CVS drugs Flashcards
Name two main causes of arrhythmias
- Ectopic pacemaker activity 2. Afterdepolarisations
How are ectopic beats developed?
Ischemic myocardium depolarises spontaneously
*dominates SA node
Why do afterdepolarizations occur?
Anything prolonging AP -> triggers premature AP
What causes re-entry loops?
What’s the difference between an incomplete and a complete block?
Ischemic myocardium blocks AP from being conducted properly -> follows an alternate depolarising pathway/”re-entry” loop -> arrhythmia
Incomplete: AP can travel through ischaemic myocardium one way
Complete: can’t travel through at all
What is Wolff Parkinson White Syndrome?
Accessory pathway between heart’s upper - lower chambers via bundle of KENT (around tricuspid)
Name the 5 classes of antiarrhythmic drugs
Drugs blocking: VGNa+ channels, K+ channels, Ca2+ channels, b blockers
Other:
adenosine - lowers HR
magnesium - relaxes myocytes
HCN channel blockers
One example of a drug blocking Na+ channels
*what condition might it be given for?
Lidocaine
*slow AP upstroke, given in ventricular tachycardia
How do B adrenoceptor antagonists work in pacemaker cells and the myocardium and what does this prevent?
Block NA -> less steep pacemaker potential and reduce FOC
- prevents ventricular arrhythmias and atrial tachycardia (slows AV node conduction)
- reduces myocardium O2 requirement
Example of beta blocker
“olol” suffix: propanolol
Why do drugs blocking K+channels work? Name one exception and a syndrome where this drug can be used
Less repolarisation prolongs the AP -> can be pro arrhythmic
Amiodarone WPW syndrome (has ca2+ channel and b-blocking activity)
Why do drugs blocking the Ca2+ channels work in the heart and in vascular smooth muscle? Name an example
Slows excitability of SA node and conductibility of AV node
*slowing calcium influx/AP upstroke in pacemaker cells
Vasodilates sm muscle (lowers BP)
*Reduces calcium influx, i.e verapamil
How does adenosine work and how is administered? Which receptors does it interact with?
Acts on A1: increases K+ conductance -> cell goes into hyperpolarisation -> temporarily stops to reset rhythm
*AV pacemakers 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
*despite increases in end-diastolic volume heart cannot pump out a stronger SV
How do positive inotropic drugs increase the CO? Name 2 examples
B-agonists that increase FOC e.g: adrenaline, dobutamine
Name an example of a cardiac glycoside and 2 main things it can do for the heart
Digoxin: blocks Na+/K+ ATPase
+ve inotropic: Increase FOC
Blocks Na+/K+ ATPase -> Na+ accumulates in cell -> deactivates Na/Ca exchanger -> intracellular calcium accumulates
What is one reason you might prescribe an Angiotensin II receptor blocker over an ACE inhibitor?
Inhibiting ACE causes cough
ACE breaks down bradykinin which normally leads to sm muscle contractions in bronchioles/COUGH
Why does angina occur and what often occurs alongside it?
Heart receiving inadequate O2
*i.e atheromatous plaques, to compensate heart tries to increase HR and FOC which shortens diastole and increases O2 demand
What are the primary and secondary actions of NO?
Primary: venodilation lowers preload - FOC- O2 demand
Secondary: Vasodilation to collateral arteries improves O2 delivery to ischemic myocardium
2 heart conditions that have an increased risk of thrombus formation
Acute MI: plaque rupturing causes clots and blocked arteries
AF: atrial quivering - blood stasis and clots
3 anticoagulant drugs
Heparin, Warfarin, Novel oral anticoagulants (NOAC)
What is the mechanism of Warfarin? What are the possible cons of using it? What should you check in a patient before administering them warfarin?
Antagonizes Vitamin K (a cofactor for 2,7,9,10)
Internal bleeding, narrow therapeutic window, other drug interactions
Check patients INR
