Cardiac arrhythmias Flashcards
Normal heart rhythm
i.e. normal sinus rhythm (NSR)
Impulses are coming from SA node
Regular P waves with similar morphology
Regularly followed by QRS complex
Normal rate
60-100 bpm
What is an arrhytmia
?
irregular heart rhythm (fast, slow, irregular)
Bradycardias and cause
<60
sinus bradycardias (physiological or sinus. node disease)
problems with AVN- atrioventricular block but not always
tachycardias
BPM
types and examples from the types
greater than 100 BPM
narrow comlpex tachycardias
AFib, A flut, AT and ST (atrial and sinus tach)
SVT
broad complex
Ventricular tachycardias
“horrible looking tachycardias”
VF and torsades
What things can cause arrhtymias
- Electrolyte disturbances
- Ion channel modification or defects
- Structural/ anatomy abnormalities
- Cell damage
Fundamentals of why arrhythmias occur
- Disturbances in impulse generation
- Disturbances in impulse propagation
- Bit of both
Who is at risk of arrhythmias
Cell/structural changes
Myocardial infarction
Myocarditis
Fibrosis
Toxins (ie alcohol)
Chemotherapy
Ion channels
Long QT syndromes
Drugs (i.e. antiarrhythmics, anti-epileptics)
Situational/Environmental factors can cause cellular dysfunction
Metabolic anomalies- K, Ca, Mg levels, temperature, acidaemia, hypoxia
Normal conduction process
Specialised conduction tissues run throughout key conduction areas of the heart.
Starts at the SA node in the top right of the right atrium.
Wave of depolarisation spreads across the atria, causing them to contract.
Electrical impulse reaches the AVN, in the bottom left of the right atrium. AVN is a specialised conduction tissue. It is the only one that allows depolarisation to spread to the ventricles.
The rest of the base of the atria is electrically isolated.
AVN directs impulse to the left and right bundle branches.
Impulse is passed onto the purkinje fibres in the bulk of the myocardium in the ventricles causing ventricular systole.
Disorders in pulse formation can be due to (2)
Disorders in automaticity
Triggered activity (EADs and DADs)
What is automaticity
“The property of a fibre to initiate an impulse spontaneously- without needing prior stimulation”
2 abnormalities in automaticity
- Inappropriate discharge rate (i.e. sinus tachycardia, sinus bradycardia)
- “ectopic” pacemaker takes over and controls atrial or ventricular rhythm
Increased or abnormal automaticity
Sinus tachycardia- SA node activating too quickly
Ectopic atrial tachycardia- abnormal focus of atrial cells that have automaticity, biphasic P waves
Junctional tachycardia- piece of tissue near AVN irregular
reason for decreased automatcity
Sinus node disease- presents as sinus bradycardia. Normal waveforms just too slow.
explain the cardaic pacemaker cells properties
- Pacemaker cells have a pacemaker potential (phase 4) enabling them to self-generate their own action potentials
- The rate of rise of ion influx at the pacemaker cell sets the intrinsic heart rate
- The SA node rate is then influenced by the autonomic nervous system
- A balance of sympathetic and parasympathetic tone sets the resting heart rate
What happens during phase 4 of a pacemaker potential
- Reaches -60mV
- Opening of slow inward (depolarising) Na+ funny channels
- Small potassium out at decreasing level as channels close
- -50 mV- opening of T-type Ca2+ channel (influx)
- -40 mV- opening of L-type Ca2+ channels (long influx) and quick upsweep to depolarising
phase 4 of a normal cardiac cell
without the external stimulus of adjaecnt ion release an action potential would never be produced as the threshold potential would never be met
what are “triggered activities”
“after-depolarizations”
These are depolarising “oscillations” in the resting membrane voltage induced by one or more preceding action potentials
i.e. unstable depolarisations (activations) that occur when the heart should be repolarising (resting)
These oscillations can trigger (or be triggered by) extra heart beats
Can trigger arrhythmias like Torsades de Pointes (polymorhphic ventricular tachycardia) or VT
What is an EAD
Early After Depolarisations arise from an abnormal membrane potential during phase 2 and 3
Lots of “aborted” action potentials usually due to changes in the ion channels
i.e increased opening of Ca and Na channels
Mechanism:
Mini spike in phase 2 and 3 of the action potential
Manifestation: prolongs QT interval (time taken for ventricular depolarisation and repolarization- “resting”), prolonging how long it takes to return to electrical baseline.
If the depolarisation occurs at the right time it can be sufficient to trigger extra heartbeats.
Possible for one EAD to trigger another, then that one triggers another and so on and so on. This creates a sustained heart rhythm disorder like Torsades de pointes.
What are DADs
Late or Delayed After-Depolarisations occur after phase 4.
Due to an increased/ altered movement of calcium.
Activate a Na/Ca exchanger triggering an AP.
what is the difference between LAD’s and DAD’s?
DAD’s happen at much more negative membrane potnetials
Outcomes of an EAD (3)
- Spike of sodium, nothing happens
- Small action potential, prolongs QT interval
- Sustained triggered activity (e.g. Torsades de Pointes) caused by early depolarisation. Influx of sodium is great enough to keep causing action potentials.
outcomes of DAD (3)
- Can sometimes do nothing- subthreshold
- Just enough to trigger an action potential (ectopic/extra beat)
- Sustained triggered activity (e.g. VT)- repeated DADs
causes of EADs
Low serum K+
Slow HR
Drug toxicity ie quinidine
Causes of DADs
- Increased serum calcium
- Increased adrenaline
- Drug toxicity ie Digoxin
- Myocardial infarction
What are the 2 forms of impulse conduction disorder
re entry
conduction block
What are the requirements for a re-entry tachycardia to take place (3)
- 2 possible routes for electrical impulse to flow down
- Two pathways must have different electrical properties, with one conducting faster- “Fast pathway” and “slow pathway”
- Impulse flows down one pathway, back up another and gets caught in a loop
when is a re-entry circuit not a problem
differeent paces, the impulses arrive at the end together
the slower pathway can be caused by:
central area of block e.g., scar tissue, refractory cells
area/ path of transient/ variable blocking e.g., dead myocytes, myocytes with different refractory period/ conduction velocity
rhythms caused by re-entry
- AV nodal Re-entrant tachycardia (AVNRT)
- AV re-entrant tachycardia (AVNRT)
- Atrial flutter
- Atrial fibrillation
- Ventricular tachycardia
Explain supraventricular tachycardia
- has 2 categories (will go into later)
- Identified on ECG’s as a regular tachycardia 130-250 bpm
- There is 1 P wave for each QRS, but they may not be visible
- QRS duration is usually narrow (normal), as after the AVN the impulse is conducted normally through the ventricles
How do accessory pathways lead to SVTs
(conductible breaks in the usually electrically insulated non-conducting strip at base of atria)
SA node fires as normal (P wave)
Reaches AVN as normal, however also reaches accessory pathway
Accessory pathways don’t have inbuilt delay so AP’s immediately pass through and activate ventricular systole.
The AVN then passes on its AP after its natural delay, remainder of ventricle catches up
Results in a slurring of the QRS complex- called delta wave
This means that there are 2 pathways for conduction; one of which is fast and one of which is slow. Therefore, a re-entry circuit can be set up.
What are the 2 types of SVT
AVNRT- Extra wire near AVN that conducts slightly slower, creating a loop
AVRT-apparently it doesn’t matter, both look similar on ECG
atrial fibrillation
Can be caused by smaller re-entry circuits above both atria
Common in those with small scarring or stretching on the atria- i.e. older people, high BP, diabetes
Wobbly and irregular baseline, no clear P waves
Electrical signals hit the AVN at random times, irregularly regular QRS complexes
atrial flutter
(“macro” circuit- usually due to extra wiring by the tricuspid valve)
Electricity goes round the atrium- shown as a sawtooth baseline on ECG
ventricular tachycardia
Most clinically prevalent when someone has had a large myocardial infarction, leaving a large section of scar tissue, some of these cells will be dead whereas others within it just conduct slower. Fast= purkinje fibre and slow = scar tissue.
Because this occurs in a large section of myocardium (ventricles), you get broad QRS complexes going round and round
Disorders of impulse conduction
conduction blocks- block to conduction going from the atria to ventricles
e.g., 1st degree to 3rd degree heart block
1st degree av block
ECG- normal activation of SAN (normal P wave), AVN has a greater delay (Prolonged PR interval)
Normal 200ms (5 small squares) here 6-7
Second degree heart block (Type 1 av wenkebach)
Somewhat normal. AVN has normal delay/ break. In wenchebach, keeps applying the breaks harder nd harder until it applied them a. little too hard and it blocks the impulse entirely.
Gradual increase in PR interval until eventually, no QRS.
Next time, foot completely off the breaks so PR interval is normal.
Somewhat pattern like
2nd degree heart block (type 2)
Randomly a P wave with occasional missing QRS. No PR interval prolongation.
3rd degree av block
Essentially AVN is dead, allows no conduction
His purkinje system has to take over as pacemaker
Sinus rhythm normal (P wave) completely unrelated to QRS complex. May find P waves in the middle of QRS complexes.
how might ischaemic heart disease cause AV block
Ischaemic heart disease is when you have atheroma (plaque) and eventual occlusion to the coronary arteries. Resultant ischaemia to myocardium.
Right Coronary Artery (RCA) usually supplies blood to critical electrical component of heart (i.e., AVN). Ischaemia to these areas can lead to sinus bradycardia or heart block
Consequences of arrhythmias
haemodynamic compromise due to CO being affected
low HR causes direct drop in CO
high HR means that ventricles can’t fill as effectively so CO drops
porlonged arrhythmia can cause
Prolonged arrhythmia can lead to
- Heart failure- CO fails to meet end organ demand
- Cardiac ischaemia and chest pain due to reduced coronary filling
- Hypotension
- Poor renal perfusion renal failure
- Poor liver perfusion liver failure
- Poor brain perfusion syncope, confusion
an inferior MI can affect from the RCA can affect what part of the ehart and cause what condition?
disrupt bf to the SA and AVN causing bradycardia and heart block
If left atrial hypertrophy what would be seen on ecg
2 p wave peaks
if right atrium hypertrophy what would happen to ecg
taller p wave
