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Cardiovascular > Cardiac arrhythmias > Flashcards

Cardiac arrhythmias Flashcards

1
Q

Describe atheroma formation

A

Prolonged exposure to lipid-rich particles, cholesterol (LDL) and abnormal function of endothelium= deposits in sub-endothelium- local inflammation
Vulnerable to clot formation and occlusion

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2
Q

What are the risk factors associated with atherosclerosis?

A

age, male sex, genetics, hypertension, diabetes, cholesterol, smoking, hyperlipidaemia

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3
Q

What is angina pectoris?

A

Atherosclerosis of the coronary arteries (pain free at rest, exert= myocardial ischemia and chest pain)

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4
Q

How do thrombi form?

A

Ruptured plague= highly thrombogenic surface exposed to bloodstream= platelet adhesion and clot formation
Partial or total occlusion of blood flow- endogenous thrombolytic mechanisms break clot down/ allow to progress

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5
Q

Describe cardiac dysfunction

A

Maladaptive response= reduced cardiac output- sympathetic NS activation, renin-angiotensin system activation (baroreceptors)- vasoconstriction so increase pressure (afterload) increase in volume (preload)- increase cardiac work- impaired- oedema

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6
Q

What are the key problems with the maladaptive regulatory response (SNA, RAS)?

A

Dysfunction of blood vessels, increased volume load on heart, increased pressure load on heart/blood vessels, imbalance of blood/oxygen supply to the heart and work of pumping, increased resistance (stiff) of arterial blood vessels, high levels of circulating lipid (cholesterol), tendency to platelet activation, tendency to thrombosis

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7
Q

What are the types of drugs used in treatment of cardiac dysfunction?

A
  • Diuretics (furosemide)= reduce sodium and water overload
  • beta-blockers (atenolol)= reduce SNS (work and oxygen demands of the heart)
  • Alpha-blockers (doxazosin)= reduce vasoconstriction
  • Calcium channel blockers (amlodipine)= relax arteriole muscle
  • Angiotensin- Converting Enzyme inhibitors (Ramipril)= reduce effects angiotensin system activation
  • Nitrates (glyceryl trinitrate)= relax veins and arteries
  • Lipid-lowering drugs (statins)= reduce cholesterol/ anti-platelet drugs (aspirin)= reduce adhesion
  • Anticoagulants (warfarin)= reduce blood clot formation
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8
Q

What is the structure of the myocardium?

A

Giant syncytial structure allowing easy cell-to-cell electrical conduction and depolarisation

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9
Q

Where are the right and left bundles?

A

Right bundle- right ventricle/ left bundle- anterior and posterior fascicles in left ventricle

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10
Q

How much of diastolic filling is passive?

A

70%

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11
Q

How does myocardium contract?

A

Pacemaker cells are unstable- depolarise spontaneously
Electrical activity produces the characteristic ECG
Sodium ions enter, then calcium= contraction of myocardial cell, potassium flows out to repolarise (energy intensive)

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12
Q

What are the clinical consequences of arrhythmias?

A

Altered heart rate (usually too fast)= reduced ventricular filling= reduced cardiac ejection= reduced efficiency (less cardiac output for a given amount of work)
reduced blood pressure/ syncope= heart failure/ angina/ death
reduced blood pressure/ syncope= heart failure/ angina/ death

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13
Q

What is automaticity?

A

Cells that are normally quiescent starting to depolarise spontaneously- ischemia death, cells take on spontaneous activity, wave of depolarisation, starts from wrong place in chain of events, contract in disordered way, rapid heart rate

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14
Q

What is re-entry?

A

Re-entry of the wave of depolarisation back to higher levels allowing rapid circus movement, more rare, part of the heart no longer responds/ depolarises, some of wave can travel wave and re affect part of the heart that would normally be quiescent, circular motion of activity- 200 circuits per minute

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15
Q

What are the causes of cardiac arrhythmias?

A

Coronary heart disease= ischaemia within the conduction system and myocardium- energy produced by oxygen to make ATP= stability of cardiac cells, maintaining concentrations of ions
Occasional= drugs (beta blockers)/ electrolyte imbalance (potassium and calcium)
Rare= congenital abnormalities- structure of the heart, ion channels

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16
Q

What are the classes of cardiac arrhythmias?

A

Atrial- atrial fibrillation or atrial flutter/ AV node- supraventricular tachycardia (SVT)rare due to circus movement/
ventricular- ventricular tachycardia (VT), ventricular fibrillation (VF)/ heart block- complete heart block impulses starting in SAN cannot get to ventricles

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17
Q

What is atrial fibrillation?

A

(1 second= 3 depolarisation) 200 bpm, compromised in output from left ventricle= angina/ SAN no longer leader of depolarisation, travel across atrial cardiac myocytes, no concerted contraction, 600 times per second, AVN cannot conduct that quickly so 200 bpm/ irregular firing

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18
Q

How is atrial fibrillation diagnosed/ tested for?

A

irregularly irregular pulse, apicoradial deficit= every time aortic valve closing some wont have pulse to feel because heart will have contacted when ventricles are not filled with blood, disordered atrial discharge (400-600 bmp)

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19
Q

What are the symptoms of atrial fibrillation?

A

Palpitations, dyspnoea (breathlessness), pulmonary oedema

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20
Q

What are the clinical consequences of atrial fibrillation?

A

Rapid heart rate= reduced ventricular filling= reduced cardiac output

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21
Q

Describe the aetiology of atrial fibrillation

A

Ischaemic heart disease (coronary), thyrotoxicosis= overactivity, rheumatic heart disease= rheumatic fever, cardiomyopathy alcohol, PE (pulmonary embolism), ASD (atrial septal defect), infiltration- very common in elderly

22
Q

What are the treatment aims for atrial fibrillation?

A

Slow ventricular response rate with drugs= digoxin, beta blockers, verapamil (calcium channel blockers), amiodarone
Treat reversible cause (thyrotoxicosis)
Reduce risk of thromboembolism with warfarin
Restore sinus rhythm with drugs/ DC cardioversion

23
Q

Describe Digoxin

A

Foxglove plant, combination of sugar, lactone, steroid/ cardiac glycoside acting on sodium/potassium ATPase by inhibition so increase sodium in cells so increase availability of calcium/ broken down to digitoxin in the body/ major therapeutic action= reduced/ slow conduction through AV node, increased force of contraction

24
Q

What is the dose of Digoxin?

A

62.5-250 micrograms per day orally (can be given IV) long half life so loading dose

25
Q

What are the adverse effects of Digoxin?

A

Anorexia, nausea, vomiting (GI upset) visual disturbances, AV block, arrhythmias- promoted by hypokalaemia, caution in renal failure (depends on renal excretion), low therapeutic index (digoxin levels can be measured)

26
Q

Describe beta-blockers

A

Heart rate and myocardial contractility (receptors), relatively b1 selective (others= metoprolol and bisoprolol), propranolol non-selective/ reduce sympathetic NS activity at heart= reduce excitability of conduction system= reduce ventricular response rate/ AF, hypertension and angina indications

27
Q

What is the dose for beta-blockers?

A

50 mg per day orally

28
Q

What are the adverse effects of beta-blockers?

A

Mostly related to beta blockade type A- lethargy, bronchospasm, reduced peripheral perfusion, hypotension, heart block

29
Q

What is Supraventricular tachycardia?

A

Can effect younger patients/ presentation= palpitations, rapid regular pulse (160-180/min)/ problem- rapid re entry through AV node

30
Q

What is the Bypass tract?

A

Anatomical defect allows conduction from atria to ventricles

31
Q

What is anterograde conduction?

A

Ander certain circumstances after depolarisation through AVN bypass tract no longer refractory or blocked by anterograde conduction

  1. forward conduction of impulses through a nerve.
  2. in the heart, conduction of impulses from atria to ventricles.
32
Q

What is retrograde conduction?

A

Sends onward depolarisation back through atrial myocytes to AVN - circus activity so SAN no longer involved

33
Q

What can be used to treat supraventricular tachycardia?

A

Vagal stimulation manoeuvres (secretion of ACh and slowing down of conduction system), carotid massage sinus at jaw, Valsalva exhale against closed glottis, eyeball pressure, diving reflex

34
Q

What is the immediate treatment of supraventricular tachycardia?

A

Adenosine 3-12 mg IV slow conduction through AVN until cleared for a few seconds/ verapamil 5-10 mg IV longer effect/ drugs fail and rapid control required= synchronised DC cardioversion

35
Q

How is supraventricular tachycardia?

A

Verapamil orally/ Surgical ablation- radio frequency energy

36
Q

Describe Adenosine

A

Natural endogenous purine/ mechanism of action= A1 receptors in AVN (potassium channels), hyperpolarisation of conduction tissue, transient blockage of conduction through the AVN, temporarily abolishes re entry through the AVN/ indications= supraventricular tachycardia

37
Q

What is the dose of adenosine?

A

3-12 mg IV, rapid cellular uptake actions last only 20-30s

38
Q

What are the adverse effects of adenosine?

A

Chest pain dyspnoea, dizziness, nausea, clinical effect reduced by theophylline but increased by dipyridamole, can be used to distinguish diagnosis from other arrhythmias

39
Q

Describe Verapamil

A

Calcium channel blocker (centrally acting)/ blocks voltage sensitive L type calcium channels, reduces conduction through the SA and AV nodes= reduced force of contraction of heart- vasodilation/ SVT, AF, angina, hypertension

40
Q

What is the dose for Verapamil?

A

40-120 mg orally 8 hourly rarely used IV

41
Q

What are the adverse effects of Verapamil?

A

Constipation, heart block, bradycardia, low BP- Never give IV verapamil to patients on beta blockers because of danger of precipitating asystolic cardiac arrest

42
Q

What is ventricular tachycardia?

A

Series of 3 or more ventricular ectopic beats, increased automaticity of ventricular tissue, serious often causes significant haemodynamic disturbance with hypotension, heart failure, may deteriorate to cardiac arrest, cause= myocardial ischaemia (reperfusion) (beats driven in ventricles)

43
Q

What is the treatment of ventricular tachycardia?

A

Lignocaine (lidocaine) IV- historical/ amiodarone IV/oral/ other drugs procainamide, disopyramide/ Failure- DC cardioversion

44
Q

Describe Lidocaine

A

Class 1 membrane-stabilising anti-arrhythmic drug (local anaesthetic)/ blocks sodium channels in excitable tissues, reduced excitability and cardiac conduction, negative inotropic effect (reduced contractility)/ ventricular arrhythmias only (post MI), local anaesthesia

45
Q

What is the dose for Lidocaine?

A

Dose almost completely metabolised by liver, must be given IV, plasma half-life is only 2 hours so requires infusion

46
Q

What are the adverse effects of Lidocaine?

A

CNS drowsiness, confusion, convulsions

47
Q

Describe Amiodarone

A

Class 3 anti-arrhythmic drug / prolongs cardiac action potential, blocks potassium channels, iodine containing/ highly effective multipurpose antiarrhythmic, atrial and ventricular arrhythmias

48
Q

What is the dose of Amiodarone?

A

Extensively bound in tissues- large volume of distribution, over long elimination half-life of 30 days, oral loading period required then 200 mg daily, IV infusion in emergencies

49
Q

What are the adverse effects of Amiodarone?

A

Major disadvantage is toxicity
Adverse- reversible corneal microdeposits, photosensitivity, slate-grey discolouration, pneumonitis, pulmonary fibrosis, thyroid dysfunction, hepatitis

50
Q

What is heart block?

A

activity of atria happening Separately from ventricles- pacemaker (reversible atropine

51
Q

Describe the Vaughan- Williams Classification of antiarrhythmic drugs

A

Class 1=1 membrane-stabilising drugs (block sodium channels) A- quinidine, procainamide, B- lidocaine, mexilitine, C- flecainide
Class 2- beta blocking drugs- atenolol
Class 3=3 drugs that prolong cardiac action potential- amiodarone, bretylium, sotalol
Class 4=4 calcium channel blockers- verapamil

Cardiovascular (52 decks)

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