pacemakers of the Heart

Movie 4-2. Pacemakers

4-2. Lecture: Where is the Pacemaker? Time: 1:47 minutes Learning Objectives 1. Know what a sinus rhythm looks like. 2. Understand how an SA nodal rhythm is different from an AV nodal rhythm. 3. Appreciate the looks of an idioventricular rhythm.

41 Figure 4-2. Intracellular Electrode

SA node ECG mV Threshold potential 60 - 80 bpm -50 P P -60

AV node 40 - 60 bpm mV

-50

-70

20 - 40 bpm Purkinje fber P P P P

mV

-70 -90

Fig. 4-2. Pacemakers of the heart. ECG records of sinus (SA), nodal (AV), and idioventricular (Purkinje) rhythms are shown with the action potentials of pacemaker cells responsible for these rhythms. Typical ranges of heart rates for these different rhythms are also indicated. Note that heart rate depends upon the maximum diastolic potential, the threshold potential, and the slope of phase 4 depolarization (see Episode 1, Fig.1-7 for review).

B. Regular Rhythms (Sinus, AV-nodal pen. Then shift the paper by one RR inter- and Ventricular Rhythms. val and see if all the pen marks still match with R waves. If they do, the rhythm is The rhythm of the heart is said to be regu- regular. Such a regular rhythm may origi- lar when the distances between succeed- nate in the SA node, the AV node, or the ing R (or S waves) are equal. The easiest His-Purkinje system (Fig.4-2). way to test this is to place a piece of paper on the ECG tracing and mark the position The normal pacemaker for the heart, the of the peaks of several R waves with a SA node, usually fires 60 to 80 times/min.

42 However, with exercise or stress the SA different resting membrane potentials and node may fire well over 100 times/min. different rates of phase 4 depolarization (see Fig.4-2). Sinus rhythm is characterized by a narrow QRS complex (<0.10 seconds) which is preceded by a P wave. When the SA node fails (as in the sick sinus syndrome), the AV node can substitute as the pacemaker. AV nodal rates are usually between 40 to 60 beats/min.

AV nodal rhythms are characterized by a narrow QRS complex that is not preceded by a P wave (or by a small, inverted P wave just before or after the QRS com- plex).

When the AV node fails to conduct im- pulses (as occurs with a third degree AV block), a focus in the His-Purkinje system of the ventricles usually picks up the beat. The rate of such idioventricular rhythms is, however, quite slow, usually between 20 to 40 beats/min. Idioventricular rhythms are easily identified. The QRS complexes are usually large and wide (>0.12 seconds) and occur independent of any P waves. (The P waves occur at a faster rhythm that bears no relationship to the QRS com- plexes.)

These differences among the intrinsic pace- maker activities of the SA node, AV node, and His-Purkinje systems are caused by

43 Sinus Arrhythmias

Movie 4-3. Sinus arrhythmias

4-3. Lecture: Sinus arrhythmia Time: 2:08 minutes Learning Objectives: 1. Appreciate different end-diastolic volumes in right and left ventricles on inspiration. 2. Understand how the Bainbridge Reflex speeds up the heart rate on inspiration. 3. Know how the Baroreceptor Reflex is involved in sinus arrhythmia.

44 C. Irregular Rhythms are rapidly depolarized by impulses con- ducted normally over the His-Purkinje sys- (1) Sinus Arrhythmia tem), and each QRS complex is preceded by a P wave. Therefore, this is a sinus An irregular (or absent) heart rhythm is rhythm (originating in the SA node). The called an arrhythmia. Arrhythmias are ab- change in rhythm (i.e., changing distances normal, unless they are caused by the cy- between R waves) is related to respiratory clic changes of inspiration and expiration. excursions. Sinus arrhythmia is expected The heart rate speeds up on inspiration in a young, healthy person. It is caused by and slows on expiration; this is sinus ar- a decrease in vagal tone to the SA node rhythmia (see Fig.4-3,A). The QRS com- on inspiration. plexes are narrow (indicating the ventricles

Figure 4-3

A Sinus Arrhythmia (normal)

B Sick Sinus Syndrome Tachycardia Bradycardia

Fig.4-3. Arrhythmias originating in the SA node. In sinus arrhythmia (A), the SA node generates im- pulses more rapidly during inspiration than during expiration. This is normal. In the sick sinus syn- drome (B), the SA node sporadically increases (tachycardia) or decreases (bradycardia) its firing fre- quency. This is abnormal.

45 (2) Sick Sinus Syndrome Purkinje system cannot always be relied upon to pick up a rhythm when the SA When cells in the SA node are not function- node suddenly fails, patients with this con- ing reliably (for instance, with diminished dition are often given an artificial pace- blood flow to this region), the SA node maker. may fire impulses rapidly one moment and slowly the next (Fig.4-3,B). The resulting (3) Wandering Atrial Pacemaker abrupt onset of tachycardia and/or brady- cardia has given this condition the descrip- The heart may also beat irregularly be- tive name tachycardia-bradycardia syn- cause of a constantly changing pacemaker drome, also called the sick sinus syn- focus outside of the SA node in the atrium drome. Because the AV node or His- (see Fig.4-4). This is noticed on the ECG record by irregularly spaced QRS com-

Figure 4-4. Wandering atrial pacemaker

P P' P" P

Fig.4-4. Wandering atrial pacemaker. As the pacemaker changes to different foci in the atria, the P wave changes from one beat to the next and the rhythm becomes irregular.

46 plexes with a normal, narrow configura- tion. However, they are preceded by P waves that change in shape from one beat to the next. For example, when a focus close to the AV node fires, the atria depo- larize in a retrograde direction, resulting in an inverted P wave (labeled as P' in Fig.4-4). A changing atrial pacemaker with a rhythm over 100 beats/min is not called a Wandering Pacemaker but is referred to as multifocal atrial tachycardia. This ar- rhythmia is frequently associated with chronic obstructive pulmonary disease.

47 3

Ectopic Beats Premature Beats

Movie 4-4.

4-4 Lecture: Premature Beats Time: 4:05 minutes Learning Objectives:

1. Distinguish between premature beats arising in the atria, AV node, and ventricles. 2. Know how to recognize premature beats on taking a person's pulse. 3. Understand why premature beats are followed by a “compensatory pause”.

49 Figure 4-5

A. Premature Atrial Contraction

P P P P Compensatory pause PAC

B. Premature Nodal Contraction

P P High focus Middle focus Low focus

C. Premature Ventricular Contraction

Fig.4-5 Premature contractions. Premature contractions may originate in ectopic foci in the atria [PAC (A)], in the AV node [PNC (B)], or in the ventricles [PVC (C)].

(4) Ectopic Beats plies, these beats come too early. Because a wave of depolarization from these early (a) Premature Beats beats renders the heart refractory to the next scheduled beat, there is a longer Premature beats (or premature contrac- pause between the premature beat and tions) are often caused by an irritable fo- the next beat, called a compensatory cus in the atria (PAC), the AV node (PNC), pause (see Fig.4-5,A). Sometimes a prema- or the ventricles (PVC). As the name im-

50 ture beat will reset the SA node. This will ceding P wave. The wide QRS complex re- change the heart rate following the prema- flects the slow spread of impulses via gap ture beat. junctions (instead of via the Purkinje fibers) from an irritable focus in one ventricle to A premature atrial contraction (PAC) the other. As the two ventricles depolarize (Fig.4-5,A) is recognized by a normal QRS in succession - rather than simultaneously complex (<0.10 seconds), preceded by a P - two sequential vectors result, instead of wave. The shape of the P wave and the PR just one summation vector. The initial vec- interval of the PAC vary depending upon tor is directed toward the leads overlying the site of its origin in the atria. the ventricle where the ectopic beat origi- nates, resulting in a tall R wave. The sec- A premature nodal contraction (PNC) ond vector is in the opposite direction and (Fig.4-5,B) is identified by the absence of a is associated with delayed depolarization P wave or (more rarely) by inverted P of the other ventricle, resulting in a deep S waves just before or after a normal QRS wave. Sometimes PVCs arise in the inter- complex (<0.10 seconds). The P wave, if ventricular septum from where impulses seen, is inverted because the wave of are more evenly conducted to right and left atrial depolarization occurs retro- grade ventricles. These PVCs are therefore nar- from AV node toward the SA node. When rower than those arising, for instance, in the irritable focus is high in the AV node, the lateral wall of the left ventricle. an inverted P wave may be seen just be- fore the QRS complex. When the focus is Ectopic beats can be detected by taking a low in the AV node, an inverted P wave person's pulse. Premature beats are often may be seen just after the QRS complex. weak or are not felt at all, because they oc- Most often, the irritable focus is in the mid- cur too early when the left ventricle is not dle of the AV node and the inverted P completely filled. Left ventricular contrac- wave is buried within the QRS complex tion at this lower filling volume results in a and cannot be seen at all. diminished stroke volume that may not generate a sufficient pulse wave to be felt A premature ventricular contraction (PVC) at the radial artery in the wrist. However, (Fig.4-5,C) is easily recognized by its wide closure of heart valves associated with the QRS complex (>0.12 seconds) with large R beat is readily heard with a stethoscope. and/or S waves and the absence of a pre- The difference in the beats/min heard with

51 the stethoscope over the heart and the beats/min felt at the wrist is called the pulse deficit. It is a clinical estimate of the number of premature beats. An ECG trac- ing is, of course, required to determine their origin (PAC, PNC, or PVC).

Ectopic beats are common in healthy young people and seem to be more fre- quent in tired or anxious individuals who drink coffee, smoke cigarettes, or con- sume alcohol. Nevertheless, such prema- ture beats are not to be dismissed as insig- nificant, especially in patients with heart or lung diseases. Ectopic beats are especially significant for a patient who has been ad- mitted to an intensive care unit for an acute myocardial infarction.

52 Dangerous PVCs

Movie 4-5.

4-5. Lecture: Dangerous PVCs Time: 4:45 minutes Learning Objectives: 1. Know when PVCs are considered dangerous. 2. Be able to recognize multifocal PVCs. 3. Understand why the R on T phenomenon presents a danger. 4. Know when PVCs are equivalent to a burst of ventricular tachycardia. 5. Be able to recognize coupled beats such as bigemini or trigemini.

53 Figure 4-6. Multifocal PVCs (b) Dangerous PVCs A a b Malignant PVCs are dangerous because they may cause the ventricles to fibrillate. When such PVCs are noticed, beta- R-on-T phenomenon adrenergic blockers or other drugs --de- B R pending upon the underlying condition T T --are sometimes used to diminish their fre- quency. The PVCs listed in Table 4-1 are considered dangerous. Run of >3 PVCs = Ventricular tachycardia C

Table 4-1. Dangerous PVCs

1. Frequent PVCs, i.e., more than 6 per Bigemini minute D PVC PVC 2. Bursts of 3 or more PVCs 3. Coupled PVCs ( couplets, bigemini, trigemini, etc.) 4. Multifocal PVCs 5. R on T phenomenon Trigemini E PVC PVC Any PVC that falls on the T wave of the preceding beat (R on T phenomenon, Fig. 4-6,B ) may trigger ventricular fibrillation. During the T wave the ventricle is partially depolarized (at the endocardium) and par- tially repolarized (at the epicardium), and Fig. 4-6. Dangerous PVCs. PVCs are considered dangerous when they (A) are multifocal, (B) fall many cells are in states of relative refracto- on the T wave of the preceding beat, (C) occur in riness or hyper-excitablity (see discussion runs of more than three beats (which is consid- of refractoriness in episode 1 ). This makes ered equivalent to ventricular tachycardia), or are closely coupled as in bigemini (D) or trigemini the ventricle more susceptible to stimuli (E). In addition, frequent (more than 6/min) PVCs from PVCs, which may induce circular cur- require close attention (not shown). rents to flow around different regions of the ventricle. These repetitive circular

54 movements of impulses may, in turn, in- duce ventricular tachycardia, flutter, or even fibrillation. The more frequent the PVCs, the more likely such malignant events to occur.

PVCs arising from the same locus in the ventricle (unifocal PVCs with identical con- figurations) are less serious than PVCs aris- ing from multiple foci (multifocal PVCs with different configurations, Fig.4-6,A) be- cause any one of these foci of irritation may induce ventricular tachycardia.

Not infrequently, PVCs are coupled directly (couplets) or with one normal beat in be- tween (bigemini, Fig. 4-6,D) or two normal beats in between (trigemini, Fig. 4-6,E), and so forth. Such coupled beats are often seen with digitalis toxicity and may give rise to more dangerous ventricular arrhyth- mias. When PVCs occur in bursts of three or more, the condition is considered equivalent to a run of ventricular tachycar- dia (Fig. 4- 6,C), and immediate measures should be taken to prevent the rhythm from deteriorating into ventricular fibrilla- tion.

55 Escape Beats

56 Movie 4-6

4-6. Lecture: Escape Beats Time: 2:10 minutes Learning Objectives; 1, Appreciate the need for escape beats. 2. Be able to recognize the origin of escape beats.

Escape Beats

57 Figure 4.7 Escape beats

Missing P-wave Atrial escape beat P P P

Nodal escape beat

Ventricular escape beat

Fig. 4-7 Escape beats. When the SA node fails to initiate an impulse (and a P wave), an escape beat is initiated by an ectopic focus located in the atria, AV node, or ventricles.

When the normal pacemaker in the SA node fails to depolarize, another focus usu- ally picks up the beat (Fig. 4-7). This focus may be in the atria, the AV node, or the ventricles. Called an escape beat, this looks just like a premature beat, except that it comes later than expected.

58 4

Tachycardias Fast Atrial Rhythms

Movie 4-7

4-7 Lecture: Sinus tachycardia and PSVT. Time: 10:24 minutes Learning Objectives:

1. Give examples of conditions causing “sinus tachycardia”. 2. Explain how the re-entry phenomenon causes PSVT.

60 Figure 4-8

A Sinus tachycardia

100-150 bpm

B PAT C PNT

150-250 bpm 150-250 bpm

D PSVT

150-250 bpm

E Atrial futter (3:1 conduction) F Atrial fbrillation 250-350 bpm (atria) >350 bpm (atria)

Ashman phenomenon

Fig.4-8. Fast heart rates originating above the ventricles. These include (A) sinus tachycardia, (B) paroxysmal atria tachycardia (PAT), (C) paroxysmal (AV)nodal tachycardia (PNT), (D) paroxysmal supraventricular tachycardia (PSVT), which is either PAT or PNT, (E) atrial flutter (in this example, with a 3:1 conduction through the AV node), and (F) atrial fibrillation (this example also shows a PVC-like beat due to aberrant conduction --a so-called Ashman beat).

61 Fast Rhythms Originating in the Atria tients with atrial flutter or atrial fibrillation. Therefore, supraventricular tachycardias Tachycardia is defined as a heart rate of (or atrial flutter or fibrillation) are seldom more than 100 beats/minute. Tachycardia life threatening; whereas, ventricular tachy- is a useful mechanism for increasing car- cardia (or ventricular flutter or fibrillation) is diac output, but only up to a point. At very life threatening and requires immediate in- rapid heart rates, diastole is shortened tervention. more than systole and, since cardiac filling occurs during diastole, there is not enough (1) Sinus Tachycardia time to adequately fill the heart with blood Sinus tachycardia results from in- before it contracts during systole. Moreo- creased sympathetic and decreased ver, the faster the heart beats, the more parasympathetic stimulation of the SA oxygen (and thus the more coronary blood node. As discussed previously in Epi- flow) it requires. However, blood flows sode 1, this raises the resting mem- through the coronaries to the left ventricle brane potential of SA nodal cells closer primarily during diastole because vessels to threshold (vagolytic effect) and in the subendocardium of the left ventricle speeds the upward drift of phase 4 de- are compressed during systole. With a polarization (sympathetic effect). As a shortened diastole, less blood reaches consequence, heart rate increases muscles that need it even more than be- above normal to values ranging from fore. 100 to 150 beats/min.

When the atria or ventricles are stimulated Sinus tachycardia is seen, for example, to contract at very rapid rates, they stop with exercise, excitement, pain, or in pa- pumping blood altogether. The chambers tients in circulatory shock. The ECG trac- first flutter and then fibrillate as different ing shows normal QRS complexes, each patches of muscle contract chaotically and preceded by a normal P wave (see the wall merely quivers. Fortunately, the Fig.4-8,A). Sinus tachycardia is an impor- ventricles are usually protected from such tant sign that the sympathetic nervous sys- rapid barrages of stimuli by the AV node, tem has been activated, and the reason for which limits the number of impulses arriv- this must be carefully sought (e.g., is the ing at the ventricles, so that the ventricles patient anemic, hypoxic, or hypotensive?). still contract and pump effectively in pa-

62 (2) Paroxysmal Supraventricular Tachy- flux into AV nodal cells. A variant of this cardia (PSVT) condition, PAT with block, is usually due to digitalis toxicity. In this situation, the atria (a) Paroxysmal Atrial Tachycardia (PAT) beat between 150 to 250 times/min, but In paroxysmal atrial tachycardia (PAT) the not all impulses [e.g., every other one (in a heart rate suddenly increases to a rate be- 2:1 block)] are conducted through the AV tween 150 and 250 beats/min. The epi- node, so that the ventricles beat slower sode may terminate just as suddenly than the atria. within seconds, minutes or hours. The tachycardia is often initiated by a PAC, that (b) Paroxysmal Nodal Tachycardia has an abnormally long PR interval. The The etiology and treatment for paroxysmal QRS complexes are of normal duration, nodal tachycardia (PNT, Fig. 4-33,C) is the and P waves can be identified before each same as it is for PAT. This is fortunate be- QRS complex - but only at the slower cause the two conditions cannot be distin- heart rates (4-8,B). At higher rates, the P guished at fast heart rates and are, there- waves become superimposed on the pre- fore, simply referred to as paroxysmal su- ceding T waves (as the duration of diastole praventricular tachycardia (PSVT, is shortened) and P waves cannot be iden- Fig.4-8,D) or, if not paroxysmal, simply as tified with certainty (Fig. 4-8,D). supraventricular tachycardia (SVT).

PAT is quite common in otherwise healthy individuals, but the condition is also fre- quently encountered in patients with aber- rant conductive pathways between atria and ventricles (Wolff-Parkinson-White or Lown-Ganong-Levine syndromes).

As discussed in Episode 1 (Michelle), PAT can often be terminated by increasing va- gal tone by the Valsalva maneuver, gag- ging, carotid sinus massage, or by admini- stration of drugs such as adenosine or verapamil which decrease calcium ion in-

63 Movie 4-8

4-8. Lecture - Atrial flutter and fibrillation. Time: 5:41 Learning Objectives 1. Draw the EKG pattern of atrial flutter with a 4:1 block. 2. Appreciate how a diagnosis of atrial fibrillation is suspected prior to taking an EKG.

(3) Atrial Flutter (4) Atrial Fibrillation

The P waves in atrial flutter occur rapidly In this condition the atria fibrillate above (250 to 350/min) and resemble the teeth of 350 times/min, and distinct P waves are re- a saw. Not all impulses are conducted by placed by small fibrillation waves. The AV the AV node, so the ventricular rate is node conducts only some of these im- slower but usually regular. Thus, only every pulses, so that the ventricular rate is unpre- third or fourth flutter wave may be con- dictable (Fig. 4-8,F). At times an impulse ducted to the ventricles (a 3:1 or 4:1 block gets through early, while one of the bundle [Fig. 4-8,E]). branches is still refractory and the other is not. This causes wide QRS complexes be- cause each ventricle is depolarized sequen-

64 tially rather than simultaneously. Such ab- cosides (e.g. digoxin) which is usually normal beats, which look like PVCs, are preferred if the patient has congestive characteristic of atrial fibrillation. This is heart failure in addition to atrial fibrilla- the Ashman phenomenon. tion.

Atrial fibrillation is common in older peo- (b) Early on in atrial fibrillation --prior to re- ple. Even though the P waves of fibrillation structuring of the atria -- attempts are may not be clear on the ECG, a diagnosis sometimes made to restore the rhythm is readily made based on the (usually) ran- to normal with electrical or chemical car- dom spacing of the QRS complexes. The dioversion or (more permanently) with QRS complexes are narrow because con- catheter ablation of irritable foci. duction over the Purkinje system is nor- mal, except for the occasional Ashman Atrial fibrillation is initiated by abnormal im- beats already mentioned. Because the ven- pulses that arrises from cells in one of the tricles contract at different end-diastolic fill- four pulmonary veins and then spreads to ing volumes, left ventricular stroke volume the atria. By making non-conducting scars and pulse pressure vary from beat to beat. with a burst of radio waves or extreme This causes the pulse to be irregular with cold at the junction of the pulmonary veins respect to both rhythm and magnitude, and the left atrium, the atrium is insulated i.e., the pulse in atrial fibrillation is from erratic electrical impulses, thereby al- irregular/irregular. lowing normal conductive pathways in the atria to re-established themselves. Since The treatment of atrial fibrillation is aimed most clots form in the left atrial append- at (a) controlling the ventricular rate, (b) age, this pocket is sometimes closed off controlling the rhythm, and (c) preventing a either by ligation (placing a loop around it stroke from emboli that brake off from from the outside) or by threading an clots formed in the left atrium (especially in umbrella-like filter into the appendage. the appendage) and travel to the brain. (c) Short of the surgical procedures men- (a) The ventricular rate is brought below tioned above, clot formation in the left 100 bpm by using drugs that slow AV atrium is traditionally prevented with war- conduction, such as beta-adrenergic farin (e.g., Coumadin) or with newer agents blockers (e.g. metoprolol) or cardiac gly- such as apixaban (e.g., Eliquis), which

65 does not have the dietary restrictions of Coumadin (e.g., avoidance of green leafy vegetables such as kale because it is rich in vitamin K -- an antidote for Coumadin).

66 Fast Ventricular Rhythms

Movie 4-9

4-9 Lecture: Fast rhythms originating in the ventricles. Time: 6:26 minutes Learning objectives

1. Make sure you can you distinguish “Ventricular Tachycardia” from “Paroxysmal Supraventricu- lar Tachycardia”. 2. Know what ventricular fibrillation looks like on a cardiac monitor. 3. Know the signs and symptoms of ventricular fibrillation. 4. Know what steps to take in resuscitating a person with ventricular fibrillation.

67 Fast Rhythms Originating in the Ven- Figure 4-9 tricles A Ventricular Tachycardia (1) Ventricular Tachycardia Ventricular tachycardia consists of three or more broad (>0.12 sec.) QRS complexes that occur more frequently than 100/min Torsade de Pointes (Fig.4-9,A). The arrhythmia may be toler- B ated well or may be associated with a de- creased cardiac output and shock. The atria beat independently in this condition, because the AV node is rendered refrac- Ventricular Flutter tory to conduction by retrograde depolari- C zation from the ventricles. In a variant form of ventricular tachycardia, Torsade de Poin- tes, the QRS complexes constantly change as if they were twisted about a D Ventricular Fibrillation point (Fig.4-9,B). This pattern may be seen in hypomagnesemia, hypokalemia, or fol- lowing an overdose of antiarrhythmic coarse fne agents such as quinidine that prolong the Q-T interval (i.e., prolong systole).

(2) Ventricular Flutter and Fibrillation A heart in ventricular flutter generates a Fig.4-9 Fast rates originating in the ventricles. These include (A) ventricular tachycardia, (B) rapid sequence of quite evenly spaced torsade de pointes, (C) ventricular flutter, and complexes that are rounded on top (D) coarse and fine ventricular fibrillation. (Fig.4-9,C). Such a tracing is an ominous sign that ventricular fibrillation is soon to follow. In contrast to ventricular flutter, ven- lar wall become rapidly depolarized in a fu- tricular fibrillation is chaotic and unorgan- tile effort that has been likened in appear- ized (Fig.4-9,D). In this condition the ventri- ance to a bag of worms. No blood is cle quivers as different patches of ventricu- pumped by the ventricles as they fibrillate,

68 and within seconds a person with this con- dition loses consciousness. Not long there- after, centers responsible for maintaining the respiratory rhythm fail as well, and res- piratory arrest follows. The heart, deprived of oxygen, continues to fibrillate for a while - first in a coarse, erratic pattern and then in a finer, smoother pattern that ends in a flat line (asystole), where all traces of elec- trical activity have vanished from the heart.

69 Mechanisms of Arrythmias

Figure 4-10 A Increased Automaticity

Ventricular Muscle Cell

+20 mV Threshold -70 -90 Normal Ischemia PVC B Triggered Activity

Ventricular Muscle Cell R +20 mV T -70 Threshold -90 After depolarization PVC

C Reentry Phenomenon

SA node Retrograde conduction in (b) Normal conduction Slow conduction in (a) due to One Way AV node local ischemia Two Way

Pathway (a) Pathway (b)

Normal PSVT

Fig.4-10. Mechanisms of Arrhythmia.

(A) Increased automaticity is illustrated for an ischemic focus in the left ventricle, which depolarizes spontaneously and gives rise to a PVC. (B) Triggered activity is illustrated for a ventricular muscle cell with an after-depolarization that triggers a PVC. Note that the PVC is closely coupled to the first beat and falls on its T wave (the R on T phenomenon). (C) Re-entry phenome- non is illustrated in the case of PSVT. Normally a single impulse travels from the SA node over dual pathways (a and b) around the AV node to the ventricles and, in the process, inscribes a single normal complex on an ECG tracing. Normally these pathways a and b function only as one-way streets for impulse traffic toward the ventricles because of their long refrac- tory periods. In the re-entry phenomenon conduction of impulses has been slowed in pathway a, because of ischemia. This delayed impulse is now conducted retrograde through pathway b,which is no longer refractory and thus open to two-way im- pulse traffic. The impulse is shown to circle repeatedly around the AV node, each time stimulating the ventricle to depolarize and resulting in a burst of complexes on the ECG tracing. (Note that the initial impulse that moved rapidly down pathway b is not shown in the graph.)

70 Mechanisms of Cardiac Arrhythmias (2) Triggered activity may also cause ven- tricular fibrillation or other arrhythmias. The Atrial or ventricular arrhythmias may be action potentials of ventricular muscle caused by three basic mechanisms: (1) cells, for instance, may not return to base- automaticity, (2) triggered activity, or (3) re- line during phase 3 repolarization but may entry (see Fig.4-10). (1) Automaticity re- instead oscillate (presumably due to an ab- sults from an increased rate in the sponta- normal delay in negative feedback signals) neous depolarization of one or more ec- close to threshold. Such after-potentials - topic foci. When muscle cells in the left provided they reach threshold - could in- ventricle become ischemic, their resting duce another depolarization that would be membrane potentials become less nega- closely coupled to the first beat. Such pre- tive, causing voltage-sensitive calcium mature contractions (PVCs) would tend to channels to open and the potential to drift fall within the vulnerable period of the car- toward threshold during phase 4 of their ac- diac cycle, i.e., during the T wave, when tion potentials (see Fig.4-10,A). Further- some parts of the ventricle are already re- more, because myocardial ischemia is usu- polarized while other parts are not. This im- ally associated with increased circulating balance in refractoriness of ventricular tis- levels of epinephrine and because epineph- sues predisposes to reentry of the impulse rine (acting via beta1-adrenergic receptors) initiated by the PVC. The resulting circular increases the “open time” of calcium chan- flow of currents is probably a major cause nels, the tendency for depolarization dur- of ventricular fibrillation. (3) The re-entry ing phase 4 is further enhanced. In this phenomenon is the most common mecha- way, coronary insufficiency may convert a nism for atrial and ventricular tachycardia, normally quiescent (contractile) ventricular flutter, and fibrillation. The principle is illus- muscle cell to a pacemaker cell that peri- trated for paroxysmal supraventricular odically generates a PVC. If many such tachycardia (PSVT) in Figure 4-10,C. For ischemic cells in different parts of the ven- reentry to occur, the impulse must travel tricle were to depolarize when the ventricle along a pathway that splits into two was not refractory, such multifocal PVCs branches and then re-unites into a com- could be partly responsible for the chaotic mon path, thereby forming a circle by rhythm seen in ventricular fibrillation. which a single impulse can reenter the original pathway over and over again to produce a burst of rapid contractions in-

71 stead of just one. Reentry of the impulse into its recent path, of course, requires that the impulse must be conducted retrograde in one branch of the circular conductive pathway (branch b). Normally, this retro- grade conduction does not occur because both branches (a and b) are refractory (the sodium channels are still inactivated) for a short interval after the impulse has passed. However, under certain conditions, such as ischemia or a PAC at an inopportune time, conduction in one branch (a) may be slowed, because the slope of phase 0 is decreased in ischemia, providing sufficient delay for the healthy branch (b) to repolar- ize before the slow impulse from the ischemic branch arrives. Since the healthy branch (b) is no longer refractory, once re- polarized, the impulse arriving from the ischemic branch will now be conducted ret- rograde along the healthy branch and can reenter the ischemic branch (a) to be con- ducted once more to the ventricles. These cycles repeat over and over.

72 5

Heart Blocks Atrio-Ventricular Blocks

Movie 4-10

4-10 Lecture: A-V blocks. Time: 6:38 minutes Learning Objectives:

1. Be able to recognize a 1st degree AV block and understand why some medications can pro- duce this effect. 2. Distinguish between the two types of 2nd degree AV block. 3. Appreciate the relationship between P-waves and QRS complexes in a 3rd degree AV block. 4. Know which patients with an AV block need an artificial pacemaker.

74 Figure 4-11. AV blocks A Normal First Degree AV Block

P-R < 0.2 sec P-R > 0.2 sec

B Second Degree AV Block, Mobitz I (Wenckebach Phenomenon)

P-R P-R P-R drop beat

C Second Degree AV Block, Mobitz II (2:1 Block)

P P P P P

D Third Degree AV Block P P P P P P

Fig.4-11. Atrioventricular conduction blocks. In first- degree AV block, the PR interval is greater than 0.20 seconds (A). In second-degree AV block, the PR interval becomes progressively longer until a P wave is not followed by a QRS complex; this cycle then repeats itself [Mobitz I, or Wenckebach phe- nomenon (B)]. Alternatively, in Mobitz II (C) there is a sudden (intermittent) loss in AV conduction so that, for instance, every other P wave is not followed by a QRS complex (in the example of a 2:1 block given). In third degree AV block (D), P waves and QRS complex- es are independent of each other, ex- hibiting an idioventricular rhythm.

75 AV blocks followed by a QRS complex. Mobitz I is commonly seen with digitalis toxicity and (A) First Degree AV Block subsides upon lowering the dosage of digi- In first degree AV block conduction of im- talis. pulses through Mobitz II is also an intermittent form of AV the AV node is delayed, resulting in prolon- block, but unlike Mobitz I, it occurs sporadi- gation of the PR interval beyond 0.2 sec- cally. In other words, every now and then, onds (1 large box), (Fig. 4-11,A). This may without warning, a P wave is simply not fol- be due to increased vagal tone, drugs lowed by a QRS complex. Mobitz II is the (e.g., digitalis, propranolol, verapamil), or result of more serious and more perma- heart disease (e.g., rheumatic fever). nent damage to the conducting system lower down in the AV node, closer to the (B) Second Degree AV Block bundle of His. Mobitz II thus serves as a In second degree AV block some impulses warning that a complete (permanent) AV arriving at the AV node from above are not block may follow. Therefore, patients with conducted, so that only every second (2:1 Mobitz II are usually given artificial ventricu- block), every third (3:1 block), or every lar pacemakers. fourth (4:1 block) P wave is followed by a narrow QRS complex (Fig.4-11,C). (C) Third Degree AV Block In third degree AV block (or complete AV The second degree AV block may be vari- block) no impulses from the atria are con- able or intermittent. Two forms are distin- ducted through to the ventricles guished, Mobitz I (or Wenckebach Phe- (Fig.4-11,D). Thus, the atria beat in a sinus nomenon) and Mobitz II (Fig.4-11,B and C). rhythm and the ventricles beat at a much In the Wenckebach Phenomenon conduc- slower idioventricular rhythm. Conse- tion through the AV node becomes progres- quently, there is no consistent relationship sively longer during a series of impulses un- between the P waves and the QRS com- til conduction is completely stopped; then plexes. The QRS complexes are character- the cycle repeats over and over again. This istically wide with large deflections, as is results in a clustering of beats that is read- true for PVCs. Because the ventricles beat ily recognized on the ECG tracing. The PR slowly, there is more time for them to fill interval is progressively lengthened from during diastole. Stroke volumes are, ac- one beat to the next until a P wave is not

76 cordingly, greater than normal, which is readily recognized by a bounding pulse found on physical examination. On occa- sion, the right atrium will contract simulta- neously with the right ventricle. Because the tricuspid valve is closed at that time, blood is forced backward into the jugular veins in the neck to produce a cannon a- wave, i.e., a marked exaggeration of the normal a-wave. Indeed, this is how a diag- nosis of complete AV block was made be- fore the ECG machine was invented. Pa- tients with a third degree AV block usually require an artificial ventricular pacemaker.

77 Bundle Branch and Fascicular Blocks

Movie 4-11

4-11 Lecture: Bundle Branch Blocks. Time: 6:16 minutes Learning Objectives: 1. Describe the genesis of the QRS complex in lead V1 in a patient with a right bundle branch block. 2.Describe the genesis of the QRS complex in lead V5 in a patient with a left bundle branch block.

78 Figure 4-12 Right Bundle Brand Block Left Bundle Branch Block Leads: V1 or V2 Leads V5 or V6

R' R' R R

S QRS > 0.12 seconds QRS > 0.12 seconds

Right Bundle Brand Block Left Bundle Branch Block

1 S R' 2 R 3 R 2 1 3 R'

Lead V1 Lead V6

Fig.4-12. Bundle branch blocks. Right bundle branch blocks (RBBB) show R,R' complexes in leads V1 and V2, while left bundle branch blocks show R,R' complexes in V5 and V6. The QRS complexes are more than 0.12 seconds (the width of 3 small boxes). The cardiac vectors responsible for these complexes are illustrated.

79 (3) Bundle Branch and Fascicular Blocks to right), but this notch is often obscured by left ventricular depolarization, so that (A) Bundle Branch Blocks only a wide R wave is seen.

When either the right or the left branch of RBBB is commonly seen in people with the common bundle of His has been dam- normal hearts. By contrast, a new LBBB is aged, depolarization of the blocked ventri- frequently associated with heart disease cle is delayed because conduction occurs (e.g., myocardial infarction). Because depo- more slowly via gap junctions between larization of one ventricle is delayed with a muscle cells. This delay in depolarization bundle branch block, Q waves may appear results in QRS complexes that are abnor- in some leads even without a myocardial mally wide, more than 0.12 seconds (> 3 infarction. One must, therefore, be very small boxes) (see Fig. 4-12). With right bun- cautious in making a diagnosis of myocar- dle branch block (RBBB) an RR' pattern (or dial infarction in patients with bundle RSR' complex) is seen in leads V1 and V2. branch blocks and rely more heavily on The R wave results from depolarization of changes in cardiac enzyme levels in the the left ventricular portion of the interven- blood. tricular septum (from left to right), the S wave (or the notch between R and R') from (B) Fascicular Blocks left ventricular depolarization (from right to The left bundle gives rise to an anterior left) and the R' wave (i.e., the second up- and a posterior branch. When either ward deflection) from delayed depolariza- branch is blocked, the QRS complex is tion of the right ventricle (from left to right). slightly widened (0.10-0.12 seconds), but With left bundle branch block (LBBB) an not to the same degree as is seen with RR' pattern (often without a notch be- LBBB (>0.12 seconds). Block of the ante- tween R and R') is seen in leads V5 and rior branch (anterior hemiblock) causes left V6. In LBBB the R wave is from depolariza- axis deviation; whereas, block of the poste- tion of the right ventricular portion of the rior branch (posterior hemiblock) causes interventricular septum (from right to left) right axis deviation. (Fig.4-13). To make the and the R' wave from delayed depolariza- diagnosis of a hemiblock you usually need tion of the left ventricle (from right to left). to document a change in the QRS axis, The notch between R and R' waves is due to right ventricular depolarization (from left

80 Figure 4-13

Left axis A B deviation

0o 0o

Right axis deviation Posterior fascicle Anterior fascicle blocked blocked +90o +90o

Fig. 4-13. Hemiblocks in the fascicles of the left bundle branch. Hemiblock of the posterior fasci- cle (A) results in right axis deviation of the mean QRS vector in the frontal plane; whereas, a hemiblock of the anterior fascicle (B) results in left axis deviation.

which requires a previous ECG for compari- son.

81 Abberant Conduction

Figure 4-14

A Normal B Wolf-Parkinson-White C Lown-Ganong-Levine Syndrome Syndrome

Bundle of Kent (accessory James fbers pathway)

Preexcitation

Short PR, Short PR, delta wave, normal QRS, Delta PSVT often PSVT often wave

PR < 0.12 seconds PR < 0.12 seconds PR < 0.12 seconds

Fig.4-14. Aberrant conduction from atria to ventricles via accessory pathways. (A) In the normal heart the ventricles are insulated from the atria, except for impulses conducted via the AV node. (B) In the Wolff-Parkinson-White Syndrome, impulses are conducted from atria to ventricles via the bundle of Kent, which pre-excites the ventricles and results in a short PR interval and a slow upstroke of the R wave (a delta wa.ve). (C) In the Lown-Ganong-Levine Syndrome, impulses are conducted around the AV node via the James fibers, which shortens the PR interval. Note that both syndromes are associ- ated with frequent episodes of PSVT.

82 (4) Aberrant Conduction lar pattern. Another potential problem with this condition is that the safety mechanism Impulses normally spread from the SA of the AV node has been by-passed. If pa- node over the atria by three specialized tients with this syndrome should develop conductive pathways that end at the AV atrial fibrillation, for instance, impulses will node. Thus, the ventricles are electrically be conducted to the ventricles via the ac- insulated from the atria, except for im- cessory pathway at much higher rates pulses conducted through the AV node than is usually seen in patients with atrial (Fig. 4-14,A). fibrillation. Because of these various com- plications, the accessory pathway is some- (A) Wolff-Parkinson-White Syndrome times interrupted surgically in patients with In patients with the Wolff-Parkinson-White Wolff-Parkinson-White syndrome. syndrome there is an abnormal accessory pathway (the bundle of Kent) from atria to (B) Lown-Ganong-Levine Syndrome ventricles (see Fig.4-14,B). Impulses by- In patients with the Lown-Ganong-Levine passing the AV node via the bundle of syndrome one of the atrial conduction path- Kent reach the ventricles a little earlier than ways by-passes the AV node to terminate usual, so that the PR interval on the ECG at the bundle of His (Fig. 4-14,C). This ac- is characteristically shorter than normal cessory pathway (the James fibers) results (i.e., <0.12 sec). Moreover, the early arrival in rapid conduction of impulses from atria of the impulse pre-excites the ventricle to ventricles. However, pre-excitation of (therefore, this condition is also called the ventricular muscle is not seen in this condi- Pre-excitation Syndrome) resulting in a tion, because impulses spread to the ventri- slow upstroke of the R wave, which is cles over the Purkinje system as usual. called a delta wave. Thus, the ECG in this syndrome shows a characteristically short PR interval (< 0.12 Patients with Wolff-Parkinson-White syn- seconds) and a normal QRS complex (< drome have recurrent episodes of paroxys- 0.10 seconds). Patients with this condition mal supraventricular tachycardia (PSVT), experience frequent episodes of PSVT, be- because impulses traveling down the bun- cause impulses may be conducted down dle of Kent to the ventricle may be con- the James fibers and reenter a circular ducted retrograde through the AV node pathway via retrograde conduction back to the atria in a self- sustaining circu- through the AV node.

83 6

Potassium Imbalance The EKG in Potassium Imbalance

Movie 4-12

4:12 Lecture: Potassium Imbalance Time: 10:08 minutes Learning Objectives:

1. A patient with absent bowel sounds and no deep tendon reflexes has hypokalemia: a. What would you expect to see on her EKG? b. Why are her deep tendon reflexes diminished? c. What does this have to do with the Nernst Equation? 2. A patient in diabetic ketoacidosis has tented T-waves. a. What do you suspect? b. Why is his heart hyper-irritable?

85 (5 ) Potassium Imbalance Figure 4-15 In hyperkalemia, when the serum potas- sium ion concentration rises from a normal value of about 4 mEq/L to about 7 mEq/L, Severe hyperkalemia the PR interval is prolonged and T waves + [K ] = 9 meq/L Wide QRS, become tall and peaked (i.e., tented T P fat P wave, waves)(see Fig. 4-15). As potassium levels prolonged P-R reach about 9 mEq/L, the QRS complex Moderate hyperkalemia widens and ventricular fibrillation or car- [K+ ] = 7 meq/L T diac standstill is imminent. In hypokalemia, Peaked when the serum potassium ion concentra- T wave tion falls from 4 mEq/L to about 2 mEq/L, Normal T waves are flattened, and U waves ap- [K+ ] = 4 meq/L pear. With a further decline in serum potas- sium, cardiac standstill or fibrillation result.

Moderate hypokalemia [K+ ] = 3 meq/L T U U wave

Severe hypokalemia [K+ ] = 2 meq/L

Prominent U wave, fat T wave

Fig.4-15. The ECG in hyperkalemia and hypoka- lemia. Characteristic ECG patterns are depicted as serum potassium concentration is raised from its nor- mal value of 4 mEq/L to 9 mEq/L or lowered to 2 mEq/L.

86 Figure 4-16

Fig. 4-16. Effect of Extracellular Potassium on Membrane Excitability. A. The resting membrane potential of a muscle cell is shown to be similar to the potassium diffusion potential, which is calculated from the concentration of intracellu- lar potassium (Ki) and extracellular potassium (Ko) with the Nernst equation. B. Resting membrane potentials and ac- tion potentials are shown for subjects with a normal serum potassium (Ko, 4 meq/L), decreased serum potassium (2 meq/L), or increased serum potassium (8 meq/L). In the subject with hypokalemia, the resting membrane potential is further removed from the threshold at which an action potential (leading to muscle contraction) is initiated, so that a larger than normal stimulus is required to initiate a response (the subject is hyporeactive). In the subject with hyperka- lemia, the resting membrane potential is closer to threshold than normal, so that a smaller than usual stimulus initiates a response (the subject is hyperreactive).

87 Figure 4-17

Fig. 4-17. Emergency measures in hyperkalemia. In hyperkalemia (serum K+>6.5 mEq/L) serum po- tassium concentration may be rapidly reduced by stimulating sodium-potassium exchange pumps in muscle or liver cells by injecting a selective beta2-adrenergic agonist or insulin. (Glucose must be given with insulin to avoid hypoglycemia.) Another method for lowering serum potassium is to stimulate sodium-hydrogen ion antiporters with sodium bicarbonate. Bicarbonate lowers hydrogen ion concentration in extracellular fluid, causing outward diffusion of hydrogen ions and inward diffu- sion of sodium ions on antiporters. The resulting increase in intracellular sodium concentration, in turn, stimulates sodium-potassium exchange pumps, which increases potassium uptake by cells and lowers potassium concentration in extracellular fluid.

Hyperkalemia tends to depolarize myocar- dial cells, i.e., it moves the resting mem- brane potential closer to threshold; whereas, hypokalemia tends to hyperpolar- ize cells, i.e., it moves the resting mem- brane potential away from threshold (see Fig. 4-16).

88 Emergency measures for hyperkalemia in- clude administration of calcium ions, which raises the threshold of (contractile) myocardial cells, administration of sodium bicarbonate, which enhances the ex- change of extracellular for intracellular po- tassium ions, or administration of beta2- adrenergic agonists, which stimulates the sodium/potassium exchange pump (see Fig. 4-17).

Emergency measures for hypokalemia in- clude a very slow infusion of a very dilute solution of potassium chloride, because raising plasma levels - even very briefly - above about 9 mEq/L will result in ventricu- lar fibrillation.

89 7

Review

True-False Questions

91 Review 7-1: Please decide whether the statement is True or False

Question 1 of 10 Measuring the pulse deficit is a way of determining the number of ectopic beats per min- ute without an ECG tracing.

A. true

B. false

Check Answer

Multiple Choice Questions

93 Review 7-2: Please choose the one best answer.

Question 1 of 10 An EKG tracing with a QRS complex of >0.12 sec with an R,R’ pattern in V5 suggests

A. Wenckebach phenomenon

B. Left bundle branch block

C. Left ventricular hypertrophy

D. Left axis deviation

Check Answer Drag Label to Target

95 0.2 sec Review 7-3, Please drag label to target. Paper speed: ECG 25 mm/sec Question 1 of 9 Machine About heart rates---

75 bpm 150 bpm Beats/min

100 bpm

3 seconds 150 bpm 100 bpm Beats/min 75 bpm

Check Answer

Interactive Questions

97 Interactive 4-1. This man complains of a headache. His blood pressure is 190/120 mmHg. His pulse is regular at 75 bpm.

What is your diagno- sis?

Does he have atrial fibrillation?

98 Interactive 4-2. This student felt palpitations. She was studying for an exam, drink- ing a lot of coffee, not sleeping.

Is this an escape beat?

What is this beat?

99 Interactive 4-3. Please answer the questions below.

A. Cardiac Vectors

P S

T Q When might you see ECG R + this wave?

B. Waves c What changes would +1 a e you expect in sinus f bradycardia with a mV 0 1st degree AV block? b -1 d C. Intervals k g j +1

mV 0 h -1 i

0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 Seconds Interactive 4-4

How would the ac- tion potential of his AV nodal cell differ from normal?

What medicine --he may be taking-- could have this effect? Interactive 4-5

What reflexes are involved in generating this rhythm?

What is the rhythm? Interactive 4-6

Is the mean QRS axis normal in this 65 year-old man?

What is his rhythm? An EKG taken 3 days ago showed a much taller R- wave and very small S-wave in this lead. What might have happened recently? Interactive 4-7

What does this sug- gest?

What is the mean QRS axis?

What is the rhythm? Interactive 4-8

What is the rhythm?

What could have trig- gered this rhythm? Interactive 4-9. This 66 year-old woman is taking digoxin for con- gestive heart failure.

What is your diagno- sis?

Does she have brady- cardia? Essay or Small Group Questions

107 Heart Rates Escape Beats

1. How can you determine a patient’s 8. How can you distinguish an escape heart rate from an ECG record? beat originating in the atria from beats origi- nating in the AV node or ventricles? Pacemakers Sinus Tachycardia 2. Can you distinguish a sinus rhythm from an AV-nodal rhythm or from an idiov- 9. What are examples of conditions caus- entricular rhythm on an ECG record? ing “sinus tachycardia”?

Sinus Arrhythmia Paroxysmal Supraventricular Tachycar- dia (PSVT) 3. How and why may the respiratory cycle influence the heart rate? 10. How does the re-entry phenomenon cause PSVT. Premature Beats Atrial Flutter and Atrial Fibrillation 4. How can you distinguish between pre- mature beats arising in the atria, AV node, 11. How would you suspect that a person and ventricles? (Make a drawing.) has atrial fibrillation even before taking his/ her ECG? 5. What is a “Pulse Deficit”? Ventricular Tachycardia 6. Why are premature beats followed by a “compensatory pause”? 12. Can you distinguish “ventricular tachy- cardia” from paroxysmal “supraventricular Dangerous Premature Ventricular Con- tachycardia”? tractions (PVCs) Ventricular Fibrillation 7. You are watching the cardiac monitor of a patient who has had a myocardial infarc- 13. Can you recognize ventricular fibrilla- tion. You notice PVCs. When are you con- tion on a cardiac monitor? cerned that these PVCs may signal a dan- gerous arrhythmia, e.g. ventricular fibrilla- 14. What are the signs and symptoms of tion? ventricular fibrillation?

108 15. What steps are you going to take to re- 24. What does a sudden change in the suscitate a person with ventricular fibril- mean QRS axis suggest? lation? Potassium Imbalance 16. Why is epinephrine or vasopressin used in ventricular fibrillation? 25. How would you detect (with an ECG tracing) dangerously low or high serum 17. What is the mechanism of action of potassium concentrations in a patient? Amiodarone? 26. Why are sluggish deep tendon reflexes Atrio-ventricular Blocks associated with hypokalemia?

18. How do you distinguish a first degree 27. What steps could you take in the emer- AV block from a second or third de- gency treatment of hyperkalemia? gree AV block?

19. What is the Wenckebach Phenome- non?

20. How is a first degree AV block related to phase 0 of the AV action potential?

21. Can you name medicines that can cause a first degree AV block?

22. Which patients with an AV block need an artificial pacemaker?

Bundle Branch and Fascicular Blocks

23. How would you recognize “right” or “left” bundle branch blocks on an ECG tracing and which one is potentially more harmful?

109 Integrative Questions

110 Integrative 4-1 This is the heart of a 21 year-old woman who noticed her heart suddenly racing. She is not dizzy or short of breath, nor does she have any chest pains.

2. What are you go- 3. What are you go- 4. What are you go- 5. What are you going to do now? ing to do first? ing to consider next?ing to try next?

1. What is her rhythm? Integrative 4-2. “I can’t breathe --Doc --can’t catch my breath --please give me something to help me breathe,”gasps the 30-year old woman in distress. You hear wheezing sounds as she breathes in and out with great effort. The spaces above her clavicles cave in on inspiration. The nurse has attached her to the moni- tor shown here.

3. What is her rhythm 2. Why this sPO2? and why?

5. How can you help her?

1. What is her prob- 4. Is her BP normal? lem? Integrative 4-3. “I can’t breathe --Doc --can’t catch my breath --please give me something to help me breathe,”gasps the 56-year old man in distress. You hear moist crackles (rales) as he breathe in. His neck veins are distended and he has 3+ pitting edema in both legs. The nurse has attached him to the monitor shown here.

3. What is his rhythm 2. Why this sPO2? and why?

5. How can you help him?

1. What is his prob- 4. Is his BP normal? lem? Integrative 4-4. This patient comes into your office.

1. What is your diag- 2. What next? 3. What next? nosis?

4.What now? Integrative 4-5. You are shopping in the Mall when you see an elderly woman collapsing. She is unconscious, not breathing, no pulse. 1. What are you going to do? 4. What next?

2. EMS arrives. You see this rhythm on their moni- tor. What are you going to do?

5. The EMS inserts an endotracheal tube. Why?

3. One of the EMS has given you an Ambu-bag with oxygen flowing into it and has inserted an IV line into the patient’s arm. What next? Integrative 4-6. Seconds after defibrillating the woman in 4-5 you look up at the monitor. This is what you see. 5. “She is taking fu- rosemide - 40 mg 3. What is her prob- daily,”a bystanders 1. What is this lem? says holding up a bot- rhythm? tle he has taken from her purse. What are you going to do with this information?

2. What now? 4. Are you going to 6. What now? shock her again? Integrative 4-7. You gave the woman with PEA from 4-6 a bolus of normal saline. Her blood pressure is now 60 mmHg by palpation. She is still unconscious, gasping for air every now and then. Here is her rhythm strip from the EMS defibrillator.

3. What could be re- 1. Can you stop 5.Now what? CPR? sponsible for her ab- normal rhythm?

2. Does she have a 4. Isn’t there anything 3rd degree AV block? you can do for her? 8

EKG Quizzes EKG Quiz A

119 EKG Quiz A: Please select the one best answer.

Question 1 of 10 76 year-old man waiting for a procedure in the electrophysiology lab.

A. atrial flutter with 4:1 AV block

B. wandering atrial pacemaker

C. sinus arrhythmia

D. atrial fibrillation

Check Answer EKG Quiz B

121 EKG Quiz B: Please choose the one best answer.

Question 1 of 10 65-year old man is feeling weak and dizzy.

A. sinus tachycardia

B. PSVT

C. hypokalemia

D. left bundle branch block

Check Answer EKG Quiz C

123 EKG Quiz C: Please choose the one best answer.

Question 1 of 10 83 year-old man complains of dizziness.

A. right bundle branch block

B. premature AV nodal beats

C. 1st degree AV block

D. ventricular escape beats

Check Answer EKG Quiz D (Advanced)

125 EKG Quiz D - Advanced : Please choose the one best answer.

Question 1 of 10 75 year-old woman complaining of palpitations.

A. inferior infarct, age unknown

B. right axis deviation

C. wandering atrial pacemaker

D. PVCs

E. A and D

F. A and C and D

Check Answer EKG Quiz E (Advanced)

127 EKG Quiz E (Advanced). Please select the one best answer.

Question 1 of 10 A 73 year-old man brought in by his daughter because of syncopal episodes.

A. inferior infarct, age unknown

B. right bundle branch block

C. 3rd degree AV block

D. left axis deviation

E. A and C

F. A and B and C and D

Check Answer 9 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