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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)
- Wall tension
- Nueral regulation (affect heart rate and contractility)
- Humoral regulation
- Myogenic tone
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
- Ang II
What types of vessels does atherosclerosis occur within?
Signs of ACS
- Chest pain (substernal vise-like)
- Arm pain
- Back pain
- Lasts 5-30 min
- Can have no signs!
- Arm pain
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
- Increase O2 supply: dilate conduit arteries at stenosis, increase subendocardial blood flow, increase collateral blood flow, decreased platelet activation
Why does GTN (nitroglycerin) relax large coronary arteries much more than small ones?
Bc of enzymatic (mtALDH) release of NO. Other nitrovasodilators have similar effect on all size arteries
First pass hepatic metab, short duration
What is the benefit of a sublingual tablet or spray of GTN?
Avoid first pass effect. Rapid onset. (but only ladts 30-60min)
In what forms amyl nitrite used?
Inhalant (limited use)
Isosorbide dinitrate (ISDN)
3-5 hr duration. Administer 3-4 times/ d
Isosorbide mononitrate (ISMN)
Longer action than ISDN. Dose 2 times/d. Minimal first pass effect.
Adverse effects of nitrates?
- Tolerance (interrupt therapy 8-12 hrs)
- Orthostatic hypotension
- Reflex tachycardia
- Gi distress (oral) or skin irritation (patch)
- Contraind w PDE5 inhibitors
Why are nitrates contraindicated w PDE5 inhibitors?
PDE5 inhibtors increase cGMP too (inhibit breakdown to GMP) so result is hypotension (drop of over 25mm hg)
Sildenafil, tadalafil, vardenafil
PDE5 inhibitors used to treat ED
Propranolol metoprolol atenolol nadolol
- B-adrenergic blockers
- Blocking B1 effects: decrease heart rate and contractility and decrease renin release
- Blocking B2 effects: potentiate a-adrenergic effects (vasoconstriction) and may exacerbate vasospasm
- Use for ACS in combo w nitrates
- Adverse fx: bronchospasm, hypoglycemia, hyperlipidemia, myocardial depression, bradycardia, reduced exercise tolerance, sleep disturbances, cold extremities, impotence, rebound w discontinuation ( bc upregulation of receptors)
Cardioselective ca channel blockers. decrease contractility, decrease heart rate, decrease arterial pressure (decr O2 demand) and vasodilate arteries and prevent coronary and cerebral vasospasm (increase O2 supply)
What are the uses of ca channel blockers?
ACS, HTN, supraventricular arrythmias, cerebral hemmorhage or vasospasm
What are the adverse effects of ca channel blockers?
Dizziness, nausea, headache, flushing, hypotension, edema, arrythmias, reflex tachycardia, gingival hyperplasia
Nifedipine, amlodipine, felodipine, nicardipine, nimodipine
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?
B-blockers, ARBs, ACEIs
What types of treatment exist for HF?
- Drugs that: decrease preload (loop diuretics/ thiazides/ spironolactone)
- Decrease afterload (ACEIs, ARBs, vasodilators), improve contractility (adrenergic agonists, phosphodiesterase inhibitors, cardiac glycosides) and interrupting compensatory responses (various)
Complex syndrome where ventricle cannot fill or eject blood properly. Can be structural or functional problem. 80 percent of ppl w HF are over 65.
Cardinal signs of HF
Dyspnea, fatigue (leads to exercise intolerance), and sometimes fluid retention (may lead to pulmonary congestionand edema)
Describe starling relationship
Increase filling pressure leads to increase stretch and increase SV
What 3 factors influence myocardial performance (SV)?
Preload, afterload, ionotropic state ( which is influenced by contractile properties of the muscle, autonomic nerves, circulating catecholomines)
What 4 things can cause cardiac remodeling?
Direct sympathetic nervous stimulation, elevated cardiac filing pressures, Ang II, and aldosterone
Signs and symptoms of HF
- Compensatory hemodynamic abnormalities
- Dysreg of Ca homeostasis which impairs contraction and rekaxation (uptake of Ca by Na/Ca exchanger)
- Dysreg of contractile proteins
- Desensitization of B-adrenergic receptors leads to reduced Ca uptakr into SR
Describe the sequelae of HF
- Decrease in CO activates neurohumoral sysrem
- Compensation maintains perfusion to organs
- Increase in volume leads to wall stress and hypertrophic remodeling
- Nuerohumoral activation directly induces apoptosis of myocytes
What are the 5 cardiovascular adaptation mechanism associated with HF?
- Abnormal baroreflex control (interpret high bp as normal)
- Cardiac hypertrophy (at lower ionotropic state)
- Altered renal function (SNS induces constriction of glomeruli and stimulatesrenin release)
- Vasoconstriction (SNS, RAAS, ADH)
What is the most useful test to evaluate pts with HF?
- Echocardiogram and Doppler flow to see abnormalities of myocardium, heart valves, or pericardium. See whether
- L ventricular ejection fraction is preserved or reduced?
- L ventricle is normal or abnormal?
- Other structural changes of valves, pericardium, or rt ventricle?
What are causes of high cardiac output HF?
Anemias and thyrotoxicosis
Describe the stages of HF
- A: risk for HF but no structural abnormalities
- B: structural heart disease but no signs of HF
- C: structural heart disease w prior or current symptoms
- D: refractory HF
Treatment of stage A HF?
- Treat HTN, dyslipidemia, cease drugs and alcohol.
- Drugs: ACEIs, ARBs
Treatment of stage B HF?
- Treat HTN, dyslipidemia, cease drugs and alcohol.
- Drugs: ACEIs, ARBs, B-blockers
Treatment of stage C HF?
- Same as stage A and B but restrict salt intake.
- Drugs: diruretics, ACEIs, B-blockers
- Some pts may take aldosterone antagonists, digitalis, hydralazine/nitrates
Treatment of stage D HF?
- End of life care.
- Heart transplant, mechanical support, experimental surgery/drugs
Where does renin come from?
Juxtaglomerular cells of the kidney
How do ACE inhibitors work?
Potent arterial dilators to reduce afterload and increase SV and CO
What is the first line of therapy for HF?
ACEIs. (Esp for all pts with reduced LVEF). Often combined with a B-blocker.
What are contraindications of the use of ACEIs?
Adverse reactions (angioedema) or impaired renal function (AngII helps perfuse kidney)
Side effects of ACEIs?
Hypotension, hyperkalemia, kidney failure in pts with impaired renal function, angioedema, cough
Captopril, enalapril, ramipril, lisinopril, quinapril, fosinipril
ACE inhibitors. Stop conversion of Ang I to Ang II. Inhibit breakdown of bradykinin (a vasodilator)
What is the mechanism of AT1 angiotensin receptor blockers (ARBs)?
Block actions of Ang II/III: cardiac remodeling, vasoconstriction, release of aldosterone. do NOT prevent brsdykinin breakdown
What 3 types of bb reduce risk of death from HF?
Who should take cardiac glycosides? (digoxin, digitoxin, ouabain)
- HF pts in atrial fibrillation or severe HF ( also should be on ACEIs or ARBs, bb, and diuretics.
- Also used for arrythmias
Mechanisms of glycosides?
- Inhibition of na/k ATPase to increase intracellular Ca andincrease force of contraction
- Sensitizebaroreceptors to decrease SNS
- Inhibit na/k ATPase inkidney which lowers na resorption so lower renin secreted
Toxicity of glycosides?
- Electrical: arrythmias, heart block, etc
- Increased tox w hypokalemia, hypercalcemia, hypothyroidism
- Clarithromycin, quinidine, verapamil increase tox
Spironolactone and eplerenone
Aldosterone antag: used in pts w severe HF or L vent dysfunc after MI. Class C or D HF- low dose with ACEI reduces mortaliy. USE W DIRURETICS. Risk of life-threatening hyperkalemia.
How do vasodilators allow the heart to function more effectively?
- Reduce preload
- Reduce afterload
- (decrease filling pressures and volume)
T or F: arterial dilators increase CO and promote diuresis
T or F: venous dilators decrease preload and also increase coronary art flow which may increase ventricular func.
T or F: hydralazine decreases renal blood floe
F. Its used in pts who cant tolerate ACEIs
What is treatment for pts w refractory HF in the hospital?
Ionotropic agents: dobutamine, dopamine, milrinone. SHORT TERM USE
Stimulates b adrenergic feceptors on heart. Increases contractility. Stimulates a2 receptors at high doses to venoconstriction (makes HF worse). Tachycardia can provoke ischemia in pts w CAD
B agonist. For pts w systolic dysfunc. Stimulates b1 and b2 receptors (ionotropy dominates)
Side effects of dobutamine
Tachycardia and arrythmias
cAMP phosphodiesterase inhibitors
- Inamrinone, milrinone
- Used for advanced HF. Accelerate relaxation so more time for ca to enter cells and increase contraction
Define pacemaker potential
Slow inward movement of calcium and na. Change it to alter rate of depolarization.
Most common sustained arrythmias
Connects signal bt SA node and AV
What dental devices shouldn't be used near a pt w a cardio dryer defibrillator or pacemaker?
Ultrasonic scalers, composite curing lights, electrosurgical units (anything emitting electromagnetic waves)
Types of drugs for arrythmias
- Na blockers (1): slow upstroke of AP and block spontaneous depolarization
- K blockers (3): increase duration of AP
- Ca blockers (4): slowing spontsneous depolarization
- B blockers (2): prolonging AV conduction
Where do thrombi develop in atrial fib?
Left atria. Risk for brain infarcts.
Treatment of a fib
Warfarin and aspirin to decrease clot risk
Atrial based arrythmias
Sinus tach, sinus bradycardia, atrial flutter
Premature ventricular contraction (PVCs), ventricular tach, ventricular fib
Impaired av transmission
- First degree: PR interval increased
- 2nd degree: ventricular rate irregular
- 3rd degree: ventricular rate slow but regular
Wolf Parkinson white syndrome
Tachycardia with accessory path
Dangerous. May progress to v-fib. Electrical loops in ventricle. Risk of quinidine and disopyramide
- Electrical loops in atria.
- Causes: HTN, age, HF, autonomic imbalance, channelopathies, atrial stretch, reduced atrial contraction, ca overload
disopyramide, flecainide, lidocaine, mexiletine, moricizine, procainamide, propafenone, quinidine
Na channel blockers to treat HF. Oral meds except lido which is given after ischemia through IV. slows upstroke of AP. RISK OF OTHER ARRYTHMIAS, WORSEN HF, and AV BLOCK. cimetidine reduces clearance
Amiodarone, dofetilide, sotalol
K channel blockers. Inhibit repolarization (prolong AP). WARFARIN increases effectiveness. Amiodarone also acts on na channeks. Sotalol is also a bb.
Bepridil, diltiazem, verapamil
- Ca channel blockers. Decrease conduction thru AV node, decrease firing in the SA node, reduce slope of pacemaker potential.
- Sfx: hypotension (esp w inhlational anesthetics), AV block, bradycardia, gingival enlargment
Slows AV conduction. Inhibitory on nerves (caffeine/theophylline reduce effects) Given IV. short lived side effects are dyspnea, bronchospasm, hypotension. Dipyridamole amplifies.
Propranolol, metoprolol, atenolol, timolol, Esmolol
Bb used in arrythmias. Decrease conduction thru AV node (reduce slope ofpacemaker potential). Side effects are fatigue, worsening of HF, hypotension, ED, bronchospasm
IV for torsades des pointes