Trivia: Cardiac Pharmacology Exam! Quiz

Spontaneous, intrinsic rhythm generated by the AV node cells

Spontaneous, intrinsic rhythm generated by the SA node cells

The making of paces

Conduction of charge from the atria to the ventricles

Spontaneous firing of the purkinje system

If you drink a glass of milk, you'll get tacchycardias

Calcium channels, due to their fast conduction, decrease the action potential and time for repolarisation

Calcium channels, due to their slow conduction, prolong the action potential and time for repolarisation

Calcium channels decrease arrhythmias

Increased conduction capacity

Voltage dependent plasma membrane

Intracellular

Extracellular

Neurotransmitter-mediated

Pressure dependent

L-type channels, which form part of the his-purkinje system and increase transmission rate of electrical signals

B-type channels, which are important in transmission of electrical conduction and stimulation of the valves of the heart

J-type channels, which are important in working myocardium and specialised conducting regions of the heart

L-type channels, which are important in working myocardium and specialised conducting regions of the heart

B-type channels, which increase cardiac contraction and spread equally through the two sides of the heart

No more than a few milliseconds

No more than a few seconds

No more than two microseconds

No more than a minute

No more than necessary

Sodium channels open, prolonging depolarisation and causing a plateau

Calcium channels open, triggered by sodium ion depolarisation, and the slow influx maintains the plateau

Outward potassium conduction is blocked, maintaining the depolarisation

Potassium channels open, increasing the rate of depolarisation and prolonging cardiac contraction

Sodium channels close, increasing the rate of depolarisation.

Closure of calcium channels

Closure of sodium channels

Re-opening of potassium channels and efflux of ions

Closure of potassium channels

Opening of sodium channels and influx of sodium

Anatomic heart disease

Myocardial infarction

Drugs

Circulating hormones

Age

Re-entry

Electrolyte imbalance

Delayed after-depolarisation

Ectopic pacemaker activity

Heart block

Abnormally raised Na+, which causes an influx of ions and triggers abnormal action potentials, causing VT

Abnormally raised K+, which causes an influx of ions and triggers abnormal action potentials, causing VT

Abnormally raised Ca2+, which causes an influx of ions and triggers abnormal action potentials, causing VT

Abnormally low Na+, which causes an efflux of ion and decreases cardiac reactivity, causing bradycardia

Abnormally low Ca2+, which causes an efflux of ion and decreases cardiac reactivity, causing bradycardia

The impulse conducted to the atria doesn't die out in surrounding refractory tissue after contraction, and instead re-excites the myocardium

The impulse in the sinoatrial node doesn't die out in surrounding refractory tissue after contraction, and instead re-excites the myocardium

The impulse in the sinoatrial node travels through the ventricles and back up to the node again, triggering a premature impulse and sudden contraction

The impulse conducted to the ventricles doesn't die out in surrounding refractory tissue after contraction, and instead re-excites the myocardium

The impulse in the atrioventricular node travels through the ventricles and back up to the node again, triggering a premature impulse and sudden contraction

It's a safety mechanism, so if the AV node is damaged, pacemaker activity can continue.

It's a safety mechanism, so if the SA node is damaged, pacemaker activity can continue.

It's a safety mechanism, so if the purkinje fibres are damaged, contractile activity can continue.

It's additional contractility, so if increased volume load occurs, more tissue can contract to cope with the increased demand

It's additional pacemaking, so if increased volume load occurs, more tissue can contract to cope with the increased demand

If they don't fire, can cause bradycardias

If they're inappropriately firing, can cause bradycardias

If they don't fire, can cause tacchyarrhythmias

If they're in the wrong place, can interfere with valvular function

If they're inappropriately firing, can cause tacchyarrhythmias

Fibrous or ischaemic damage to the conducting system (usually SA node)

Atria and ventricles firing independently of each other, with atria supplied by ectopic pacemakers

Fibrous or ischaemic damage to the conducting system (usually AV node)

Atria and ventricles firing independently of each other, with ventricles supplied by ectopic pacemakers

Dilatation of the chambers obliterates the conducting system, causing heart failure

SA node - atrium - AV node - purkinje fibres - ventricle

SA node - purkinje fibres - AV node - atrium - ventricle

AV node - purkinje fibres - atrium - SA node - ventricle

Ventricle - AV node - purkinje fibres - atrium - SA node

Atrium - SA node - purkinje fibres - AV node - ventricle

High calcium causes influx of ions into the cell transiently, which increases the normal after-depolarisation waves (can be seen as peaked T waves)

Can be caused by cardiac glycosides, NA or phosphodiestesterase inhibitors that increase intracellular calcium

Mediated by high levels of extracellular calcium

Increased normal after-depolarisation waves trigger a repetitive discharge and contraction that is independent of pacemaker stimulus

Can occur in the non-pacemaker cells of the heart.

Binding rates of ATP to actin and myosin fibres

Troponin, to which Ca2+ binds and triggers a conformational change