Dysrhythmias and Congenital Heart Defects

Back to Pathophysiology! Yay!

If you've forgotten everything about ECGs and the conducting system of the heart, I suggest re-reading my post about the heartbeat- it covers a lot of the basics on how the heart is meant to function. And that's important, because now we're going to find out what happens when the rhythm is out of whack and you have a dysrythmia (or arrhythmia)!

Dysrhythmias

Causes

There are a lot of causes for dysrhythmias/arrythmias, such as damage to the conduction system, electrolyte disturbances, thyroid disease, infection, drugs and so forth.

Monitoring

The ECG, mentioned in my post about the heartbeat, is pretty much the most important diagnostic tool for detecting arrhythmias. Other options include the Holter monitor, which is a portable ECG that a patient wears for 24 hours. The Holter monitor records continuously over this time period. Another type of portable ECG is the event recorder, which a patient can wear for a longer period of time, but it won't record until the patient presses a button to indicate that something is happening (maybe they are feeling faint, or getting palpitations etc.)

Classifications

Arrythmias can be classified in different ways. They can be classified according to heart rate- tachyarrythmias are above 100 beats/min and bradyarrythmias are below 60 beats/min. They can be classified according to rhythm- regular or irregular. Finally, they can also be classified according to origin- supraventricular or ventricular.

I'm going to take you through a few conduction abnormalities, grouped according to where they occur. Bear in mind that not all of these are necessarily pathologic- pretty much all healthy people have tachycardia when they exercise or are stressed, for example. Also, athletes might have a lower resting heart rate than usual (bradycardia).

• SA Node
• Sinus tachycardia- a regular heartbeat between 100 and 160 beats/min.
• Sinus bradycardia- a regular heartbeat lower than 60 beats/min.
• Sick sinus syndrome- caused by damage to the SA node. Characterised by somewhat irregular alternating tachycardia and bradycardia.
• Atrium
• Premature atrial contractions (PAC)- ectopic beats from irritable atrial muscle cells cause early atrial contraction.
• Atrial flutter- an atrial rate 160-350 beats/min. The ventricles maintain a normal, regular rhythm due to the delay at the AV node.
• Atrial fibrillation- an atrial rate over 350 beats/min that does not show up as a P-wave on the ECG. Ventricles beat slowly and irregularly. There is a risk of thrombosis due to blood pooling in the atria (the atria are not contracting properly and pushing their blood into the ventricles).
• AV Node
• Supraventricular tachycardia- signals from the AV node or above cause the ventricles to beat at 150 beats/min or faster. No P-wave appears on the ECG as it is masked by the many QRS complexes.
• Heart block- delay or stoppage of conduction at AV node or bundle of His
• First degree- PR interval longer than 0.2 seconds (normal 0.12-0.2 seconds). Benign- usually only discovered by coincidence.
• Second degree type 1 (Mobitz 1)/Wenckebach: PR interval becomes progressively longer with every beat until QRS is dropped.
• Second degree type 2 (Mobitz 2): PR interval consistent, but not all QRS waves appear.
• Third degree- complete stoppage of transmission between atria and ventricles, causing atria and ventricles to contract independently. Atria contract at the normal rate- ventricles much slower (30-45 beats/min).
• Ventricles
• Premature ventricular contractions (PVCs)- ectopic beats from ventricular cells, causing early contractions. If there's only one or two it's not an issue, but it's a concern if there's several of them.
• Bundle branch block- conduction defect in any one of the bundle branches. Appears as a wide QRS complex on the ECG.
• Ventricular tachycardia (VT)- ventricles beat very fast. This can be dangerous, as this reduces the time for ventricular filling, in turn reducing stroke volume and cardiac output
• Ventricular fibrillation (VF)- MEDICAL EMERGENCY, requiring CPR, defibrillation and/or IV drugs. Ventricle muscle fibres contract independently and rapidly, so they don't provide enough combined force to eject blood. This leads to zero cardiac output.

Symptoms

Arrythmias can range in severity. They can be asymptomatic, or they can lead to palpitations, dizziness, hypotension, syncope and even cardiac arrest (which I'll talk about in a bit).

Treatment

Just like with angina, it's important to try and treat the cause if you can. This can involve correcting electrolyte disturbances, treating thyroid problems, curing infections and so on. If this can't be done, or if the condition doesn't improve, then there are other things that might help. The β-blockers and calcium channel blockers that I mentioned in my post about coronary artery disease might help, as well as digitalis. Pacemakers can also help in SA nodal disease and heart block. In an emergency, defibrillators can save lives.

Cardiac Arrest

Really bad arrythmias (*cough*ventricular fibrillation*cough*- it's probably not the only one though) can lead to cardiac arrest, which is basically when the heart stops beating. It can be classified into two categories: shockable and non-shockable. This basically just refers to whether you can fix it with a defibrillator or not. Shockable forms of cardiac arrest include ventricular fibrillation, as well as pulseless ventricular tachycardia. Non-shockable forms include pulseless electrical activity, as well as asystole. Asystole is defined as not having a heartbeat for longer than 1 second.

Congenital Heart Defects

Causes

Congenital heart defects are structural defects that develop while the baby is still in utero. These might be due to genetic factors such as chromosomal abnormalities, or due to environmental factors such as infection, alcoholism or diabetes in the mother.

Classifications

Congenital heart defects can be classified according to function or structure. Functional classifications are acyanotic or cyanotic- i.e. do they make the child turn blue due to lack of oxygen? Structural classifications refer to the part of the heart that has been affected. Septal defects affect the septa dividing the left and right sides of the heart, valvular defects affect the valves, vascular defects affect the arteries and veins, and so on.

Treatment

Some congenital heart defects correct themselves spontaneously. If not, surgical repair might be possible. Drug therapy and other supportive measures may also need to be used.

Now let's look at some specific heart defects!

Ventricular Septal Defect

Ventricular septal defect- the so-called "hole in the heart"- is the most common congenital heart defect. As the name implies, it's a hole in the interventricular septum (the wall between the two ventricles). Ventricular septal defect is acyanotic- that is, it doesn't turn babies blue.

Usually blood flows through the hole from left to right, as the left ventricle has a higher pressure. This is also known as a left-to-right shunt. This causes less blood to flow around the systemic circulation and more blood to flow around the pulmonary circulation, which can lead to pulmonary hypertension. Over time, pressure can build up in the right ventricle, and when the pressure here exceeds that of the left ventricle, a right-to-left shunt can develop. This results in Eisenmenger's syndrome, which is cyanotic because a right-to-left shunt is essentially directing deoxygenated blood to the systemic circulation.

Tetralogy of Fallot

The tetralogy of Fallot is a collection of four (tetra = four) structural defects that occur together:

1. Narrowing (stenosis) of the pulmonary valve
2. Thickened right ventricle wall due to the extra effort to pump blood through the narrowed valve
3. Ventricular septal defect
4. Aorta moved a little more to the right so that it is over the "hole in the heart."

Another post down!