Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

59 Cards in this Set

  • Front
  • Back
action of CV drugs?
1) alteration of myocardial contractility or HR
2) alteration of conduction of the cardiac AP
3) vasodilation or vasoconstriction of coronary and peripheral vessels
myocardium is one of the more poorly?
perfused tissues in the body
(coronary circulation receives only 4% of the CO)
myocaridal O2 supply
1) HR
2) coronary perfusion pressure
3) arterial O2 content
4) coronary artery diameter
myocardial O2 demand
1) HR
2) preload
3) afterload
4) contractility
the most common cause of angina is the build up of?
Tx of pts with significant coronary artery disease aims to achieve?
an "even" myocardial oxygen balance
anti-anginal drugs are used to?
1) reduce preload (Nitrates)
2) reduce HR (beta-bloekers)
3) reduce myocardial work (beta-B)
4) reduce oxygen consumption (beta-B)
5) maximize coronary vasodilation (Ca channel B)
anti-anginal drugs
1) Nitrates
2) Glyceryl trinnitrate (NTG)
3) beta-blockers
4) Ca antagonists
What is the drugs of first choice for angina?
main action of Nitrates?
1) venous (low dose) or
2) venous and arterial (higher doses)
vosodilation from Nitrates is mediated by production of?
1) nitric oxide (NO) and
2) increased levels of intracellular guanosine 3',5'-monophosphate (cGMP) in vascular smooth muscle
Glyceryl trinitrate (NTG)
1) a short acting nitrate
2) suration of action of 30 min
3) useful in preventing angina attacks than in stopping them
longer acting nitrates?
1) isosorbide dinitrate (Isordil)
2) isosorbide mononitrate (Imdur)
Nitrates are best used "intermittently", allowing a few hrs without treatment in each 24 hrs period, WHY?
because people develop tolerance to Nitrates, and blood vessels become hypo- or non-reactive to the drugs
unwanted effects of Nitrates?
1) dilation of cranial vessels = headache
2) tachycardia
3) hypotension
4) development of tolerance to nitrates
beta blockers are used to?
1) prevent angina
2) treat HTN
atenolol (Tenormin) and metoprolol (Lopressor) are the drug of choice because?
they are cardioselective
(only work on beta-1 receptors, and not the beta-2 receptors elsewhere in the body)
side effects of beta blockers?
1) bronchoconstriction
2) cold extremities
3) worsening of PVD
4) hypoglycemia
5) impotence
Why beta blockers are not good choice for CHF pts?
because CHF pts need a "sympathetic drive" to the heart to maintain adequate CO, and blockade of beta-1 receptors in these pts can worsening heart failure
calcium antagonists act by?
blocking the Ca channels which open in response to depolarization of the cell memb. (voltage sensitive channels).
3 sub-groups of Ca antagonists
1) papaverine derivatives (Verapamil)
2) benzothiazepines (Dilt)
3) dihydropyridines (Nifedipine, Norvasc)
Ca antagonists reduce?
afterload (by arterial vasodilation)
action of Ca antagonists?
1) reduce afterload
2) dilate coronary arteries
3) reduce cardiac work
4) improve myocardial O2 balance
adverse effects of Ca antagonists?
1) postural hypotension
2) flushing
3) peripheral edema
4) constipation
5) negative inotropic effect (should not be used in pts in cardiac failure) = esp. Verapamil
1) arrythmias of sinus origin
2) ectopic thythms
3) conduction blocks
4) pre-excitation syndromes
1) arrhythmias of sinus origin
electorical conduction follows the normal pathway
1) too fast
2) too slow
3) irregular
2) ectopic rhythms can be due to?
1) abnormal automaticity (spontaneous discharge)
2) re-entry
re-entry tachycardias involve?
the cardiac impulse being transmitted to a functional "ring" of conducting tissue, one side of which has a unidirectional (one-way) block
re-entry mechanisms are implicated in?
1) A-flutter
2) SVT
3) VT
3) conduction blocks can occur at the level of?
1) AV node (1st, 2nd, and 3rd degree blocks) or
2) His-Purkinje fibers (BBB)
4) in pre-excitation syndromes, what is bypassed by an accessory pathway?
the normal delay at the AV node
this bypass will leads to?
premature ventricular depolarization
2 examples of pre-excitation syndromes?
1) Wolf-Parkinson-White
2) Lown-Ganong-Levine
classification of anti-arrythmic drugs are based on?
Vaughan-Williams classification
(basis of mechanisms of action)
1) Class 1?
membrane stabilizing drugs
2) Class 2?
3) Class 3?
prolongation of AP and refractory period
4) Class 4?
calcium antagonists
Class 1: membrane stabilizing drugs:
fast depolarization of the cell memb. is inhibited by?
blocking the inward flux of Na ions
Class 1 is further sub-divided into 3 groups
1) 1a: Quinidine, Procainamide, Disopyramide
2) 1b: Lidocaine, Mexiletine, Tocainide, Phenytoin
3) 1c: Flecainide
Class 2: beta-blockers
1) reduce automaticity
2) increase the AP duration in the ventricles
3) increase the refractory period at the AV node
ex of beta-blockers
1) propranolol (Inderal)
2) metoprolol (Lopressor)
3) esmolol (Brevibloc)
Class 3:
1) prolongation of AP
2) prolongation of refractory period
1) amiodarone (Cordarone)
2) bretylium
Class 4: Ca antagonists
Verapamil (Calan)
1) slows conduction at the AV node
2) Tx for SVT
Class 4: Digoxin (Lanoxin) is the only anti-arrythmic drug for the A-fib that does not have?
1) negative inotropic or
2) vasodilator effects
Digoxin is used for?
1) heart failure
2) arrythmias (control HR in Afib)
direct action of Digoxin is?
1) to block the Na/K ion exchange pump = > Ca in cell = > contractility
2) slows the conduction of AP at the AV node
Digoxin also acts indirectly by increasing?
parasympathetic activity via the vagus nerve = slows AV node conduction
high doses of Digoxin can cause?
serious arrythmias
1) complete heart block
2) vent. ectopic beats
3) V-tac/V-fib
side effects of Digoxin?
1) N/V
2) visual disturbance
3) headache
factors enhance Digoxin toxicity?
1) hypokalemia
2) hypomagnesimia
3) hypercalcemia
4) hypoxia
5) acidosis
6) myocardial ischemia
the dose of Digoxin must be reduced in?
1) renal failure
2) drugs (amiodarone, verapamil, quinidine)
Class 4: Adenosine is a naturally occuring molecule which is a metabolite of?
adenosine monophosphate
Adenosine acts via?
specific adenosine receptors
Adenosine cause?
1) coronary vasodilation
2) reduce conduction at the SA and AV nodes
Adenosine is useful in treating?
re-entry SVT
Adenosine does not work for?
half-life of Adenosine?
very short, 10 sec
Adenosine is useful in diagnosing broad complex tachycardia as either SVT ro vent in origin, because?
1) short duration of action
2) low incidence of adverse effects