REFLECTIONS ON ARRHYTHMIAS

REFLECTIONS ON ARRHYTHMIAS

Any severe, untreated arrhythmias can cause cardiac failure, and they are often the consequence of ischaemic heart disease. For this reason, they are discussed after those two diseases.

Arrhythmias may be due to problems at any level of the conducting system of the heart. The most common cardiac arrhythmia is atrial fibrillation, with “incidence increasing with age (Framingham data indicate a prevalence of 76 per 1000 males and 63 per 1000 females aged 85-94 years)”.

Learning about the conducting system of the heart (illustrated below) for me, for the first time, was quite burdensome. It didn’t really electrify me at the beginning. But the more one thinks about it, the more incredible it becomes. It is a truly fascinating system, which deserves our greatest attention. The details of the workings of this system can be found in any decent physiology textbook. I could not summarise it better than Harun Yahya, when he concludes his chapter on the topic in his book, ‘The Miracle of Electricity in the Body’:

“In order for your heart to work with perfection, it needs electrical signals. In order for those signals to be produced, the sodium, potassium and calcium ions need to be present at particular levels in the blood. Bearing in mind that these levels are regulated by organs such as the kidneys, intestines, stomach and lungs, it’s even more evident that such a system cannot be the result of a fictitious mechanism such as evolution.

First of all, there is a technology in the heart far superior to that of any man-made device. But most important of all, is that there would be no purpose for the heart to come into being by chance on its own. Together with the heart, there must be blood vessels thousands of kilometers (miles) in total length, as well as liquid blood to fill those vessels, kidneys to filter the blood, lungs to give oxygen to the blood and absorb carbon dioxide, a digestive system to provide nutrients for the blood, a liver to refine these nutrients, a nervous system to regulate the working of the heart, a brain to manage the body as a whole, a skeletal system to keep the body upright, and a hormonal system to assist the heart’s operations—are all present at the same time. The way that all these and thousands of other elements come together in the most harmonious manner possible is one of the many proofs of a flawless Creation.”

The conducting system thus is an example of the truest irreducible complexity. It could not come about by chance. One of its most interesting aspects is the structural relationship it has with the heart muscle tissue itself. Take for instance what is known as the PR interval, a 120 – 200 ms illustration of creative genius. It is actually a period of delay, as explained by Guyton, one of the greatest cardiovascular physiologists of all time:

“..so that the cardiac impulse does not travel from the atria into the ventricles too rapidly; this delay allows time for the atria to empty their blood into the ventricles before ventricular contraction begins. It is primarily the A-V node and its adjacent conductive fibers that delay this transmission into the ventricles”.

This delay, as explained by Guyton again, is caused “mainly by diminished numbers of gap junctions between successive cells in the conducting pathways, so that there is great resistance to conduction of excitatory ions from one conducting fiber to the next. Therefore, it is easy to see why each succeeding cell is slow to be excited.” The AV node hence is a gate-keeper.

Now, one wonders what would have happened if there were a normal number of gap junctions. There would have been no time for the atria to empty into the ventricles, and the same sort of picture we have with atrial fibrillation, which we are going to talk about in a bit, but perhaps without the palpitations, will occur. The worst case scenario would be the combination of atrial fibrillation with the condition Wolf-Parkinson-White where the AV node is byassed, and death will result very quickly because the ventricles will fibrillate without the delay.

Another example is the relationship of the size of chambers to the electrical system. This is illustrated in diseases like atrial fibrillation and ventricular fibrillation, which are often caused by larger chambers than normal, causing the phenomenon of ‘re-entry’, whereby the electrical impulse, having passed its suspected distance, encounters no refractory period of the heart, and continues to conduct, and irritate encountered muscle after; the heart does not rest, it keeps beating, eventually haphazardly, and death would result.


Cardiac arrhythmias can be divided broadly into tachycardias and bradycardias, which I shall discuss next.





1. TACHYCARDIAS

Tachycardias are more common and can be classified thus:



This is where the heart beats too fast, defined usually as a heart rate > 100; it may be sinus, supraventricular or ventricular in origin, depending on the site of initial depolarization. For ease of discussion, atrial flutter and fibrillation may be classified as supraventricular tachycardias. Re-entrant tachycardias are the other types of SVT. SVTs are narrow complex tachycardias. Ventricular tachycardia may be monomorphic, polymorphic (Torsades de pointes) or bidirectional, or at its worst, ventricular fibrillation.
All tachycardias carry a risk of cardiac failure, and in some cases, cardiac arrest; AF carries the additional risk of thromboembolism and stroke.

Tachycardias may present with palpitations, dizziness, angina, shortness of breath, syncope, cardiac arrest, or sudden death; they may also be symptomless. The history should focus on symptoms and possible underlying etiologies.

An ECG with a long rhythm strip will allow diagnosis of the tachycardia, if present at the time of the test. For infrequent symptoms, 24-hour Holter monitoring (with a diary of events) may catch and record the rhythm disturbance. Electrophysiologic studies may reveal an arrhythmogenic focus, and response to treatment may be assessed, but this is only available in specialized centers.

We shall discuss each of those tachycardias now.



SINUS TACHYCARDIA

In this condition, the heart just beats faster than it normally does. It can be caused by a number of things:


TACH FEVER

• Thyrotoxicosis
• Anaemia / Adrenaline (e.g. exercise, iatrogenic, phaechromocytoma)
• Congestive heart failure / Clot (e.g. DVT, PE, MI) / Caffeine & Cigarettes & Cocaine
• Hypotension
• FEVER

All these conditions can be put under one category – stress. By stressing the heart, the human body releases adrenaline, the hormone responsible for the fight-or-flight response. Describing this reaction, Harun Yahya states the following:

“The human body sometimes needs to be stronger, more resistant and to exhibit a higher performance than normally. For example, when a person has to defend himself or escape, the heart needs to beat faster and to pump more blood.

For situations like these, the necessary precautions have been taken, and another system has been installed in the human body. In case of any extraordinary situation, the adrenal glands secrete the hormone adrenaline. In comparison with its size, this hormone molecule makes a very long journey to the heart. Reaching there, the hormone commands the heart cells to contract more speedily. The adrenal cells producing this hormone know which language those heart cells will understand. At the same time, they are aware that the body must be more resilient and therefore, the heart needs to beat faster. The heart cells obey this command and begin beating faster, and in this way, the body is provided with more of the oxygen it needs in emergency situations.

The famous Israeli physicist and molecular biologist Gerald L. Schroeder refers to this special system:
“Muscle cells and especially muscle cells of the heart have large numbers of receptors designed to pass adrenaline, a stimulant hormone. At the sensation of danger (sensation did I say? I wonder just which carbon atom is experiencing this emotional trauma?), our reptilian response of fight stimulates the release of large doses of adrenaline in to the blood. Taken up by the heart muscles, the beat increases dramatically, pumping oxygen-rich blood to power hungry muscles in arms and legs. Cells along the small intestine are constructed to absorb glucose, amino acids and fatty acids, the products of food digestion and transport these products to the adjacent bloodstream, where they’ll be carried to the membranes of cells.”

As you have seen, it is astonishing how cells made up of unconscious atoms immediately identify this danger, declare a state of emergency, and take the relevant measures. This series of events requires consciousness and cannot, of course, be the work of chance. Our Almighty Lord created all of these cells and inspires in them the knowledge of what to do, and when.”

Because it is a ‘natural’ response, it ought not to be treated unless it is causing problems itself; for example, in a myocardial infarction, where the blood supply to the heart is limited anyway, the heart beating faster would increase its oxygen demands, worsening things. Other than that, let nature take its course, and the sinus tachycardia should resolve with the resolution of that cause.

ON ATRIAL FIBRILLATION

The next condition we will discuss is the most common arrhythmia. It affects about 5% of people aged 75 and over. Despite the fact that it has many prognostic and therapeutic implications as causing increased overall morbidity and mortality, as Lip and Beevers explain:

“Atrial fibrillation is sometimes regarded as a fairly trivial and unimportant disorder and is often neglected, probably because many patients have few symptoms. In fact, some patients with chronic atrial fibrillation may require long term treatment with potent antiarrhythmic and anticoagulant drugs, which may have important pharmacological interactions and adverse effects”.

It is possible that greater awareness of the condition, and its close cousin, atrial flutter, would become greater if people become more aware of the diseases of their leaders. Indeed, this is what happened in England after former Prime Minister Tony Blair was treated for the condition in 2004. He contributed to several ‘Arrhythmia Awareness weeks’, stating in one:

"I would like to congratulate the Arrhythmia Alliance and their partner organisations on their third Arrhythmia Awareness Week. This year the week will culminate in the first Heart Rhythm Congress fir which I would also like to add my congratultions and best wishes.”

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Another leader who suffered atrial fibrillation is the father of his best friend and the current US president, former president George Bush. His story is of greater interest than Tony Blair’s, since it highlights one of the most important risk factors for atrial fibrillation, namely thyroid disease.

Apparently, Bush senior was jogging at Camp David one Saturday afternoon (May 4, 1991), and developed shortness of breath, chest tightness, and excessive tiredness. He was examined by the White House physician, who discovered him to have a rapid irregular heartbeat. An ECG confirmed atrial fibrillation, and “Graves disease was diagnosed immediately after the occurrence of atrial fibrillation. Bush had been feeling increasingly tired over the preceding two weeks, had lost nine pounds in two months, and had seen his handwriting deteriorate. Physical examination disclosed a fine tremor of his hands and slight enlargement of his thyroid gland (goiter). Bush was hyperthyroid.”



Another American president who was afflicted with atrial fibrillation was William Taft, who we described earlier in the section on hypertension, attributing it mainly to his obstructive sleep apnea and obesity. As Tosos says:

“On July 10, 1913, Taft developed a fainting feeling while playing golf, and had to sit down. The episode was blamed on his aggressive dieting. In retrospect, it may have been the first episode of atrial fibrillation, which became fully manifest circa 1923 in the paroxysmal form. By August 1924 he was taking three digitalis pills a day. It is possible, but unclear, that he was chronically in atrial fibrillation by September 1926. His blood pressure at this time was 160-165/100 and his heart rate 50-55/minute and irregular”.

It is most likely that his atrial fibrillation was related to his hypertension, since that is its most common cause, accounting for over 50% of cases. But he had additional recognised risk factors – namely his obstructive sleep apnea (even when corrected for its hypertensive effects, as the following diagram shows) and ischaemic heart disease (as stated by Marx (1960), "For some years Chief Justice Taft has had a very high blood pressure, associated with general arteriosclerosis and myocarditis. ... He has no fevers and suffers no pain. His present serious condition is the result of general arteriosclerotic changes”).





A BRIEF HISTORY OF ATRIAL FIBRILLATION

It is very interesting to know that the condition was likely recognised by the Chinese, just like blood pressure, as it is mentioned in the same book, ‘The Yellow Emperor's Classic of Internal Medicine’ (Huang Ti Nei Ching Su Wen), "When the pulse is irregular and tremulous and the beats occur at intervals, then the impulse of life fades; when the pulse is slender (smaller than feeble, but still perceptible, thin like a silk thread), then the impulse of life is small." The following table, from the ‘ABC of Atrial Fibrillation’, summarises key events in the history of the condition:

HISTORY OF ATRIAL FIBRILLATION

 Adams, 1827 - Probably the first to recognise the condition clinically but as a "sign of mitral stenosis"
 Hope, 1839 - Identified irregular pulse in association with mitral stenosis-exercise worsened the total irregularity, whereas it abolished an intermittent pulse
 Marey, 1863 - Published a pulse tracing of atrial fibrillation from a patient with mitral stenosis
 Vulpian, 1874 - Observed atrial fibrillation in vivo (dog)
 Engelman, 1894 - Reported atrial fibrillation caused by multiple foci in the atria
 Einthoven, 1900 - Invented the electrocardiograph
 Lewis, 1909 - Recorded atrial fibrillation with electrocardiograph; studied mechanisms of the condition
 Rothenberger and Winterberg, 1909 - Identified "arrhythmia perpetua" and "fibrillation of the auricles"
 Bouilland, 1935 - Found that digitalis reduced the ventricular rate dramatically even though irregularity of pulse persisted
 Lown, 1969 - Recommended cardioversion of atrial fibrillation

Because atrial fibrillation is an ECG diagnosis, Einthoven’s contribution must be regarded as the key event in its history.

RISK FACTORS FOR ATRIAL FIBRILLATION

The atria will not fibrillate provided their conducting fibres are adequately perfused, not irritated, and are expected to conduct over their allocated distance. If irritated by infection (e.g. sepsis due to pneumonia), excessive amounts of thyroxine (thyrotoxicosis) or alcohol, or if the atria are enlarged because of valvular disease, heart failure or hypertrophy (e.g. due to hypertension), or if the atria are inadequately perfused through ischaemic heart disease, then atrial fibrillation will ensue. These causes be recalled by the rude mnemonic ‘A SHIT’:

• Alcohol
• Stenosis (mitral or tricuspid)
• Hypertensive heart disease (including pulmonary hypertension e.g. secondary to COPD)
• Ischaemic heart disease / Infection (e.g. pneumonia)/ Idiopathic
• Thyrotoxicosis

The irregularity caused by atrial fibrillation in structural defects is due to the increased size of the atria increasing the distance that the cardiac electrical excitatory impulse must travel, eventually becoming so long and predisposing to circus movements.

The condition highlights another example of irreducible complexity. A normal cardiac structure and function, a normal blood pressure and vasculature, a normal thyroid and absence of infection (therefore a functioning immune system) are all necessary to spare the heart the torment of atrial fibrillation.

There are three types of AF – recalled by 3P:

• Paroxysmal (reverts spontaneously to sinus rhythm)
• Persistent (reverts with electrical or pharmacological intervention)
• Permanent (does not revert; also known as chronic AF)

Clinically, the patient suffers with cardiac symptoms (especially palpiations but also dizziness, chest pain, and shortness of breath), cardiac failure, stroke, or symptoms of the cause. On examination, there is an irregularly irregular pulse and the apical rate is greater than the rate at the radial artery. The first heart sound is of variable intensity. The ECG shows absent P waves and irregular narrow complex QRS complexes (unless there is associated bundle branch block). The reason for this is that numerous small depolarization waves spread in all directions through the atria. Because the waves are weak and many of them are of opposite polarity at any given time, they usually almost completely electrically neutralize one another, and the P-wave is absent.





ATRIAL FIBRILLATION – top ECG is normal to compare

MANAGEMENT OF ATRIAL FIBRILLATION

Acute AF is treated as per the following algorithm:



Therefore treatment is aimed at CRAP:

 Cardioversion
 Rate control
 Anticoagulation
 Preventing recurrence

Thus, the treatment can be divided into:

• Anticoagulant (heparin acutely if <48 hrs, warfarin long term)/ Amiodarone
• Beta-blockers
• Calcium channel blockers / Cardioversion (chemical e.g. fleicanide, or electrical)
• Digoxin

Most patients are put on digoxin; β-blockers or diltiazem are used if left ventricular function is good. These control the rate. But to revert the AF to sinus rhythm, cardioversion (DC or chemical) is necessary.

DC cardioversion is used if AF has been present for < 1 year and cardiac function is not too bad. Chemical cardioverters include AF:

• Amiodarone
• Fleicanide

Patients should be anticoagulated to reduce the risk of emboli. If the patient has contraindications to warfarin, aspirin should be considered.

If there is no improvement, the patient should be considered for radiofrequency ablation of the AV node and permanent pacing.

ATRIAL FLUTTER

This is due to circus movement of continuous atrial depolarization. As the AV node cannot conduct that fast, it is usually transmitted with a degree of block.

The causes and treatment are similar to those for atrial fibrillation; amiodarone and sotalol may chemically cardiovert, slow the ventricular response, or act as prophylactic agents. The ECG shows a "sawtooth" appearance to the baseline at 300 bpm due to flutter or F waves. The ventricular rate is usually divisible into this, e.g., 150 bpm in 2:1 block, or 100 bpm in 3:1 block.



RE-ENTRANT TACHYCARDIAS

There are two major groups of this – AV nodal re-entry tachycardia (AVNRT) and AV-rentry tachycardia (AVRT) (which involves an abnormal connection between the atria and the ventricles some distance from the AV node). The classical example of the latter is Wolff-Parkinson-White syndrome.
AVNRT is usually called SVT, presents as a narrow complex tachy

SVTs are narrow complex tachycardias. The ECG is as follows:


Their management involves the ALS algorithm; ABC, MOVE and:

ABCDE

• Adenosine (3 mg bolus, repeated every 2 minutes 6 mg  12 mg  12 mg) / Amiodarone 300 mg over 1 hour; repeat once)
• Beta-blocker (Esmolol 40 mg IV over 1 minute followed by infusion 4 mg/min)
• Calcium channel antagonist (verapamil 5-10 mg IV) / Cardioversion (if adverse signs) / Catheter ablation (long term)
• Digoxin (500 mcg IV over 30 minutes)
• Excitation (vagal manaeuvers)



Wolff-Parkinson-White is an interesting condition, because it highlights the importance of a normal anatomy of the heart. It is rare, affecting only 0.15% of people, although it does affect some famous people, such as the singers Meat Loaf, who said, “his most frightening near-death experience was also the most recent. He says, "The worst incident was in 2003 when I had Wolff-Parkinson-White Syndrome (a rapid heart rate). I thought I'd had a heart attack on stage”, and Marlyn Manson.

It highlights to us the qualities of the normal AV node, and its wide difference to the ‘bundle of Kent’, which is the aberrant pathway of conduction in the condition, allowing for antegrade as well as retrogade conduction between the atria and ventricles. It is as if, by knowing about the condition, God is asking the patient and medical professional learning about it, to be grateful for the way things are. It is as if He is saying, “Imagine if you had an accessory pathway, like the bundle of Kent”! It is as if He is saying, be grateful for the refractory period that I have bestowed your normal conduction. Without it, death may occur, in the form of ventricular fibrillation.

In knowledge of the possible aetiology of WPW (most cases have unknown aetiology), we will understand how important the precise genetic make ups of our hearts are, and how even the slightest error can lead to disaster.

“Mutations in the PRKAG2 gene cause Wolff-Parkinson-White syndrome. A small percentage of all cases of Wolff-Parkinson-White syndrome are caused by mutations in the PRKAG2 gene. Some people with these mutations also have features of hypertrophic cardiomyopathy, a form of heart disease that enlarges and weakens the heart (cardiac) muscle. The PRKAG2 gene provides instructions for making a protein that is part of an enzyme called AMP-activated protein kinase (AMPK). This enzyme helps sense and respond to energy demands within cells. It is likely involved in the development of the heart before birth, although its role in this process is unknown.

Researchers are uncertain how PRKAG2 mutations lead to the development of Wolff-Parkinson-White syndrome and related heart abnormalities. Research suggests that these mutations alter the activity of AMP-activated protein kinase in the heart, although it is unclear whether the genetic changes overactivate the enzyme or reduce its activity. Studies indicate that changes in AMP-activated protein kinase activity allow a complex sugar called glycogen to build up abnormally within cardiac muscle cells. Other studies have found that altered AMP-activated protein kinase activity is related to changes in the regulation of certain ion channels in the heart. These channels, which transport positively charged atoms (ions) into and out of cardiac muscle cells, play critical roles in maintaining the heart's normal rhythm.”

The disaster may be noted in association with other cardiac and non-cardiac abnormalities, which may be recalled by ‘EINSTEIN’S MATHS’:

• Ebstein’s anomaly
• MVP
• ASD
• Thyrotoxicosis
• Hypertrophic cardiomyopathy
• Sex ratio (M > F; remember Einstein was male!)

It may be noted on an ECG with detection of WPW:

• Wave (delta) seen in V1
• PR interval shortened
• Widened QRS complex due to the delta wave

Wolf-Parkinson-White Syndrome





In Low Ganong Levine, a similar condition, there is an abnormal conduction pathway between the atria and bundle of His, the PR is shortened, but the QRS is normal.

Treatment of both is via ABCDE (as all SVTs) - with the important exception being the contraindication of digoxin and verapamil, since they may accelerate conduction down the accessory pathway by blocking the AV node. Adenosine is also not a very good idea, but can be used, provided full anti-resusciation measures are available. Radiofrequency ablation is crucial if electrophysiological studies show a high conducting potential of the accessory pathway.

VENTRICULAR TACHYCARDIA & FIBRILLATION

These two are the most common causes of cardiac arrest, which we shall discuss in the next section. As such they are the most important arrhythmias, and deserve a detailed discussion.

They are broad complex tachycardias, that can be monomorphic (usually due to an anatomically abnormal substrate such as myocardial infarction scar tissue causing a reentrant circuit) or polymorphic – also known as ‘torsades de pointes’ – due to abnormal triggered activity in ventricular myocardium that prolongs the QT interval.

In learning about the causes of VTs and ‘long QT syndromes’ (with which ‘torsades des pontes’ VTs are commonly associated) we learn about other irreducibly complex system called the ventricles.

The most common underlying cause for VT is myocardial ischaemia and infarction. The most important trigger for attacks is a low or high magnesium and potassium. From this we already learn that the functioning of the ventricles is completely dependent on a finely tuned biochemical (electrolyte) balance and perfusion of the ventricles. Another not uncommon cause is HOCM and other cardiomyopathies, and indeed, it is usually VT that kills patients with these conditions – for instance Marc-Vivien Foe, and why they are traditionally given amiodarone. In knowing this, the normal, precise anatomical architecture of the heart is highlighted.

The long QT syndromes, the other causes of ventricular tachycardia, can be caused by a number of things, most commonly is the obvious ischaemic heart disease. Surprisingly, but appropriately, the condition is discussed by Harun Yahya in his book on ‘The Miracle of Electricity in the Body’ – although what he is actually describing is two inherited syndromes, Romano-Ward syndrome and Jarvell-Lange-Nielsen syndrome , and not all long QT causes. There are other causes of QT syndromes as I shall outline next.

He writes in a section headed, ‘The Flawless Creation Needed for the Heart to Work Shows That There Is No Room for Chance in the Creation of Mankind’:

“QT syndrome is an inherited condition involving defects in the potassium channels in the heart, which impairs the heart’s ability to transmit electricity. Those suffering from QT risk sudden death from excessive exercise or even a nightmare.

The heart’s electrical activities need to be simultaneous if the organ is to properly perform all its functions. The body’s natural pacemaker, which regulates the rhythm of the heartbeat, sends an electrical signal to every cardiac cell for their contractions to begin. In order for the heartbeat to occur, the potassium channels must open and the potassium ions have to be permitted to leave the cell. In QT syndrome, however, as a result of functional defects in these channels, the cells’ acquisition of electrical properties for the next beat is delayed. When the heart is stimulated excessively by emotion or exercise, the defective channels don’t allow enough potassium to depart, and this electrical irregularity can lead to the sudden death.”

There are other causes of long QT intervals highlight not just the importance of normal genetic make up (as the above syndromes do), but the importance of a normal temperature regulation (to avoid hypothermia), normal immune system (so as to avoid rheumatic heart disease), and normal pancreas, adrenal glands, kidneys, liver (which hydroxylates vitamin D), intestines, bone and parathyroids (so as to avoid hypokalaemia and hypocalcaemia). Mitral valve prolapse is associated with, if not a cause of the condition, and in knowing this, we know that normal valves are essential to avoid the condition.

A number of drugs cause the problem too, and in knowing this we come to appreciate the marvels of a normal drug metabolic system – most importantly the liver and the kidneys – in those to whom we administer those drugs. Without them, they will end up in VT, and eventually cardiac arrest. Among those drugs are STEAK:

 Sotalol
 Tricyclic antidepressants / Terfenadine / Tamoxifen
 Erythromycin & clarithromycin
 Amiodarone / Antipsychotics (phenothiazines) / Antimalarials (quinine)
 Ketoconazole

It is for this reason that great caution should be exerted when administering those drugs to any patient with cardiac, renal or liver problems. They will be more sensitive to them.

Again, like in atrial arrhythmias, the patient can present with palpitations, shortness of breath, chest pain, and other symptoms. The ECG may show:



The treatment involves the VT protocol if with pulse; if pulseless need to treat as cardiac arrest; ABC & MOVE, looking for and treating any underlying cause (e.g. hypokalaemia), then if no resolution, use LAMB

• Lidocaine
• Amiodarone
• Magnesium sulphate / Mexilitene
• Beta blockers

If drugs are not successful, use DC cardioversion; over the long term, patients need to have a PCI or CABG for severe CAD, and need to have an implantable cardiac defibrillator inserted.