Vasodilator (esp arterioles) Stimulation of guanylyl cyclase. Tx of mild/mod htn. Side effects COMMON (headache, nausea, dizziness, sweating, angina/arrythmias w ischemic heart disease, lupus)
Vasodilator (esp arterioles). Activates k channels for hyperpolarization. Reflex increase in cardiac func also fluid retention. Tx of mild/mod htn. Sfx: chf, tamponade, reflex tacycardia, hair growth (ROGAINE)
Vasodilator ( esp arterioles). Activates k channels. Salt and water retention. Tachycardia and increased CO. Tx of htn emergencies and malignant htn). Sfx: fluid retention and hyperglycemia, hyperuricemia
Vasodilator. Generates NO which activates guanylyl cyclase. Acts on arteries and veins to reduce preload and afterload. Use to produce hypotension in surg and htn emergencies (IV in hospital) RAPID decr in MAP
Vasodilator( esp veins). Generates NO which activates guanylyl cyclase. Use for hypotension in surg and htn emergencies. Sfx: headache, short action, tolerance
Vasodilator. Prostacyclin (PGI2). Uses cAMP. Counteracts thromboxane A2. Use as potent antihypertensive but administer continuously thru IV ( use for pulmonary htn).
Non-selective endothelin receptor blocker. Use for pulmonary htn. Sfx: edema, headache, inhibition spermatogenesis, resp tract infection, decrease hematocrit, hepatic effects
What is the initial approach to tx htn?
Thiazide diuretic. Then use combos. Secondary approach is ACEI, ARBs, Ca channel blockers, or other vasodilators
Implications of anti-htn meds in dentistry?
Sedation w centrally acting drugs, NSAIDs antagonize anti-htns, orthostatic hypotension, sensitivity to catecholamines (adrenergic blockers), dry mouth, gingival hyperplasia (ca channel blockers), angioedema and cough (ACEI)
What are the major determinants of myocardial oxygen consumption?
Heart rate, contractility, wall stress
Coronary blood flow is mainly regulated by what?
Myocardial oxygen consumption (MVO2)
But also by autoregulation (arterioles constricting/relaxing)
Nueral regulation (affect heart rate and contractility)
3 types of acute coronary syndrome?
Stable (occurs w exercise etc), unstable, acute
Also variant (aka Prinzmetals) with vasospasm wo stenosis and microvascular angina which occurs in females more and has no stenosis
Drug classes to treat ACS and mechanisms?
Nitrovasodilators (increase supply and decrrease demand)
B receptor antagonists (decrase demand)
Ca channel blockers (increase supply and decrease demand)
Misc drugs ( alleviate causes)
Determinants of oxygen supply to the heart?
Coronary blood flow and oxyfen extraction
As MVO2 increases, what happens to coronary blood flow?
Also increases (myocytes tell arterioles to dilate)
cAMP, cGMP, and hyperpolarization of k channels all do what to VSM?
What is the effect of reactive oxygen species on VSM?
Prevents activation of cGMP. No relaxation. Can occur with
What types of vessels does atherosclerosis occur within?
Signs of ACS
Chest pain (substernal vise-like)
Lasts 5-30 min
Can have no signs!
What is the most important drug type used for ACS?
They release NO like normal endothelium
Reduce O2 demand:
Venodilator, arterial dilator, reduce wall stress, but have indirect reflex increase in hrart rate and contractility
Dihydropyridine ca channel blockers. Decrease art pressure, decrease heart rate (reduce O2 demand) and vasodilate epicardial arteries and stenoses and prevent coronary and cerebral vasospasm (increase O2 supply)
New class of antianginal. Piperazine derivative (partial fatty acid ox inhibitor). Shifts ATP production to that from glycolysis. Inhibits late na channel to decrease na and ca inside ischemic myocytes). Minimal effect on heart rate and bp (use w other drugs in refractory pts). Improves exercise tolerance. Works better in males.
How would you treat chronic stable angina?
B blockers and aspirin (81mg). If contraindiacted to use bb (reynauds, asthma, depression, diabetes, some arrythmias) use ca channel blockers. Nitrates are cheap and safe but tolerance and side fx limit monotherapy (so use in combo). Also, STATINS to reduce high cholesterol
What is the chronic treatment of unstable angina?
Reduce demand and prevent vasoconstriction with nitrates, b-blockers, ca channel blockers (prevent vasospasm). Stabilize plaques with statins. Prevent platelet aggregation/activation w aspirin, clopidogrel, glycoprotein IIb/IIa blockers. Limit thrombus formation w heparin and THROMBIN INHIBITORS (hirudin, hirulog)
Prasugrel, clopidogrel (Plavix)
Thienopyridines. Req hepatic biotransformation. Noncomp irreversible ADP antagonist at P2 receptors. Blocks ADP mediated activation of glycoprotein GP IIa/IIb. INHIBITS PLATELET AGGREGATION. Use w aspirin. ACS (esp stents!) MI and sroke. Side fx: neutropenia
What is the treatment of acute angina/ MI?
MONA. also b blockers blunt increase in heart rate from GTN
Implications for dentistry and pts with angina?
Meds should be near (GTN in office), sit before stand, pts taking b-blockers should avoid other cardio depressants and LA w NE, gingival hyperplasia w ca channel blockers
What 3 categories of drugs provide mortality benefit in HF when used alone?