cardiovascular drugs 2 Flashcards
Factors that cause influx of calcium into cells
Ach
Bradykinin
Sheer stress
Mechanism of nitrates
Activate guanylyl cyclase
Causes conversion of GTP -> cGMP -> GMP
cGMP relaxes myosin like chain
What regulates end diastolic volume (preload)
SNS
RAAS
What regulates heart rate/contractility
SNS
Ca2+
What regulates TPR
SNS
RAAS
Side effects of nitrates
Postural hypotension
Headache
Dizziness
What do beta blockers do
Decrease frequency
Decrease force of contraction
Therefore decrease CO
Also inhibit renin release - so inhibit RAAS
Ivabradine
Blocks pacemaker current in nodal tissue - reduce cardiac rate
Ivabradine will reduce Na+ entry through If channels - slow rate of depolarisation
Doesn’t alter force of contraction
Alternatives to ivabradine
Long acting nitrates
Nicorandil
Ranolazine
Secondary prevention of hypercholesterolaemia
Statins
Aspirin
ACE inhibitors and ARBs - decrease workload
Treatment for ACS
Pain relief - Dimorphine u-opioid receptors Oxygen Aspirin Clot busting drugs Beta blockers ACE inhibitors Anticoagulant
Treatment of Heart failure (digoxin)
Digoxin - binds to Na/K ATPase and inhibits - more Na+ in heart muscle cells - inhibits Na+/Ca2+ exchanger more Ca2+ in muscle = stronger contraction
Increases SV
Also slows heart rate by increasing AV delay
Treatment of dysrhythmias
Amiodarone - K+ channel blocker increases refractory period of ventricular myocytes
Diltiazem
Used as an antianginal and antiarrhythmic
Blocks Ca2+ channels
Slows nodal rate and vasodilator coronary arteries
Not a DHP
What does NO do to vasodilate
Relaxes vascular smooth muscle cells - dephosphorylates myosin
