Cardiovascular drugs Flashcards
what are contraindications for treating a patient with a history of cardiovascular conditions
- had acute or recent myocardial infarction (within previous 3-6 months)
- unstable or recent onset of angina pectoris
- uncontrolled congestive heart failure
- uncontrolled arrhythmias
- uncontrolled hypertension
- had recent cerebrovascular accident (stroke within previous 6 months)
what should you discuss with a patient’s physician regarding their cardiovascular status
- patient’s medical condition
- meds taken
- what your treatment entails
- any treatment modifications required to safely treat patient
what is the cardiovascular system
- comprises of the heart and blood vessels
- function is to supply blood and oxygen to the body through the beating of the heart and the vasculature
what happens when the body’s demand for oxygen increases
- the vasculature contracts or dilates to direct blood flow to the areas of the body requiring more oxygen
what causes the cardiovascular system to fail
- either when the heart does not contract sufficiently or
- there is blockage of a blood vessel (atherosclerosis)
what are some examples of cardiovascular disorders
- hypertension
- angina pectoris
- congestive heart failure
- arrhythmias
what is hypertension
- increase in arterial pressure due to the fact that the amount of blood in the vessel is greater than the space available in the blood vessel
- blood pressure is regulated by the sympathetic nervous system and the kidneys
- normal = 120/80
what are goals for patients with hypertension with or without risk factors/history
- hypertension without risk factors/history = > 140/90
- hypertension with risk factors/history = > 130/80
what are major risk factors for hypertension
- smoking
- obesity
- sedentary lifestyle
- alcohol
- stress
- male
- family history of cardiovascular disease
- postmenopausal woman
- sodium intake
what is primary/essential hypertension
- blood pressure that doesn’t have a known secondary cause
- cause unknown
- majority of cases
what is secondary hypertension
- known cause
- only small population with hypertension have an underlying disease known to raise blood pressure
what is cardiac output
- amount (volume) of blood pumped out per minute by a ventricle of the heart
what is total peripheral vascular resistance
- resistance offered by the systemic blood vessels to the flow of blood
what is blood volume
- total amount of blood in the body (~5 L)
what is stroke volume
- amount of blood pumped by a ventricle in one contraction
what is the calculation for cardiac output
- heart rate X stroke volume
what is afterload
- resistance of blood vessels to blood flow
what is preload
- volume of blood returned to the heart before it beats
what is contractility
- forcefulness with which the heart contracts
what are some lifestyle modifications that will help with hypertension prevention/management
- reduce weight
- limit alcohol consumption
- increase aerobic physical activity
- restrict sodium intake
- stop smoking
what are diuretics
- first class of antihypertensive drugs in the 1950s
- still used as a first line drug because fewer adverse side effects
what are the 3 classes of diuretics
- thiazides
- loop diuretics
- potassium-sparing diuretics
what is the mechanism of action for diuretics
- increase urinary excretion
- block reabsorption of sodium in renal tubules -> increase in sodium and water excretion in the kidneys -> decrease in blood pressure and edema
- decreases blood volume
what is a common dental side effect of diuretics
- xerostomia
what are thiazide diuretics
- most common diuretic for hypertension
- inhibit sodium reabsorption back into the blood
- antihypertensive effects last for at least 24 hours, allowing once daily dosing
what else is lost in the urine when using thiazide diuretics
- potassium is also lost in the urine
- will cause hypokalemia
- needs to be replaced by foods or potassium supplement
what are some negative effects of thiazide diuretics
- increase serum lipids
- cause hyperglycaemia - decrease effectiveness of anti diabetic drugs
- increase uric acid levels (will cause gout)
- non steroidal anti-inflammatory drug (eg ibuprofen) decreases the antihypertensive effect of thiazides
- black liquorice increases potassium depletion
what are some negative effects of loop diuretics
- more loss of fluids than with thiazides
- potassium lost in the urine
- prototype: furosemide (lasix)
- rapid onset (within one hour)
what are potassium-sparing diuretics
- prototype: spironolactone (aldactone)
- no loss of potassium occurs
- no problems with development of arrhythmia
what do alpha 1 adrenergic receptor antagnostics do for the cardiovascular system
- prototype: prazosin (minipress)
- vasodilator (inhibits contraction of smooth muscles)
- lowers peripheral vascular resistance
- blocks alpha 1 receptors
- lowers blood pressure
what do beta adrenergic receptor antagonists do for the cardiovascular system
- drugs block the effects of catecholamines (ep EPI, NE) at beta-adrenergic receptors
- decrease heart rate and lower cardiac output
- selective beta 1 receptor blockers act directly on the heart and not on the bronchioles or pancreas (OK in diabetics and asthmatics)
what do angiotensin-converting enzyme inhibitors (ACE inhibitors) do
- inhibit angiotensin-converting enzyme (ACE) in the kidney, which reduces synthesis of angiotensin II (a vasoconstrictor)
- preferred drug for patients with diabetes and hypertension
what are adverse effect of angiotensin-converting enzyme inhibitors
- dizziness, headache, cough, xerostomia, orthostatic hypotension, angioedema
- will have drug interactions with NSAIDs
what are angiotensin-II receptor blockers (ARB)
- blocks angiotensin II receptors on vascular muscles
- fewer side effects
- NSAIDs drug interaction
- prototype: losartan (cozaar)
what are calcium channel blockers (CCBs)
- calcium responsible for vascular smooth muscle contraction
- CCBs cause vasodilation
- CCBs inhibit calcium entry into vascular smooth muscle cells
- orthostatic hypotension and gingival enlargement
what are direct acting vasodilators
- direct acting vasodilators relax smooth muscle cells, which surround blood vessels by an unclear mechanism
- usually used in combination with other antihypertensive agents for the treatment of moderate to severe hypertension
what are antiangina drugs
- metabolic demands of the heart exceed the ability of the coronary arteries to supply adequate blood flow to the heart
- myocardial ischemia, atherosclerosis
- classical symptoms are squeezing chest pain that radiates to the left, both or right arms and to the jaw
what are stable antiangina drugs
- chest pain (angina) is intermittent on exertion but relieved by rest
what are unstable antiangina drugs
- oxygen demand exceeds oxygen supply at rest and the frequency and severity of attacks increases
what are variant angina antiangina drugs
- due to a heart spasm
- risk of heart attack
what are goals of treatment of angina
- reduce morbidity and mortality and control the angina
- restoring balance between heart oxygen supply and demand
- increasing oxygen supply or
- decreasing oxygen demand
what are some drugs that treat angina
- nitrates
- beta 1 blockers
- calcium channel blockers
- aspirin: platelet inhibition
- lifestyle modifications
- cholesterol reduction
- homocysteine reduction
- patients with unstable angina are at high risk for heart attack and require antiplatelet drugs
what are nitrates
- relax vascular smooth muscles and cause vasodilation
- prototype: nitroglycerin (specific for the use of angina)
- sublingual nitroglycerine: initially at the onset of acute chest pain and continue for prevention of attacks with the patch or ointment form (2%)
- sublingual form is used initially because of its fast onset within seconds
what drugs might nitrates interact with
- viagra (hypotensive)
what are beta-blockers
- reduce mortality and decrease myocardial oxygen demand by decreasing heart rate, contractility and tension
- used in the following patients: stable angina who require long-term treatment; angina + hypertension
- cardioselective beta 1-blockers should be used
what are some cardioselective beta 1-blockers
- atenolol
- timolol
- metoprolol
what are calcium channel blockers
- reduce anginas symptoms but do not reduce mortality
- useful in variant angina (and hypertension)
what is aspirin
- antiplatelet drug
- inhibits platelet aggregation (clotting)
- reduces mortality in patient with unstable angina and prevention of strokes
what is heart failure
- weak heart muscles
- output of the heart is insufficient to supply adequate levels of oxygen for the body
- impaired heart contraction and circulatory congestion
what is cardiac hypertrophy
- enlargement of the heart
what happens when there is left sided heart failure
- congestive lung failure
- lung symptoms
- shortness of breath
what happens when there is right sided heart failure
- edema in lower limbs
what are heart failure drugs
- reduce cardiac workload (decrease preload)
- reduce oedematous fluid (preload) with diuretics
- directly increase heart contractions (positive ionotropic effect) with cardiac glycosides
what do vasodilators do for heart failure
- increase cardiac output and blood pressure (ACE inhibitors, angiotensin-II receptor blockers, calcium channel blockers, and direct vasodilators)
- beta-1 blockers (eg carvedilol) -> reduce sympathetic stimulation to the heart
what are diuretics
- prototype: furosemide (lasix)
- reduce systemic or peripheral (body) or pulmonary (lung) edema
- adverse side effects: loss of electrolytes (potassium) and xerostomia
what do ACE inhibitors do
- ACE inhibitors (ACEI)
- prototype: captopril (capoten)
- slow or prevent the progression of heart failure
- decrease the work and oxygen
- used when digitalis has failed
what are cardiac glycosides
- prototype: digoxin (Lanoxin)
- found in foxglove plants; digitalis
- treatment: CHF and heart arrhythmias
- direct effects on heart
- increased cardiac output
- improve circulation
- positive ionotropic effect, increase heart contraction
- negative chronaotropic effect, decrease heart rate
what are some adverse side effects glycosides
- narrow therapeutic index
- carefully monitor serum levels
- hypokalemia (low potassium) – heart arrhythmias
- visual disturbances
what is an arrhythmia
- arises in different parts of the heart
- the sinoatrial (SA) node paces the heart by stimulating the nerves
- impulse travels through the heart
- arrhythmia occurs when there is a change in the rhythm of the heart
how do antiarrhythmic drugs work
- suppress the arrhythmia by blocking either autonomic function or calcium, potassium, or sodium channels, which slow conduction of the cardiac impulse
what are the four classes of antiarrhythmic drugs
- class I: sodium (Na) channel blockers, class IA, IB, IC
- class II: beta-adrenergic blockers
- class III: potassium (K) channel blockers
- class IV: calcium (Ca) channel blockers (CCBs)
what are class I antiarrhythmic drugs
- Na blockers
- largest group
- prototype: quinidine, lidocaine (xylocaine)
- class IB: used in ventricular arrhythmias
what is the mechanism of action for class I antiarrhythmic drugs
- block sodium entry into the cell, thereby preventing transmission of the nerve impulse and reducing the rate of depolarization
what are class II antiarrhythmic drugs
- beta blockers
- used for the prevention and treatment of supra ventricular arrhythmias
- prototype: metoprolol (lopresor)
what are class III antiarrhythmic drugs
- prototype: amiodarone (cordarone)
- potassium channel blockers
- prolong the action potential duration and refractory period
- for supra ventricular and ventricular arrhythmias
what are class IV antiarrhythmic drugs
- calcium channel blockers
- prototype: diltiazem (cardizem) and verapamil (isoptin)
- supra ventricular arrhythmias
what is the role of epinephrine in cardiac patients
- the low dose of epinephrine injected in dental anaesthesia stimulates beta 2-receptors
- dilation of blood vessels (coronary arteries) supplying the heart
- increased coronary artery blood flow
- positive inotropic (force of contraction)
- positive chronaotropic (rate of contraction)
- increase in cardiac output, heart rate and systolic pressure (in large doses)
how much epi can we give to cardiac patients vs normal patients
- in normal healthy patients: maximum amount of EPI = 0.2 mg per appointment
- in patients with clincally significant cardiovascular impairment: maximum amount of EPI = 0.04 mg per appointment
what are lipids
- lipids (fats) important to humans
- triglycerides: synthesized by the liver
- cholesterol: mostly obtained from diet
- insoluble in blood, so they are transported in blood in the form of lipoproteins
what are lipoproteins
- complexes containing different percentages of triglycerides, cholesterol, proteins, and phospholipids
what are the 3 types of lipoproteins
- VLDL (very low-density lipoprotein): triglycerides and cholesterol and transported in the blood in the form of VLDL
- LDL (low-density lipoprotein): highest amount of cholesterol is carried by LDL, ‘bad’ cholesterol
- HDL (high-density lipoprotein): transports cholesterol to the liver where it is eventually removed form the body, ‘good’ cholesterol
what are triglycerides
- most common lipid
- major storage form of fat in the body
- serves as important energy source
- accounts for 90% of total lipids in the body
what is cholesterol
- gets into the body by foods you eat and what the liver makes
- LDL transports the highest amount of cholesterol to various sites in the body
- LDL is considered the ‘bad’ cholesterol
- HDL also transports cholesterol from the tissues to the liver where it is broken down and excreted in the faces = good cholesterol
- elevated levels of LDL cholesterol responsible for the development of CAD and other disorders
- the LDL:HDL ratio is an important factor in predicting cardiovascular disease
- a high cholesterol level (hypercholesterolemia) contributes to the development of atherosclerosis
how do you manage hyperlipidemia
- lipid-lowering drugs are indicated in patients with high risk or coronary artery disease because of multiple risk factors
what are the targets for hyperlipidemia
- lowering triglycerides
- lowering total cholesterol
- lowering LDL/HDL ratio
what are HMG-CoA reductase inhibitors/statin drugs
- prototype: atorvastatin (Lipitor)
- primarily reduce LDL-C
- inhibit HMG-CoA reductase, which results in less cholesterol formation
what are side effects of HMG-CoA reductase inhibitors
- hepatotoxicity
- myopathy
- rhabdomyolysis
what are possible drug interactions for HMG-CoA reductase inhibitors
- erythromycin + clarithromycin/increase statin levels
- grapefruit juice
what are bile acid sequestrants
- used prior to the discovery of statin drugs
- lower blood cholesterol
- these drugs bind bile acids, which contain high amounts of cholesterol
- only 20% decrease in LDL
- more adverse side effects than statins
what are fibric acid drugs
- reduce triglyceride levels
- can displace other highly protein bound drugs (ie warfarin) from their receptors, causing elevated plasma levels
- prototype drug is fenofibrate (lipidil)
what is nicotinic acid
- natural product: a vitamin
- lowers triglycerides and LDL-C and increasing HDL-C
- contraindicated in diabetes and people with peptic ulcer disease
- gastric irritation. glucose intolerance, flushing, skin problems, myalgia
what are combination drugs
- latest approach to drug management for LDL-C reduction
- amlodipine/atovastatin (caduet) and ezetimibe/simvastatin (Vytorin)
- may be superior to the statin drugs
- these drugs not only block absorption of cholesterol (cholesterol absorption inhibits) from food but also reduce the cholesterol that the body makes in the liver
what is the pathogenesis for atherosclerosis
- adherence of platelets to the blood vessel wall (platelet aggregation)
- causes coagulation and blood clotting
- leads to formation of a thrombus (blood clot)
what are anticoagulant drugs
- retard coagulation and prevent the occurrence of a thrombus
- prototype drugs: heparin: injectable, warfarin (Coumadin): oral and injectable
what are indications for anticoagulant drugs
- thromboembolic disorder
- artificial heart valve
what is warfarin
- anticoagulant drug
- metabolized by CYP3A4 enzymes in the liver
- erythromycin, clarithromycin (biaxin) inhibit these enzymes resulting in elevate warfarin levels
- increased risk for bleeding with concomitant administration of aspirin and other non steroidal anti-inflammatory drugs
what INR is recommended for periodontal debridement procedures
- less than 1.5-3
what are anti platelet drugs
- inhibit platelet aggregation
- aspirin
- prevent arterial thrombosis in patients with heart disease and stroke, heart attacks
- clopidogrel (plavix)
- prevention of heart attack, stroke in patients with recent heart attack and stroke
what are special conditions related to pacemakers
- if a client reports having a pacemaker, or any other implanted device
- a medical consultation may be required prior to initiating dental hygiene care
- consultation if the implant has been inserted within the last 6 months
- most dental hygiene/dental procedures unlikely to interfere with a shielded pacemaker or ICD
- manufacturers of the dentspyl/cavitron ultrasonic scaler advise users not to operate the unit if the operator or client has an implanted cardiac device (but no reported incidents)
pacemaker and ICD is what for endocarditis
- a negligible risk factor for endocarditis
- prophylactic antibiotic coverage for dental hygiene treatment not recommended
how do lead aprons help with pacemakers
- covering unshielded pacemakers with a lead apron may offer protection from electrical interference
- care should be taken not to place electric cords over the client’s chest
- or operate the magnetostrictive hand piece within 6 inches of the implanted cardiac device
can you use epinephrine or other vasoconstrictors with pacemakers
- they are contraindicated
- used with caution (reduced dose with careful monitoring) in clients with pacemakers and implanted defibrillators
- observable symptoms of a malfunction include difficulty breathing, dizziness, light-headedness, changes in pulse rate, swelling in chest, , ankles, arms, wrists, chest pain, prolonged hiccuping and muscular twitching -> emergency protocol
why are people with gum disease more likely to suffer from strokers or coronary artery disease (theories)
- oral bacteria affect the heart when enter blood stream -> attach to fatty plaques in the coronary arteries (heart blood vessels) -> contribute to clot formation
- inflammation caused by periodontal disease increase plaque buildup -> contribute to swelling of the arteries
what is the relationship between periodontal disease and Mls/Strokes
- periodontal disease can also exacerbate heart conditions
- people diagnosed with acute cerebrovascular schema (stroke) found more likely to have an oral infection when compared to those in the control group
what conditions are recommended for prophylaxis antibiotics
- artificial heart valves
- a history of infective endocarditis
- a cardiac transplant that develops a problem in a heart valve
- heart valve scarred by rheumatic fever
- certain specific, series congenital hear conditions, including:
- unrepaired or incompletely repaired cyanotic congenital heart disease, including those with palliative shunts and conduits
- a completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure
- any repaired congenital heart defect defect with residual at the site or adjacent to the site of a prosthetic patch or a prosthetic device
prophylactic antibiotic regimens for oral and dental procedures
- take 30-60 mins before dental procedures
- oral amoxicillin
- unable to take oral medications: ampicillin or cefazolin, or ceftriaxone
- allergic to penicillins or ampicillin – oral cephalexin or clindamycin or azithromycin or clarithromycin
- allergic to penicillins or amphicillin and unable to take oral medications: cefazolin or ceftriaxone or clindamycin
