Drugs on the CVS Flashcards
Name two main causes of arrhythmias
- Ectopic pacemaker activity
2. Afterdepolarisations
How are ectopic beats developed?
Damaged myocardium (due to ischemia) can become depolarised spontaneously - these can dominate the SA node
Why do afterdepolarizations occur? Name one factor that makes you more at risk
They occur due to anything prolonging the AP - which can trigger a premature AP to fire
a QT interval is normally 400-440 ms (don’t want it >440)
Having high intracellular calcium puts you more at risk as this means the threshold can be reached too fast causing a premature AP
What do re-entry loops cause and why do they occur?
What’s the difference between an incomplete and a complete block?
Re-entry loops are caused by ischemic myocardium that ‘blocks’ an AP from being conducted through it properly, instead the AP then follows an alternative route which it can loop around depolarising myocardium improperly. This causes an arrhythmia
Incomplete block: AP can travel through the ischaemic myocardium one way
Complete block: AP cannot travel through that ischaemic myocardium at all
What is Wolff Parkinson White Syndrome? What are 2 pathways the AP can loop in this syndrome, and which specific heart structure does it use + where is it?
WPW is when you have an accessory pathway between your heart’s upper and lower chambers - using the Bundle of KENT around the tricuspid valve
- AP spreads down and re-enters the atria starting another AP from the SA node
- Other accessory pathways allow the atrial depolarization to spread into the ventricles (not through HIS), rejoin HIS and bring an AP back up in the wrong direction to the AV node
Name the 5 classes of antiarrhythmic drugs
- Drugs blocking Voltage-sensitive Na+ channels
- Antagonists of B adrenoceptors
- Drugs blocking K+ channels
- Drugs blocking Ca2+ channels
- Other: adenosine, HCN channel blockers, magnesium
Why do drugs blocking Na+ channels work? Name one example, how and when is it given?
They slow the upstroke of the AP - lengthening the absolute refractory period and slowing the readiness the tissue has to accept another AP
E.g: Lidocaine: Given IV if the patient shows signs of ventricular tachycardia (prevents automatic firing of depolarised ventricular tissue)
How do B adrenoceptor antagonists work in pacemaker cells and the myocardium? Name an example, and their suffix…
They block the sympathetic action:
In pacemakers: drugs block NA so the gradient of pacemaker potential is less steep - cell reaches threshold slower
In myocardium: drugs act on B1 to reduce FOC
Suffix: “olol”, E.g; propanolol
Why are B-blockers beneficial? (Name 3 things)
- Reducing the sympathetic activity in the heart prevents ventricular arrhythmias
- Reducing the HR and FOC also reduces the O2 requirement of the heart
- Slowing conduction in the AV node prevents atrial tachycardia
Why do drugs blocking K+channels work?
Why are they not generally used? Name one exception and a syndrome where this drug can be used
Blocking K+ channels means less K+ ions are able to leave the cell during repolarisation, therefore the AP becomes prolonged and the absolute refractory period lengthened
Not generally used as since they tend to be pro-arrhythmic
Exception: Amiodarone, used in Wolf Parkinson White syndrome as it has other actions including Ca2+ channel blocking and some B-blocker activity
Why do drugs blocking the Ca2+ channels work in the heart and in vascular smooth muscle? Name an example
This slows Ca2+ influx in pacemaker cells, reducing the AP upstroke and also slowing conduction in the AV node
*In vascular smooth muscle: reducing the Ca2+ influx reduces contractions and acts as a vasodilator which lowers the BP
E.g: verapamil
How does adenosine work and how is administered? Which receptors does it interact with?
IV administered, acts on A1 receptors at the AV node
Increases K+ conductance, putting the cell in so much hyperpolarisation that the heart momentarily stops to reset the rhythm. Therefore, they pause the AV pacemakers so they can’t transmit excess atrial systoles into more ventricular systoles
What will happen to Starling’s Curve in heart failure?
X: End diastolic volume
Y: Stroke Volume
Shifts right and reduces in height - as despite increases in end-diastolic volume the heart is incapable of pumping out a stronger stroke volume
How do positive inotrope drugs increase the CO? Name 2 examples and a scenario where these might be used.
They are B-agonists that increase the FOC
e.g: adrenaline, dobutamine
Used in cardiogenic shock if it’s reversible
Name an example of a cardiac glycoside and 2 main things it can do for the heart
Digoxin: blocks Na+/K+ ATPase
Increase FOC
1. Normally, Na+ pumped out favors an extrusion of K+, but since this channel is blocked Na+ accumulates inside the cell
- Normally, the Na+ and Ca2+ exchanger pumps Na+ inside the cell (and Ca2+ out) - but due to its intracellular accumulation this is no longer favourable
- Intracellular Ca2+ accumulates - causing greater FOC/ a positive inotropic effect
Increase vagal activity (parasympathetic) which slows the HR and AV conductance
