Range of symptoms for arrhythmia
From nothing to sudden death none, palpitations fatigue dizziness, loss of conciouness angina-like pain (rare) decompensation of heart failure circulatory collapse and death
What is the most common clinically significant arrhythmia? Why does it pose a risk?
Atrial fibrillation 1-2% prevalence in elderly Doesn't affect CO greatly, but presents high risk for atrial thrombi formation and stroke
How do you diagnose an arrhythmia?
1) anamnesis 2) Resting ECG 3) ECG on physical exercise 4) ECG on vagal/valsalva maneuver 5) Invasive electrophysiology study 6) test for arrhythmias that occur very infrequently, ie only once every day/few hours, with long term observation- Holter monitor, Implantable Loop Recorder 7) Genetic testing
Risk factors for arrhythmias
Vegetative changes (growths) Abnormal blood ion concentrations Ischemic heart disease Cardiomyopathies, degenerative disease Heart failure Hypertrophic hearts Genetic problems Drugs Electric shock
Anything that increases heterogeneity of refractory time of different heart regions
What are possible mechanisms of Bradycardias (Bradyarrhythmias)
Depressed or failing Sinus Node Conduction problems
What are possible mechanisms of Tachycardias (Tachyarrhythmias)
Re-entry Abnormal Automaticity, Triggered Activity (review audio for this one)
What is abnormal automaticity? How does it arise?
Any mycardial cell is capable of automaticity, abnormal automaticity is when an abnormal region is initiating contractions. Particularly when the resting potential increases towards 0, in the ranges of -60mV thru -10mV.As cells depolarize, their intrinsic frequency of AP firing increases.
Risk factors that enhance it: Ischemia, Hyperkalemia, low pH, catecholamines
Hyperkalemia raises the resting membrane potential (high K+ plasma concentration means less K+ leaks out of the cell, meaning a more positive cell interior, thus depolarization) The raised membrane potential also inactivates many NA+ channels, effectively raising the threshold potential, and weakening contraction.
In acute mild hyperkalemia increases excitability due to increased membrane potential, but soon decreased excitability due to Na+ channel inactivation.
What is Torsades de poinets?
TdP tachycardia, A polymorphic ventricular tachydardia that can arise if there is a very long QT interval
Often preceeded by a series of short-long-short RR intervals
risk factors: low blood potassium or low magnesium.
Hypokalemia lowers the resting membrane potential to even more negative.
It also provides less driving force for the inward K+ current which repolarizes the cell, resulting in a longer QT interval.
Hypomagnesemia lowers Na/K ATPase activity because magnesium is an essential cofactor of the pump. This prolongs repolarization, making a longer QT interval.
Treatments: can be magnesium administration, or pacemaker implantation which are programmed to fire in order to prevent long QT intervals.
What can trigger EADs?
What can these lead to?
Long QT time can trigger Early After Depolarizations.
These can lead to TdP-tachycardia, torasades de pointes.
Because the EAD causes a subsequent compensatory pause, this increase the R-R interval. If there is a longer R-R interval, there is a longer QT interval, increasing the likelyhood to TdP-tachycardia.
Also, strong sudden sympathetic activation/effects can trigger EADs and TdP-tachycardia
What are DADs and what can tirgger them?
Delayed after depolarizations.
Can be triggered in animal models by increasing tachycardia.
After a very high rate of stimulated tachycardia, sustained recurring DADs may be triggered.
Triggers: Accumulation of intracellular Ca++ causes spontaneous delayed afterpotentials.
Tachycardia, digitalis toxicity, overdrive pacing, ischemia, heart failure, Sympathetic activation
Treatment: Adenosine, Ca-Antagonists.
Conditions require for Reentry phenomenon to start?
What factors can increase the risk for reentry?
Unidirectional block (may be transient)
A sufficiently short refractory period, with differing refractory periods for the two parallel paths.
Hypertrophy of an atria or ventricle (increases the path length of conduction)
Hyperthyroidism, Vagal stimulation (both decrease the refractory period in the atria).
Important: Vagal stimulation decreases refractory period in atrium
Increases refractory period in the AV junction.
What is WPW?
Wolf Parkinson White syndrome:
A pre-excitation disorder due to the presence of an extra conducting fiber bundle, the Accessory bundle of Kent.
This bundle links the left atria to the left ventricle down the left marginal border.
Conduction down this bundle is faster than normal because it bypasses the slowing effect of the AV junction.
This represents two parralel pathways.
These pathways have different conduction characteristics
Therefore, a properly timed premature contraction (which occurs commonly) can very easily produce a re-entry tachycardia called AVRT (AV Reentrant Tachycardia). This occurs commonly in WPW syndrome patients.
Two types of AVRTs:
Orthodromic AVRT: excitation goes from the atria down to the ventricles, then conducted back upwards to the atria by the accessory bundle.
Narrow QRS signal
Antidromic AVRT: Conduction downwards through accessory fiber, then back upwards through the AV junction.
very wide QRS
How can you terminate reentry phenomena?
Vagal maneuvers such as Valsalva maneuver or Carotid massage.
This is NOT because the vagal maneuver slows the heart rate, this only works if the heart is under normal sinus rythm
Under an AVRT, the sinus node is irrelevant.
The vagal tone affects the AV node by increasing the refractory period, thus providing a halting point at the AV junction, and suddenly halting it.
Why is WPW syndrome dangerous
It is NOT because of the reentry phenomenon, the AVRT tachycardia is not actually very dangerous
Supraventricular tachycardias are not very dangerous.
But Atrial fibrillation can develop and that is very dangerous.
Because WPW patients can bypass the AV node which usually has a long enough refractory period to halt any transmission of the high frequency fibrillation from the atria down to the ventricles. But WPW patients can bypass this and transmit the fibrillation from atria to ventricles, resulting in FBI tachycardia. (fast broad irregular tachycardia), which can proceed to ventricular fibrillation.
What is brugada syndrome?
A genetic disorder, resulting in channel dysfunction in the sodium channels, causes large ST elevations, can lead to ventricular fibrillation and sudden death.
How is NSTEMI treated?
The treatment of NSTEMI is identical to the treatment of unstable angina.
Fundamentally, the first step in treating NSTEMI is to stabilize the heart muscle to prevent further damage. This can usually be accomplished by administering oxygen, morphine, beta blockers, aspirin, Plavix, and a statin drug.