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Pharmacology > Cardiovascular drugs > Flashcards

Cardiovascular drugs Flashcards

1
Q

what are contraindications for treating a patient with a history of cardiovascular conditions

A
  • 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)
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2
Q

what should you discuss with a patient’s physician regarding their cardiovascular status

A
  • patient’s medical condition
  • meds taken
  • what your treatment entails
  • any treatment modifications required to safely treat patient
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3
Q

what is the cardiovascular system

A
  • 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

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4
Q

what happens when the body’s demand for oxygen increases

A
  • the vasculature contracts or dilates to direct blood flow to the areas of the body requiring more oxygen
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5
Q

what causes the cardiovascular system to fail

A
  • either when the heart does not contract sufficiently or

- there is blockage of a blood vessel (atherosclerosis)

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6
Q

what are some examples of cardiovascular disorders

A
  • hypertension
  • angina pectoris
  • congestive heart failure
  • arrhythmias
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7
Q

what is hypertension

A
  • 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
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8
Q

what are goals for patients with hypertension with or without risk factors/history

A
  • hypertension without risk factors/history = > 140/90

- hypertension with risk factors/history = > 130/80

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9
Q

what are major risk factors for hypertension

A
  • smoking
  • obesity
  • sedentary lifestyle
  • alcohol
  • stress
  • male
  • family history of cardiovascular disease
  • postmenopausal woman
  • sodium intake
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10
Q

what is primary/essential hypertension

A
  • blood pressure that doesn’t have a known secondary cause
  • cause unknown
  • majority of cases
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11
Q

what is secondary hypertension

A
  • known cause

- only small population with hypertension have an underlying disease known to raise blood pressure

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12
Q

what is cardiac output

A
  • amount (volume) of blood pumped out per minute by a ventricle of the heart
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13
Q

what is total peripheral vascular resistance

A
  • resistance offered by the systemic blood vessels to the flow of blood
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14
Q

what is blood volume

A
  • total amount of blood in the body (~5 L)
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15
Q

what is stroke volume

A
  • amount of blood pumped by a ventricle in one contraction
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16
Q

what is the calculation for cardiac output

A
  • heart rate X stroke volume
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17
Q

what is afterload

A
  • resistance of blood vessels to blood flow
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18
Q

what is preload

A
  • volume of blood returned to the heart before it beats
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19
Q

what is contractility

A
  • forcefulness with which the heart contracts
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20
Q

what are some lifestyle modifications that will help with hypertension prevention/management

A
  • reduce weight
  • limit alcohol consumption
  • increase aerobic physical activity
  • restrict sodium intake
  • stop smoking
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21
Q

what are diuretics

A
  • first class of antihypertensive drugs in the 1950s

- still used as a first line drug because fewer adverse side effects

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22
Q

what are the 3 classes of diuretics

A
  • thiazides
  • loop diuretics
  • potassium-sparing diuretics
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23
Q

what is the mechanism of action for diuretics

A
  • 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
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24
Q

what is a common dental side effect of diuretics

A
  • xerostomia
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25
Q

what are thiazide diuretics

A
  • most common diuretic for hypertension
  • inhibit sodium reabsorption back into the blood
  • antihypertensive effects last for at least 24 hours, allowing once daily dosing
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26
Q

what else is lost in the urine when using thiazide diuretics

A
  • potassium is also lost in the urine
  • will cause hypokalemia
  • needs to be replaced by foods or potassium supplement
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27
Q

what are some negative effects of thiazide diuretics

A
  • 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
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28
Q

what are some negative effects of loop diuretics

A
  • more loss of fluids than with thiazides
  • potassium lost in the urine
  • prototype: furosemide (lasix)
  • rapid onset (within one hour)
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29
Q

what are potassium-sparing diuretics

A
  • prototype: spironolactone (aldactone)
  • no loss of potassium occurs
  • no problems with development of arrhythmia
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30
Q

what do alpha 1 adrenergic receptor antagnostics do for the cardiovascular system

A
  • prototype: prazosin (minipress)
  • vasodilator (inhibits contraction of smooth muscles)
  • lowers peripheral vascular resistance
  • blocks alpha 1 receptors
  • lowers blood pressure
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31
Q

what do beta adrenergic receptor antagonists do for the cardiovascular system

A
  • 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)
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32
Q

what do angiotensin-converting enzyme inhibitors (ACE inhibitors) do

A
  • inhibit angiotensin-converting enzyme (ACE) in the kidney, which reduces synthesis of angiotensin II (a vasoconstrictor)
  • preferred drug for patients with diabetes and hypertension
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33
Q

what are adverse effect of angiotensin-converting enzyme inhibitors

A
  • dizziness, headache, cough, xerostomia, orthostatic hypotension, angioedema
  • will have drug interactions with NSAIDs
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34
Q

what are angiotensin-II receptor blockers (ARB)

A
  • blocks angiotensin II receptors on vascular muscles
  • fewer side effects
  • NSAIDs drug interaction
  • prototype: losartan (cozaar)
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35
Q

what are calcium channel blockers (CCBs)

A
  • calcium responsible for vascular smooth muscle contraction
  • CCBs cause vasodilation
  • CCBs inhibit calcium entry into vascular smooth muscle cells
  • orthostatic hypotension and gingival enlargement
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36
Q

what are direct acting vasodilators

A
  • 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
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37
Q

what are antiangina drugs

A
  • 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
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38
Q

what are stable antiangina drugs

A
  • chest pain (angina) is intermittent on exertion but relieved by rest
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39
Q

what are unstable antiangina drugs

A
  • oxygen demand exceeds oxygen supply at rest and the frequency and severity of attacks increases
40
Q

what are variant angina antiangina drugs

A
  • due to a heart spasm

- risk of heart attack

41
Q

what are goals of treatment of angina

A
  • reduce morbidity and mortality and control the angina
  • restoring balance between heart oxygen supply and demand
  • increasing oxygen supply or
  • decreasing oxygen demand
42
Q

what are some drugs that treat angina

A
  • 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
43
Q

what are nitrates

A
  • 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
44
Q

what drugs might nitrates interact with

A
  • viagra (hypotensive)
45
Q

what are beta-blockers

A
  • 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
46
Q

what are some cardioselective beta 1-blockers

A
  • atenolol
  • timolol
  • metoprolol
47
Q

what are calcium channel blockers

A
  • reduce anginas symptoms but do not reduce mortality

- useful in variant angina (and hypertension)

48
Q

what is aspirin

A
  • antiplatelet drug
  • inhibits platelet aggregation (clotting)
  • reduces mortality in patient with unstable angina and prevention of strokes
49
Q

what is heart failure

A
  • weak heart muscles
  • output of the heart is insufficient to supply adequate levels of oxygen for the body
  • impaired heart contraction and circulatory congestion
50
Q

what is cardiac hypertrophy

A
  • enlargement of the heart
51
Q

what happens when there is left sided heart failure

A
  • congestive lung failure
  • lung symptoms
  • shortness of breath
52
Q

what happens when there is right sided heart failure

A
  • edema in lower limbs
53
Q

what are heart failure drugs

A
  • reduce cardiac workload (decrease preload)
  • reduce oedematous fluid (preload) with diuretics
  • directly increase heart contractions (positive ionotropic effect) with cardiac glycosides
54
Q

what do vasodilators do for heart failure

A
  • 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
55
Q

what are diuretics

A
  • prototype: furosemide (lasix)
  • reduce systemic or peripheral (body) or pulmonary (lung) edema
  • adverse side effects: loss of electrolytes (potassium) and xerostomia
56
Q

what do ACE inhibitors do

A
  • ACE inhibitors (ACEI)
  • prototype: captopril (capoten)
  • slow or prevent the progression of heart failure
  • decrease the work and oxygen
  • used when digitalis has failed
57
Q

what are cardiac glycosides

A
  • 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
58
Q

what are some adverse side effects glycosides

A
  • narrow therapeutic index
  • carefully monitor serum levels
  • hypokalemia (low potassium) – heart arrhythmias
  • visual disturbances
59
Q

what is an arrhythmia

A
  • 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
60
Q

how do antiarrhythmic drugs work

A
  • suppress the arrhythmia by blocking either autonomic function or calcium, potassium, or sodium channels, which slow conduction of the cardiac impulse
61
Q

what are the four classes of antiarrhythmic drugs

A
  • 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)
62
Q

what are class I antiarrhythmic drugs

A
  • Na blockers
  • largest group
  • prototype: quinidine, lidocaine (xylocaine)
  • class IB: used in ventricular arrhythmias
63
Q

what is the mechanism of action for class I antiarrhythmic drugs

A
  • block sodium entry into the cell, thereby preventing transmission of the nerve impulse and reducing the rate of depolarization
64
Q

what are class II antiarrhythmic drugs

A
  • beta blockers
  • used for the prevention and treatment of supra ventricular arrhythmias
  • prototype: metoprolol (lopresor)
65
Q

what are class III antiarrhythmic drugs

A
  • prototype: amiodarone (cordarone)
  • potassium channel blockers
  • prolong the action potential duration and refractory period
  • for supra ventricular and ventricular arrhythmias
66
Q

what are class IV antiarrhythmic drugs

A
  • calcium channel blockers
  • prototype: diltiazem (cardizem) and verapamil (isoptin)
  • supra ventricular arrhythmias
67
Q

what is the role of epinephrine in cardiac patients

A
  • 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)
68
Q

how much epi can we give to cardiac patients vs normal patients

A
  • 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
69
Q

what are lipids

A
  • 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
70
Q

what are lipoproteins

A
  • complexes containing different percentages of triglycerides, cholesterol, proteins, and phospholipids
71
Q

what are the 3 types of lipoproteins

A
  1. VLDL (very low-density lipoprotein): triglycerides and cholesterol and transported in the blood in the form of VLDL
  2. LDL (low-density lipoprotein): highest amount of cholesterol is carried by LDL, ‘bad’ cholesterol
  3. HDL (high-density lipoprotein): transports cholesterol to the liver where it is eventually removed form the body, ‘good’ cholesterol
72
Q

what are triglycerides

A
  • 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
73
Q

what is cholesterol

A
  • 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
74
Q

how do you manage hyperlipidemia

A
  • lipid-lowering drugs are indicated in patients with high risk or coronary artery disease because of multiple risk factors
75
Q

what are the targets for hyperlipidemia

A
  • lowering triglycerides
  • lowering total cholesterol
  • lowering LDL/HDL ratio
76
Q

what are HMG-CoA reductase inhibitors/statin drugs

A
  • prototype: atorvastatin (Lipitor)
  • primarily reduce LDL-C
  • inhibit HMG-CoA reductase, which results in less cholesterol formation
77
Q

what are side effects of HMG-CoA reductase inhibitors

A
  • hepatotoxicity
  • myopathy
  • rhabdomyolysis
78
Q

what are possible drug interactions for HMG-CoA reductase inhibitors

A
  • erythromycin + clarithromycin/increase statin levels

- grapefruit juice

79
Q

what are bile acid sequestrants

A
  • 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
80
Q

what are fibric acid drugs

A
  • reduce triglyceride levels
  • can displace other highly protein bound drugs (ie warfarin) from their receptors, causing elevated plasma levels
  • prototype drug is fenofibrate (lipidil)
81
Q

what is nicotinic acid

A
  • 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
82
Q

what are combination drugs

A
  • 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
83
Q

what is the pathogenesis for atherosclerosis

A
  • adherence of platelets to the blood vessel wall (platelet aggregation)
  • causes coagulation and blood clotting
  • leads to formation of a thrombus (blood clot)
84
Q

what are anticoagulant drugs

A
  • retard coagulation and prevent the occurrence of a thrombus
  • prototype drugs: heparin: injectable, warfarin (Coumadin): oral and injectable
85
Q

what are indications for anticoagulant drugs

A
  • thromboembolic disorder

- artificial heart valve

86
Q

what is warfarin

A
  • 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
87
Q

what INR is recommended for periodontal debridement procedures

A
  • less than 1.5-3
88
Q

what are anti platelet drugs

A
  • 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
89
Q

what are special conditions related to pacemakers

A
  • 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)
90
Q

pacemaker and ICD is what for endocarditis

A
  • a negligible risk factor for endocarditis

- prophylactic antibiotic coverage for dental hygiene treatment not recommended

91
Q

how do lead aprons help with pacemakers

A
  • 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
92
Q

can you use epinephrine or other vasoconstrictors with pacemakers

A
  • 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
93
Q

why are people with gum disease more likely to suffer from strokers or coronary artery disease (theories)

A
  • 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
94
Q

what is the relationship between periodontal disease and Mls/Strokes

A
  • 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
95
Q

what conditions are recommended for prophylaxis antibiotics

A
  • 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
96
Q

prophylactic antibiotic regimens for oral and dental procedures

A
  • 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

Pharmacology (21 decks)

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