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Year 2 Foundation in Clinical Practice 2 > Cardiac Arrhythmias > Flashcards

Cardiac Arrhythmias Flashcards

1
Q

the normal heart rate range

A

60-100 beats / min

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2
Q

functions of the following ;
SA node
AV node

A

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)

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3
Q

the stages involved in the generation of myocardial cell action potential, and what happens during these stages

A

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)

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4
Q

in auto-rhythmic cells, the influx of which ions generates an action potential

note this is not the same as in myocardial cells

A

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

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5
Q

in auto-rhythmic cells AP, at the peak or close to it, which ion channels open

A

K+ opens generating a outward current
(repolarization, similar to other excitable cells).

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6
Q

what do these indicate on an ECG;
P wave
QRS wave
T-wave

A

P-Wave – atria depolarise

QRS- wave – ventricles depolarize, (atria
repolarize)

T-wave – ventricles
repolarise

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7
Q

Cardiac Arrhythmias description and what it could lead to

A

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

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8
Q

two main types of arrhythmia

A

Bradycardia: the heart rate is slow (< 60 b.p.m).

Tachycardia: the heart rate is fast (> 100 b.p.m).

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9
Q

examples of supraventricular Tachyarrhythmias(same as tachycardia)

A
  • 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

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10
Q

examples of ventricular tachyarrhythmias

A

Ventricular tachycardia (can be monomorphic or polymorphic)

  • Torsades de pointes (prolonged QT interval)
  • Ventricular Fibrillation
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11
Q

examples of bradycardia

A

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

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12
Q

the three main mechanisms that lead to arrythmias

A

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.

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13
Q

the main nerve in the parasympathetic nervous system, and its main functions ?

A

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

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14
Q

some factors that can affect automacity, and lead to bradycardia

A

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.

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15
Q

some factors that affect automacity, thereby causing tachycardia

A

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

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16
Q

what is referred to by triggered activity, as a mechanism leading to arrythmias

A

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.

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17
Q

the two main types of trigerred activity

A

Early after depolarization (EAD)
* Delayed after depolarization (DAD)

EAD more dangerous, and can be fatal very rapidly

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18
Q

EAD description

A

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

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19
Q

the main causes of EAD

A

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.

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20
Q

name some class of drugs that can increase the risk of EADs

A

Anti arrhythmics(easp class 1 and class 3)
antibiotics
antipsychotics
antidepressants
antiemetics

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21
Q

what happens in torsades de pointes

A

“Torsades de pointes” refers to a life-threatening heart rhythm disturbance where the ventricles of the heart beat rapidly and irregularly

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22
Q

causes of DAD

A

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

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23
Q

how digoxin toxicity causes DAD

A

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

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24
Q

what is meant by re-entry in arrhythmias

A

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.

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25
the types of reentry
AF, atrial flutter, AVNRT, AVRT, VT, VF ## Footnote AVNRT (Atrioventricular Nodal Reentry Tachycardia) (Atrioventricular Reentry Tachycardia) VF (Ventricular Fibrillation), use the same logic for the rest
26
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.
27
causes of sinus tachycardia
Increased automaticity, leading to decreased BP or low O2 activating baroreceptors/chemoreceptors Anaemia, hyperthyroidism, Sympathomimetic drugs, phaeochromocytoma, pain , anxiety ## Footnote 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)
28
causes of torsades de pointes
hypokalaemia hypomagnesemia QT prolonging medications
29
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
30
main reason/ cause of multifocal atrial tachycardia
decreased O2 (esp in COPD) ## Footnote most common cause is COPD
31
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.
32
general cause of VF (ventricular fibrillation)
multiple reentrant circuits
33
anti- tachycardia agents are a subset of anti-arrhythmic agents, true or false
true ## Footnote 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)
34
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
35
the main neurotransmitters of the autonomous nervous system,i.e parasympathethic and sympathetic
parasympathetic - acetylcholine sympathetic- noradrenaline or norepinepherine and adrenaline/epinepherine
36
the two main classes of anti-bradycardia agents
Beta-adrenoceptor agonists like epinephrine Muscarinic receptor antagonists like atropine
37
Class I Anti-Arrhythmic Agents are further divided into how many subclasses, name these classes
3 class 1a class 1b class 1c ## Footnote note that Class I Anti-Arrhythmic Agents aka sodium channel blockers
38
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
39
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 ## Footnote Quinidine, Disopyramide, Procainamide(class 1a) Lidocaine, Phenytoin, Mexiletine(class 1b) Flecainide, Propafenone(class 1c)
40
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 ## Footnote beta 1 receptors mainly found in the heart while beta 2 receptors mainly found in the lungs
41
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
42
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. ## Footnote note that the constrictive role is not significant enough to cause problems( in terms of increasing bp further)
43
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
44
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 ## Footnote very long half-life (25-60 days) blocks the AV node as well, leading to bradycardia
45
where do Class IV Anti-Arrhythmic Agents, especially NDHPs(Verapamil, Diltiazem) mostly work in the heart ? what do they do(their function) ## Footnote note Class IV Anti-Arrhythmic Agents aka calcium channel blockers
they Act preferentially on SA and AV nodes it causes slow phase 0 rise of AP (L-type), thereby prolonging repolarization of the AV node. it also increases the effective refractory period
46
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
47
which receptor does adenosine work on
Stimulates P1 purinergic receptor (A1, A2)
48
adenosine functions
it is an anti-arrhythmic agent that opens G-protein coupled K+ channels, thereby inhibiting SA and AV node conduction It also inhibits Calcium influx, decreasing Calcium dependent action potentials ## Footnote has a very short half life
49
in which cases do we use adenosine
in SVT (Supraventricular Tachyarrhythmias )
50
digoxin MoA
Digoxin inhibits Na⁺/K⁺-ATPase, leading to: ✅ Increased intracellular calcium → stronger heart contractions(positive inotrope). this is particularly helpful in heart failure Digoxin also enhances vagal tone by acting on the vagus nerve, leading to: ✅ Slower heart rate (negative chronotropic effect) ✅ Reduced AV node conduction (useful in atrial fibrillation)
51
name some non pharmacological treatments for arrhythmias(name the specific example/type of arrhythmias that they can be used for )
vagal manoueuvres- for SVT DC cardioversion- for AF AV node Ablation( usually last treatment option) ## Footnote Vagal maneuvers are techniques that stimulate the vagus nerve to slow the heart rate. E.g. holding your breath and bearing down, immersing your face in ice-cold water (diving reflex), coughing, putting pressure on your eyelids Direct current cardioversion (DCCV) is a procedure that uses an electric shock to restore a normal heart rhythm Ablation is a medical procedure that destroys or removes tissue or a body part
52
does DC cardioversion alter underlying causes of AF
no
53
causes of AF
**Cardiac causes**, such as hypertension, valvular heart disease, heart failure, and ischaemic heart disease **Systemic causes**, such as excessive alcohol intake, hyperthyroidism, electrolyte depletion, infection, or diabetes mellitus
54
symptoms of AF
*Breathlessness. *Palpitations. *Chest discomfort. *Syncope or dizziness. *Reduced exercise tolerance, malaise/listlessness, decrease in mentation, or polyuria
55
name some conditions associated with AF ## Footnote these can be caused by AF
stroke PSVT- returns to normal within 7days
56
# , how do we confirm a diagnosis of AF
By arranging a 12-lead ECG. if there are no p waves, a chaotic baseline and an irregular ventricular rate that that is indicative of AF ## Footnote this is gold standard in confirming AF diagnosis
57
Drugs for AF treatment
Rate control with Beta blockers or calcium channel blockers. use digoxin if both do not work rhythm control with amiodarone or cardioversion antocoagulants, thus warfarin/ DOACs **(if moderate to high risk of stroke )**
58
in which case can we not use beta blockers or calcium channel blockers in AF ? when do we opt for rhythm control in AF?
if patient is in cardiac failure if rate control not worked or still have symptoms
59
drugs used in the prophalyxis of SVT
beta blockers, CCBs
60
treatment of SVT
rate control with beta blockers or CCBs Vagal manoeuvres to help with the rate Cardioversion or cardiac ablation in severe cases
61
how do we treat ventricular tachycardia ## Footnote note it is oftn due increased SNS
Use Beta Blockers Sodium Channel Blockers Lidocaine (Type 1b) - **best post MI** Type 3 antiarrhythmics, esp. Amiodarone
62
how do we treat torsades de pointes ## Footnote note this is due to increased QT interval( QT Syndrome)
discontinue drugs that increase QTI Intravenous Magnesium Sulphate
63
how do we treat cardiac arrest
CPR to maintain perfusion Adrenaline- Administered every 3-5 minutes during the resuscitation attempt. It works by **stimulating alpha and beta receptors, leading to vasoconstriction and improved blood flow to vital organs.** amiodarone (**in cases of VF or VT**, where the patient is unresponsive to defibrillation)
64
VT and VF are shockable rhythms, true or false
true means patient can be defibrillated if need be
65
important counselling points for beta blockers
Take the medication as prescribed, at the same time each day, with or without food. Do not alter the dosage or discontinue without consulting your healthcare provider Be vigilant for signs of bradycardia (slow heart rate) or hypotension (low blood pressure), such as lightheadedness, dizziness, or fainting, and report to HCP asap **In pregnant women,** beta blockers can pose risks like intra-uterine growth restriction, neonatal hypoglycemia, and bradycardia; these risks are heightened in cases of severe hypertension. Regular monitoring of blood pressure and heart rate is essential to ensure the medication's effectiveness and adjust dosages if necessary. Beta blockers should be used with caution in patients with asthma or chronic obstructive pulmonary disease (COPD), as they may exacerbate respiratory symptoms. In patients with diabetes, beta blockers can mask symptoms of hypoglycemia, such as rapid heartbeat.
66
important counselling points CCBs
Take the medication as prescribed, at the same time each day, with or without food Do not alter the dosage or discontinue without consulting your healthcare provider. common side effects are Swelling of the ankles or feet, Dizziness or lightheadedness, especially when standing up quickly, Flushing or warmth. there may be signs of allergic reaction if serious adverse effects Regular monitoring of blood pressure and heart rate is essential to ensure the medication's effectiveness and adjust dosages if necessary. Some CCBs should be avoided in heart failure patients as they can worsen cardiac function. Discuss with your healthcare provider if you are pregnant, plan to become pregnant, or are breastfeeding, as some CCBs may not be recommended provide lifestyle advice ## Footnote Elderly Patients: May be more sensitive to the effects of CCBs, especially the risk of low blood pressure
67
68
We can use CCBs in decompensated heart failure , true or false
False , they should NOT be used in decompensated heart failure
69
Some drugs that decrease potassium levels in the blood
Diuretics (loop and thiazide )
70
We cannot use beta blockers In decompensated heart failure , true or false
True , especially IV beta blockers
71

Year 2 Foundation in Clinical Practice 2 (23 decks)

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