Full transcript
0:05Hello everyone and welcome to our module
0:07on EKG basics. The EKG is a visual
0:10representation of electrical activity as
0:13it moves through the heart. So in order
0:14to understand EKGs, we need to review
0:16how electricity moves through the heart
0:18under normal conditions. So normally the
0:20SA node located on the right atrial free
0:22wall is the pacemaker of the heart and
0:24it depolarizes and sends a wave of
0:27depolarization spreading to myioytes in
0:29the left atrium and the right atrium.
0:31From there depolarization funnels
0:33through the AV node and then goes to the
0:34his bundle and then the left and right
0:36bundle branches and finally it reaches
0:38the perkingi fibers which are embedded
0:40in the myioytes of the left ventricle
0:42and right ventricle and when the
0:43perkingi fibers deolarize they lead to
0:45ventricular deolarization.
0:48Shown on the screen is a typical example
0:50of electrical activity as it moves
0:52through the heart as depicted by the
0:53EKG. The EKG picks up electrical
0:56activity and plots it versus time. So
0:58time is always the x-axis and the y-axis
1:00is electrical activity. And anytime
1:02there's an electrical event in the
1:04heart, it can generate either a positive
1:06or negative deflection of the EKG. A
1:08positive deflection is upward, a
1:09negative deflection is downward. So each
1:11of the waves represents some electrical
1:13event in the heart. So let's go through
1:15what each of them represent right now.
1:16The Pwave is the first event in the
1:18cardiac cycle and that represents atrial
1:20depolarization. The Pwave is followed by
1:23this flat section of the EKG tracing and
1:25that section is caused because it takes
1:28time for electricity to move through the
1:30AV node, His bundle, bundle branches and
1:32perkingi fibers. Once electricity moves
1:34through all of these structures, it
1:36reaches the ventricles. And when the
1:38ventricles deolarize, they generate the
1:40largest section on the EKG. That's
1:42called the QRS complex and it represents
1:44ventricular depolarization.
1:46This complex can include a negative
1:48deflection called a Q-wave, a positive
1:51deflection called an Rwave, and another
1:53negative deflection called an S-wave.
1:55Following the QRS complex, there is
1:57something called the T-wave, which
1:58represents repolarization of the
2:00ventricle. You do not see a wave showing
2:03repolarization of the atria. That's
2:05because atrial repolarization occurs at
2:07the same time as the QRS complex and
2:09therefore atrial repolarization is
2:11embedded within the QRS complex. So
2:14here's a normal 12 lead EKG and it's
2:16called a 12 lead EKG because there are
2:1812 different recordings of the
2:20electrical activity of the heart. The
2:22leads each have a name. Leads one, two,
2:24and three are always shown on the left
2:26side of the tracing. Next comes AVR,
2:28AVL, and AVF. This is followed by the V
2:31leads V1 2 and three and V4 5 and V6.
2:34Along the bottom of the EKG, there are
2:36often one or more so-called rhythm
2:38strips. Here, V1 is shown as a rhythm
2:40strip and lead two as a rhythm strip. On
2:42these rhythm strips, multiple QRS
2:44complexes are recorded in a row so that
2:46you can better determine the heart
2:47rhythm. And I've expanded lead two at
2:50the top of the screen so that you can
2:51see that each lead has a Pwave, a QRS
2:53complex, and a T-wave just like we
2:55talked about on the last slide. So most
2:57students understand the Pwaves and the
2:59QRS complexes and what they represent.
3:01But what's often tricky to understand is
3:03what each of the different leads on the
3:05surface EKG represent. Notice that the
3:08QRS complex in lead 2 is all pointing
3:10upward. Notice that the QRS complex in
3:13lead AVR is all pointing downward.
3:15Notice that in lead V3, the QRS complex
3:18is pointing slightly upward and slightly
3:20downward. We have to explain this. All
3:22these leads are recording depolarization
3:24of the same left ventricle. So why does
3:27lead V2 show the QRS complex as upward,
3:30lead AVR as downward, and lead V3 as
3:32partly upward and partly downward?
3:34That's the second key point about EKGs
3:36that we have to explain, and that's what
3:38we're going to talk about next. So let's
3:40go back to this drawing of electrical
3:42activity as it moves through the heart.
3:43And let's imagine that the left and
3:45right ventricles are deolarizing. When
3:47that happens, we have electrical
3:48activity moving in lots of different
3:50directions. Some is moving this way to
3:51deolarize the left ventricle. Some is
3:53going this way to deolarize the right
3:55ventricle. But if we could sum up all
3:57those electrical forces, we would get a
3:58summation vector that looks like this.
4:01Each of the 12 different EKG leads is
4:03going to look at this summation vector
4:05from a different vantage point. And
4:07therefore, each of the 12 leads is going
4:09to show the QRS complex, which
4:11represents ventricular deolarization as
4:13a different shape because it's looking
4:15at the same summation vector of forces
4:17from a different vantage point. To make
4:19this easier to understand, let's imagine
4:21we have a car moving down the street
4:22being watched by person one and person
4:25two. Person one will say that the car is
4:27moving away from them. Person two will
4:29say that the car is moving towards them.
4:31They're both correct. They're both
4:32watching the same phenomena. It's just
4:34that they are observing it from a
4:35different vantage point. And that's what
4:37each of the 12 leads on the EKG does. It
4:39observes electrical depolarization of
4:41cardiac structures from a different
4:43point of view. Here's another drawing of
4:46the heart. And once again, I've shown an
4:47arrow representing the summation vector
4:49of electricity as it moves through
4:51cardiac structures. On this drawing,
4:53I've also shown the vantage point for
4:55all of the EKG leads. So, let's see if
4:57we can make sense of this. Now, so lead
4:59AVR views electrical activity in the
5:01heart from the right side of the heart.
5:03This means that all electrical activity
5:05from the point of view of lead AVR is
5:07moving away from the lead. And when
5:09electrical activity moves away from a
5:11lead, it generates a negative deflection
5:13on the surface EKG. Contrast lead AVR
5:16with leads one and AVL. They view
5:18electrical activity from the left side
5:20of the heart. So they will see that
5:21summation vector of forces moving
5:23towards them. And when electrical
5:25activity moves towards an EKG lead, it
5:27generates an upward deflection on the
5:29surface EKG. Leads 2, three, and AVF
5:32view electrical activity from the
5:33inferior portion of the heart. And leads
5:36V1 through V6 view electrical activity
5:39across the heart with V1 being more
5:41towards the right side and V6 being more
5:43towards the left side. So now let's look
5:45at a normal 12 lead EKG and see if we
5:47can make sense of it. Here's lead AVR
5:49and notice that the QRS complex is going
5:51entirely downward. That's because lead
5:53AVR is positioned on the right side of
5:55the heart and it sees all electrical
5:57activity moving away from it. Lead V6,
6:00on the other hand, is located on the
6:02left side of the heart. It sees all
6:03electrical activity moving towards it.
6:05Therefore, the QRS complex is entirely
6:07upward. Lead V3 is in the middle and so
6:10it has some of the QRS going upward and
6:12some going downward. So all these leads
6:14are looking at the same electrical
6:15phenomena. All the QRS complexes
6:18represent depolarization of the same
6:20ventricle but they look different
6:21because each lead is looking at this
6:23phenomena from a different point of
6:25view. So here's a summary slide of the
6:27key points that we've just discussed.
6:29These are very important for you to
6:30understand in order to interpret EKGs.
6:32Key point number one is that the
6:34different waves like the Pwave and the
6:36QRS complex represent repolarization and
6:38depolarization of structures in the
6:40heart. Key point number two is that EKGs
6:43have 12 leads and each lead watches the
6:45same thing but from a different vantage
6:47point. And when the electrical activity
6:48moves towards a lead that generates an
6:50upward deflection. When it moves away
6:52from a lead that generates a negative
6:54deflection. Let's briefly discuss
6:56cardiac pacemakers. As I mentioned
6:58earlier, the SA node is the dominant
7:00pacemaker of the heart under normal
7:02conditions. There are however other
7:04pacemakers that exist but they are
7:05slower and therefore the essay node
7:07dominates them and controls the
7:09depolarization rate of the heart.
7:11However, if the essay node fails one of
7:13the other pacemakers can take over. So
7:15as you may know a normal heart rate is
7:17about 60 to 100 beats per minute. That's
7:19the rate at which the essay node
7:20deolarizes. However, if the essay node
7:22were to fail for any reason the AV node
7:24could begin to deolarize the heart, but
7:26it can only do so at a rate of about 40
7:28to 60 beats per minute. The hiss bundle,
7:30the bundle branches and the perkingi
7:32fibers can also potentially become
7:33pacemakers. However, they are at even
7:36slower rates of about 25 to 40 beats per
7:38minute. You should be aware that
7:39conduction velocity, in other words, the
7:41speed with which electricity moves
7:43through the heart is slowest in the AV
7:45node. This is very important
7:47physiologically. By slowing conduction
7:49through the AV node, the heart has more
7:50time for the ventricle to fill with
7:52blood and this helps make the organ a
7:54more effective pump. conduction velocity
7:56is fastest in the perkingi fibers and
7:58the conduction of electrical activity
8:00through the atria and ventricular
8:02myioytes is in the middle between these
8:03two extremes. If we go back to this
8:05slide, the reason that the QRS complex
8:08does not follow immediately after the
8:10Pwave is because it takes time for
8:12electrical activity to move through the
8:13AV node bundle bundle branches and
8:15perkingi fibers. Most of this time is
8:18occupied by conduction moving through
8:20the AV node. That's because that's where
8:22conduction is slowest. Let's talk about
8:24how you can determine heart rate from
8:25the surface EKG. You can do this by
8:27figuring out how much time passes
8:30between two QRS complexes. Remember,
8:32each QRS complex represents
8:34depolarization of the left ventricle. In
8:36other words, it represents a heartbeat.
8:38So, the time between QRS complexes
8:40varies with the heart rate. And if you
8:42can figure out that time, you can
8:43calculate the heart rate. So, the way
8:45this is done is by figuring out how many
8:47boxes pass between two QRS complexes.
8:49And there are two types of boxes.
8:51So-called big boxes are represented by
8:53the dark lines. I'm marking one big box
8:55with my pen here. Between each big box
8:58are five smaller boxes. So the small
9:00boxes represent 40 milliseconds of time
9:03and the big boxes represent 200
9:05milliseconds a time. So if you want, you
9:07can count up how many milliseconds pass
9:09between two QRS complexes and do the
9:11math and calculate the heart rate.
9:13However, no one really does it that way.
9:15The way it's done is by using a quick
9:17method, which involves figuring out how
9:18many big boxes pass between two QRS
9:21complexes. So to do this, you need to
9:23identify a QRS complex that falls on a
9:25solid line like this one right here. You
9:28then figure out how many big boxes pass
9:30before the next QRS complex. You can see
9:32that one passes, two, three, so about
9:35three and a half, just a little under
9:37four big boxes pass before the next QRS
9:40complex. Once you know how many big
9:42boxes, you can determine the heart rate.
9:43If there were just one big box between
9:45the QRS complexes, the heart rate would
9:47be 300. If there were two, it would be
9:49150. If there were three, it would be
9:51100. Each additional big box represents
9:54a heart rate of 300 divided by the
9:56number of big boxes. So, in other words,
9:58three to five big boxes between a QRS
10:00complex is a normal heart rate, a heart
10:02rate between 60 and 100. And that's what
10:04we've got here. We've got about three to
10:06four big boxes, which represents a heart
10:08rate of somewhere around 75 or so, a
10:11normal heart rate. And this is the
10:13simple way that everyone does to eyeball
10:14the heart rate. You just look at how
10:15many big boxes are between the QRS
10:18complexes. Divide the number 300 by the
10:20number of big boxes and that will
10:21estimate the heart rate for you. Next,
10:24we're going to talk about determining
10:25something called the QRS axis, which can
10:28be important in different disease
10:29states. And in order to understand the
10:31QRS axis, we need to go back to this
10:33picture, which shows the summation
10:34vector of electrical forces moving
10:36through the heart. Normally, that
10:38summation vector moves downward and
10:40toward the right. If the heart is
10:41oriented normally and electrical
10:43activity is being conducted normally
10:45from the SA node to the ventricles. Now
10:48let's suppose we took a grid and laid it
10:49directly over the heart and labeled it
10:51such that 0 degrees was to the right,
10:53positive 90° was to the bottom plus 180°
10:57was to the left and negative 90° was to
11:00the top. If we did this, a normal QRS
11:03vector, meaning a QRS vector generated
11:05by normal depolarization of the SA node
11:07with a heart in the normal orientation
11:09inside the chest, would generate an axis
11:12that was between minus30 and positive
11:1490°. In other words, it would usually be
11:16in this bottom right hand quadrant here,
11:17or else it could go a little bit up into
11:19the top left hand quadrant, but it would
11:21never go beyond negative 30 degrees. And
11:23this is what's called a normal QRS axis.
11:25This is where the axis is located in
11:27patients who have normal hearts
11:28depolarizing under normal conditions. It
11:31turns out that there are a number of
11:32conditions that can shift the QRS axis
11:34to the left. This is called a left axis
11:37deviation. This happens when the QRS
11:39axis is between minus30 and minus 90.
11:42There are a number of things that can do
11:43this. Some of them that are worth
11:45knowing include a left bundle branch
11:46block. This can also occur when you have
11:48a ventricular rhythm like ventricular
11:50tacocardia. This is a heart rhythm that
11:52is not originating in the SA node, but
11:54instead is coming from the ventricle
11:56itself. There are also some conditions
11:58that can cause a right axis deviation.
12:00This occurs when the QRS axis is between
12:02positive 90 and plus 180. And some of
12:05the conditions that can do this include
12:06a right bundle branch block, right
12:08ventricular hypertrophy, and there are
12:09many, many others. With that in mind,
12:12let's talk about how you can determine
12:14the QRS axis using the surface ECG. In
12:17order to do this, we're going to look at
12:19specific leads on the ECG and decide
12:21whether the QRS is pointing mostly up
12:23like this, that's a positive deflection,
12:25or mostly downward, which is a negative
12:27deflection. And we're going to start by
12:29looking at lead one. Lead one, when
12:31there is a positive or upward
12:32deflection, creates a vector of
12:34electricity going in this direction
12:36towards 0 degrees. When lead one is
12:38negative, it creates a vector going in
12:40this direction away from 0 degrees. The
12:42next lead we'll look at is lead AVF.
12:45Lead AVF is an inferior lead. When there
12:47is a positive deflection in lead AVF,
12:50that is a vector of electricity going
12:51downwards towards 90°. And when there's
12:54a negative deflection in lead AVF, that
12:56is a vector going away from 90°. So we
12:58can take these two vectors, the vector
13:00for lead AVF and the vector for lead
13:02one, and sum them together, and we might
13:04get a vector something like this. And
13:05that is the QRS axis. And I've cleared
13:08away my ink so I can show you that a
13:10normal QRS axis would have a summation
13:12vector somewhere between -30 and plus
13:1490. And because a normal axis includes
13:17this area here from 0 to minus30, many
13:19people instead of using lead AVF use
13:22lead 2. Lead 2 instead of going from +
13:2590 to - 90 is actually out here at plus
13:2860°. And so if you use lead V2 together
13:31with lead V1, then anytime both of those
13:33leads are positive, you will have an
13:35access somewhere in here, which is
13:36normal. So that's what many people do.
13:38If you've got a positive QRS vector in
13:41lead one, that means you've got a line
13:43going in this direction. And if you have
13:44a positive QRS vector in lead 2, that
13:47means you have a line going in this
13:48direction. And therefore, their
13:50summation is going to be somewhere in
13:52this range here, which is normal. Now,
13:54in reality, nobody ever calculates an
13:56exact number for the QRS axis. Instead,
13:59most of us use a quick method to
14:01determine whether the axis is normal,
14:03leftward deviated, or rightward
14:04deviated. So, let me go over that quick
14:06method. Now, to use the quick method,
14:08you first glance at lead AVR. Lead AVR
14:10should always be negative. If lead AVR
14:13is upright, it usually means the limb
14:15leads are reversed. In other words, it
14:16means someone has put the leads on the
14:18patient incorrectly. So, to use the
14:20quick method in actual practice, you
14:22start by glancing at AVR to make sure
14:23the leads are properly positioned. And
14:25if they are, AVR will be negative as
14:27shown in this picture on the screen.
14:29Once you determine that the leads are
14:30placed appropriately, you then look at
14:32just two leads on the 128 EKG, leads one
14:34and two. If they're both positive, like
14:36I've shown on the screen here, then the
14:38axis is between 0 to 90 and the axis is
14:40normal. And most of the EKGs you'll look
14:42at have a normal axis. So, this is a
14:44quick way to rapidly determine that the
14:46axis is normal and that you don't need
14:47to go any further looking for whether
14:49it's a left or right deviation. If
14:51they're not both positive, then you have
14:53a left or right axis deviation and you
14:55need to figure out which one you have.
14:57For a left axis deviation, all you need
14:59to do is look at lead two. If lead 2 is
15:01negative, it means the axis is between
15:03minus30 and minus 90 and therefore you
15:05have a left axis deviation. The one
15:07exception to this is sometimes lead 2
15:09will look like I've shown here where
15:11it's partly upward and partly downward.
15:13This is called a physiologic left axis
15:15which is slightly to the left but still
15:17within normal limits. To determine
15:19whether you have a right axis deviation,
15:21all you need is lead one. If the QRS
15:23complex is negative in lead one, like
15:25I've shown here, then you have a right
15:26axis deviation, which is between 90 and
15:29180 degrees. So, here's a summary of the
15:32quick method, which is what most
15:33cardiologists I know use in actual
15:35practice. You look at AVR quickly to
15:37make sure it's negative, which tells you
15:38the leads have been placed properly. You
15:40then look at lead one and two. If
15:41they're both positive, the axis is
15:43normal. If lead two is negative, you
15:45have left axis deviation. And if lead
15:46one is negative, you have right axis
15:48deviation. And I've shown you the shapes
15:50of all these on the screen here so you
15:51can remember them. I'll finish this
15:54module by going through the different
15:55time intervals in the surface EKG. And
15:57I'll start with the PR interval. This is
15:59the time from the start of the Pwave to
16:01the start of the QRS complex. And a
16:03normal PR interval is 120 milliseconds
16:05to 200 milliseconds in duration. And
16:08it's very easy to identify PR
16:10prolongation with your eye. That's
16:11because remember what I told you before,
16:13a big box represents 200 milliseconds in
16:16time. So if the PR interval is longer
16:17than one big box in duration, then the
16:20PR interval is prolonged. And you can
16:22develop a prolonged PR interval from
16:23firstdegree AV block and I talk about
16:25this and other forms of AV block in a
16:27separate video. You can also develop a
16:29short PR interval if you have a bypass
16:31track caused by the wolf parkinson white
16:33syndrome and I talk about WPW in its own
16:35video as well. Next is the QRS interval.
16:38This is the time from the start of the
16:40QRS complex to the end of the QRS
16:42complex. And a normal QRS interval is
16:44less than 120 milliseconds in duration.
16:47And I told you before that a small box
16:49in the surface EKG represents 40
16:51milliseconds. This means that a normal
16:53QRS complex should be less than three
16:55small boxes in duration. And if we look
16:58at this blown up image on the top right
16:59side of the screen, you can see that the
17:01QRS complex starts and ends before three
17:04small boxes have passed. Therefore, this
17:06is a normal QRS complex. And there are a
17:08number of causes of a prolonged QRS
17:10complex, but some of the most common are
17:12bundle branch blocks. You develop a QRS
17:15interval prolongation in a right bundle
17:17or left bundle branch block. And in the
17:19video on aven bundle branch blocks, I
17:20talk in detail about how to recognize
17:22right and left bundle branch blocks.
17:24Next is the QT interval. This is the
17:26time from the start of the QRS complex
17:28to the end of the T-wave. The QT
17:30interval varies with your heart rate.
17:32So, in order to determine whether a QT
17:34interval is normal, you need to
17:36determine the heart rate and then
17:37correct the QT interval. This is not
17:39something I recommend you worry about
17:41doing as a medical student. A rule of
17:43thumb you can use, however, is that the
17:45T-wave should end before you are halfway
17:47between two QRS complexes. So, if we
17:50take the space between these two QRS
17:52complexes and mark the halfway point,
17:53you can see that the T-wave in this
17:55example has finished before that halfway
17:57point. And that's what you see in a
17:59patient who has a normal QT interval.
18:01There are relatively few causes of a
18:03short QT interval, but one that you
18:04should definitely know is hypercalcemia.
18:06On the CCG on the left side of the
18:08screen, you can see that the T-wave
18:10begins almost immediately after the QRS
18:12complex. There is no flat portion of the
18:14EKG between the QRS and the T-wave. And
18:16this is what you can see in patients who
18:18have an elevated calcium level. There
18:20are a number of causes of a prolonged QT
18:22interval. These include hypocalcemia.
18:24That's easy to remember. It's the
18:25opposite of the cause of a short QT
18:27syndrome. also a number of drugs
18:29especially anti-arithmics and also the
18:31long QT syndrome which we'll talk about
18:33in a second to understand why calcium
18:35affects the QT interval let's review the
18:38role of calcium in the meiocy action
18:40potential calcium is responsible for
18:42phase two of the meioy action potential
18:44this is called the plateau phase and in
18:46this phase calcium is moving into
18:48myioytes in the setting of hypocalcemia
18:51there's less driving force to move
18:53calcium into meioytes so it takes longer
18:56for calcium to fill the cell and this
18:58phase is going to continue until enough
19:00calcium has gotten inside of the
19:01meioytes. Therefore, in the setting of
19:03hypocalcemia,
19:04this plateau phase, phase 2, is drawn
19:07out and it takes longer for meiocytes to
19:09depolarize and repolarize. That means
19:12that it will take longer for the QT
19:14interval to occur because that phase of
19:16the EKG represents the time required for
19:19myioittes in the ventricles to
19:21depolarize and repolarize. There is a
19:23special form of ventricular tacoc cardia
19:25called torsad deance. This word means
19:28twisting of the points and it's a form
19:30of ventricular arhythmia that occurs
19:31with the QRS complexes getting smaller
19:33and then larger and then smaller again.
19:35And this is the feared outcome of QT
19:37prolongation. If your QT interval
19:39becomes prolonged, you will develop
19:41torsad plants which results in cardiac
19:43arrest and can result in death. And this
19:45is why anti-arithmic drugs which prolong
19:47the QT interval are dangerous because if
19:50they prolong it too much this arhythmia
19:52will develop and that's how patients can
19:53die from taking anti-ythmic drugs. You
19:56can also get torsad plants from
19:57hypocalemia and hypommagnesmia. This is
20:00not related to QT prolongation. This is
20:02related to effects of these electrolyte
20:04abnormalities on ventricular
20:05depolarization. Rarely you can get
20:08torsad plants from hypocalcemia. It's
20:10interesting. Hypocalcemia prolongs your
20:12QT interval. However, it's uncommon for
20:14hypocalcemia to lead to sorsad deplants.
20:17I told you that one of the causes of a
20:19prolonged QT interval was something
20:20called the long QT syndrome. There is a
20:23congenital disorder called the
20:24congenital long QT syndrome that is
20:27caused by abnormal potassium and sodium
20:29channels in the heart. This is a very
20:31rare disorder, but the reason they may
20:33ask you about it on the USML step one
20:35exam is because it's a way to test your
20:37underlying knowledge of the basic myiocy
20:40action potential. Shown in blue on the
20:42screen here is a normal cardiac myioite
20:45action potential. Shown in red is what
20:47the action potential can look like when
20:49either the sodium channels or the
20:50potassium channels are abnormal. Sodium
20:52channels are responsible for this phase
20:54of the action potential. Potassium
20:56channels are responsible for this phase.
20:58If either the sodium or potassium
21:00channels are abnormal, the meiocy action
21:02potential can get drawn out as I've
21:04shown in this red example on the screen.
21:06When it takes longer for me to
21:08depolarize and repolarize that results
21:10in a prolonged QT interval on the
21:12surface EKG and that's what happens to
21:14children born with the congenital long
21:16QT syndrome caused by abnormal potassium
21:18or sodium channels. The way this may be
21:20presented in a board question is as a
21:22patient with a family history of sudden
21:24death. The reason there is a family
21:25history of sudden death is because the
21:27congenital long QT syndrome runs in the
21:29family and other family members have
21:31died of torsad plants caused by a
21:33prolonged QT interval. A classic
21:35scenario is a young patient who has
21:37recurrent seizures. The patient is not
21:39really having seizures. They're actually
21:41passing out from torsad to ponance and
21:43the EKG will show a long QT interval.
21:45There is also a variant of the
21:47congenital long QT syndrome that has
21:49been well described called the Jerel and
21:51Lang Neielson syndrome. This occurs in
21:53Norway and Sweden. It results in the
21:55long QT syndrome in association with
21:57congenital deafness. It's very rare, but
21:59they sometimes ask you about this on
22:00board exams. Much more common than the
22:02congenital long QT syndrome is the
22:04acquired long QT syndrome. This is where
22:06a patient has a normal QT interval on
22:08their EKG but acquires a prolonged QT
22:11interval because of a drug they are
22:13taking. This is commonly caused by a
22:15number of anti-arithmic drugs which I
22:16discuss in another video. It's also
22:18commonly caused by levofluxin which is a
22:21fuoroquinolone antibiotic. It can also
22:23be caused by haldol which is an
22:24antiscychotic and it can be caused by
22:26many many other drugs. And importantly
22:29for families and family members who have
22:31the congenital long QT syndrome, they
22:33need to avoid all these drugs. If their
22:35QT is prolonged at baseline from the
22:37long QT syndrome and then they take one
22:39of these drugs, it can be potentially
22:41fatal. Let me mention peaked T- waves.
22:43These are T- waves that are unusually
22:45tall like these I've shown on the screen
22:47here. This is classically seen in
22:48hypercalemia. It can also occur very
22:51early on when patients develop eskemia.
22:53These are called hyperacute T- waves and
22:55they often preede ST segment elevation
22:57in acute eskemia. Lastly, I'll mention
23:00Uavs. This is a deflection that comes
23:02after the T-wave, hence the name Uwave.
23:04It's usually an upward deflection just
23:06like the T-wave. The origin of Uaves is
23:08not clear. One of the prevailing
23:09theories is that it might represent
23:11repolarization of the perkingi fibers,
23:12although there are other theories.
23:14Uwaves can be seen on a normal EKG but
23:17the classic situation in which prominent
23:19U waves are seen is in the setting of
23:21hypocalemia.
23:22And that concludes our module on EKG
23:24basics.