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.

Matters Of The Heart-Monitoring Electrical Activity (Part 2)

When you look at a Full EKG (that page with a bunch of different squiggly lines on it) you notice that each lead's squiggly line is shapped differently. This is because they are examining the heart from a different angle.

Imagine you are sitting at home reading this blog article about electro-chemical activity in the heart and your spouse or lover comes in to tell you s/he bought you a new car!
You are supprised and excited the first question you ask is, 'What kind of a car is it?'
Your loved one says excitedly, 'go see'

It's sitting in the driveway right now. You run out the front door and you see the outline of the car from the front: the windshield and the headlights. From here you will probably be able to tell if the car is a passenger sudan or an SUV/Truck. But to make sure you need to examine the car from the side.

In awe, your eyes are fixed on the car as you walk diagonally towards the side of the car. Now you can see the outline of the car from the side: the wheels and the sidedoors. From here you will probably be able to identify the car's features and further diffentiate the car type: For example, if it has an open truck bed, hatchback etc.

But if you still aren't sure of the make or model. You continue to walk towards the back of the car. Now you can see the rear tires, license plate, and the make/model.

You identify the car as the one you've wanted since you turned 16 (but hadn't been able to buy) and you turn to your loved one and say: 'What the flip were you thinking?! We can't afford this!'

The same principles involved in you identifying the new car apply to identifying the patterns of electrical activity in the heart on a Full 12-Lead EKG.

Electrical activity in a heathy heart starts in the atria (with the SA node in the upper righthand corner) and decends downward and to the left to the apex of the heart (I had to draw an arrow on my chest to visualize it).

A electrode sensor placed on the left side of the body will detect this electrical movement as an upward spike.

A sensor placed on the right side of the body will detect this electrical movement as a downward spike.

But it gets more specific then simply looking at the heart from either the right or the left side. Cardiologists (heart doctors) often need to pinpoint an ischemic area, or EKG technicians need to identify a specific kind of heart conduction abnormality that may not be visible from a simple side view.

This is why several different Limb and Chest Leads were developed.

Limb Lead Sensors-

Along with the diagonal (right upper to left lower) arrow on my chest, I also drew on my arms. RA, LA, RL, LL. These represent the locations on my limbs where electrode sensors could be placed if I were to have my heart examined via EKG-Limb Leads.

Right Leg Sensor-
Because the electrical activity moves from upper right to lower left, though, the right leg doesn't sense much of it (cuz it's traveling in towards the left leg). This means that the right leg electrode (RL) is not usually used. And when it is, it's usually used as a ground (negative) sensor.

Left Leg Sensor-
This location is used as a positive electrode sensor in leads II and III and AVF. It is used as a negative electrode sensor in leads AVR (along with the negative sensor in the left arm) and AVL (along with the negative sensor in the right arm).

Right Arm Sensor-
This location is used as a negative electrode sensor in leads I and II, as well as in AVF (along with the right arm(, and AVL (along with the left leg). It is used as a positive electrode sensor in the AVR lead.

Left Arm Sensor-
This sensor is used as a positive electrode sensor in lead I, and as a negative (ground) sensor in lead III. It is also used as a negative sensor in AVF (along with the right arm) and AVR (along with the left leg), and it as used as the positive sensor in AVL.

(Whew! It's a good thing the machine is in charge of determining the polarity of the sensors. I just want to know what the squiggly lines mean)

Bipolar Limb Leads-

Lead I- Because this lead is taken from the right arm to the left arm (with the right arm being negative and the left arm being positive) it captures the movement of the heart's depolarization wave from the left side of  the heart.  PQRST complexes appear roughly in their characteristic forms as described in Part 1.

Lead II- Because this lead is taken from the right arm to the left foot (with the right arm being negative and the left foot being positive), it captures the movement of the heart's depolarization wave from roughly the front/right angle of the heart (or maybe its the bottom, hard to tell from a two dementional picture). From this lead, the P Wave and the T wave of the PQRST complex appear to have a higher ampletude then compared to Lead I. The QRS complex also has a slightly different shape; although still tall and narrow, the R wave has a higher ampletude and the S wave has a lower negative ampletude.

Lead III-
This lead from the left arm to the left foot (with the left arm being a negative electrode sensor and the left leg being a positive electrode sensor). It captures electrochemical 'movement' of depolarizing cells from the lower right side of the heart. When the PQRST complex is seen from this lead, the P Wave is even taller then when it was seen from lead II, the T wave is of a lower ampletude, and the QRS complex is similar to the QRS complex as seen in lead II.

Unipolar Limb Leads-

AVF-
This lead runs between the two negative (ground) electrode sensors in the right and left arms to the positive sensor electrode in the right foot. It captures the electrical wave of depolarization from the front/center of the heart. This view appears similar to those in leads II (because it is right next to it, in between leads II and III).

AVR-

This lead runs between two negative electrode sensors in the left arm and left leg to a positive electrode sensor in the right arm. It captures the movement of depolarization energy from the upper righthand corner of the heart. When seen from this view, the PQRST complex has inverted P and T waves. The QRS complex has a prominent Q wave, and an R wave.that is of a smaller ampletude than leads II or III.

AVL-

This lead runs between two negative elecrode sensors, one in the right arm and one in the left leg, and a positive sensor in the left arm. It captures the wave of depolarization through the heart from the upper left corner. The PQRST complex has an inverted P wave and an upright T wave, the QRS complex is of a smaller ampletude (compared to leads I, III, AVF) and the R wave is more prominent than the S wave.

Chest Leads-

They are placed in six different positions on the chest (From right to left, numbered V1-V6).

Unlike the bipolar limb leads, the chest leads only have positive electrode sensors placed in six different positions on the chest. These positive electrode sensors  make a positive deflction on the EKG squiggly line.

This means that the leads placed on the right side of the heart (V1 and V2) will have QRS complexes with prominent S waves and diminished Q waves. As the placement of subsequent electrodes moves to the left side of the chest (where the left ventricle and apex of the heart are) the QRS complexes will look more tall and peeked (because the depolarization wave is moving toward them!)

I can now sense the pattern that, because the left ventricle is responsible for cardiac output, the "classic" view of the PQRST complex from an EKG/telly box is taken from the leads that view the heart from this side. Good to know!

Matters Of The Heart-Normal and Abnormal Heart Rhythyms (Part 1)

ATRIAL RHYTHMS-

Normal Sinus Rhythm

The impulse for this rhythm originates from a cluster of myocytes and nerve cells called the SA Node (the 'pacer' in a healthy heart). 
On an EKG strip, it appears with the normal pattern of PQRST complexes with a consistant rate and rhythm (with equal distance between identical waves of neighboring complexes).

The rate for this rhythm is 60-100 PQRST 'heartbeats' per minute.

Sinus Arrhythmia

The impulse for this rhythm also originates from the SA Node. However, the SA Node paces at a faster rate when the patient is taking a breath (respiratory inspiration), and paces at a slower rate when the patient is releasing a breath (respiratory expiration). This is because taking a breath stimulates the the SA Node via the sympathetic nervous system, and  releasing a breath stimulates the parasympathetic inhibition of the pacing impulse.

This mechanism is not inherently pathologic, in fact, it functions in most human beings. The difference in heart rate during inspiration and heart rate during expiration is called 'Heart Rate Variability' and is an indicator of resiliency after Myocardial Infarct.

Sometimes the SA Node doesn't work, this could be because it's not getting enough oxygen or because the tissue that makes up the SA Node has died. When this happens, we have what is called a

Wandering Pacemaker

A wandering pacemaker is a clump of atrial cells (atrial foci) that generate an electrical impulse. Often there are several sites within the atria that act as foci and can generate an electric impulse, this will be reflected in the shape of the 'P' waves on the EKG strip.

Because the pacer generating a given heartbeat comes from a different location compared to different heartbeat, the PQRST complexes are often dissimillar in appearance. Their rhythm is irregular,  the rate is usually 60-80 beats per minute (less then 100 bpm).

Multifocal Atrial Tachycardia (MAT)

This rhythm is similar to that of a wandering pacemaker, except that it's fast! Three or more atrial foci are involved in this rhythm and the rate is over 100 bpm. It is often seen in patients with Chronic Obstructive Pulmonary Disease (COPD) and in heart disease patients who have digitalis toxicity (too much digoxin (a heart disease medication) in their system).

Atrial Fibrillation

In this rhythm, multiple atrial foci are firing all at the same time: this appears as a bunch of a bunch of small spiked deflections of various ampletude instead of 'P' Waves on a 'PQRST' complex.
Despite the multiple 'pacer' impulses, these impulses only occassionally are able to travel through the AV Node to initate ventricular contraction. This causes the ventricular rate to also be irregular.

In this rhythm, the atria does not depolarize or contract syncronously, this increases the risk that blood will become stagnant and not move from one compartment to another. This is dangerious because it contributes to clot formation which can travel to another part of the body and cut off circulation to parts of the body (causing severe acute problems such as occlusive stroke, heart attack, or pulmonary embolism).

Matters Of The Heart-Monitoring Electrical Activity of the Heart (Part 1)

Assessment findings like blood pressure readings, heart sounds, and observable signs and symptoms associated with cardiovascular malfunction are an importiant part of a full cardiovascular assessment. But once you suspect a heart ailment, you need to use a diagnositc tool called an ElectroKardioGram (or EKG). This machine is like a camera, except for instead of measuring wavelengths of light, it measures electrical activity in various locations of the heart. This is very importiant because in many cases the electrical activity of the heart is altered even before other signs and symptoms of an illness or malfunction manifest themselves. This allows a cardiac problem to be treated earlier, and decreases the chance of death (mortality).

An EKG machine has 12 'leads' created by 'electrode' sensors that are basically adhesive stickers that attach to specific locations on the patients chest or body. These electrode sensors create the 'leads' that act as a camera for electrical activity.

Positive electrode sensors detect when a wave of positively charged ions are moving (depolarization) towards them and record the impulse as an upward deflection on the squiggly line (very scientific term, I know) along a strip of graphing paper or recording device called an EKG strip.

The horazontal plane on an EKG strip represents time elapsed, the vertical plane on an EKG strip represents electrical voltage being generated.

These electrodes can also sense when a wave of positively charged ions (depolarization) is moving away from them. This is recorded as a downward deflection on the squiggly line.

Leads

Three of the leads are 'Bipolar limb leads'. This means that a pair of electrodes (one functioning as a positive sensor and another functioning as a negative sensor) work together to form an EKG reading from one of three angles. These leads are numberd: I, II, III.

Another three 'limb leads' are called 'Augmented limb leads' formed from one positive electrode senser and two negative electrode sensors. These leads are numbered: AVR, AVL, and AVF. Each of these reveal the electrical activity of the heart at a different angle.

Additionally, there are also six 'chest' leads'-created by positive electrode sensors arranged on the chest horazontally (no negative electrode sensors). They are numbered V1, V2, V3, V4, V5, V6 and they reveal the electrical activity along the front of the heart from various angles.

Each of these leads form a page of squggly lines called a full EKG.

(Each of the lines look a bit different from each other, and are still confusiong to me. But never fear! I will investigate further and include my findings in a future post!)

Wave Amplitude:

An upward deflection on the squggly line means that a positive wave of depolarized cells is moving towards the positive electrode sensor.

In a healthy individual, the quiggly line often forms a pattern of waves chararacteristic of a healthy cardiac cycle.
These waves are named for letters in the alphabet (But not ABCDE, because that would sound weird)

They are called PQRST

Factors such as the shape and the length of each wave, the length of the intervals between each wave, the length of overall complexes and the frequency of complexes or sets of waves are really importiant to assess when interpreting an EKG reading.

Lets go over the waves one at a time:

P-

This wave is usually a small upward deflection on the squiggly line, rounded at the top. It indicates depolarization/contraction in the atria.

In between the P wave and the next wave in the PQRST complex is a brief 'pause' that appears as a flat 'baseline' called the PQ segment or PQ Interval. This 'delay' is caused by the impulse being conducted through the AV Node, Bundle of His, Left and Right Bundle Branches, and Perjinki fibers. It allows time for blood to move from the atria to the ventricles.

QRS-
Even though these are actually three 'waves' they all indicate ventricular depolarization and the beginning of ventricular contraction/systole so they are often treated as one wave. The initial wave is a small downward deflection called the Q wave (not always visable). The second wave is tall, slender and has a peaked top; it is called the R wave. The third is usually medium-sized downward deflection called the S wave.

After this QRS complex, the squiggly line becomes horazontal again in a segment called the ST interval. This area represents the plateu or 'slow' phase of ventricular repolarization. (The heart is still physically contracting or 'pumping' at this time, but electrically it begins to revert to it's polarized state.) The ST Interval is an importiant area to assess, because if this segamented is elevated or depressed it can indicate a myocardial infarct.

T-

This wave occurs at the end of the of the PQRS complex and represents the end/'rapid' phase of ventricular repolarization. It appears as a wide, round upward deflection on the squggly line.

The whole process starts over after an isoelectric pause...Allowing the ventricles relax and the atria fills up with more blood.

Matters Of The Heart-Heart Sounds/BP Assessment

When you listen to the heart via a stethoscope you hear two distinct sounds infamously known as the 'Lub-Dub' (or if you wanna be all scientific, 'S1' and 'S2')

The First Sound in the cycle ('Lub'/'S1') is louder then the second. It is made by the closing of both of the Atrio-Ventricular Valves. They close after the ventricles have filled with blood and are about to be pumped out to their respective destinations.

There is a short period between the 'Lub' and the 'Dub'. During this time, the semilunear valves open and the ventricules are activelly pumping/pushing blood into pulmonary and systemic circulation: this time period is called Systole.

(When you take someone's blood pressure with a sphignomanometer, your aim is to achieve two numbers. The first indicates the amount of pressure the heart is pushing blood out during Ventricular Systole or ventricular contraction. This is called Systolic Blood Pressure)

The Second Sound ('Dub'/'S2') is slightly softer, and it is made by the semilunear valves closing after the ventricles have pumped blood through them.

Immediately after 'Dub'/'S2' sound, the heart is at 'rest' (the ventricles that provide cardiac output to pulmonary/systemic curculation are recieving blood, not pumping it.) This time period is known as Ventricular Diastole.

(Again, when you take someone's blood pressure with a sphignomanometer, your aim is to recieve two numbers, the second number is the amount of pressure in the systemic circulation when the heart is NOT pumping blood into them. This number is called Diastolic Blood Pressure.)

Sometimes other sounds--not consistant with the 'lub-dub' pattern--are heard when auscultating (listening for) heart sounds with a stethoscope. At times this is because the valves are not closing simultaneously (resulting in 'Split' heart sounds), or there is turbulent blood flow (resulting in a 'heart murmur')

Blood Pressure Readings

Typically when the Atria are contracting (atrial systole) the Ventricles are relaxing (ventricular diastole). When we check the blood pressure on a patient, we are measuring left ventricular systole and diastole (Because it reflects the amount of blood being pumped out of the heart and towards the rest of the body).

Blood pressure readings will vary depending on the individual patient's normal values. Commonly recognized 'Normal' blood pressure readings are 120/80, (or '120 systolic over 80 diastolic') Blood pressure is measured in millimeters of mercury (abbreviated as mmHG).

Hypertension-

A blood pressure reading equal to or greater than 140 systolic and/or 90 diastolic is often considered too high. Prolonged hypertension causes damage to blood vessels; increasing risk for hypoxia, infarct, and aneurysm.

Hypotension-

A blood pressure reading of less then 90 systolic and/or 60 diastolic is often considered too low. Hypotension often displays more acute signs and symptoms-such as fatigue, weakness, dizziness (esspecially with position changes), poor urine output/renal failure, and altered level of consiousness.

Matters Of The Heart-Physiology (Part 2)

As I mentioned earlier, the upper and lower chambers of the heart are electrically insulated from each other by the Atrio-Ventricular Valves (which are made of, like, collagen or something and are not the electrically-reactive myocytes). This means that the Sinoatrial node (SA Node) does not directly stimulate the ventricles to contract.

This sounds like it would be a problem, but it is really a good thing. If the SA Node directly stimulated both the atria and the ventricles, they would contract/pump at the same time. There would be no pause to allow time for each compartment to fill with blood, and cardiac output (Abbreviated as CO, it means the amount of blood the heart pumps out per minute) would be deminished.

The Pathway Through the Atrio-Ventricular Node-

The pathway for electric stimulation to pass between the atria and reach the ventricles is through the Atrio-Ventricular Node (Also called the AV Node). It is a nerve-thingy that picks up the electro-chemical depolarization and carries it to the ventricles.

The AV Node is responsible for the brief delay that occurs between atrial and ventricular contraction. The conduction is carried through the AV Node to the nerve fibers called 'The His Bundle', which then separates into the Left and Right Bundle Branches (Servicing the Left and Right ventricles, respectively) Eventually these branches terminate in the Purkinje Fibers that directly depolarize the myocytes in the ventricles.

(Note: The ion used to transmit the electrical stimulation (aka depolarization) through ventricles system is calcium which, apparently, is slower then Sodium at conducting a depolarization impulse. This  becomes esspecially importiant when a person has a calcium imbalance).

Matters Of the Heart-Anatomy (Part 1)

The heart is comprised of four compartments, all of them recieve and pump blood to and from different areas.

The two upper compartments (or chambers) are called the atria. They are comparitively small and are in charge of recieving blood and pumping it to the lower chambers of the heart.

The Heart Chambers:

The Right Atria
Recieves blood from most of the body. (The head, arms legs, stomach, liver, kidneys etc.)

The Left Atria
Recieves blood from the lungs.

Both are very importiant for the ciruculation of oxygenated blood.

The two lower chambers of the heart are called the Ventricles. They are in charge of pumping blood to locations outside of the heart.

The Right Ventricle

Recieves blood from the Right Atria and pumps it to the lungs so it can become oxygenated.

The Left Ventricle

Recieves blood from the Left Atria so it can be pumped (and supply oxygen to) the body's organs.

These compartments are separated from each other by specialized structures: the muscular septum and the valves.

The Septum

The right and left heart are separated by a substance called septum, which is primarily made out of muscle and bundles of nerve tissue. This structure functions as a barrier (so blood going to different locations doesn't mix). It's myocytes also to physically pump blood, and the nerve bundles help in the conduction of electrical impulse from the top of the heart to the bottom.

The Valves

The upper and lower heart is separated by a series of 4 (four) valves. They have two primary functions:

1) Preventing the backflow of blood

2) Insulate the upper heart from the lower heart electronically (this is importiant, we will see why in Physiology Part 2)

The Four Valves:

The Atrio-Ventricular Valves

These two valves are relatively large and are located in between the atria and ventricles of the heart. They are:

The Tricuspid Valve-

This valve is on the right side of the heart, in between the right atria and the right ventricle. It has three little cusps (that kind of look like parachutes) that close when the right ventricle is full to prevent it from spilling blood back into the right atria.

Bicuspid Valve (sometimes called the Mitral valve just to make things confusing)-

This valve is on the left side of the heart; between the left atria and the left ventricle. It is made out of two little parachute-like cusps that prevent blood from flowing backward into the left atria and the lungs/pulmonary system.

The Semilunar Valves

There are two more valves in the heart. They act as doorways in-between the ventricles and the arteries that the ventricles empty into. They are called the Semilunar valves because they are shaped like a half-moon.

The Pulmonary Valve-

This valve is located in-between the right ventricle and the artery that carrys blood to the lungs so it can become oxygenated blood (this artery is called the 'Pulmonary Artery'). This valve is importiant because it prevents blood from flowing backward into the heart.

The Aortic Valve-

This valve is located in-between the Left Ventricle and the artery that carries blood to the bodies to supply oxygen to them (this artery is called the 'aorta') This valve is importiant because it prevents blood from flowing backward into the left ventricle of the heart.

Matters Of The Heart-Physiology (Part 1)

Just like the rest of the body, the heart is made up of cells. The muscle cells in your heart are called myocytes (myo means heart in latin or something, and cytes means cell).

These cells are really special because they have the ability to generate an electrical impulse by pumping electrically charged ions (Sodium is the most importiant ion just in case you were curious, but calcium and pottassium also have a role in conduction) in and out of their cell membranes. This process is called depolarization/repolarization.

During the short time the heart is not beating, the inside of the myocyte is negative and the outside is positive (this state is called 'polarized').

(Depolarization)

When the cell is getting ready to contract,  ions that carry a positive electrical charge enter the cell until the inside becomes positively charged and the outside of the cell becomes negatively charged. This is the electrical activity that causes the heart to contract. It is called depolarization because the electric 'poles' of the cell have switched.

Repolarization

Afterwards, the cells return to their resting state, positively-charged ions are transported outside of the cell and the cell becomes 'polarized' with the inside of the cell being negatively charged and the outside of the cell being positively charged.  This is called repolarization because the cell is returning again to its resting, 'polarized' state.

As I mentioned earlier, any myocyte in the heart can generate electrical activity strong enough to stimulate the other myocytes to depolarize/repolarize in concert with its own 'beat', This means that any of them can act as a cardiac 'pacer' for the rest of the heart to respond to. '

In a heathly heart, this 'pacer' is usually located in the right upper corner of the heart. This location is called the Sinoatrial node (or just the SA Node) This is where the 'Heartbeat' starts.

Matters Of The Heart

You want a heart! You don't know how lucky you are not to have one. Hearts will never be practical until they can be made unbreakable.-The Wizard of Oz (From the movie: 'The Wizard of Oz)

At the end of last year, I got my Advanced Cardiovascular Life Support (ACLS) card (which is like a CPR card, only you get to do more stuff like give drugs, evaluate heart rhythm and work in concert with a group of other people focusing on saving someone's life).

I've always admired the teamwork behind ACLS teams. (I also find it facinating the ways in which they defuse the tension, but I'll talk more about that another time).

Contrary to the way a "Code Blue" is depicted in TV and movies, the atmosphere surrounding the ACLS team working on a "code" is often calm and controlled. This is partially because of the ACLS algorithms: Everyone involved in the code knows what their job is, everyone knows what everyone else's job is, and they know how to communicate with each other.

It's really facinating to watch and be a part of, and this class helped me understand the process a lot better.

As I was preparing to attend the class, I read the 2010 ACLS textbook from the AHA One short paragraph I'd found in the book was a bit disheartening. I will paraphrase here:

There is not evidence that [Insert drug name here] increases rates of survival to hospital discharge or neurologic outcome after resuscitation from cardiac arrest. However, [insert drug name here] has been shown to increase short-term survival to hosptial admission when compared to placebo.

WHELL HOW the FLIP is this more effective than Basic Life Support (BLS) where you just hit them on the chest a bunch of times, shock them with electricity (if you have an AED), and WAIT for the ACLS team to arrive??

DIS' IS SUPOSTA BE THE MAGIC PART!!

The ACLS team can put an exhaustive effort into bringing a 'dead' person back to 'life', but unless the disease, injury, or imbalance that caused the heart to stop beating properly in the first place is corrected, the patient will 'die' again as soon as the drugs effects wear off.

BOOOO!

ACLS is not a miracle cure. For the most part, all it can do (and is meant to do) is buy time.

PS. If you though this post was going to have something to do with the metaphorical heart in control of human emotion, I'm sorry.