Matters Of The Heart-Misc.

Artifical Pacemakers-

People who have a severe heartblock would normally not have sufficient cardiac output to perform activities of daily living. However thanks to a relatively small battery, some wire, and a doctor who is brave enough to put them inside your chest, a patient with heart block can live many more years with adequate cardiac output to live an active and healthy life.

There are some importiant things to remember when caring for people who have artificial pacemakers:

1) Don't take their blood pressure on the arm closest to the pacer battery!! (Sorry, old CNA habit)

2) This type of rhythm will appear different from a regular PQRST complex, depending on where the pacer is positioned in the heart. Don't freak out if you see a tall, very narrow pacing spike followed by a wide ventricular complex; this just means the artificial pacer is in the ventricles.

3) There are different types of artificial pacers, someof them are temporary and worn outside of the body, some of then are internal, some of then also contain defibrillators (which show up as a REALLY TALL spike/waveform)

Heart Transplant

In a heart transplant, the portion of the patient's atria that has the SA node is not.removed when the new heart is put.in. Because of this, there will be two P waves on the PPQRST complex: the first one is native to the patient, the second from the donor heart.

A heterotopic heart transplant (in which the native heart is not removed) there are two sets of PQRST wavelengths. (Because the patient has two hearts). One is upright, and one is inverted.

This blog series has been my studies compiled from the book called 'Rapid Interpretation of EKG'S' By Dale Dubin.

If you are interested in learning about heart physiology and EKG interpretation, I highly recommend this book. :)

Matters Of The Heart-Electrolyte and Drug Imballance

There are electrolyte imballances that cause certian arrhythmias:

Potassium

(acts as a partner to sodium, helps stablize the myocyte's electrical energy during repolarization)

Too much potassium is called Hyperkalemia, and results in peaked T waves, flattened P waves, and a wide QRS complex on an EKG.

Too little potassium is called Hypokalemia, and results in flat T waves as well as the creation of another wave after the T wave (called a U wave...)

These signs will increase in severity as the electrolyte imbalance increases.

Calcium

This ion functions in the AV node, his bundle, and branches. It also excellerates ventricular depolarization/repolarization.
Hyper calcemia results in a short QT interval (shortens everything except for the P wave, because that's the atria and calcium speeds up the ventricles.)

Hypocalcemia results in a prolonged QT interval.

There are also certian arrhythmias associated with drug toxicity:

Digitalis

Digoxin is a drug that treats Atrial fibrillation by slowing the SA node (it also inhibits the AV node from being receptive to the extra atrial impulses).
However, the theraputic range for this drug is narrow, and too much can cause heart block, premature beats, or both!

If the toxicity progresses, eventually the irritation and heart block will cause ventricular rhythms such as Ventricular tachycardia and fibrillation from taking over.

It's importiant to monitor drug levels in patients who take digoxin, as well as look for the charactaristic, 'dipping' ST segment depression.

Quinidine

Is another antiarrhythmic. Like Digoxin, it is for the treatment of A Fib. It works as a sodium channel blocker, it lengthens depolarization and repolarization. On an EKG strip, toxicity with this drug appears as wide, notched P and QRS waves, a depressed ST segment, and a U wave present. If not corrected, this toxicity can also lead to Torsades de Pointes.

Matters Of The Heart-Hemibock

Sometimes a heart attack's worst damage is not to the myocardial damage itself, but to the nerve bundles that help distribute the depolarization to the ventricals. An occlusion in arteries supplying oxygent to particular bundle brances can cause a type of heart block called a hemiblock.

Cardiac Circulation

Even though the heart is filled with blood, this is not the same blood that supplies the heart with nutrients. After the blood leaves the heart for the aortia, two main arteries break off almost immediately and lead back towards the heart from the outside.These are called coronary arteries and they are the ones that supply the heart with nutrients. The most importiant for supplying the nerve fibers with nutrients are the two following:

Anterior Decending section of the Left Coronary Artery

Right Coronary Artery

Stupid Memory Thingy:

Yesterday I was trying to memorize which artery goes to which nerve bundle (because they kinda twist around and branch out like fingers to supply different areas) So wrote an outline that would help me remember:

I took a pin and wrote 'Right Coronary Artery' on the thumb and pinkie of my dominant hand.

The three middle fingers of my dominant hand I wrote 'Anterior Decending Left Coronary Artery' (or I would have, but it was too long so I wrote 'ADLCA')

On my non-dominant hand I wrote out the sections of the nerve fibers below the atria:

The AV node is my wrist

The Bundle of His is my hand

My thumb is the Right Bundle Branch

My index finger is the anterior segment of the left bundle branch

My ring finger is the Posterior Segment of the Left Bundle branch.

Now when I hold my hands together and fold my fingers over like I'm going to say a prayer (with my dominant hand's thumb on top) an outline forms that tells me which arteries suppy which sections of the AV conduction system:
The right coronary artery (on my thumb) is supplying blood to the AV Node and the His Bundle (on my wrist and the top part of my hand). (On my Pinkie) It is also supplying the posterior divistion of the Left Bundle Branch.

The Anterior Division of the Left Coronary Artery on my three middle fingers suppies the right bundle branch, the anterior segment of the left bundle branch, as well as also supplying the Postertior division of thet left bundle branch.

It helped me visualize the bundle branch fasicles and the arteries that serve them. I think it would have been more convenient to reverse the hands, because I normally rest the thumb of my non-dominant hand on top when I fold my hands, but it still worked.

Types of Hemiblock-

Hemiblocks are catergorized by the section of the bundle branches in which they disrupt electrical energy.

Anterior Hemiblock blocks the anterior division of the left bundle branch.

(The Anterior Division of the Left Coronary Artery supplies this area with blood)

On an EKG, this block will be revealed by a slightly widened QRS and an altered Q wave in lead I, as well as an altered S wave in lead III (abreviated S1Q3). (Left Axis Deviation)

Posterior Hemiblock Blocks the posterior divistion of the left bundle branch

(This area is supplied by both the Anterior Division of the Left Coronary Artery and the right coronary artery)

On an EKG, this block will be revealed by a normal or slightly widened QRS complex and an altered S wave in lead I, as well as an altered Q wave in lead III. (Abrevieated S1Q3). (Right Axis Deviation)

Right Hemiblock (or Right Bundle Branch Block) blocks the right bundle branch.

(This area is supplied by the Anterior Decending Left Coronary Artery)

On an EKG, this block shows minimal Right Axis Deviation, because the net electrical activity of the heart is moving away from this area anyway. However, this type of block often occurs with an anterior hemiblock (because they are supplied by the same artery!).

Complete Heart Block (involving the AV node/Bundle of His)

(Supplied by the right coronary artery)

The atria and ventricles will beat indepenedently of each other at an inherent rate.

Intermittent Mobitz

This happens when two of the three bundle branch pathways to ventricular depolarization are blocked, but the third still works intermittently.

This will appear as a bundle branch block of the perminently disabled fasicles, with an occasional missing QRS complex that is blocked by the remaining semi-functional bundle branch.

Because the atria are conductiong electricity normally, the P wave will always be present (and not premature), even when it is not conducted to the ventricles. (The problem is below the atria, so there are no premature atrial beats.)

Matters Of The Heart-Escape and Premature Beats/Rhythms

Escape Beats and Rhythms

So remember back when I was talking about how each of the myocites has a property called automaticity...which means it can generate an electrical impulse and become a pacer foci for the other myocardial cells to respond to?
This is supposed to act as a safeguard it keeps the heart beating even when the normal pacing is disturbed. But sometimes this pacing activity persists even after normal SA node pacing has resumed.

These automaticity foci are said to escape the normal SA node conduction. When this happens for only one or a few beats (because the SA node had resumed pacing activity) it is called an "escape beat". When it happens for an extended period of time, it is called an escape rhythm.

For instance, lets say a patient's SA node.has stopped pacing activity and the patient had gone into Sinus Arrest. After a short pause, an automaticity foci in the atria picks up pacing activity and the rhythm becomes an atrial escape rhythm. On an EKG strip, this rhythm looks very similar to the PQRST waveform (but the P waves might be of a slightly different shape), with a rate of 60-80 bpm.

If Sinus Arrest occurs and no automaticity foci pick up pacing activity, an automaticity foci in the atrio-ventricular junction will start to pace depolarization. This is called a junctional escape rhythm. On an EKG strip thse will be noted to pace slower then atrial foci (40-60bpm)  and because of the retrograde dispursement of the depolarization, P waves may not be visable. If P waves are visable, they will be inverted and may be before or after the QRS complex. 

If a ventricular focus is not stimulated from a pacer from the atria or the AV junction, it's own pacers will escape and an a ventricular escape rhythm will be seen on an EKG strip. This type of rhythm is slow (the ventricles only pace 20-40bpm). The depolarization wave goes backward, so QRS complexes are wide, and the P waves are inverted.

Premature Beats-

If the heart is under stress from certian drugs, hormones, sympathetic simulation, a deficit of certian elctrolytes, or lack of oxygen  (even if normal SA node pacing and conduction are intact) the foci may become irritable and produce an extra heartbeat. This is called  premature beat and can occur at any of the three levels of the heart: Premature Atrial Beats, Premature Junctional Beats, Premature Ventricular Beats. On an EKG strip, these types of pacing activity will appear as an "early" PQRST-like complex that may disrupt another waveform whose appearance will vary depending on the site of origin:
Altered P waves=Premature atrial beat
Absent or retrograde P waves=premature junctional beat
Retrograde P waves and wide QRS complex=Premature Ventriclar Beat...more commonly called a Premature Ventricular Complex (PVC).

Sometimes multiple 'premature' impulses occur in a series, such as in bumigeminy (every other beat is premature) or trigeminy (every third beat is premature). If stressors are unrelieved this may progress to a run of premature beats, and eventually (if it continues to be unrelieved) it may convert to a dangerous heart rhythm like ventricular tachycardia.

Matters Of The Heart- Identifying Heart Blocks

Sometimes there are disruptions the depolarization conduction system. These disruptions are called heart blocks.

If you remember, in a "normal healthy" heart the pacer impulse originates in the SA Node and is conducted through the atria until it hits the AV Node. From the AV Node it is conducted through the bundle of his, leading through the right and left bundle branches, terminating at the the perjikie fibers.

A heart block can occur at any of these points.

SA Node:

Sinus Block occurs when one of the following takes place:

The SA node does not generate and impulse for a PQRST cycle(resulting in a 'skipped beat' on the EKG).

Or

The SA Node generates a depolarization impulse, however it is blocked from leqving the SA Nose, so surrounding tissues are not stimulated to depolarize.

In an EKG, this will appear as a flat baseline segment (an extended "pause" between PQRST cycles).

Sick Sinus Syndrome

The SA Node is under distress and paces at a very slowly and no automaticity foci in the atria, AV Junction, or ventricles are attempting to pace the atria because they are also in distress.

AV Block

This is when the depolarization impulse from the SA node is parially or completely blocked at the AV node, bundle of HIS, or the bundle branches.

First Degree AV Block-

This is not a true heart block, it is merely a slowing of the impulse conduction through the atria. This results in a delay between atrial depolarization and ventricular depolarization. On the EKG reading this is manifested by a PR Interval lasting at least 0.2 seconds.

Second Degree AV Block-

There are two sub-types of heart block in this catergory:

Type I (AKA Wenckebach)

This type occurs when when conduction is slowed at the AV Node in progressive degrees until the a 'P' wave is entirely blocked from producing a QRS response in the ventricles. This is manifested on the EKG strip as a progressively lengthening PR interval until there is a 'P' wave without a QRS complex following it (there is just s baseline segment, followed by another 'P' wave belonging to the next PQRST complex, and the cycle of increasing PR interval length starts again).

Type II (AKA Mobitz)

In this type of heart block, the disruption of the depolarization impulse occurs in the Bundle of His or the Bundle Branches. 'P' waves from the SA Node are blocked at a consistent ratio (such as 4 'P' waves to 1 QRS complex, or 3 'P' waves to 1 QRS complex). On an EKG strip, the PR interval is consistent in the PQRST complex; however, there may be several 'P' waves that do not initiate ventricular depolarization.

These two subtypes of heart block are distinct from each other. However, in some instances they can be confused with each other:

Imagine you pick up an EKG strip and you see the following pattern repeated: two P waves followed by a QRS complex. You don't notice a variable PR interval but, because of the ratio of two atrial depolarizations to one ventricular depolarization, it is difficult to tell.

This rhythm is an 2:1 AV block. There is a method to determine wheither the block is in the AV node or the bundle brances using the vagal manuver to increase parasympathetic stimulation (slowing) of the AV node so that (if it is in the AV node) the ratio of P waves to QRS complexes changes or (if it is in the branches) it may eliminate the block.
This procedure can be helpful, however it can also make the rhythm worse. In a hospital setting is recommended to get a test called an EP to help diagnose this type of block.

Third Degree AV Block-
In this type of block, the atria and ventricles are completely isolated from each other electrically. Both the atria and the ventricles have their own, independent pacers that 'beat' at an inherent rate (the ventricles usually much slower) and there is NO association between the P wave and the QRS complex (AV dissociation). A patient with this type of heart block can deteriorate very quickly, monitor closely and keep in mind that the patient will most likely require an artificial pacemaker to maintain cardiac output.

Ventricular Block

Bundle Branch Block-

When either of the bundle branches (right or left) is damaged, conduction to the ventricle it serves is delayed. On an EKG strip you may see this as a 'Split' or 'Joined' QRS complex. It is wide (often greater then 3 mm) and may have two peaks (one signifying the depolarization of each ventricle).

This will appear most clearly in the chest leads on the far right or left of the heart (V1, V2, V5, V6).

Matters Of The Heart-'Reading' an EKG Strip

When you assess a patient's heart rhythm by looking at an EKG strip, you are primarily looking for the following:

1) Heart Rate
2) Rhythm
3) Axis
4) Hypertrophy
5) Infarction

1) Rate

There is a way you can quickly determine a patient's heart rate by looking at a short section of an EKG strip, it involves memorizing the following numbers:

300, 150, 100, 75, 60,50

(If the heart rate is lower, you will have to count it out by the other method I will show you shortly)

As I mentioned earlier, the horizontal plane on an EKG strip represents time elapsed. Vertical lines mark out time intervals: with bolder lines marking 0.2 second (or 1/300 minute) intervals, and thinner lines marking 0.04 second intervals.
Using this we can determine the rate by counting the number of bold lines in between an interval of QRS complexes. The procedure follow thus:

First:
Find an 'R' wave that falls on (or nearly on) a bold virtical line.

Second:
Use the numbers! Count down with the numbers 300-150-100-75-60-50 using the bold vertical lines.
Find the next bold vertical line to the left of the first and say (or think) '300' (have you reached the next 'R' Wave in the neighboring QRS complex? No? Keep going!)
Find the next bold vertical line to the left of the '300' line and say (or think) '150' (have you reached the next 'R' Wave? No? Keep going!)
Find the next bold vertical line to the left of the '150' line and say (or think) '100' (have you reached the next 'R' Wave? No? Keep going!)
Find the next bold vertical line to the left of  the '100' line and say (or think) '75' (have you reached the next 'R' Wave? No? Keep going!)
Find the next bold vertical line to the left of the '75' and say (or think) '60' (have you reached the next 'R' Wave? No? Keep going!)
Find the next bold vertical line to the left of the '60' line and say (or think) '50' (have you reached the next 'R' Wave? No? Whell that's too bad, cuz you have bradycardia and determining an accurate heart rate won't work with this method :P)

For Bradycardia-

Count the number of PQRST cycles on a six second EKG strip and multiply by 10 (ugh, this one is sooo hard!)

There is also a mathmatical method in which you take into account the fact that the thin lines are one millimeters apart and represent 1/1500th of a second:

Heart Rate=1500/Milimeters in between similar waves

2) Rhythm

I've already talked about rhythms (organized by their pacer orgin, in my previous blog post titled, 'Normal and Abnormal Heart Rhythms'

It is very importiant to know what all of those squiggly lines mean, because you can determine where the heart is having problems by how some of the waves are shaped, or if some are missing, or if they look like they're not supposed to.

3) Axis

Remember when I told you I wrote an arrow on my chest to get an idea of how the electrical activity in my heart moved, and how it the way each of the different leads would 'see' the PQRST complex? 

Well I didn't know it at the time, but that arrow was an axis (actually, the arrow itself is a vector...but it represents an axis: the direction in which the depolarization is moving within the myocardium...particularly the ventricles)

In a normal, healthy heart, this conduction moves from the AV Node, through the bundle of His and the left and right bundle branches (located in the ventricular septum) to the perjinke fibers, and endocardal tissues. Because the heart is angled towards the left, and because the left ventricle is larger and thicker-walled than the right, more depolarization energy is used there. This contributes to the overall 'downward and to the left' vector.

Additional factors, affect the direction of the axis: including tissue hypertrophy and infarction. If the tissues in the heart are hypertrophied (enlarged) a greater degree of depolarization energy (and thus, the ventricular axis) is directed in the direction of the hypertrophied tissue.

If there is infarction, there is no electrical/depolarization activity in the affected tissue. Therefore, the direction of the vector/axis is deviated.

We measure the axis in degrees.

Imagine a circle on the front of your chest:

90 degrees is the direction of your belly button.

-90 degrees is the direction of your neck.

0 degrees is to the left side of your heart

180 degrees is to the right side of your heart

(In a 'normal healthy' heart, the ventricular axis is located approximately at 40 degrees)

If your heart was displaced (instead of facing towards the left, it was facing towards the right) the Vector would be displaced in the same direction. (This might sound far-fetched, but this type of deviation isn't unheard of. Sometimes electrodes need to be reversed in order to pick up the correct lead).

Now things get a bit tricky...
Remember in that blog post I wrote about monitoring the electrical activity in the heart? The one where I started talking about the polarity of all of the electrode-sensor leads? This factors into determining the axis in a specific lead.

I'll use an example:

The left side limb leads where the Left Arm has a positive electrode sensor are Lead I and AVL. This means that they are 'looking' at the positive wave of depolarization from the left side. In these leads, the QRS complexes of a 'normal healthy' heart will be upright (because the wave of depolarization is moving towards them!)

Imagine for a moment that you are looking at a full EKG page of squiggly lines. You first examine lead one and you notice (gasp!) that the QRS complexes are inverted!
This is called Right Axis Deviation (R.A.D) It can occur if the left side of the heart has been severely damaged, or the right side of the heart is severly hypertrophied.

The same principle applies to all of the limb leads, you just have to remember where the positive and negative sensors are located and you can find out where and if the axis has deviated from the normal range. This helps to determine areas of the heart that might be damaged.

4) Hypertrophy

For the definition of hypertrophy, please see the entry in the 'Axis' subheading.

The chest leads are usefull in identifying areas of hypertrophy in the heart. Because the chest leads consist of positive electrode sensors only, they can detect positive impulses moving in the direction of the sensor. This is usefull for determining the location of hypertrophy because the greater degree of depolarization energy used in this type of tissue will produce waves that appear abnormal in the nearby lead.

For example, in lead V1 a 'P' wave will appear as two waves (one positive and one negative) when hypertrophy is present where the V1 is positioned. You can further differientiate between right and left atrial hypertrophy by comparing the two 'P' wavelengths. If the first is larger, the hypertrophy is primarily on the right side of the atrium, if the second is larger; the hypertrophy is primarily on the left atrium.

Hypertrophy in both the ventricals is seen as an abnormally elongated 'R' wave in V1 (particularly visible, because this view is on the right side of the heart and the waveform of the 'R' is oriented upwards in this lead.)

In order to determine which ventricle is affected with hypertrophy, look at the other chest leads:
If the large R wave becomes smaller in leads V2, V3, V4 (as the sensors move to the left side of the heart) then right ventricular hypertrophy is present.

If the waveform is of very high ampletude, with exagerrated 'S' wave in V1, changing to a large 'R' wave in V5 (of greater then 35mm deapth total of the two) and an inverted and asymmetrical 'T' wave in leads V5 and V6, then left ventricular hypertrophy is present.

5) Infarction

I briefly defined infarction in under the subheading 'axis', it refers to an area of tissue that is dying: either the oxygen supply has been cut off and the tissue is in destress (Ischemia), the tissue has sufferd damage due to loss of oxygen (Injury), or the tissue has died in the affected area (Necrosis).

It is most commonly the left ventricle that suffers from myocardial infarct, therefore in order to assess if infarct has taken place we will need to look at the leads on that side and note the altered electrical/depolarization energy flow in the QRS (ventrical) complexes.

A common finding in ischemia of the left ventricle is a symmetrically inverted T wave.

In myocardial injury, the ST segment will be elevated (unless the injury occured just below the endocardial lining, then the ST segment will be depressed).

In myocardial necrosis, the ST segment is elevated and the Q wave is prominent (at least 0.04 seconds in length, or one small 1mm square on the graph). If this type of Q wave is present in the lead views (except for the AVR lead, because that one apparently will LOOK like a Q wave when its actually an R wave...cuz it looks at the heart from the wrong angle...yeah, its confusing), note the leads on which the promenent Q wave is visible (except for the AVR cuz its probably not a Q wave at all)

More notes on necrosis infarction: Reguardless of where the infarct is located, there are electrochemical markers that will help identify the area. Necrotic myocardial tissue CANNOT conduct electricity, therefore the cannot conduct a depolarization impulse and a chest electrode will not be able to sense electrical activity when it is placed over he area of infarct...
It WILL, however, pick up on the electrical activity on the OTHER SIDE OF THE HEART!

For example, a elecrode sensor placed in front of necrotic tissue on the left side of the left ventricle will pick up the depolarization impulse on the RIGHT side of the ventricle (in the septum). And the impulse from this area of the heart will be moving from the endometrial lining (on the inside chambers of the heart where the perjinke fibers are) TO the epicardium on the outside of the heart. This means the depolarization wave (as seen from this lead) will be moving in the opposite direction compared to the the depolarization wave seen in a 'normal healthy' heart.

Prominent Q waves in leads V1-V4 indicate anterior infarction. (The Q wave is promenent because the chest leads are picking up the depolarization of the septum better then they normally would because of the necrotic "hole").

Promenent Q waves in leads I and AVL indicate lateral infarction.

Promenent Q waves in leads II, III or AVF indicate inferior infarction.

Posterior infarction is easy to miss (because we don't place chest leads on the back of the heart!) However, it is very severe so we need to look for them carefully. They will produce ST depression and large R wave in leads V1, V2. The large Q wave may be present in lead V6. If this type of infarction is suspected, it is importiant to do a mirror test, in which the EKG strip in leads V1 and V2 is inverted and read from the "blank" side of the strip (hold up to a light source to assist with visuallization.) Look for the "Q waves with ST elevation" in this mirror view. These will indicate posterior infarction (Which I think are really the R wave and the ST depression).

Matters Of The Heart-Normal and Abnormal Heart Rhythms (Part 2)

Atrial Rhythms Continued-

Bradycardia-
This rhythm is defined as abnormally slow heart action. Although heart rates will vary from individual to individual, a heart rate of less then 50 bpm is usually considered bradycardic. If a slow heartbeat is accompanied by any signs and symptoms of poor cardiac output (such as dyspnea, fatigue, dizzyness (esspecially with movement) and cyanosis), this rhythm will need to recieve medical attention.

Although I placed this in the catergory of atrial rhythms, this rhythm can actually originate from anywhere in the heart:
SA node- With simulation of the parasympathetic nervous system.
Atria Foci-which has an inherent range of 80- 60 bpm, but can become depressed to run at even lower rates.
Junctional foci-Which have an inherent rate of 60-40bpm.
And Ventricular Foci-Which have an inherent rate of 40-20 bpm.

Tachycardia-

This rhythim occurs when the heart rate is greater than or equal to 100 beats per minute. (In this instance, the SA node acts as the pacer). In many cases, this rhythm is a response to sympathetic stimulation from stressors such as exercise, dehydration, or pain. When this is the case, the rhythm is not inherently harmful and the rate will decrease when the stressors are relieved.

Atrial Flutter-
This rhythm is similar to Atrial Fibrillation; in both, irritable automaticity foci in the atria stimulate depolarization. However, in a fib, several pacers emit an impulse simultaneously, in Atrial Flutter one pacer emits an impulse at a rate of 250-350 beats per minute. Not all of these 'pacer' impulses are conducted to the ventricles. This contributes to the 'sawtooth' appearance of multiple small ampletude 'P' waves (meaning they indicate atrial depolarization) precieding a QRS complex.

Depending on the ratio that the atrial pacer is able to simulate the ventricles to contract, this rhythm can be hard to identify (Sometimes the ratio can be 2 'P' waves to one QRS, which looks similar to a PQRST complex in tachicardia) Sometimes healthcare professionals suggest the patient perform a vagal manuver (such as carotid massage, testing the gag reflex or bearing down with breath held) this stimulates the parasympathetic nervious system to lower the heart rate...If atrial flutter is the rhythm, the 'sawtooth' pattern will become more visable.

There is another rhythm in which it is helpful to use the vagal manuver to lower the heart rate, it is called Supraventricular tachycardia

Atrial/Junctional Rhythms-

Supraventricular Tachycardia-
The location of the 'pacer' for this rhythm can be in the atria (this is sometimes called Atrial Tachycardia), it may also be found in or near the AV Node or Bundle of His. (this is sometimes called Junctional Tachycardia)

However, in many cases, it is impossible to distinquish the location of the pacer because it is firing so fast (150-250 bpm) and every supraventricular impulse is conducted to the ventricles. (Fortunately, both types of supraventricular tachycardia are treated in pretty much the same way)
If the onset of these types of tachycardia is sudden, it is called 'Paroxymal' Paroxysmal Supraventricular Tachycardia (PST).

One treatment for this rhythm is to (as I mentioned above) perform a vagal manuver. There is also a drug called adenosine that interupts the electrical conduction of the heart, allowing normal pacing to resume.

Ventricular Rhythms-

Ventricular Tachycardia-

This rhythm has one irritated foci acting as pacers for ventricular depolarization. This rhythm is rapid (150-250 bpm), and because the route of electrical depolarization is reversed (usually it ends, not starts in the ventricles) the ventricular contractions appear dissimilar to the normal QRS complexes and are wide and tall.

This rhythm indicates the heart is in severe stress and (if persistant) is not able to provide an adequate cardiac output to maintain consiousness. If the rhythm persists, it will progress to ventricular fibrillation. 

Torsades de Pointes-

This rhythm is a subtype of ventricular tachycardia. The name is french for 'Twisting of Points' which is pretty much how this rhythm looks on an EKG strip: Multiple ventricular depolarization complexes that gradually grow, and then deminish, in ampletude. (Rate 250-350 bpm). This rhythm is thought to be caused by two ventricular pacing sites (foci) competing to be the dominant pacer. It is most often associated with severe magnesium deficiency. (Magnesium is primarily intracellular an has a role in maintaining muscle tone).

Ventricular Flutter-

This rhythm originates from a single irritable foci in the ventricles, which paces at a rate of 250-350 bpm. It is similar in appearance to the wide ventricular complexes of Torsades de Pointes, however the waves are smooth (because there is still only one irritable foci acting as pacer). This is a sign of degeneration of the rhythm from V-Tach to V-Fib.

Ventricular Fibrillation-
Multiple uncoordinated and irritated foci attempt to pace the ventricles. This rhythm appears as a series of wide, rapid (350-450bpm) waves of low ampletude. In ventricular fibrillation, depolarization is not able to produce contraction. This rhythm requires immediate ACLS intervention.