Ischaemic Heart Disease Treatment Flashcards
Definition of IHD:
Narrowing of lumen of coronary arteries - imbalance
Regulation of cardiac workload EDV HR Contractility TPR
- End Diastolic Volume (preload) regulated by sympathetic system, RAAS, (contractility of venules; RAAS (Na+ and H2O retention)
- Heart Rate (sympathetic system/ Ca2+)
- Contractility (sympathetic system/Ca2+)
- Total peripheral resistance (sympathetic system, RAAS)
Imbalance in demand and supply
Increase HR, force and TPR = Decrease thrombus, atheroma and vasoconstriction
Stable angina definition
Predictable pattern of pain
Relieved by rest and worse during exercise
Nitrate action
Increase cGMP = Decrease calcium and ventilation
Increase NO = dilate some CA
Nitrate side effects
- Postural hypotension
- Reflex tachycardia
- Headache
- Dizziness
- E.g. Gylceryl trinitrate (GTN)
Reflex tachycardia
Due to sympathetic NS
In response to change in blood flow or blood pressure
Beta blocker action
Decrease frequency and force of contraction
Inhibit renin release from kidney and inhibit RAAS
Beta blocker side effects
- Bronchoconstriction
- Fatigue
- Contraindicated in patients with peripheral vascular disease
- Potential bradycardia
- E.g. bisoprolol
Calcium ion channel antagonists
Decrease frequency and force contraction (phenylalkylamine/benzothiazepines)
Increase arteriole dilation (dihydropyridines)
Decrease Cardiac workload
Ivabradine
Blocks pacemaker current in nodal tissue of heart
Side effects:
◦ Luminous phenomena (Ih) in retina
◦ Blurred vision
◦ dizziness
Ivabradine decrease cardiac rate
Reduce Na+ entry through If channels and slow depolarisation of SAN and reduce firing frequency
Isosorbide mononitrate
Long acting nitrate
Decrease preload
Ranolazine
Reduce work done by heart
Trimetazidine
◦ Rebalances energy metabolism in the cell
◦ Preferentially moves potassium in the heart muscle cells to use glucose and not fatty acids
Reduce hypercholesterolemia
Drugs designed to inhibit uptake from GI tract or reduce production in liver
Statins
Decrease production of cholesterol in liver by inhibiting HMG CoA enzyme
Stimulate liver cells to express LDL receptors and allow liver cells to scavenge LDL-C from plasma
Antiplatelet agents
Antiplatelet agents (aspirin/clopidogrel)
ACE inhibitors
Eg. Ramipril
Decrease heart workload
ARBs (losartan)
Decrease heart work load
Prasugrel
pro-drug like clopidogrel and needs to be activated in the liver
MI diagnosis
- Pain
- Sweating
- Tachycardia
- Cold clammy skin
MI treatment
• Beta blockers
◦ Decrease cardiac workload, prevents arrhythmias E.g. metoprolol/bisoprolol-short acting
• ACE inhibitors
◦ Decrease cardiac workload, prevents remodelling development of heart failure E.g. Ramipril
• Anticoagulant
◦ In case of long term bed rest, prevents thrombus formation E.g. warfarin
Metoprolol/bisoprolol-short acting
Decrease cardiac workload - prevent arrhythmias
Beta blocker
MI treatment
Ramipril
ACE inhibitor
Decrease cardiac workload
Prevent remodelling development of HF
MI treatment
Warfarin
Anticoagulant
In case of long term bed rest, prevent thrombus formation
Digoxin
Binds Na+/K+ ATPase and inhibits action
Increase levels of Na+ ions inside the heart muscle
Increase inhibits Na+/Ca2+ exchanger - build up of Ca2+ ions
Treatment of dysrhythmias
Amiodarone
K+ channel blocker that increase refractory period of ventricular myocytes and can terminate arrhythmias
Amiodarone
K+ channel blocker that increase refractory period of ventricular myocytes and can terminate arrhythmias
Treat dysrhythmias
Nitrate-cGMP pathway
Guanylyl Cyclase (GTP -> cGMP) Sildenafil -> PDE (cGMP -> GMP)
Acetylcholine and bradykinin
Increase Ca2+ entry in cell
- > NOS (L-arg-> NO)
- > sGC (GTP -> cGMP) = relaxation
Peripheral vascular disease contraindicated with
Calcium channel antagonists
Contraindication with BB (asthmatics) -> CCBs
Verapamil
Diltiazem
Cardiac selective CCBs can cause
Bradycardia
Heart Block
CCBs mechanism of action
Block L-type channel in SAN and AVN
Slow rate of depolarisation
Decrease ventricle contractn
Luminous phenomena in retina
Ivabradine
Antiplatelet agent mechanism of action
Release ADP which acts on P2Y12 receptors to stimulate platelet expression of GPIIb/IIIa