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Pharmacology Exam 5 > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Atrial action potentials compared to ventricular

A

shorter plateau due to larger K+ outflow current than Ca2+ current
Do not have Na+ channels, must target the Ca2+ channels

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2
Q

Arrythmia

A

Timing or path of electrical depolarization is altered:

  1. abnormal initiation of cardiac action potential (site or timing)
  2. abnormal conduction pathway
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3
Q

Ectopic pacemaker

A

tissue that does not have automaticity spontaneously generates an AP
Usually following ischemia (O2 is out for K+/ATPase)

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4
Q

After-depolarization

A

multiple APs initiated by single incoming AP

  • Early depolarization - AP rise off plateau (prolonged AP from K+ channel blocker)
  • Delayed after depolarization (Ca2+ overload)
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5
Q

Early depolarization

A

K+ channel blocker

Torsade de pointes

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6
Q

Delayed after depolarization

A

Digoxin

Ca2+ overload (rise from RP)

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7
Q

Abnormal conduction pathway

A
  1. Non-conductive tissue in the center
  2. Unidirectional block so anterograde impulse is extinguished by retrograde is transmitted
  3. Retrograde impulse do not enter refractory tissue
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8
Q

Treat re-entry arrythmias

A

Increase the refractory period (K+ channel blocker)

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9
Q

Types of arrythmias

A
  1. Premature ventricular beat
  2. Atrial or ventricular tacchycardia (HR 100-200bpm)
  3. Supraventricular tachycardia
  4. Paroxysmal tachycardia
  5. Flutter (rapid regular contractions 200-350bpm)
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10
Q

Atrial flutter

A

Treat with Ca2+ Channel blocker

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11
Q

Vaughan williams classification

A
  1. Na+ channel blocker (fast tissue)
  2. Beta-blocker (slow tissue)
  3. K+ channel blocker (re-entry arrythmia)
  4. Ca2+ channel blocker
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12
Q

Quinidine (1a)

A

Block Na+ and K+ channels
Risk of torsade depointes
GI disturbances
Quinidine syncope
Cinchonism = cinchona (from quinidine) - tinnitus, dizziness, blurred vision, headaches
Thrombocytopenia, hepatitis, angioedema, fever
Not first line

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13
Q

Procainamide (1a)

A

Na+ channel blocker

K+ channel

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14
Q

Lidocaine (1b)

A

Na+ channel blocker ONLY in depolarized state
Block nerve conduction through nerves (work locally)
Bind to open channel and block = causes cell to stay in inactivated state for long time
Use dependent blockade
Target unhealthy, depolarized tissue > normal healthy = fewer cardiac effects
Short 1/2 life = need IM or IV

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15
Q

Flecainide (1c)

A

Potent Na+ channel blocker
His purkinje system, supraventricular arrythmias
ONLY use short-term because increased death do to proarrythmic

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16
Q

Propanolol (2)

A

Block B-Adrenergic receptor (ca2+ channel in the slow tissue AV and SA node)
Decreased HR and contraction
LONG-TERM survival benefits
Good for mild-moderate CHF (remodeling of the heart), but BAD for severe CHF (because reduce strength and rate of contraction)
Supraventricular arrythmias (decrease AV conduction, block re-entry arrythmia thru AV)

Adverse: too much B blocking = block SA and AV node, worsened angina w/ withdrawal (due to upregulation of adrenaline receptors), dyspnea

17
Q

Amiodarone (3)

A 
K+ channel blocker - prolonged AP duration
BLOCKS EVERYTHING (Na+, Ca2+, A and B-adrenergic receptors) - effective, but side effects
LONG 1/2 life - extensively tissue bound (2 weeks-3 months) *side effects may be later*
75% long-term adverse effects
Side effect profile is well defined -- still widely used
18
Q

Amiodarone side effects

A

Tissue bound - microdeposits in eye, skin (photosensitivity, blue grey skin)
Neurologic side effects (channels in brain) - motor tremor
Hypotension
**Life threatening pulmonary toxicity (MOST WORRISOME - MONITOR LUNG FUNCTION)

19
Q

Amiodarone drug interactions

A

Drug in tissues for long time

  • Digoxin and warfarin
  • w/ B-blocker or Ca2+ channel blocker can cause AV block and sinus arrest, worsen CHF
20
Q

Sotalol (3)

A

B-blocker
L-isomer NON-selective B- blocker
D-isomer blocks K+ channels (torsade de pointes)

21
Q

Dofetilide (tikosyn) (3)

A

Selective blocker of ONLY CARDIAC K+ channels
Adverse: torsades de pointes
FEW extracardiac effects
only in clinics with special training

22
Q

Verapamil and Dilitazem (4)

A

Ca2+ channel blockers
suppress upstroke of AP (decrease excitability and contractibility at SA and AV node)
First choice for supraventricular tachycardia
Short 1/2 life = 4min (heart can stop for minutes)
Adverse: reflex tachycardia, VFIB (misdiagnose), AV block, constipation
interact with digoxin

23
Q

Adenosine

A

Adenosine receptor agonist
Open K+ channel (hyperpolarize AV node) = stop transmission
IV bolus or paroxysmal tachycardia - SHORT HALF LIFE (SECONDS) - better than verapamil, not life-threatening if heart stops (heart stops for seconds)

24
Q

PR interval

A

AV node conduction time

Increased by CA2+ blockers

25
Q

QRS complex

A

Purkinje fiber/ventricular conduction time

Prolonged by Na+ channel blockers

26
Q

QT interval

A

ventricular AP

Prolonged by K+ channel blocker (torsades de pointes)

27
Q

CHF treatment

A 
Reduce workload of heart
Restrict Na+
Give diuretics
ACE inhibitors 
B blockers
aldosterone antagonists
28
Q

Digoxin

A

Cardiac glycoside
BOTH direct effects on heart and indirect on autonomic nervous system
Direct&raquo_space; CHF
Ionotropic effect inhibit Na+/K+/ATPase, and parasympathomimetic
NARROW TOXIC RANGE
Not first line

29
Q

First line treatments for CHF

A

Diuretics
Ace inhibitors
Beta blockers

30
Q

Diuretics

A

Reduce salt and water retention (decrease BP and afterload and preload)
loop diuretics&raquo_space; K+ diuretics

31
Q

ACE inhibitors

A

Block conversion of angiotensin I to angiotensin II (active)

reduce preload by decreasing Na+ reaborption = H20 excretion

32
Q

Angiotensin AT1 Receptor antagonist (losartan)

A

Block AT1 receptor before angiotensin II effects
Same as ACE inhibitor effects
only for patients that do not tolerate ACE

33
Q

Mineralocorticoids (aldosterone) blockers

A

Prevent aldosterone from uptaking Na+ and H20

act like ACE and AT1

34
Q

Bet blockers

A

improve mortality by reducing ventricular remodeling

NOT USED IN SEVERE

35
Q

Vasodilators (hydralazine)

A

Activate K+ channel in VSM = K+ enter and hyperpolarize the cell and less likely to contract
Reduce afterload
Use instead of dihydropyrimidines to avoid CA2+ channel blockers

Pharmacology Exam 5 (3 decks)

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