Week 4: Arrhythmias Flashcards
1
Q
What is the normal PR interval for normal sinus rhythm
A
0.12 and 0.2 of a second
2
Q
What is the normal QRS duration for normal sinus rhythm
A
0.04 and 0.1 of a second
3
Q
What are the 4 abnormal rates of sinus rhythm
A
Tachycardia (too fast)
Bradycardia (too slow)
Sick sinus syndrome (irregular clumbing of R waves)
Sinus arrest
4
Q
What are the 3 conduction pathway disturbances you can have?
A
- Escape rhythms (usually from sinus arrest)
- Atrio-ventricular blocks
- Accessory pathways
5
Q
What are the 3 major classes of dysththmias you can have
A
- Abnormal rates of sinus rhythm (beating too quickly (tachycardia), too slowly (bradycardia), irregularly, erratic)
- Disturbances in the conduction system (abnormalities to the rhythm of action potential production and/or conduction system to the various parts of the heart)
- Abnormal sites of impulse initiation (ectopic)
6
Q
What is an escape rhytm and what are the 2 standard types of them
A
- These are the rhythms that are produced when the AV node, bundle of his, bundle branches or the purkinje fibres become the new pacemakers of the heart
- They start as a result of damage to the Sinoatrial node that forces it to become electrically silent. This results in a period of sinus arrest (no ECG or electrical activity), which allows the AV node to become spontaneously active taking over the role of pacemaker in the heart
Junctional escape rhythm
Ventricular escape rhythm
7
Q
what is a junctional escape rhythm and what would it show on an ECG
A
- Is the first escape rhythm to arise, produced by the AV node
- Its inherent automaticity is 40 – 60 bpm
- An ECG that showed a junctional escape rhythm would not have a normal P wave (as there is no atrial contraction)
- However, it would have a normal QRS-T complex as we still get depolarisation of the ventricles in the normal sequence (septum, free wall of ventricles etc.) however at the slower rate that is characteristic of the AV node
8
Q
What is a ventricular escape rhythm, what rate of automaticity would it have, what would it should on an ECG
A
- Is the escape rhythm that arises from the bundle of his, bundle branches or the purkinje fibres (is often these fibres) within the ventricle
- Its inherent automaticity is 15 – 40 Aps / min
- The reason ventricular escape rhythms are often facilitated by the purkinje fibres is that damage to the heart that is severe enough to destroy the AV node, chances are the bundle of his and bundle branches will be damaged to. Leaving the purkinje fibres to take over pacemaker duties
- An ECG that showed a ventricular escape rhythm would have no P wave, and a QRS complex that is abnormally wide (as we are not getting the normal sequence of AV node – bundle of his – bundle branches – ventricular free walls that provides the QRS complex)
9
Q
What is an AV block
A
- Is when we have normal sinus rhythm in the atria, but because of a malformed or damaged AV node, the conduction is blocked
- This usually is as a result of an issue with the AV Node, but may sometimes be caused by defective bundle of his or bundle branches (we are not covering bundle branch blocks)
10
Q
What are the types of AV blocks you can have (just list names)
A
First degree AV Block
Second degree (Type 1 or Type 2) AV Block
Third degree AV Block
11
Q
What is a first degree AV block and what does it display on an ECG
A
- This degree of AV block results in a normal rhythm, with each QRS complex being associated with a P wave
- The wave of depolarisation is just delayed, with a PR interval that is greater than 0.2 of a second (usually more than 5 squares)
12
Q
What is a second degree AV block
A
Can be type 1 or type 2
- Not all atrial depolarisations produce ventricular polarises when this type of block exists, that is not all P waves are associated with QRS complexes
- The pattern that arises of blocked P waves determines the type of second degree AV block, either Type 1 or Type 2
13
Q
What is second degree type 1 av block and what does it show on an ECG
A
- Type 1 or Wenckebach or Mobitz type 1 show a progressively increasing PR interval until a P wave is not conducted, that is until we drop a beat. We would have an orphan P wave and no ventricular contraction (no QRS complex). This pattern is then repeated
14
Q
What is second degree AV block type 2 and what does it show on an ECG
A
- Type 2 or Mobitz Type 2 shows a normal and consistent PR interval (with no PR prolongation) until suddenly a QRS complex is lost –> results in reduced cardiac output
15
Q
What is a third degree AV block and what would you see on an ECG
A
- involves a complete block of electrical continuity between the atria and the ventricles (that is, no P waves are connected to the QRS complex)
- As a result, this block produces an escape rhythm (as the bundle branches and purkinje fibres have their own inherent rhythm of 15 – 40 bpm)
- Abnormally wide QRS complex’s will be evident
- Patients will experience bradycardia of 15 -40 bpm of the ventricle which will compromise cardiac output
16
Q
What is a pre-excitation syndrome and what does it show on an ECG
A
a congenital heart defect that introduces an accessory conduction pathway
causes a pre-excitation syndrome where the right ventricle becomes excited, producing action potentials ahead of schedule (passes straight from atria to ventricles without going through the AV node)
- This results in depolarisation of the ventricles unusually quickly which shortens the PR interval, whilst also forming what’s known as the delta wave
- The QRS complex will be abnormal (slightly wider because of the delta wave), instead of the Q caused by depolarisation of the septum, we get a delta wave
17
Q
What are the 6 dysrhythmias caused by ectopic pacemakers
A
- Premature atrial complexes
- Atrial flutter
- Atrial fibrillation
- Premature ventricular complexes
- Ventricular tachycardia
- Ventricular fibrillation
18
Q
What are the 3 mechanisms behind ectopic pacemakers
A
- Abnormal automaticity
- Triggered activity
- Re-entry
19
Q
what is abnormal automaticity
A
- This happens when contractile myocytes that should otherwise lack automaticity spontaneously depolarise and produce action potentials ahead of schedule
20
Q
explain the 3 mechanisma behind abnormal automaticity
A
ISCHAEMIA:
- Contractile myocytes require oxygen to produce ATP so that they can contract
- This ATP also powers the sodium/potassium ATPase and the calcium ATPase that maintain normal ion gradients across the cells membrane
- Reduced oxygen levels as a result of ischemia, reduce the ATP levels in the cell, thus disabling the pumps and altering the ion gradients
- Eventually this results in spontaneous depolarisation and inappropriate automaticity in the contractile myocytes
- Electrolyte imbalances (particularly hypokalaemia):
is another cause of this abnormal automaticity which can be caused by renal problems, excessive vomiting, diarrhea
- Abnormally leaky channels that release Na+ or Ca2+
can cause spontaneous depolarisation if too many ions are leaked (usually pumps put these right back into the cell). This can particularly be an issue if there is not enough ATP to power the pumps
21
Q
explain what an early after depolarisation is and why.
A
- Are second action potentials that are triggered early on in the relative refractory period (phase 3)
- This can be explained by voltage gated calcium and sodium channels recovered from inactivation before the membrane potential is below their threshold of activation
22
Q
explain what an delayed after depolarisation is and why.
A
- Are depolarisations that occur after the repolarisation phase is complete ahead of the sinus rhythm
- This occurs during Phase 4
- DADs are associated with high intracellular Calcium and sarcoplasmic reticulum calcium level. This trigger calcium to be released from the sarcoplasmic reticulum which evokes an action potential
23
Q
what does digoxin do and what is digitalis toxicity
A
- Delayed afterdepolarisation is suggestive of heart failure and is often associated with Digitalis toxicity (too much of a drug builds up causing DADs) and excessive catecholamine stimulation
- Digoxin is actually also the drug that treats this, it is a poison which blocks sodium/potassium ATPase which in small concentrations has a positive ionotropic (force of contraction of ventricular myocytes) effect
- This drug in high amounts however contributes to DADs. This is because the digoxin blocks the sodium/potassium ATPase, there is an overload of calcium under resting conditions. The SERCA loads more calcium into the SR than normal, this then spontaneously dumbs the calcium at rest (leading to a spontaneous depolarisation during stage 4) leading to an early depolarisation ahead of the sinus rhythm
24
Q
What can one re-entry loop lead to and what can multiple re-entry loops lead to?
A
ventricular tachcardia and ventricular fibrilation
25
what are the 3 requirements for re-entry to occur
a functional or anatomical loop
The absolute refractory period of the re-entered segment of muscle must be shorter than the conduction time around the loop
Unidirectional conduction block within the loop (something that allows AP’s to only go in one direction, can be caused by transient ischemia taking away their ability to produce action potentials)
26
Explain a re-entry loop
Normal wave of excitation sweeps from endocardium to epicardium. When wave of excitation meets the arteriole, it splits and tries to go around it. However, the ischaemic myocytes on one side stop the progression of the wave of excitation (unidirectional block). Whilst the wave of excitation sweeps around the arteriole, blow flow is restored (reason the block is unidirectional is that the ischaemia is transient). The myocytes are therefore able to produce an action potential and therefore trigger a wave of excitation which hits them from the epicardial side (opposite to normal). Therefore, the myocytes more endocardial to the transiently ischaemic myocytes /unidirectional conduction block are either in RRP or at rest and can produce an action potential. Hence, abnormal activation of the former ischaemic myocytes re-excites their neighbours etc. This generates a re-entry wave which is self-propagating around the arteriole and throughout the ventricles creating a circus movement of the wave of excitation.
27
what is a premature atrial complex, whats it caused by and what does it have on an ECG
- Occurs when atrial depolarisation is initiated by cells other than the SA node pacemaker cells within the atria
- This can be caused by inappropriate automaticity, an early afterdepolarisation or delayed afterdepolarization in atrial contractile myocytes, it will result in a premature atrial complex, which is also known as a premature atrial contraction (PACs)
- Simply put, we have atrial depolarisation caused by cells other than the sinoatrial node and the conduction system to create an ectopic beat
- Each one is followed by a compensatory pause until sinus rhythm can re-establish itself
28
What is an atrial flutter and what will it look on an ECG
- Is a very serious form of atrial tachycardia
caused by a re-entry loop
- This will look like a saw tooth pattern of P waves, however will have a slower rate of ventricular depolarisation (as during much of the P waves, the AV node will be in an absolutely refractory state, thus not all atrial depolarisations are conducted)
29
what are some of the possible causes of the re-entry of the atrial flutter
- Acute alcohol toxicity
- Underlying heart disease
- Fluid overload
- Atrial ischemia
30
what is atrial fibrilation
Is characterised by chaotic depolarisation of the atria, which is accompanied by a ventricular depolarisation that is irregular and variable
Involves multiple and constantly changing re-entry loops, which result in chaotic and disorganised contraction of the atria
31
what are 2 methods of treating atrial fibrilation
It is treated by cardioversion with electric shock across the long axis of the heart (base to apex). It is timed with the peak depolarisation of the ventricles (R wave) which depolarises the entire heart simultaneously, the heart then repolarises simultaneously, restoring sinus rhythm
Anti-arrhythmic drugs are also used to treat atrial fibrillation. These include: calcium channel blockers, beta blockers, digitalis, amiodarone
32
what are premature ventricular complex, what are they caused by and what do they have on an ECG
Caused by spontaenous depolarisation of the ventricles
As with premature atrial complexes, PVCs are usually caused by inappropriate automaticity (associated with ischemia and electrolyte imbalance) or triggered activity (DADs or EADs)
As repolarisation will obviously follow a different path, the T wave is inverted
As depolarisation follows an unusual sequence, the QRS complex is usually an abnormally long
The PVC will be ahead of the sinus rhythm, before we get a compensatory pause before the next sinus beat
33
what is monomorphic ventricular tachycardia, what is it caused by and what would you see on an ecg for it
Re-entry loop in the ventricles causing rhythm to exceed 100bpm
A characteristic ECG of ventricular tachycardia at high rates will see the QRS complexes combine with T waves to form large, wide, undulating waves, with individual parts of the wave form being un recognisable (if the waves look the same they are known as monomorphic)
Re-entry is the most common underlying mechanism or cause of ventricular tachycardia
34
what is polymorphic ventricular tachycardia, what is it caused by and what would you see on an ecg for it
This is a non-sinus tachycardia which is polymorphic, meaning that the shape of the wave changes as you go along (the wave gets larger, then smaller then larger then smaller)
This is known as torsade de pointes, and is especially associated with Long QT syndrome (early afterdepolarisations)
Is associated with a drop in cardiac output meaning it is quite serious (significant reductions in arterial pressure)
35
what is the difference between polymoprhic and monomorphic ventricular tachycardia
Polymorphic: This is a non-sinus tachycardia which is polymorphic, meaning that the shape of the wave changes as you go along (the wave gets larger, then smaller then larger then smaller). Is associated with a drop in cardiac output meaning it is quite serious (significant reductions in arterial pressure)
Monomorphic: A characteristic ECG of ventricular tachycardia at high rates will see the QRS complexes combine with T waves to form large, wide, undulating waves, with individual parts of the wave form being un recognisable (if the waves look the same they are known as monomorphic)
36
what is ventricular fibrilation, what is it caused by and what would you see on an ecg?
Is caused by multiple re-entry waves working its way through the ventricles
VF is characterised by rapid, chaotic electrical rhythm which is completely uncoordinated
Cardiac output of patients with VF is significant diminished making it potentially lethal
Ventricular tachycardia often progresses to ventricular fibrillation as the single loop re-entry loop that causes VT, can split into two re-entry loops which continue to multiply causing the degeneration of VT into VF
it is just one fukced up ecg
37
inappropriate automaticity often results from ischaemia. Define ischaemia and explain how ischaemia compromises the ability of the contractile myocyte to maintain its resting membrane potential
ischaemia - inadequate supply of blood --\> decreased o2 --\> decrease ATP
atp is needed to power the Na/K atpase and therefore it cannot maintain the resting membrane potential as this pump cannot function properly without atp
38
which phase of the action potential do early afterdepolarisations occur
phase 3
39
which phase of the action potential do delayed afterdepolarisations occur
phase 4
40
how would a prolonged action potential duration predispose your patient to EADs
voltage gated calcium and sodium channels have recovered from inactivation before resting membrane potential is below their threshold.
41
how does elevated calcium levels in the myoplasm and the sarcoplasmic reticulum trigger DADs
increase calcium + high SR calcium --\> Sarcoplasmic reticulum overload which releases calcium causing depolarisation
42
inappropriate automaticity and triggered activity (EADs, DADs) will most likely produce which dysrhythmia?
pre mature atria or ventricular complexes
43
a single re-entry loop will most likely cause which type of dysrhythmia?
atrial flutter or ventricular tachycardia
44
a prolonged PR interval is which type of
first degree av block
45
consistent P waves with a random loss of QRS complex is which type of dysrythmia?
second degree type 2 av block
46
how is a second degree type 2 av block treated
Is treated with an artificial pacemaker, which couples the QRS complexes to P waves
47
what arythmia have nice rhythmic P waves but very abormal and slow QRS and t complex's. The QRS complex is abnormally wide and produced by the Bundle branches and purkinje fibres.
third degree av block
48
what is an example of a pre-excitation syndrome
Wolff-Parkinson-White Syndrome is an example of one of these pre-excitation syndromes
49
what is characteristic about a pre-excitation syndrome (accessory pathway)
has a delta wave
