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Flashcards in Exam I Deck (136):

The management of cardiovascular disease according to the prevention guidelines for hypertension are:

● 40 minutes of exercise 3-4 days a week
● Eat lots of fruit, veggies
● Reduce Sodium intake


The management of cardiovascular disease according to the prevention guidelines for obesity are:

● Team-based treatment
● Weight loss strategies based on BMI
● diet, exercise still best bets


The management of cardiovascular disease according to the prevention guidelines for cholesterol are:

● Overall health status and risks guide treatment
● “Bad cholesterol number” no longer main factor guiding treatment
● Decisions for drug treatment based on discussions with healthcare provider


The management of cardiovascular disease according to the prevention guidelines for risk assessment are:

● Calculators used to assess your personal risk set stage for discussions with healthcare provider
● Risks for African-Americans specified for the first time
● Stroke risks included for the first time


______________, are the firs line of defense for treatment of hypertension.



Regarding Diuretics,
the need for intervention for patients with DM/kidney disease or under and over 60 are:

■ 140/90 60 y.o
■ DM or kidney disease and


What are the AHA/ACC BP guidelines?

■ Systolic 140-159
■ Diastolic 90-99
■ If higher, lifestyle changes + medications


will ___________ urine formation.
Most _________the kidney tubular _________of Na+ which is __________ with an accompanying volume of water



__________ BP
__________peripheral resistance
__________ cardiac output
__________ blood volume



MOST diuretics are ___________ by kidney ________ secretion.
Drugs are secreted into _____________ then _______ from the body

- tubular
- tubule


What are the 8 kinds of classes of diuretics?

1) Mercurials
2) Thiazides
3) Loop (high ceiling)
4) Carbonic anhydrase inhibitors
5) Potassium-sparing diuretics
6) Osmotics
7) Acidifying agents
8) Xanthines


First class of diuretics are_____________



What is the MOA (mechanism of action) for Mercurials?

Block Na reabsorption by releasing Hg ions to interact w/ sulfhydryl group of Na transport receptors in tubules


Blocking Na+ reabsorpation causes a ____________ of CL- transport, resulting in...?

Decreased Cl transport in ascending loop of Henle → risk of hypochloremic alkalosis


_________First choice agents for hypertension and congestive heart failure



Most commonly prescribed diuretic __________



What is the MOA for Thiazide?

○ inhibition of active Na reabsorption in proximal and distal tubule
○ inhibition of carbonic anhydrase = decrease H for exchange with Na


What are the desired effects of Thiazide on
-BP, plasma volume, EC fluid, CO, starling's law, and peripheral resistance ?

1) Lowers BP
2) decreases plasma volume
3) decreases extracellular fluid
4) Decreased cardiac output that eventually normalized

5) Starling’s law= if decrease amount of blood returning to the heart (preload), heart doesn't have to work as hard to eject blood back into the systemic circulation

6) Decreased peripheral resistance
7) Normalization of cardiac output after several days


What are the Preparations for Thiazide?

○ hydrochlorothiazide (HCTZ)

■ Use: hypertension, edema from congestive heart failure & nephrotic syndrome


What are the complications for Thiazide?

Complications= xerostomia, lichenoid drug reaction, photosensitivity
○ chlorothiazide (Diuril)


What are the Loop diuretics MOA?

1) Inhibition of active Na reabsorption in ascending Loop of Henle by blocking Cl reabsorption
(inhibits Na-K-Cl symporter)

2) major loss of volume


Drugs are toxic due to such rapid loss of ____________.



All loop diuretics are ototoxic to _______ degree (causes ____________, ________/_________)

-hearing loss


What are the preparations for Loop diuretics?

○ fureosemide (Lasix)

■ Use: hypertension, edema from congestive heart failure & renal/hepatic disease)
○ ethacrynic acid (Edecrin)
○ bumetanide (Bumex)
○ torsemide (Demadex)


What are the Potassium-sparing (retaining) diuretics
1)Receptor sites are where?
2) Increase excretion of what?
3) blocks effect of?
4) Prevents loss of ?

1) Competes with aldosterone for receptor sites in DISTAL renal tubules

2) INCREASE Na, Cl and water excretion while conserving K and H

3) blocks effect of aldosterone

4) prevents usual loss of K+


What is the Potassium-sparing (retaining) diuretics preparation?

○ spironolactone (Aldoactone)
○ triamterene (Dyrenium)
○ eplerenone (Inspra)


What is the MOA of Carbonic anhydrase inhibitors?

1) Inhibits carbonic anhydrase
2) exchange of H+ decreased
3) Na+/water excretion increased


Carbonic anhydrase inhibitors are __________ diuretics that work on ___________ and _________



Carbonic anhydrase inhibitors are used primarily for what?

Glaucoma & adjunctive therapy for congestive heart failure


Carbonic anhydrase inhibitors:

_______________ aqueous humor production(eye)
Retard _________ and __________ discharge from the CNS neurons (anticonvulsant properties)



What are the preparations for Carbonic anhydrase inhibitors?

1) acetazolamide (Diamox)
2) methazolamide (Neptazane)
(not used very much)


Osmotic diuretics (urea):

Are used in _____________ situations when need to __________ blood volume.
Used when patients kidney ____________.

-shuts down


Osmotic diuretics MOA?

1) Cause major diuresis at Bowman’s capsule in proximal convoluted tubule

2) These drugs are filtered but NOT reabsorbed (water follows solute)


Preparations for Osmotic diuretics?

urea (Ureaphil)


Acidifying Agents (ammonium):

-Rare, but if used for treatment of ____________ states or metabolic ____________.
-Used in _____________ to produce a large amount of chloride
-_________ acidity by _________ free H+ [ ]

- hyperchloremic
- alkalosis
- emergency room


Acidifying Agents (ammonium): MOA? Preparation?

MOA = Increases amount of Cl in urine and Na stays with it= diuresis

Preparation = Ammonium chloride


_________ drugs for __________ and _________.

Xanthines are also ____________ (think caffeine)

- asthma
- stimulants (Makes you pee)


What is the MOA for Xanthines?

1) Stimulates cardiac function to increase renal blood flow and GFR

2) INCREASES cardiac output and vasodilation/blood flow to afferent arteriole Bowman’s capsule

3) INCREASE blood filtration

4) Inhibit ADH = INCREASE blood flow, decrease reabsorption of water in collecting duct


What is the Potency of diuretics (MOST to LEAST)?

Potency: loop > thiazide > carbonic anhydrase > K+ sparing


First drug of choice for HTN and congestive heart failure ?



Thiazide is the MOST commonly prescribed ____________.
HCTZ (microzide) can also be used for tx of _________ syndrome.



Loop diuretics: Ethacrynic acid (Edecrin), furosemide (Lasix) cause what ?

1) serious edema
2) acute HTN
3) pulmonary edema
4) congestive heart failure
5) hepatic/renal disease


Common side effects associated with Thiazide diuretics:

-Hypokalemia: The more _______ that accumulates in distal proximal tubule the more ____________ to counteract this effect.
-Contraindicated for patients with __________, __________ and ___________.
-Fibric acid derivates drugs used to lower ____________ block _________ of these drugs.
Causes _______ drug reaction.
Loss of ____________, __________ and _______
-Inhibits _________ secretion.
-Elevated ____________ and __________.
-Lowered ________ because ______ not firing as quickly (leading to weakness/fatigue)
- ____________ dysfunction.

-K+ salts
-high cholesterol
-Mg + (Hypomagnesaemia)
-Na+ (Hypoattremia)
-Uric acid ( Hyperuricemia)
-Cholesterol and triglycerides


What are the Loop diuretic side effects? (10)

1) Cause a major loss of volume
2) Drugs of choice for serious edema
3) Major loss of Na+ and K+ = serious electrolyte imbalances may result
4) ototoxic
5) hypocalcemia
6) nephrotoxicity (increased with Keflex)
7) Gi distress
8) CNS effects
9) causes major fluid loss and possible serious electrolyte imbalance
10) Lichenoid drug reaction


What are the Potassium-sparing specific side effects?

1) hyperkalemia
2) gynecomastia (mimic female sex hormones)
3) breast tenderness
4) menstrual irregularities
5) decreased libido in males


What are the K salt specific side effects?

1) Patients take potassium supplements to counteract K loss from diuretics.
2) Major adverse side effect: GI distress
3) ALL potassium supplements have K in the name (K-tab, Klor-Con)


What are the K salt specific contraindicated for:

1) severe renal impairment
2) taking K+ sparing
3) taking ACEIs (hyperkalemia)


What are the oral side effects associated with diuretics?

1) Xerostomia (b/c water loss)

2) aphthous stomatitis (mouth ulcers)

3) Lichenoid drug reaction: “fake” lichen planus → associated with Thiazides and Loops

4) delayed hypersensitivity reaction
-Use of NSAIDS for 3+ weeks can decrease effectiveness of diuretics


Beta blockers are _____________ and __________.
Desired effects include:
-____________ CO (even tho constrict vessels via β2)
-_______________ the work of the ________
-________________ renin secretion
-_____________ plasma volume and __________ return.
-_______________ sympathetic outflow from __________.
-_______________ peripheral resistance.
Chronotropic = + or -?
Ionotropic = + or - ?

-Cardioselective and Non-Cardioselective- (end in “olol”)
+ chronotropic
+ inotropic: force of contraction INCREASES


Describe Cardioselective drugs?

1) Cardioselective (Start with A-M)
2) block β1
3) selective more commonly used


Describe Non-cardioselective ?

1) Non-cardioselective (Start with N-Z)
2) block both β1 and β2
3) Some exceptions for the A-M/N-Z rule (mostly ophthalmic preparations for glaucoma)


Alpha 1 blockers (at postsynaptic tissues)
****-end in “azosin”
-Peripheral __________ in arterioles and venules
-___________ peripheral vascular resistance
-______ effect on cardiac _________ and _____blood flow.

-little effect on cardiac


Alpha 1 blockers are more effective when used with _____________ or ___________

- β-blocker


Alpha antagonists can block _________ that mediate contraction of ___________ such as the trigone and sphincter muscles of the bladder, leading to _________ resistance to urinary outflow.
This can be used to Tx ______

-Alpha 1 receptors
-nonvascular smooth muscle
-BPH (enlarged prostate)


ACE inhibitors (ACEIs):

End in _________.

Prevent conversion of ___________ to __________ .
______________ vasoconstriction.
Decreases __________, __________, and _________.
Increases in __________ activity.
Overall ____________ and __________ ____________lower BP.

- “pril”
-angiotensin I to angiotensin II (potent vasoconstrictor)
-inhibit → causes vasodilation
- blood volume and BP, aldosterone secretion
and Na and water retention.
- Plasma renin activity
-blood volume


Angiotensin II receptor blockers (ARBs) :

end in ________.
blocks__________& _______ secreting effects of angiotensin II
_______ plasma renin level causes decreases in BP by: _____________, decrease ________ & _________ retention. = Results in _______
Preferred over _______ b/c action is at the receptor = _____ side effects, better tolerance.

- vasoconstrictor & aldosterone
- increases
- Na and water
-result: reduction of BP
- fewer


Renin inhibitors:

binds to _______ reducing levels of angiotensin I, angiotensin II and __________.

does not ________ plasma renin activity
(seen in ACEIs & ARBs)

- renin
- aldosterone
- increase


Ca channel blockers (CCBs) :

inhibits _____ from entering “slow-channels” or ______________ of vascular smooth muscle and myocardium during __________
produces ________ of coronary vascular smooth muscle and coronary ________
________ myocardial oxygen delivery (good for angina too)
●Used for:
__________, ________ and __________.

- Ca
-select voltage-sensitive areas
- relaxation
- vasodilation

●Used for:


Centrally Acting Antihypertensives:

Used less often due to what ?
When is it used?

-to adverse events
- other drugs are ineffective


Alpha agonist stimulates what on brainstem and activates what kind of neuron?

-Alpha 2 on brainstem
-activates inhibitory neuron


How does Alpha agonists affect sympathetic outflow?

Decreases sympathetic outflow from CNS


How is Alpha agonist administered?

-orally or via transdermal patch


Alpha agonist decreases what 4 things?

1) peripheral resistance
2) renal vascular resistance
3) HR
4) BP


Alpha 2 agonist, Clonidine (Catapres) causes what adverse effects?

1) Dizziness & sedation
2) Rapid elevation of BP if sudden discontinuation
3) Xerostomia
4) Parotid gland swelling & pain
5) Dysgeusia (unpleasant taste)


Catecholamine release blockers:

● block granular uptake and storage (depletion) of NE = decrease SNS (due to lack of NT supply)
● decrease vascular smooth muscle tone and cardiac output
● reserpine (Serpasil):
○ decrease BP via depletion of NE and Dopa
○ causes sedative effects
○ crosses BBB (used to treat agitated psychoses/schizophrenia)
○ causes mental depression and risk for suicide
● guanethidine (Ismeline): no longer in US
○ uncouples action potential from exocytotic release of NT = blocks AP


Common side effects of Diuretics (antihypertensive medications)



Common side effects of ) Beta blockers - overactivity of PANS (antihypertensive medications)

■ GI upset
■ Xerostomia
■ Weakness and fatigue
■ Orthostatic hypotension
■ Sedation
■ Depressed mood
■ Sexual dysfunction (Impotence in men = #1 reason for poor compliance)

■ Contraindications:
● Congestive Heart Failure
○ already have decreased cardiac output
● Asthma
○ dont want to block β2 in case of bronchoconstriction
○ use cardioselective beta blocker
● Heart block
○ decrease heart rate and force of contraction
● Diabetes
○ decrease glycogenolysis and glucagon secretion= hypoglycemic
○ use cardioselective beta blocker


Common side effects of Alpha 1 Blockers (antihypertensive medications)

■ Orthostatic hypotension
● worse with exercise, alcohol
● drowsiness or excitation
● headache
■ CV
● Tachycardia
● Arrhythmias
● Palpitations
● Peripheral edema


Common side effects of ACE Inhibitors (antihypertensive medications)

■ Chronic dry cough (significant reduction of quality of life)
● cough syrups/lozenges have no effect
● watch for caries
● Cough mediated by increased bradykinin release in bronchial tree
■ Angioneurotic edema with first dose
■ Angioedema


Common side effects of ARB inhibitors (antihypertensive medications)

■ CNS: dizziness, fatigue, insomnia, headache
■ Upper respiratory infection
● most often seen in patients taking losartan
● dry cough
■ GI: diarrhea
■ Pain: muscle cramps, leg and back pain
■ Angioedema (more common in ACEIs)
■ Teratogenicity
■ NSAIDS may decrease effectiveness


Common side effects of Renin Inhibitor (antihypertensive medications)

■ headache
■ dizziness
■ cough
■ Upper respiratory infection


Common side effects of Catecholamine Release Blockers (antihypertensive medications)

■ Side effects due to increase in PNS activity
● Lethargy
● Nasal congestion
● Contraindicated in patients with peptic ulcers (increased HCL secretion)


Identify at least one generic and brand name drug of each class of antihypertensive medication (Mercurials)

1) Thiomerin
● Generic Name = mercaptomerin
2) Mercuhydrun
● Generic Name = meralluride


Identify at least one generic and brand name drug of each class of antihypertensive medication (Thiazide Diuretics)

1) Microzide (HCTZ)
● Generic Name = hydrochlorothiazide

2) Diuril
● Generic Name = chlorothiazide


Identify at least one generic and brand name drug of each class of antihypertensive medication
Loop (High Ceiling Diuretics)

1) Lasix
● Generic Name = furosemide

2) Edecrin
● Generic Name = ethacrynic acid

3) Bumex
● Generic Name = bumetanide

4) Demadex
● Generic Name = torsemide


Identify at least one generic and brand name drug of each class of antihypertensive medication ( Potassium-sparing diuretics)

1) Aldactone
● Generic Name = spironolactone

2) Dyrenium
● Generic Name = triamterene

3) Inspra
● Generic Name = eplerenone


Identify at least one generic and brand name drug of each class of antihypertensive medication ( Carbonic Anhydrase Inhibitors)

1) Diamox
● Generic Name = acetazolamide

2) Neptazane
● Generic Name = methazolamide


Identify at least one generic and brand name drug of each class of antihypertensive medication (Osmotic diuretics)

1) Ureaphil
● Generic Name = urea


Identify at least one generic and brand name drug of each class of antihypertensive medication
( Beta Blockers)

■ Cardioselective (block beta1) = “-olols” and start with A-M; more commonly used

1) Tenormin
○ Generic Name =atenolol

2) Betoptic
○ Generic Name =betaxolol

3) Zebeta
○ bisprolol
4) Brevibloc
○ Generic Name =esmolol

5) Lopressor, Toprol
○ Generic Name =metoprolol

6) Bystolic
○ Generic Name =nebivolol


Identify at least one generic and brand name drug of each class of antihypertensive medication
( Beta Blockers)

■Noncardioselective (block beta1, beta2) = start with N-Z

1) Corgard
○ Generic Name =nadolol

2) Inderal
○ Generic Name =propranolol

3) Betapace
○ Generic Name =sotalol


Identify at least one generic and brand name drug of each class of antihypertensive medication
(Alpha1 Receptor Blockers: end in “-zosin”)

1) Cardura
● Generic Name =doxazosin

2) Minipress
● Generic Name =prazosin

3) Flomax
● Generic Name = tamsulosin


Identify at least one generic and brand name drug of each class of antihypertensive medication
(ACE Inhbitors: end in “-pril”)

1) Lotensin
● Generic Name = benzepril
2) Capoten
● Generic Name = captopril
3) Vasotec
● Generic Name = enalapril
4) Monopril
● Generic Name = fosinopril

5) Prinivil, Zestril
● Generic Name = lisinopril
○ biggest market seller in US
○ drug of choice for tx HTN in pts w/ DM
○ causes dry cough

6) Univasc
● Generic Name = moexipril
7) Accupril
● Generic Name = quinapril
8) Altace
● Generic Name = ramipril
9) Mavik
● Generic Name = trandolopril


Identify at least one generic and brand name drug of each class of antihypertensive medication
(Angiotensin Receptor Blockers (ARBs)

1) Atacand
● Generic Name = candesartan
2) Teveten
● Generic Name = eprosartan
3) Avapro
● Generic Name = irbesartan
4) Cozaar
● Generic Name = Iosartan
5) Benicar
● Generic Name = olmesartan
6) Micardis
● Generic Name = telmisartan
7) Diovan
● Generic Name = valsartan


Identify at least one generic and brand name drug of each class of antihypertensive medication
(Calcium Channel Blockers)

1) Celan
● Generic Name = verapamil
2) Procardia
● Generic Name = nifedipine
3) Norvasc
● Generic Name = amlodipine
4) Vascor
● Generic Name = bepridil
5) Dilacor, Icardizem
● Generic Name = diltiazem
6) Plendil
● Generic Name = felodipine
7) DynaCirc
● Generic Name = isradipine
8) Cardene
● Generic Name = nicardipine


Identify at least one generic and brand name drug of each class of antihypertensive medication
(Alpha2 Agonist Drugs)

1) Catapres
● Generic Name = clonidine
2) Tenex, Intuniv
● Generic Name = guanfacine


Identify at least one generic and brand name drug of each class of antihypertensive medication
(Catecholamine Release Blockers )

1) Serpasil
● Generic Name = reserpine
2) Ismelin
● Generic Name = guanethidine


What are the calcium channel blockers that are associated with causing gingival hyperplasia as a side effect'?

1) nifedipine (Procardia) 30%
■ greatest number of cases of gingival hyperplasia for all drugs in this class

2) verapamil (Calan) 8%

3) diltiazem (Icardizem, Dilacor) 2%

4) amlodipine (Norvasc)


What are the drug interactions with antihypertensive medications of significance to dentistry.?

○ Enhanced hypotension with general anesthetics and CNS depressants
○ Prolonged action of analgesics, sedatives, and tranquilizers (think central acting drugs)
○ Potentiated response to vasoconstriction drugs
■ Use epinephrine w/ caution
■ Safe cardiac dose of epinephrine = 0.04 mg
■ Always take BP prior to injection of local anesthetics
○ OTC sympathomimetics (cold capsules and asthma tables) may counteract antihypertensives therapy
○ Use of NSAIDS for longer than 3 weeks may decrease effectiveness of some diuretics, beta blockers and ACE inhibitors
■ worst offender: indomethacin
○ Nicotine in cigars and cigarettes constricts blood vessels and increases BP


What is the important precautions to take during dental procedures when treating patients with hypertension?

○ Prevent sudden changes in posture
○ Decrease stress
○ Tissue retraction with vasopressors is contraindicated
■ Impregnated gingival retraction cord
○ Rebound hypertension may develop if hypertensive agents are abruptly withdrawn
■ (Many men quit use of beta blockers due to impotence = severe rebound hypertension

○ Diuretics make you lose potassium
○ ACEI and ARBs Increase potassium


What are Cardiac Arrhythmias?

● Produce abnormalities of the heartbeat
● Alterations in the pattern of cardiac rhythm
● In all arrhythmias, some face of the normal electrophysiologic system that governs cardiac contraction is behaving abnormally
● Caused by disease, cardiac injury or drugs


What do Cardiac Arrhythmias result from?

○ Abnormal impulse formation
■ Arise from non-traditional locations
○ Abnormal impulse conduction
■ Abnormal pathways due to blockages
○ Combination of both


What are the types of Cardiac Arrhythmias?

○ At nodal level
■ suprventricular (atrial)
■ ventricular
■ ectopic foci “emergent leaders”
● impulses that preempt the SA or AV node rate
○ At conduction level
■ normal pattern of conduction but conduction splits and goes two ways
■ reentry
■ unidirectional block (action potential is blocked from being stimulated from one side of the tissue but not from the other
■ prolonged refractory period
○ Premature contractions
■ extra systoles
■ PVC’s or PAC’s
○ Tachycardia
■ normal contractions at a faster rate
○ Flutters
■ all areas may not follow normally
○ Fibrillations
■ uncoordinated contractions
○ Bradycardia
■ normal contractions at a slower rate
○ Heart block
■ Complete= His Purkinje system cut in half
● atria and ventricles work independently
■ Partial= some areas affected more than others


Identify the indications for use of anti arrhythmic drugs and the non-pharmacologic treatments.

○ Indications
■ Paroxysmal atrial tachycardia
■ Paroxysmal ventricular tachycardia
■ Atrial fibrillation
■ Ventricular ectopic arrhythmias
■ Digoxin-induced arrhythmias

○ Non-pharmacologic treatments for arrhythmia
■ electric cardioversion
■ automatic implantable cardioverter devices
■ ablation therapy
■ pacemakers


Identify the contraindications for use of antiarrhythmic drugs.

○ Contraindications
■ Complete A-V heart block
■ Congestive heart failure
■ Hypotension
■ Known hypersensitivity to the drug


What is the use of anti arrhythmic drugs and the pharmcologic effects?

○ Used to modify or restore aberrant electrophysiologic properties of cardiac muscle to normal
■ depress parts of the heart that are beating abnormally
○ Type of arrhythmia determines drug selection

○ Pharmacologic effects:
■ change of slope of depolarization
■ raise threshold for depolarization
■ alter conduction velocity in different parts of the heart


What are the phases of anti arrhythmic drugs and how do they work ?

○ Antiarrhythmic medications:
■ Work on 1 of 5 transmembranes phases of the cardiac cycle which alters (shortens/lengthens) the phases to control rhythm.
■ 5 transmembrane phases:
● Phase 0: influx of Na ions through fast channels generates depolarization
● Phase 1: early, partial repolarization through efflux of K ions
● Phase 2: plateau where net influx of Ca through Ca channels is slightly more than the efflux of K channels
● Phase 3: predominant efflux of K ions
● Phase 4: restoration of ionic concentrations via Na/K & Na/Ca exchange pumps
○ resting membrane potential reestablished (-90mV)
● Phases 0,1,2 & most of 3 (to about -50mV= absolute refractory period
● Middle of phase 3 to beginning of phase 4 = relative refractory period
○ Absolute (Effective) refractory period:
■ Cells cannot respond to a stimulus
■ Term is synonymous with depolarization
■ Mechanism that protects the heart from all other ectopic impulses
○ Relative refractory period:
■ Time when only a strong stimulus can cause depolarization
■ Occurs when repolarization is almost complete

○ Refractory periods:
■ Length of time between each of the refractory periods varies between individuals
■ Affected by:
● medications, recreational drugs, disease, electrolyte imbalance, myocardial ischemia, myocardial injury

○ Non-refractory phase
■ All cells are repolarized and ready to respond in a normal fashion
○ Automaticity:
■ 3 areas of the heart which have pacemaker activity
● SA node (main pacemaker)
● AV node
● Purkinje FIbers
■ What drives automaticity?
● Spontaneous opening & closing of K channels.
● The net flow of these ions repolarizes the cell, then depolarizes to threshold

○ Cardiac Conduction:
■ Rate of depolarization (Phase 0)
● Important because informs neighboring cells that something is happening
■ Threshold and resting membrane potentials
● Important in determining how easily and how frequently cells can depolarize
● The further away from these potentials that the cell is maintained, the harder it will be to get the cell to depolarize
○ Effective Refractory Period (ERP)


What is class I (IA) of anti arrhythmic drugs in terms of their mechanism of action and site of action?

○ Class I
■ Block voltage-sensitive Na channels
■ Decrease excitability
■ Decrease conduction velocity
■ Prolong effective refractory period

● Class IA
○ Slow conduction, prolong AP, increase ERP
○ Quinidine = toxic, can produce fatal arrhythmias (made from bark of cinochona tree = overdose leads to cinchonism
○ Typically used now for life-threatening arrhythmias because of its pro-arrhythmic effects = use has been replaced by new, safer medications and non-pharmacologic interventions (radiofrequency ablation)
○ Prophylaxis after cardioversion to maintain normal rhythm
○ PVC’s, atrial fibrillation or flutter, ventricuar tachycardia
○ Site of action: atrial tissues
○ Side effect: may cause or exacerbate arrythmia
1. procainamide (Pronestyl)
a. Derivative of the local anesthetic procaine
b. Many adverse effects = reversible lupus-like syndrome in 25% of patients
c. Toxicity can cause asystole or induction of ventricular arrhythmias
d. Many CNS side effects
2. disopyramide (Norpace)
a. Causes peripheral vasoconstriction
b. May decrease myocardial contractility in patients with pre-existing impairment of left ventricular function
c. Used for treatment of ventricular arrhythmias as an alternative to quinine and procainamide


What is class I (IB) of anti arrhythmic drugs in terms of their mechanism of action and site of action?

● Class IB
○ Decrease duration of AP by shortening//decreasing of AP by shortening/decreasing repolarization (ERP) = speeds up rate so overcome ventricular ectpic foci
○ Lidocaine is drug of choice
○ Used to treat ventricular arrhythmias
■ eg. during an MI
■ lidocaine does not slow conduction, so little effect on atrial or AV junction arrhythmias
○ Side effects: CNS effects; may cause arrhythmias
○ Site: ventricles
1. phenytoin (Dilantin) = anticonvulsant/antiarrhythmic
a. Prolongs ERP and suppresses ventricular pacemaker automaticity; shortens AP in the heart
i. *gingival hyperplasia*
2. Mexiletine (Mexitil)
a. Structurally related to lidocaine
b. Serious ventricular arrhythmias, suppression of PVCs
3. tocainide (Tonocard)
a. Suppression of life-threatening ventricular arrhythmias


What is Class IC of anti arrhythmic drugs in terms of their mechanism of action and site of action?

○ Marked conduction slowing
○ Site: ventricles
○ slow conduction in all cardiac tissues
○ Approved only for use of refractory ventricular arrhythmias (life threatening)
○ Serious safety concerns
■ Cause arrhythmias because of profound effect on Na channels in healthy heart tissues as well
1. flecainide (Tambocor)
2. propafenone (Rythmol)


What is Class II of anti arrhythmic drugs in terms of their mechanism of action and site of action?

■ Beta Blockers
● Block effect of catecholamines on pacemaker cells to prolong the refractory period
● Depress automaticity, prolong AV conduction, decrease heart rate and contractility
■ Blocks Na channels (so some Class I membrane stabilizing effects as well)
■ Use: Tachyarrhythmias, atrial flutter and fibrillation, AV nodal reentrant tachycardia
■ Cardioselective and non-cardioselective agents


What is Class III of anti arrhythmic drugs in terms of their mechanism of action and site of action?

■ Blocks K channels
■ Prolong AP and prolong effective refractory period (ERP)
■ Slows heart because drug reduces amount of norepinephrine released
■ All drugs in this class may induce arrhythmias
1. amiodarone, bretylium (Bretylol)
a. Life-threatening recurrent ventricular fibrillation and or if refractory or intolerant of other antiarrhythmics
b. Contains iodine = long-term use causes blue skin discoloration due to accumulation of iodine
c. May cause thyroid disease with long-term use
d. Severe toxic effects = compliance is very poor, many patients opt to discontinue the drug
i. Pulmonary fibrosis, GI intolerance, tremor, ataxia, neuropathy, liver toxicity, photosensitivity, muscle weakness
2. sotalol (Betapace)
a. also non cardioselective beta blockers


What is Class IV of anti arrhythmic drugs in terms of their mechanism of action and site of action?

■ Calcium channel blockers
■ Slow conduction velocity and increase effective refractory period of the AV node
■ Negative chronotropic effect; also some negative inotropic effect (contraindicated in patients with congestive heart failure
1. verapamil (Calan) diltizaem (Cardizem, Dilacor)
a. drug of choice for cardiac arrhythmas (PSVT)
b. other actions: dilate coronary and peripheral arteries
c. Side effects: CNS, GI, tachycardia, hypotension, flushing, headache; gingival hyperplasia
2. Adenosine
3. Digoxin aka cardiac glycoside
a. Indicated for atrial fibrillation and flutter
b. Congestive Heart Failure - Increased intracellular Ca leading to increased contractility


What is the clinical manifestation of cinchonism associated with quinidine?

○ Cinchonism = quinidine (class 1a) use only
■ nausea/vomiting, headache, tinnitus, deafness, symptoms of cerebral congestion, vertigo, visual disturbances


What are the common side effects associated with anti arrhythmic medications?

○ The vagal blocking effects of antiarrhythmic drugs and anticholinergics can act synergistically and lead to tachycardia
○ Therapeutic effects of antiarrhythmics are increased by potassium (and reduced in hypokalemia)
○ Hypersensitivity
○ Hypotension, shock
○ Paradoxical arrhythmias
○ GI disorders


Compare and contrast typical angina with variant angina.
What is Typical?

○ Typical (exertional)
■ coronary arteries are not able to transport enough oxygen to meet myocardium demand
■ oxygen demand of the myocardium exceeds the amount of available oxygen
● ischemic heart disease
● coronary artery disease= stenosis
● history of MI
■ stress, exertion, eating, anxiety, cold, local anesthesia, pain, atherosclerotic lesions
■ if demand > available oxygen then necrosis occurs = MI


Compare and contrast typical angina with variant angina.
What is Variant (atypical, Prinzmetal’s)) ?

■ Rare (more common in males and Japanese)
■ When coronary arteries are normal:
● mainly B-2 receptors in coronary arteries = Epi cause vasodilation
○ improves blood flow to heart
● Epi on B-1: increasing oxygen demand of the heart
■ Individuals with variant angina have more Alpha-1 receptors than Beta-2 receptors in their coronary arteries (vasoconstriction)
■ Epi increases HR and cardiac output (beta-1) but now vasoconstrictors coronary arteries (alpha 1)
■ Results in lack of oxygenation due to vasospasm
■ EKG dx: elevated ST segment (not in normal/typical angina)


List several factors that may trigger an angina attack.

○ physical exertion
○ mechanical stress
○ increased contractility, pulse rate, BP
○ temperature (cold)
○ hyperventilation


What is the mechanism of action of nitrites/nitrates, beta-blockers and calcium channel blockers as it relates to the management of angina?

○ MOA: relaxation of all smooth muscle = no contraction = arterial and venous vasodilation
○ work on endothelial cells that produce nitric oxide
○ activates guanylyl cyclase which converts GTP → cGMP → dephosphorylation of light myosin chain (2ndary messenger)
○ Causes:
■ vasodilation
■ decrease preload and venous return
■ decrease work
■ decrease oxygen demand


What are the side effects of nitrites/nitrates, beta-blockers and calcium channel blockers?

○ headaches b/c fast onset of vasodilation
○ weakness, dizziness
○ flush (especially with amyl nitrate)
○ postural hypotension and syncope (increases w/ alcohol)
○ tachycardia and increase peripheral resistance
■ use B-blockers to treat tachycardia
○ rash
○ oxidation of hemoglobin to methemoglobin: blood no longer carries oxygen well
○ decrease oxygen-carrying capabilities (associated with large dosages)


Compare the rate of onset and duration of action of nitrites/nitrates?

○ rapid onset
○ rapid tolerance will develop
○ Amyl nitrate:
■ vaporole: inhale
■ onset


What are the important dental care considerations for patients taking antianginal medications?

○ limit extent of procedures per visit
○ limit Epi administration (1:100,000) in local anesthesia to 2 cartridges
■ cardiac dose = 0.04 mg Epi
○ consider local anesthetics w/o vasoconstrictor
○ can cause gingival hyperplasia


Describe the antiplatelet effects of aspirin

○ Aspirin - acetylsalicylic acid - most comprehensively studied and least expensive of all antiplatelet medications
■ Target: COX which inhibits thromboxane A2
■ Causes irreversible platelet aggregation
● effects last for life of the platelet = 7-10 days
■ Indications
● Prevention of thromboembolic conditions
● History of MI (lowers risk)
● History of stroke
■ No need to discontinue low dose aspirin therapy prior to dental treatment
● Risk to patient for having a stroke is greater than the risk for the patient having an uncontrollable bleeding incident or bleeding to death in the dental chair.
■ Discontinuing the use of aspirin increases mortality risk. 3 fold higher risk for major adverse cardiac events
● Risk was amplified by a factor of 89 in patients who had undergone stenting


Describe the anti platelet effects of thienopyridines (e.g. clopidogrel (Plavix) and other drugs.

○ clopidogrel (plavix)
■ a thienopyridine that decreases platelet aggregation with collagen
● Requires adenosine to form the clot
■ Desired effect is caused by the inhibition of the cellular availability of adenosine and adenosine uptake
■ Prevents the binding of ADP to collagen receptors which prevents platelet aggregation

○ Other anti-platlet drugs
■ ticlopidine (Ticlid)
■ prasugrel (Effient)
■ ticagrelor (Brilinta)

■ cause reversible effects on platelets depending on half life
■ watch ibuprofen and aspirin cross reaction


Discuss the dental management of patients taking combination antiplatelet therapy for percutaneous coronary intervention (stents).

○ Those concerned about peri/postprocedural bleeding must be aware of catastrophic risks of premature discontinuation
■ 12 months after implantation
■ minimum of one month for bare-metal stents
■ Restart thienopyridine as soon as possible after the procedure because of concerns of late stent thrombosis
○ Optimal treatment for many patients experiencing acute coronary syndromes
○ Provides better safety and efficacy than thrombolysis and may obviate need for bypass surgery
○ warfarin use has been associated with increased gingival bleeding and mouth ulcers
○ no need to discontinue warfarin prior to routine dental procedures


Describe the anticoagulant effects of heparin

○ Heparin
■ Naturally produced anticoagulant (antithrombin)
■ Synthetic version given by IV
■ Indications: prevention and treatment of thromboembolic disorders
■ Anticoagulation for dialysis procedures
■ Heparin glock flush used to clear IV lines
■ Produces immediate anticoagulation effects
■ Patient admitted to hospital is started on heparin and warfarin: heparin produces initial effect
■ Adverse Reactions
● Bleeding in gut, brain, GI tract
● Synergistic effect with oral anticoagulants (Coumadin), NSAIDS, alcohol
● Histamine release is possible if heparin is administered too rapidly = extensive bleeding can result
● Antidote to heparin = Protamine


Describe the anticoagulant effects of warfarin (Coumadin, Jantoven)

■ Oral anticoagulant
■ Target: Liver
■ Interferes with liver synthesis of vitamin-k dependent clotting factors
● Factors II, VII, IX, X, and proteins C and S
■ takes 4-5 days after initial administration to see effect
■ 1-2 day overlap period with heparin following warfarin administration
■ Indications:
● Prophylaxis and treatment of TE disorders (venous and pulmonary) and embolic complications that arise from atrial fibrillation or cardiac valve replacement
● Adjunct to reduce risk of systemic embolism (recurrent MI, stroke) after MI
■ Investigational: prevention of recurrent TIA
■ Metabolized in liver by P450 enzymes
■ Drugs that induce liver metabolism will decrease level of warfarin: dose will need to be increased to maintain the desired effect
● eg. phenytoin
■ Low therapeutic index: very narrow window of safety = easy to alter the level of anticoagulation
● Changes in diet, fever, antibiotics, GI disorder/flu can alter warfarin levels


Identify factors that can alter the efficacy of warfarin (Coumadin).

○ Fever
○ Flu
○ Diarrhea or vomiting
○ use of many drugs, including antibiotics
■ phenytoin
○ change in diet (consumption of leafy greens increased Vit K)
■ need Vit K to synthesize clotting factors in liver
■ Warfarin shuts off production of these clotting factors


State the antagonists to heparin and warfarin (Coumadin).

○ acetaminophen (Tylenol) and warfarin (Coumadin)
■ combination causes enhanced anticoagulation
■ dose and duration of acetaminophen should be as low as possible.
● patients taking 4 acetaminophen for longer than a week
○ INR>6.0 increased 10 fold


Discuss the indications for use for direct antithrombins (Factor Xa inhibitors).

○ apixaban (Eliquis) - thromboprophylaxis for hip/knee replacement; nonvalvular atrial fibrillation
■ best documented alternative to warfarin and aspirin for stroke prevention in the broad population with Atrial Fibrillation

○ fondaparinux (Arixtra) - thromboprophylaxis for hip/knee replacement; unstable angina; non-ST segment elevation MI; treatment of DVT/PE

○ rivaroxaban (Xarelto) - thromboprophylaxis for hip/knee replacement; treatment of DVT; nonvalvular atrial fibrillation; treatment of PE
■ good alternative to warfarin in atrial fibrillation; most data in DVT and ACS


Describe the dangers of anticoagulant medications. (from what I can find she only has a list for heparin but the main point is the same)

○ Heparin
■ Bleeding in gut, brain, GI Tract
■ Synergistic effect with oral anticoagulants (coumadin), NSAIDS, alcohol
■ Histamine release is possible if heparin is administered too rapidly = extensive bleeding can result
■ Antidote to heparin = Protamine


What are the tests used to assess the effects of heparin and warfarin (Coumadin).

○ Bleeding time test = 1 - 6 minutes
○ Prothrombin time (PT) = 10 -13 seconds

■ evaluates extrinsic pathway (II, VII, X, V)
○ Activated Partial Prothrombin Time (aPTT) = 25 to 35 seconds; used to measure the effects of heparin, which increase aPTT to 50 to 70 seconds
■ Evaluates intrinsic pathway (XII, XI, IX, VIII, X, V)
■ used first when giving IVs to reduce clotting
○ International Normalized Ratio (INR)
■ used to measure the effect of warfarin (Coumadin)
■ calibrated/standardized prothrombin test
■ INR = PT (patient)/PT (control)
■ INR = 2.0-3.0 therapeutic range for venous thrombosis, pulmonary embolism, systemic embolism, atrial fibrillation
■ INR 2.5-3.5 therapeutic range for mechanical prosthetic heart valves
■ Okay to provide dental treatment when INR falls between 2.0-3.5
■ Over 4 overdose range
■ below 2 increase for stroke and above 3.5 increase risk for hemorrhage


Name 2 thrombolytic (clot-busting) drugs and 1 antidote for tPA.

○ tPA (tissue plasminogen activator) = IV drug
■ Serine protease released from endothelial cells; binds to fibrin and activates plasminogen
■ Retavase = recombinant form given in 2 shots
■ Antidote for tPA = Epsilon AminoCaproic Acid (Amicar) = treat hemophilia and cerebral aneurysm bleeds
○ streptokinase (Streptase)
■ Enters the clot and changes conformation of incorporated plasminogen so that drug can break down fibrin
■ Very expensive, but effective for heart attacks
■ Successive exposure causes antibody production = triggers anaphylaxis upon repeated exposure
○ urokinase
■ Converts inactive plasminogen to active form of plasmin which circulates and dissolves fibrin


Describe dabigatran (Pradaxa):

○ FDA approved October 2010
○ Thrombin inhibitor
○ Prodrug = lacks anticoagulant activity
■ converted in vivo to active dabigatran
○ specific, reversible, direct thrombin inhibitor that inhibits both free and fibrin - bound thrombin
○ prevents thrombin - mediated effects, and by inhibiting thrombin - induced platelet aggregation
○ Inhibits: coagulation by preventing thrombin-mediated effects, including cleavage (furrow) of fibrinogen to fibrin monomers, activation of factors V, VIII, XI, and XIII
○ Indications: prevention of stroke and systemic embolism in Pt with non-valvular atrial fibrillation
○ Canadian labeling (not US): post operative thromboprophylaxis after total hip or knee replacement
■ knee replacement - up to 10 days
■ hip replacement - up to 35 days
○ No antidote
■ protamine and vitamin K do not reverse anticoagulant effects
○ May be removed with dialysis
■ 60% removed over 2-3 hours
○ Severe hemorrhage:
■ transfusions of frozen plasma, packed RBCs or surgical intervention when appropriate:
○ Compared to Warfarin:
■ advantages: no monthly monitoring, fewer drug to drug and diet interactions
■ disadvantages: very expensive, twice dialy dosing
■ in studies, patients who took pradaxa had fewer strokes than those taking warfarin
● RE-LY trial = randomized evaluation of Long Term Anticoagualnt Therapy
■ Adverse effects: bleeding, GI effects


Describe the mechanism of action of bile acid sequestrants, in lowering plasma lipids.

○ Bile acid sequestrants (contain “cole-” or “chole-”)
■ bind bile acids in gut
■ increase fecal loss of bile salt bound LDL
■ drug interactions: bind drugs in GI tract → GI side effects
■ preparations: cholestyramine resin, colesevelan, colestipol


Describe the mechanism of action of fibric acid derivatives, in lowering plasma lipids.

○ Fibrotic acid derivative (“fiber” sound is in the name)
■ lowers plasma triglycerides
■ increases HDLs
■ inhibits cholesterol synthesis in liver
■ preparations: clofibrate (Atromid), fenofibrate (Tricor), gemfibrozil (Lopid)


Describe the mechanism of action of niacin in lowering plasma lipids.

○ Niacin
■ decreases liver TAG synthesis necessary for VLDL production
■ decreased VLDLs decrease plasma LDLs
■ can reverse some endothelial cell dysfunction leading to thrombosis caused by high cholesterol and atherosclerosis
■ least expensive of all meds
■ side effects: facial flushing
■ used for mildly elevated cholesterol


Describe the mechanism of action of HMG CoA Reductase inhibitors in lowering plasma lipids.

○ HMG CoA reductase inhibitors (“statins”)
■ leading cholesterol lowering medications
■ inhibits rate limiting step in cholesterol synthesis
● decreases synthesis of cholesterol in liver
● increases LDL breakdown
● also may increase HDLs in some people (dec risk of coronary heart disease)
■ anti-inflammatory activity


Discuss important dental drug interactions associated with HMG CoA Reductase inhibitors (“statins”).

○ cannot take if pt has liver disease
○ alters liver function
■ must have liver testing done on regular basis
■ elevated liver enzymes dictate need to stop drug
○ myalgias
■ rhabdomyolysis: degeneration of m. tissue causing cramping and fatigue especially in lower extremities
○ RED FLAG DRUGS = promote rhabdomyolysis
■ macrolide antibiotics (erythromycin)
■ systemic (azoles) antifungals
○ multiple drug interactions: be sure to look up each medication before prescribing
○ assess risk for increased bleeding
○ assess changes in cholesterol lower medications at each visit (compliance)


What are the main effects of cardiac glycosides?

○ Summary of effects
■ Increased force of myocardial contraction
■ Decreased firing of SA node (Negative chronotropic effect)
■ Increased automaticity (Increase ectopic impulse formation = related to toxicity)
■ Slowed AV conduction
■ Prolonged refractory period of AV node
■ Diuresis
■ Decreased venous pressure
■ Decreased tachycardia
■ Decreased heart size


What is the MOA of cardiac glycosides?

■ Inhibits Na/K ATPase pump - resulting in increased Ca+ inside of cell.
● Increases contraction of the heart
● Positive inotropic effect
■ Directly suppresses AV node conduction increase ERP and decrease conduction velocity - Slows down re polarization of myocytes following AP
● Results in prolonged action potential
● Slows heart rate = negative chronotropic effect***
■ Causes diuresis ***
● Decreases venous return
● Allows heart to become more efficient
● Decreases filling pressure
● Decreases heart rate
● Decreases heart size


Describe the primary effects of cardiac glycosides on the myocardium.

○ Increase force of myocardial contraction
○ Decreases firing of SA (negative chronotropic effect)
○ Increased automaticity
○ Slowed AV conduction
○ Prolonged refractory period of AV node
○ Diuresis
○ Decreased venous pressure
○ decreased tachycardia
○ decreased heart size


Describe the margin of safety of cardiac glycosides (therapeutic index).

○ Low therapeutic index
■ therapeutic dose is approximately 50-60% of the toxic dose
● every pt. must be titrated


What are the 2 indications for the use of cardiac glycosides?

1) Cardiac heart failure (CHF)
2) Atrial fibrillation/flutter


List common side effects produced by cardiac glycosides including cardiac, gastrointestinal and central nervous system side effects.

○ Digoxin Toxicity
■ Block conduction between SA node and AV node
■ Bradycardia (lack of conduction due to AV block)
● decreases cardiac output
■ Causes arrhythmias
■ extra beats due to conduction blockage between upper and lower heart, lower may start beating on its own
■ GI effects (result from stimulation of chemoreceptor zones and vagal nucleus (parasympathetic effects)
● nausea/vomiting
● increase salivation
● anorexia
● diarrhea
● abdominal pain
■ Central Nervous system
● Headache - vasodilation, changes in edema in CNS
● Fatigue - decreased muscle tone
● Drowsiness
● Visual disturbances (blurry vision)
● Green/yellowish aura - pt. knows that he is at toxic level of digitalis if he sees aura.
○ Increased vagal output - can be blocked by atropine
○ Low therapeutic index
○ Uncoordinated arrhythmias


Identify the common cardiac glycoside used to treat congestive heart failure.

○ First discontinue drug
○ Antidote: digoxin immune fab (Digibind, DigiFab)

■ Administer potassium chloride and anti-arrhythmic meds.
● If K+ decreases, then digitalis will worsen
● Increasing K+ (antidote for toxicity) will decrease effects of digitalis


Discuss dental practice considerations when treating patients with congestive heart failure.

○ Decrease stress for the patient
○ Caution with use of local anesthetics with vasoconstrictors
○ Avoid using gingival retraction cords due to potency of vasoconstrictors
○ Do not recline patient fully: hard to breathe
○ general anesthesia decreases cardiac output and decreases perfusion = dangerous to a patient with CHF