CVS 10 Flashcards by Alyssa Conte

List 3 causes of arrhythmias.

ECTOPIC PACEMAKER ABILITY
- damaged myocardium becomes depolarised and spontaneously active
- latent pacemaker region activated due to ischaemia and dominates over SA now

AFTERDEPOLARISATIONS
- abnormal depolarisations following the action potential

RE-ENTRY LOOP
- conduction disorder
- accessory pathway

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Explain what happens during the phases of cardiac myocyte potential.

phase 0: influx of Na+ via voltage-gated sodium channels

phase 1: K+ efflux

phase 2: counterbalance of Ca2+ influx and K+ efflux

phase 3: K+ efflux begins to exceed Ca2+ influx

phase 4: Na+/K+ ATPase together with Na/Ca pumps

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What is an arrhythmia?

What are the 3 principle mechanisms?

disorder of rate or rhythm due to either abnormal impulse generation or abnormal impulse conduction

increased automaticity: establishment of a dominant ectopic pacemaker
re-entry (due to depolarisation from often ectopic pacemakers, hitting cells that are refractory)
after-depolarisation - development of a transient rapid depolarisation during or following repolarisation which has the potential to generate an AP

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What are the 2 main types of arrhythmias?

bradycardia HR<60bpm in the day and <50bpm at night

tachycardia HR>100bpm

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Tachycardias are more symptomatic when what?

List 2 examples of tachycardias and where they both arise from.

when sustained and fast

SVT - arise from atrium or AV node
VT - arise from ventricles

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List 4 things which arrhythmias may cause.

sudden death
syncope
HF
chest pain
palpitations
dizziness

(or no symptoms)

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Anything which prolongs the 1 of an 2 can allow afterdepolarisations to occur.

1: prolongs
2: action potential

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A long after depolarisation would show/affect which ECG feature?

would lead to a longer QT interval

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When do ectopic pacemakers develop?

when cells in the conducting tissue develop more rapid phase 4 depolarisations than the SA node does

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What are the basic classes of anti-arrhythmic drugs?

drugs that block voltage-gated sodium channels
antagonists of b-adrenoreceptors
drugs that block voltage gated potassium channels
drugs that block voltage gated calcium channels
drugs that dont fit in these classes i.e adenosine

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Give an example of a drug which blocks voltage-dependant Na+ channels (class I). Where is the key action of this drug?

lidocaine - on cardiomyocytes not SA node

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What medication is given IV sometimes following MIs if the patient shows signs of VT?

lidocaine

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What class of anti-arrhythmic does lidocaine belong to and what is its mechanism of action?

it blocks voltage-dependant Na+ channels - class I

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Give 2 examples of b-adrenoreceptors antagonist and mention what class they are in.

bisoprolol, atenolol, metoprolol - class II

act at b1-adrenoreceptors in the heart, decrease slope of pacemaker potential in SA node

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Bisoprolol and atenolol are what type of anti-arrhythmics? What class are they in and what is their mechanism of action?

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B-blockers slow conduction in what?

in the AV node

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Class III anti-arrhythmic drugs do what?

They’re not generally used because what?

Give an example.

they prolong the action potential by blocking voltage gated K+ channels

because they can also be pro-arrhythmic

AMIODARONE

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Amiodarone belongs to what class of anti-arrhythmics?

What is it’s mechanism of action?

What is it used to treat specifically?

class III - prolongs the action potential mainly by blocking voltage gated K+ channels and lengthening the absolute refractory period

used to treat tachycardia associated with WPW

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What class of anti-arrhythmic does verapamil belong to?

What is its mechanism of action?

class IV - BLOCKS VOLTAGE-GATED Ca2+ CHANNELS decreases slope of pacemaker action potential at SA node: decreases AV nodal conduction, decreases force of contraction - negative inotropy

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What type of medication is amlodipine?

They are not effective in preventing 1 but they do act on 2 3 4 so they are used to treat 5 and 6.

dyhydropyridine Ca2+ channel blocker

arrhythmias
2, 3, 4: vascular smooth muscle
5: HTN
6: angina

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What is the mechanism of action of adenosine?

acts on a1 receptors at AV node and enhances K+ conductance

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Which medication acts on A1 receptors at the AV node and enhances K+ conductance?

adenosine

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List the 4 features of HF.

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What medications are used for improved diagnosis in HF? What does each category do?

ACEi/ARB
- decreased vasomotor tone and blood volume
- reduced afterload and reduced preload

aldosterone antagonist e.g spironolactone
- blocks aldosterone receptors in DCT = decreased Na+ reabsorption and decreased K+ secretion

beta-blockers e.g bisoprolol
- reduced HR + negative inotropic effect
- reduced BP
- reduced myocardial oxygen demand

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List drugs used in HF which increase myocardial contractility.

cardiac glycosides e.g digoxin - inhibits Na+/K+ ATPase -> increased Na+ inhibits Na+/Ca2+ exchanger beta adrenoreceptor agonists - used in cardiogenic shock

Which medications used in HF reduce the workload of the heart?

ACEi - inhibits the action of ACE in the lungs - prevent the conversion of angiotensin I to angiotensin II - aldosterone acts on the kidneys to increase Na+ and water reabsorption

What do ACEi do? List 5 things.

- decrease vasomotor tone - reduce afterload of the heart - decrease fluid retention - reduce preload of the heart - reduce work-load of the heart

What is the action of cardiac glycosides? Give an example.

block Na+/K+ ATPase digoxin increase in Na+ conc inside the cells leads to an inhibition of the Na+/Ca2+ exchanger - increase Ca2+ conc inside cardiac myocytes: - positive inotropic effect - increased force of contraction - negative lusitropic effect

Angina is also known as what? When does it occur?

myocardial ischaemia occurs when o2 supply to the heart does not meet its need - usually pain with exertion

What medications are used to treat angina?

REDUCE WORK LOAD OF THE HEART - ACEi/ARB - b-adrenoreceptor blocks - Ca2+ channel antagonists - organic nitrates IMPROVE THE BLOOD SUPPLY TO HEART - Ca2+ channel antagonists CHOLESTEROL REDUCTION - statins ANGIO +/- STENTS - re-vascularise

What is the mechanism of action of nitrates? Give an example.

reaction of organic nitrates with THIOLS in vascular smooth muscles causes nitrite to be released nitrite (NO2) is reduced to NO GTN

How does NO cause vasodilation?

List 2 anti-platelet drugs and their mechanism of action.

aspirin: COX inhibitor clopidogrel: inhibits ADP induced aggregation

What do ACE inhibitors and ARBs do to vasomotor tone and blood volume?

They decrease vasomotor tone and reduce blood volume, leading to lower preload and afterload.

What is the mechanism of action of ACE inhibitors?

They inhibit angiotensin-converting enzyme (ACE) in the lungs, preventing conversion of angiotensin I → angiotensin II, thereby reducing vasoconstriction and aldosterone secretion.

What is the effect of blocking angiotensin II production?

↓ Peripheral vasoconstriction (↓ afterload) ↓ Aldosterone-mediated Na⁺ and water retention (↓ preload) ↓ Blood pressure overall

What is the main difference between ACE inhibitors and ARBs?

ACEi: block formation of angiotensin II. ARBs: block the receptor (AT₁) that angiotensin II binds to.

What is the mechanism of action of spironolactone?

It blocks aldosterone receptors in the distal convoluted tubule, leading to ↓ Na⁺ reabsorption and ↓ K⁺ secretion.

What’s a key side effect of spironolactone?

Hyperkalaemia (↑ K⁺)

What are the main effects of β-blockers (e.g. bisoprolol)?

↓ Heart rate (negative chronotropic) ↓ Contractility (negative inotropic) ↓ Blood pressure ↓ Myocardial oxygen demand

Why are β-blockers used in heart failure and angina?

They reduce cardiac workload and oxygen demand, improving survival in chronic heart failure.

What should β-blockers be avoided in?

Asthma or COPD (may cause bronchospasm) and bradycardia or AV block.

What is the mechanism of action of digoxin?

Inhibits the Na⁺/K⁺ ATPase pump → ↑ intracellular Na⁺ This inhibits the Na⁺/Ca²⁺ exchanger → ↑ intracellular Ca²⁺ ↑ Ca²⁺ → increased contractility (positive inotropy)

What are the main effects of digoxin on the heart?

↑ Force of contraction (positive inotropic) ↓ Heart rate (negative chronotropic) ↓ Rate of relaxation (negative lusitropic)

What conditions is digoxin used for?

Atrial fibrillation (rate control) and heart failure (symptom relief).

What is the role of β-adrenoceptor agonists in cardiac care?

Used in cardiogenic shock to increase heart rate and contractility (positive inotropy and chronotropy).

What is the mechanism of action of aspirin in clot prevention?

Irreversibly inhibits COX enzymes (COX-1 and COX-2) → ↓ thromboxane A₂ → ↓ platelet aggregation.

What is the mechanism of action of clopidogrel?

Inhibits the ADP receptor (P2Y₁₂) on platelets → prevents ADP-induced platelet aggregation.

How does heparin work?

Activates antithrombin III, which inhibits thrombin (factor IIa) and factor Xa, preventing clot formation. Given intravenously for short-term anticoagulation.

How does warfarin work?

Inhibits vitamin K epoxide reductase complex (VKORC1) → prevents activation of vitamin K–dependent clotting factors (II, VII, IX, X) → long-term anticoagulation.

What’s the main difference between heparin and warfarin in use?

Heparin: IV, fast-acting, short-term Warfarin: Oral, slow-acting, long-term

Name the two main classes of DOACs and give examples.

Direct thrombin inhibitor: Dabigatran Factor Xa inhibitors: Apixaban, Rivaroxaban

What’s the advantage of DOACs over warfarin?

Fixed dosing No routine INR monitoring Fewer food and drug interactions

Which class of antiarrhythmic drugs works by prolonging the action potential duration and lengthening the absolute refractory period?

Class III - Potassium channel blockers

lusotropy re-entry

Describe two different antiplatelet drugs used in cardiovascular disease, including their mechanisms of action.

aspirin - blocks COX-1 and COX-2 - inhibits thromboxane clopidogrel - inhibits P2Y12 ADP receptor on platelet surface and prevent them for aggregating

What is the primary mechanism by which adenosine exerts its antiarrhythmic effect?

Enhances potassium conductance and hyperpolarises AV nodal cells

Beta-blockers used in heart failure, such as bisoprolol, reduce afterload by __________ blood pressure as a result of reduced __________.

lowering sympathetic nervous activity (lower HR, reduced contractility)

Which medication used in heart failure management works by inhibiting the Na⁺/K⁺/Cl⁻ transporter in the Loop of Henle?

furosemide

Explain briefly how ectopic pacemakers can develop in ischaemic heart tissue.

What is the primary mechanism by which warfarin exerts its anticoagulant effect?

Blocks vitamin K epoxide reductase, preventing synthesis of clotting factors

Organic nitrates like glyceryl trinitrate (GTN) are converted to nitric oxide. Describe the cellular mechanism by which nitric oxide causes vasodilation.

Nitric oxide (NO) diffuses into vascular smooth muscle cells and activates guanylyl cyclase, increasing cyclic GMP (cGMP) levels. cGMP activates protein kinase G, which lowers intracellular Ca²⁺ and causes smooth muscle relaxation, leading to vasodilation.

ACE inhibitors prevent the conversion of angiotensin I to angiotensin II, thereby reducing __________ and decreasing aldosterone-mediated ___________ and water reabsorption.

vasoconstriction sodium

CVS 10 Flashcards

(63 cards)