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103 Cards in this Set

  • Front
  • Back

What is Congestive Heart Failure (CHF)

heart doesn't pump blood as well as it should

The failing heart has reduced work output per unit of O2 consumption

not all blood pumped out of heart: accumulation of blood in the heart: leads to enlarged heart

How do the drugs that treat CHF work on the heart?

reduce the O2 demands of the heart OR by increasing the function/strengthen the heart

What group of drugs treat CHF? What are these derived from?

Cardiac Glycosides (Digitalis)

foxglove plants

The cardiac glycoside that is used in the treatment of CHF?

digoxin (Lanoxin)

What is the primary use of digitalis? Secondary use?

Congestive Heart Failure

Atrial Flutter and Fibrillation

How does digitalis work?

-Increases cardiac output without an increase in O2 consumption.

LV failure: fluid accumulate in lungs

RV failure: fluid accumulates in systemic vessels-leads to edema.

cant put enough blood through kidneys for excretion

Why does digitalis depress the conductal system?

So that every impulse does not reach the ventricles.

How does digitalis act on the heart?

Receptor is an enzyme in the cell membrane called NA/K ATPase.

Blocks Na/K uptake, more calcium retention.

Increase contraction, stronger contraction.

Digitalis has a positive inotropic effect which means it does what?

increases force of contraction

increases influx of Ca2+

contraction phase enhanced

Digitalis does what to the refractory period?

(this does what 4 things)

Decreases refractory period:

atrial and ventricular muscle

more loss of K+

decreases repolarization time

can induce fibrillation

Digitalis increases cardiac output and causes what effect on the heart?

-decreases size of distended congestive heart

-diuresis from improved CV dynamics

Digitalis Increases the refractory period of the ___ Node and _________ fiber system due to ____________ stimulation (PsANS).

(What three things does this do?)



Vagus Nerve

- decreases conduction velocity

- can lead to heart block or other arrhythmias

- this is why digitalis is used in Afib

Digitalis can cause slowing of the heart rate at what does?

(this is due to what 2 things?)

Low doses

- vagus nerve stimulation

- decreases SANS activity due to restoring cardiac output

Therapeutic index of digoxin

Low therapeutic index

-hospital administration

-need to individualize doseage

Toxic cardiac reactions to digoxin

-heart block

-ectopic systoles of ventricular origin


Toxic Extra Cardiac reactions to digoxin

Visual: yellow-green, white dot, double vision

CNS: headache, drowsy, dizzy

GI: nausea/vomit (CTZ), anorexia, increase salivation, cramps, diarrhea

Treatment of digoxin toxicity (4)


-digiband (Ab to digitalis)

-Potassium supplements

-Lidocaine for ventricular arrhythmias

The drugs used first for treating CHF?

ACE inhibitor



CHF drugs that cause a decreased Preload pressure

Venule Dilators:



-salt restriction

CHF drugs that cause an increased contractabilty



CHF drugs that cause a decreased afterload pressure

Arteriole dilators:

-ACE inhibitors


-Calcium channel blockers

-alpha channel blockers

What is a cardiac arrhythmia?

an abnormal heart beat

Drugs for cardiac arrhythmias are used to:

used to modify or restore the rhythm of the heart toward normal

What is the action of cardiac arrhythmia drugs?

Cardiac Depressants!

The mechanism of action of cardiac depressants (drugs for cardiac arrhythmias)

- decrease in cardiac activity

-increase in refractory period

-decrease in pacemaker activity

What is the classification for antiarrhythmic drugs

Vaughan-Williams Classification

What is the Vaughan-Williams Classification of antiarrhythmic drugs?

Type I: Na+ blocker (membrane stabilization blocks conduction)

Type II: beta receptor blocker (reduce SANS activity)

Type III: K+ blocker (prolong action potential & repolarization)

Type IV: Ca++ blocker (slow conduction velocity at AV node)

Type I drugs:

antiarrhythmic, Na+ channel blocker.

membrane stabilization blocks conduction.

decrease conduction and depolarization. increase repolarization time.

Type I antiarrhythmic drug used in Dentistry?

lidocaine (xylocaine)

lidocaine (xylocaine)

Na+ channel blocker (stabilize membrane and block conduction)

decreases responsiveness, conduction

increases repolarization time.

How is lidocaine delivered to body?

parenterally (but effective oral derivatives are available)

lidocaine may be used in emergency situations during what?

during transport following an acute myocardial infection, this may be used.

How does lidocaine affect ventricular function

decreases automaticity in purkinje fibers therefore used for treatment of ventricular ectopic rhythms

What arrhythmia does lidocaine treat?

ventricular fibrillation

Toxicities of myocardial depressants (3)

excessive cardiac depression leading to drowsy and lethargy

nausea and vomit

various CNS disturbances

Type II antiarrhythmic drugs?

beta receptor blockers

reduce SANS activity

Type III antiarrhythmic drugs?

K+ channel blockers

prolongs the action potential and repolarization

Type IV antiarrhythmic drugs?

Ca++ channel blockers

slows conduction velocity at AV node.

used to manage life-threatening recurrent ventricular fibrillation or unstable ventricular tachycardia- assists to convert atrial fibrillation to normal sinus rhythm

Type III antiarrhythmic drugs

Side effect of Type IV antiarrhythmic drugs

gingival hyperplasia

What is angina pectoralis

severe substernal pain in chest due to inadequate blood flow

insufficient oxygen to the heart=pain

coronary muscles are spasming

Three types of Angina pectoralis?

-Chronic Stable Angina (Classic Angina of Effort)

-Variant Angina

-Unstable Angina

Chronic stable angina (classic angina of effort)

presence of atheromatous obstruction in the coronary arteries

goal: increase myocardium perfusion, decreases O2 demand

Variant Angina

coronary artery spasm

goal: prevent vasospasm

Unstable Angina

thrombi near atherosclerotic plaque

goal: correct tendency to form thrombi

Normal coronary flow

-myocardium has a smaller blood supply in relation to O2 requirement

-normal flow is regulated by physical factors such as transmural pressure during systole

-some autoregulation-adenosine

Myocardial O2 supply is determined by:

and compromised by:

coronary blood flow

atherosclerosis, arterial spasm, and platelet-fibrin thrombi

Myocardial O2 demand is influenced by:

and influenced by:

heart rate, contractability, and wall tension

exercise, smoking, cold, and eating

THe pain of angina pectoris (3)

acute attack

long-term prophylaxis

short-term prophylaxis

Classification of drugs used to treat angina pectoris

Negative Inotropic Vasodilators

Negative inotropic vasodilators:

inorganic nitrites and organic nitrates

Selected pharmacology of nitrites and nitrates: Examples

nitroglycerine (Nitrostat)

amyl nitrite (Amyl Nitrite Aspirols)

nitroglycerine (Nitrostat)

treat angina pectoris, emergency drug, sublingual, vasodilator, immediate onset

amyl nitrite (Amyl Nitrite Aspirols)

treat angina pectoris, ammonia inhalant, immediate response, causes vasodilation

Negative inotropic vasodilators: Mechanism of Action

produce nitric oxide (NO) in vascular smooth muscle.

Why are negative inotropic angina pectoris drugs only taken as needed?

Tolerance development

Adverse reactions and precations of negative inotropic drugs

throbbing vascular headaches (Nitrates)

methemoglobinemia (Nitrites)

face flushing


reflex tachycardia (palpations)



visual disturbance (dilate retinal vessels)

Drug interaction that can occur with negative inotropic vasodilators

-hypotensive effects of narcotics and antihypertensive agents

-increase intraocular pressure of anticholinergic agents


-drop in BP enhanced with PDE-5 (Viagra)

Antianginal agents in dentistry

prophylactic use of nitroglycerin in angina pt.

emergency use of nitroglycerin or amyl nitrite in treating an acute anginal attack

precautions with the use of antianginal agents in dentistry

use patients prescription and dose

know nonspecificity of drug and overdose response

short shelf life- frequently update

Beta blocker used to treat angina pectoris

Proranolol (Inderal)

decreases demand of O2 on the heart.

Calcium blocking agents used to treat angina pectoris

directly inhibit Ca++

-relaxes effect on vascular smooth muscle

arterial dilation in coronary and systemic beds

amlodipine (Norvasc)

Ca++ entry blocking agent

relaxes the vascular smooth muscle and dilates arterioles in coronary and systemic beds

What drugs are used to treat thromboembolic disorders

Anticoagulant drugs

Blood coagulation cascade phases

1. coming together of many factors to activate factor 10

2. factor 10 convers prothrombin to thrombin

3. thrombin converts fibrinogin to fibrin

What ion is essential for coagulation?


Chemistry of Heparin:

Large, highly polar molecules

Heparin mechanism of anticoagulant action:

mediated by endogenous component of plasma- heparin cofactor (antithrombin III)

neutralizes thrombin so it cannot act (antithrombin action)

what decreases the levels of antithrombin III?

estrogen (birth control decreases antithrombin III and can cause blood clots)

Naturally occurring, prevents microclots from appearing in our blood.


Onset and half life of Heparin


t1/2= 1-3 hours

Route of administration: Heparin

parenteral (NOT orally)

Clinical use of heparin

"Heparin Lock"- draw blood, put some heparin in it to prevent coagulation

Heparin anticoagulant is antagonized by what?

protamine sulfate (use if there is a heparin overdose)

What is the adverse effect of Heparin


Oral anticoagulants

Coumarin derivatives

Example of an oral anticoagulant

warfarin (Coumadin)

warfarin (Coumadin) mechanism of action:

antagonize the utilization of Vitamin K by the liver

depresses the synthesis of plasma clotting factors (2, 7, 9, 10)

decreases platelet adhesiveness

Pharmacokinetics of oral anticoagulants:

oral, but high variability in amount absorbed

highly bound to plasma protein

metabolized in liver

adverse effect of oral anticoagulats


Coumarin derivatives (oral anticoagulants) are antagonized by what?

Vitamin K

Newer orally administered anticoagulants are different how?

more predictable

don't need to monitor INR

can inhibit


-Factor 10a

Blood has the capacity to dissolve clots by means of what?

fibrinolytic system

When activated ______forms ______ to break clots



activators of the fibrinolytic system may be used in the treatment of

victims of a heart attack

Example of activators of the fibrinolytic system

tissue plasminogen activator [t-PA, alteplase (Activase)]

tissue plasminogen activator:

natural enzyme made available by genetic engineering.

prevents tissue damage by opening vessel

sooner used less tissue damage from blood clot

What is the most common complication associated with activators (thrombolytics)


If body has excessive amounts of t-PA what happens

the body doesn't clot and at a surgical risk

Platelets provide:

the initial hemostatic plug at site of injury to the vascular.

Platelet inhibitors used to prevent:

thrombosis and to alter the natural history of atherosclerotic vascular disease

Example of a platelet inhibitor


Drugs used to lower plasma lipoproteins:

high levels of lipids (cholesterol) can lead to CV disease

High cholesterol can accelerate what

development of atherosclerosis which may lead to thrombosis (blood clot) and infarction (heart attack)


bad cholesterol

put lipids on tissues


good cholesterol

takes lipids to liver

Therapeutic approach to lower plasma lipoproteins: Diet

diet low in cholesterol and saturated fats

diet high in fiber

Lower plasma lipoproteins, need to reduce all other risk factors:

smoking, hypertension, obesity, poor physical condition, diabetes

Drug therapy (last case scenerio) to lower plasma lipoproteins:

HMG-CoA reductase inhibitors (statins)

HMG-CoA reductase inhibitors AKA


How do statins work?

synthesis in liver.

inhibit exyme "rate limiting step" to decrease LDL and increase HDL

atorvastatin (Lipitor)

lower plasma lipoproteins

decrease LDL

increase HDL by inhibiting the enzyme

side effects of HMG-CoA reductase inhibitors (statins)

elevate liver enzymes

muscle pain (myopathy)

memory loss (cognitive problems)

dpse-related depletion of Coenzyme Q10