Session 3: Cardiac arrhythmias/Lipid and cholesterol metabolism Flashcards
- Understand the basis of the heart’s electrophysiological control mechanisms
- Understand the basic ways in which arrhythmias may occur
- Be able to describe the targets of drug action on the cardiovascular system
- Describe the classification of anti-arrhythmic drugs
• For the major classes of anti-arrhythmic drugs, know their:
o Mechanism of action
o Effect on the heart (incl. ECG)
o Common uses
o Common side-effects
• Know the preferred drugs for treating common cardiac arrhythmias
• Understand the basis of the heart’s electrophysiological control mechanisms LO
- To function efficiently, heart needs to ?
- How does relaxation differ in other muscles?
- Coordination of heartbeat is a result of a complex, coordinated sequence of changes in?
- Contract: sequentially (atria, then ventricles) & in synchronicity
Relax: between contractions
- Do not relax between contractions
Exhibit TETANY -> contract & hold contraction for certain length of time
- membrane potentials & electrical discharges in various heart tissues
Draw a normal ECG wave and label the segments and state what occurs in different parts

Arrhythmias
- What is an arrhythmia
- Tachycardia:
- Bradycardia:
- Heart condition where disturbances in:
- Results in ?
- A number of tests can help with diagnosis including?
- heartbeat is irregular, too fast, or too slow
- above 100 beats per minute
- below 60 beats per minute
- Arrhythmias are due to problems with the electrical conduction system of the heart.
– Pacemaker impulse formation
– Contraction impulse conduction
– Combination of the two
- Rate and/or timing of contraction of heart muscle that is insufficient to maintain normal cardiac output (CO)
- electrocardiogram (ECG) and Holter monito
There are four main types of arrhythmia:
- Extra beats -> premature atrial contractions, premature ventricular contractions, and premature junctional contractions
- Supraventricular tachycardias -> atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia
- Ventricular arrhythmias -> ventricular fibrillation & ventricular tachycardia
- Bradyarrhythmias
Draw the (ventricular) cardiac action potential

What is the effect of drugs Blocking Na channels?
Marked slowing conduction in tissue (phase 0)
Minor effects on action potential duration (APD)

Beta blockers
- What are they?
- Some block activation of all types of β-adrenergic receptorsand others are selective for one of the three known types of beta receptors, designated β1, β2 and β3 receptors.[5] β1-adrenergic receptors are located mainly in the ?
β2-adrenergic receptors are located mainly in the ?
β3-adrenergic receptors are located in ?
- Competitive antagonists that block the receptor sites for the endogenous catecholamines; adrenaline & noradrenaline on adrenergic beta receptors
- heart & kidneys
- lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle
- fat cells
Effect of beta-blockers of the AP
Diminish phase 4 depolarisation and automaticity

Draw the effect of drugs that block K channels on the cardiac AP
Increase action potential duration (APD)

Draw the effect of Calcium channel blockers on the cardiac AP
decrease inward Ca2+ currents
resulting in a decrease of phase 4 spontaneous depolarization
Effect plateau phase of action potential

Explain the AP in a cardiac myocyte

Draw the AP in the SAN

Draw the effect of Ca2+ channel blockers on the SAN AP

- What does automaticity mean?
- Draw the effect of drugs affecting automaticity on the SAN AP
- Automaticity is the cardiac cell’s ability to spontaneously generate an electrical impulse (depolarize). Cells that are dedicated to the purpose of generating an impulse to maintain a heart rate commensurate with the body’s need are called pacemaker cells

State how the SAN generates its own automaticity (session 4 CVS)

Describe the AP in the SAN

• Understand the basic ways in which arrhythmias may occur LO
State the Mechanisms of Arrhythmogenesis/Abnormal impulse generation: (4)
Triggered rhythms:
Early afterdepolarization
Delayed afterdepolarization
Automatic rhythms:
Ectopic focus -> AP arises from sites other than SA node
Enhanced normal automaticity -> ↑AP from SA node

State the causes of Abnormal conduction: (4)
Conduction block (This is when the impulse is not conducted from the atria to the ventricles)
1st degree
2nd degree
3rd degree
Reentry
Circus movement
Reflection

Explain how re-entry occurs
1-This pathway is blocked
2-The impulse from this pathway travels in a retrograde fashion (backward)
3-So the cells here will be reexcited (first by the original pathway and the other from the retrograde)

Abnormal anatomic conduction
Label the red arrow

Here is an accessory pathway in the heart called Bundle of Kent
What does the Bundle of Kent lead to?
- Present only in small populations
- Lead to preexcitation -> Wolff-Parkinson-White Syndrome (WPW)
- What is Wolff-Parkinson-White Syndrome (WPW)
- How does its ECG look?
- What does this result in ?
1.
2.
- Asymptomatic
paroxysmal supraventricular tachycardia

• Be able to describe the targets of drug action on the cardiovascular system LO
Action of drugs
Give a brief description of the drugs you would choose (in terms or mechanism) In case of abnormal generation & In case of abnormal conduction
In case of abnormal generation:
- > Decrease of phase 4 slope (in pacemaker cells)
- >Raises the threshold
In case of abnormal conduction:
↓conduction velocity (remember phase 0)
↑ERP (so the cell won’t be reexcited again)



















