CVS Arrhythmias and Drugs Flashcards
What 4 things can drugs alter in CVS?
Blood vol
HR
Heart rhythm
Force of contraction
Name some causes of tachycardia
Ectopic activity, AF, Aflutter, afterdepolarisations, reentry loops (e.g WPW syndrome)
Name some causes of bradycardia
Heart block 1st 2nd 3rd degree - AVN dysfunction
Sick sinus syndrome - SAN dysfunction
Can beta blocker cause bradycardia by affecting both SAN and AVN? What other drug can from the lecture?
Yes
Ca channel blockers affect both too
What is triggered activity?
Afterdepolarisations (there are early and late ones)
Which type of after depolarisation is more common with high intracellular Ca2+ - which drug toxicity is associated with this?
Delayed
Digoxin
Which type of afterdepolarisation is more common in AP prolonged? Why? What drug can cause this?
Early
Because it lengthens the QT interval which predisposes to arrhythmias
K+ channel blockers can cause this due to increasing the length of the AP
Describe how a re-entrant mechanism can occur in the heart and give an example of an arrhythmia caused by this?
Damaged area of heart - fibrotic Unidirectional block Depolarisation spreads round and the wrong way through damaged area Forms a loop Reentry tachycardia
E.g. AF (many of these in atria)
Name two things can cause damage and fibrosis to the myocardium to predispose to arrhythmias?
Dilation (e.g. from mitral stenosis/regurg)
Necrosis (e.g. from MI)
Ischaemia (Atherosclerosis)
Briefly say how and AV Nodal Reentry tachycardia is formed
Fast and slow pathways in the AVN create reentry loop
Briefly say how ventricular pre excitation can occur? Which disease?
Accessory pathway between atria and ventricles creates a large reentry loop e.g. in wolf-parkinson-white syndrome
What are the 4 classes of drugs (4 areas they act)
I Block Na channels
II Block b adrenoceptors
III Block K+ channels
IV Block Ca2+ channels
Why is an ischaemic/damaged part of myocardium susceptible to tachyarrhythmias?
Because the NaKATPase fails and this causes the cell to spontaneously depolarise and may then act as the foci
What drug would you give to prevent the complication of tachyarrhythmia? Why?
Beta blocker
Negative chronotropic and inotropic effect - stabilises activity and prevents ventricular arrhythmias
How does Lidocaine work? Which tissue does it preferentially block and why? Why does it not have a big effect on normal tissue?
Use dependent block
Binds to open or inactivated Na channels so preferentially blocks damaged depolarised tissue - so prevents automatic firing from ventricular cells.
Little effect in normal cardiac tissue as it dissociates readily - within 1AP
Blocks during depolarisation - and dissociates in time for next AP
When would lidocaine be used post MI? How is it given?
If signs of VT
Given IV
Would you use it for VT in other patients not post MI?
No use other drugs
What effect do b blockers have on the SAN AP?
Decrease the slope of the pacemaker potential and the rising phase of the AP
What has sympathetic activity got to do with arrhythmias post MI? Which drug blocks this
post MI often have increased sympa activity
Increased sympa activity related to arrhythmias
B blocker
What type of arrhythmias can b blockers prevent with their action of slowing conduction at AVN? Give an example
Prevent supra ventricular tachys
can slow rate in AF
Can beta blockers help prevent both atrial and ventricular arrhythmias?
Yes
How do beta blockers reduce O2 demand of tissue?
As it reduces workload by reducing HR and contractility
How do K+ channel blockers (class III) work? What is the danger? What is the drug exception that is used in clinical practice?
Prolong AP by blocking K+ channels and prolonging the absolute refractory period
Should prevent another AP occurring too soon but in reality can be pro arrhythmic
Except amioderone - as it affects other channels not just K+ so ends up being quite helpful
When is amioderone useful?
Wolff-Parkinson-White syndrome tachys
Supresses ventricular arrhythmias post MI
