Cardiac Arrhythmias Flashcards
the normal heart rate range
60-100 beats / min
functions of the following ;
SA node
AV node
pacemaker of the heart, initiates excitation of the heart
Conduct the electrical signal to the apex of the heart.
and, Delay transmission of action potentials slightly (so the atria can complete contraction before ventricular contraction begins)
the stages involved in the generation of myocardial cell action potential, and what happens during these stages
4(resting potential)
0(sodium channels open)
1(sodium channels close)
2(calcium channels open; the potassium channels quickly close)
3(calcium channels close; slow opening of potassium channels)
4(resting potential)
in auto-rhythmic cells, the influx of which ions generates an action potential
note this is not the same as in myocardial cells
calcium ion influx generates an action potential(depolarization), instead of sodium ions as in myocardial cell action potentials
note that there is initially sodium influx before the calcium influx n order to reach the threshold, after which calcium channels open to let them in
in auto-rhythmic cells AP, at the peak or close to it, which ion channels open
K+ opens generating a outward current
(repolarization, similar to other excitable cells).
what do these indicate on an ECG;
P wave
QRS wave
T-wave
P-Wave – atria depolarise
QRS- wave – ventricles depolarize, (atria
repolarize)
T-wave – ventricles
repolarise
Cardiac Arrhythmias description and what it could lead to
An abnormality of the cardiac rhythm
may cause sudden death, syncope,
heart failure, dizziness, palpitations or no symptoms at all
Syncope is used to describe a loss of consciousness for a short period of time
two main types of arrhythmia
Bradycardia: the heart rate is slow (< 60 b.p.m).
Tachycardia: the heart rate is fast (> 100 b.p.m).
examples of supraventricular Tachyarrhythmias(same as tachycardia)
- Sinus tachycardia - SA node fires too quickly
- Atrial tachycardia(Focal AT, Multifocal AT)
- Paroxysmal SVT (PSVT)
- Atrial fibrillation
- Atrial Flutter
note all these are supraventricular.
Paroxysmal means it comes and goes
examples of ventricular tachyarrhythmias
Ventricular tachycardia (can be monomorphic or polymorphic)
- Torsades de pointes (prolonged QT interval)
- Ventricular Fibrillation
examples of bradycardia
Sinus bradycardia – SA node not firing
1° Heart Block
2° Heart Block – Mobitz I and II
3° Heart Block
Sick sinus syndrome – both tachy and brady
Sick sinus syndrome (SSS) is a heart condition that causes abnormal heart rhythms
the three main mechanisms that lead to arrythmias
Automaticity
* Triggered activity
* Re entrant circuit
note these can lead to tachycardia as well as bradycardia
Automaticity refers to the heart’s ability to initiate its own electrical impulses, allowing the heart to beat regularly without outside signals. When automaticity is affected, the heart’s rhythm can slow down, leading to bradycardia.
the main nerve in the parasympathetic nervous system, and its main functions ?
the vagus nerve
The vagus nerve controls involuntary functions like digestion, heart rate, and immune response. connected to internal organs like the heart, brain…etc
aka the cranial nerve
some factors that can affect automacity, and lead to bradycardia
Increased vagal tone: The vagus nerve, which controls parasympathetic functions, can slow down the heart rate. This happens naturally when you’re sleeping or in athletes who have a well-trained heart.
Drugs: Some medications, like beta-blockers, calcium channel blockers, and digoxin, can lower the heart rate by reducing the heart’s ability to respond to signals or by blocking certain pathways in the heart.
Decreased metabolic activity: Conditions like hypothermia (low body temperature) or hypothyroidism (low thyroid hormone levels) can slow down metabolic processes in the body, including the heart’s electrical activity, resulting in bradycardia.
Hyperkalemia: High levels of potassium in the blood can disrupt the electrical activity of the heart, leading to a slower heart rate.
some factors that affect automacity, thereby causing tachycardia
Increased sympathetic activity
* Hypovolaemia
* Hypotension
* Hypoxia (COPD, pulmonary embolism)
* Sympathomimetics – adrenaline ,cocaine,
methamphetamine
* Pain/anxiety
* Increased metabolic activity – fever, hyperthyroidism
note, negative feedback plays a role here. eg, in hypovolaremia, there is reduced blood volume, so the heart tries to compensate by increase it’s output , there increases it’s rate
what is referred to by triggered activity, as a mechanism leading to arrythmias
Triggered activity refers to abnormal electrical impulses that occur after the normal depolarization of a heart cell. It typically arises due to changes in the normal electrical activity of the heart.
the two main types of trigerred activity
Early after depolarization (EAD)
* Delayed after depolarization (DAD)
EAD more dangerous, and can be fatal very rapidly
EAD description
occurs during repolarisation. EADs happen** if the repolarization process is delayed**, leading to an abnormal “extra” electrical impulse before the cell is fully back to its resting potential.
repolarization is the phase when the heart cell is returning to its resting state after an action potential
the main causes of EAD
Prolonged QT interval, aka QT syndrome
Decreased levels of K+, Ca2+ , Mg2, which lead to QT syndrome
EAD increases the risk of arrythmias like ventricular tarchycardia and torsades de pointes
Magnesium is a natural calcium antagonist, and its deficiency (hypomagnesemia) can make the heart more susceptible to arrhythmias by increasing intracellular calcium levels.
name some class of drugs that can increase the risk of EADs
Anti arrhythmics(easp class 1 and class 3)
antibiotics
antipsychotics
antidepressants
antiemetics
what happens in torsades de pointes
“Torsades de pointes” refers to a life-threatening heart rhythm disturbance where the ventricles of the heart beat rapidly and irregularly
causes of DAD
Increased Calcium influx to cells(main cause)
Ischaemia
- Hypoxia
- Inflammation (myocarditis)
- Stretch
- Increased sympathetic activity
- Digoxin toxicity
note the logic behind most if not all these causes is the fact that they increase calcium levels in the cell
how digoxin toxicity causes DAD
Digoxin, a cardiac glycoside, is used in heart failure and arrhythmias. It works by inhibiting the Na+/K+-ATPase pump, which increases intracellular sodium levels. As a result, the sodium-calcium exchanger (NCX) is less efficient in extruding calcium from the cell, leading to calcium overload. This calcium accumulation increases the risk of DAD. Digoxin toxicity can therefore cause arrhythmias, often via DAD
what is meant by re-entry in arrhythmias
re-entry occurs when an electrical impulse travels in an abnormal circuit rather than following the normal conduction pathway. This impulse continuously re-enters the same area of tissue, repeatedly stimulating it. This abnormal repetitive stimulation can lead to arrhythmias (irregular heart rhythms), sometimes causing very rapid heart rates.
the types of reentry
AF, atrial flutter, AVNRT, AVRT, VT, VF
AVNRT (Atrioventricular Nodal Reentry Tachycardia)
(Atrioventricular Reentry Tachycardia)
VF (Ventricular Fibrillation), use the same logic for the rest
sinus tachycardia
is a common condition that happens sometimes in response to stressful situations. Your heart beats more than 100 times per minute, but usually returns to normal after the stressful event has passed. If your symptoms continue when your body is at rest, it’s a good idea to see your healthcare provider.
causes of sinus tachycardia
Increased automaticity, leading to decreased BP or low O2 activating baroreceptors/chemoreceptors
Anaemia, hyperthyroidism, Sympathomimetic drugs, phaeochromocytoma, pain , anxiety
Baroreceptors monitor blood pressure and blood volume in blood vessels, and signal the brain to make adjustments
Phaeochromocytomas are rare tumours that start in the inner part of the adrenal gland (the medulla)
causes of torsades de pointes
hypokalaemia
hypomagnesemia
QT prolonging medications
heart block description and what it primarily leads to
Heart block is a condition that occurs when the electrical signals that control the heart’s rhythm are disrupted.
primarily leads to bradycardia
main reason/ cause of mutifocal atrial tachycardia
decreased O2 (eg in COPD)
most common cause is COPD
causes of atrial fibrilation
AF can be caused by a combination pof;
Increased automaticity → More rapid, uncoordinated electrical signals.
Re-entrant circuits → Continuous looping of electrical impulses in the atria
Triggered activity → Extra beats initiating abnormal atrial rhythms.
Electrolyte imbalances (low potassium, low magnesium) further increase the risk by prolonging repolarization(QT prolongation) and enhancing excitability.
general cause of VF (ventricular fibrillation)
multiple reentrant circuits
anti- tachycardia agents are a subset of anti-arrhythmic agents, true or false
true
anti-tachycardia drugs specifically target abnormally fast heart rhythms (tachycardia), whereas anti-arrhythmic agents address a broader range of irregular heart rhythms, including both fast and slow heartbeats (arrhythmias)
vaughan williams classification of anti-tachycardia agents
Class I: Na+ channel blockers
Class II: beta-adrenoceptor antagonists
Class III: K+ channel blockers
Class IV: Ca2+ channel blockers
others, like adenosine and digoxin
the main neurotransmitters of the autonomous nervous system,i.e parasympathethic and sympathetic
parasympathetic - acetylcholine
sympathetic- noradrenaline or norepinepherine and adrenaline/epinepherine
the two main classes of anti-bradycardia agents
Beta-adrenoceptor agonists like epinephrine
Muscarinic receptor antagonists like atropine
Class I Anti-Arrhythmic Agents are further divided into how many subclasses, name these classes
3
class 1a
class 1b
class 1c
note that Class I Anti-Arrhythmic Agents aka sodium channel blockers
how do the subclasses of Class I Anti-Arrhythmic Agents affect repolarisation
class 1a prolongs repolarization, leading to extended refractory periods, to slow conduction
class 1b shortens repolarisation, making cells recover faster after depolarisation
class 1c does not affect repolarisation, but it strongly slows electrical conduction
in descending order(from strongest to weakest), list the subclasses of Class I Anti-Arrhythmic Agents based on how strongly they block the sodium channel
Ic > Ia> Ib
Quinidine, Disopyramide, Procainamide(class 1a)
Lidocaine, Phenytoin, Mexiletine(class 1b)
Flecainide, Propafenone(class 1c)
how many geenrations of Class II Anti-Arrhythmic Agents are they, name and describe them
- 1st generation of beta-blockers: Non-selective (they block both β1 and β2 adrenoceptors). Propranolol, sotalol
- 2nd generation of beta-blockers: More cardioselective. as they are relatively selective for β1adrenoceptors. Selectivity is lost at higher drug doses. eg are Metoprolol, atenolol
- 3rd generation of beta-blockers: Also possess vasodilator actions (blockade of** vascular** beta-adrenoceptors). Carvedilol, nebivolol
beta 1 receptors mainly found in the heart while beta 2 receptors mainly found in the lungs
what do beta- adrenoreceptors antagonists/blockers do in the heart
they bind to beta 1 receptors in the heart, leading to;
Decrease in heart rate
* Decreases conduction velocity
* Decreases myocardium contractility
what do beta- adrenoreceptors antagonists/blockers do in the blood vessels
they casue vasodilation, decreasing bp, heart rate…
they can cause VASOCONSTRICTION if they bind to beta 2 adrenoceptors. this is because beta 2 receptors mainly mediate vasodilation, i.e they are responsible for dilation, especially in the lungs.
note that the constrictive role is not significant enough to cause problems( in terms of increasing bp further)
which drug is a mix of class II and class III antiarrhythmics
sotalol.
it is a;
Non selective beta-adrenoceptor antagonist
Blocks K+ channels so prolonging action potential duration
what class of anti-arrhythmic agents is amiodarone, and what does it do.
Mainly class III, but also acts as class I, II and IV
it blocks K+ channels responsible for repolarization, lengthening the refractiory period and decreasing re-entry
it also blocks Na+ block - decreases pacemaker cell discharge rate. it also blocks Ca2+ channels
it is an alpha & beta adrenoceptor antagonist - non competitive
very long half-life (25-60 days)
blocks the AV node as well, leading to bradycardia
where do Class IV Anti-Arrhythmic Agents, especially NDHPs(Verapamil, Diltiazem) mostly work in the heart ?
what do they do(their function)
note Class IV Anti-Arrhythmic Agents aka calcium channel blockers
they Act preferentially on SA and AV nodes
in which heart conditions do we use Class IV Anti-Arrhythmic Agents
- Re-entrant paroxysmal supraventricular tachycardia(Often involves AV node)
- it is also Rarely used to treat ventricular arrhythmias
