Cardiac

Question 1

Atrial action potentials compared to ventricular

Answer 1

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

Question 2

Arrythmia

Answer 2

Timing or path of electrical depolarization is altered:

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

Question 3

Ectopic pacemaker

Answer 3

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

Question 4

After-depolarization

Answer 4

multiple APs initiated by single incoming AP

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

Question 5

Early depolarization

Answer 5

K+ channel blocker

Torsade de pointes

Question 6

Delayed after depolarization

Answer 6

Digoxin

Ca2+ overload (rise from RP)

Question 7

Abnormal conduction pathway

Answer 7

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

Question 8

Treat re-entry arrythmias

Answer 8

Increase the refractory period (K+ channel blocker)

Question 9

Types of arrythmias

Answer 9

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)

Question 10

Atrial flutter

Answer 10

Treat with Ca2+ Channel blocker

Question 11

Vaughan williams classification

Answer 11

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

Question 12

Quinidine (1a)

Answer 12

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

Question 13

Procainamide (1a)

Answer 13

Na+ channel blocker

K+ channel

Question 14

Lidocaine (1b)

Answer 14

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

Question 15

Flecainide (1c)

Answer 15

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

Question 16

Propanolol (2)

Answer 16

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

Question 17

Amiodarone (3)

Answer 17

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

Question 18

Amiodarone side effects

Answer 18

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)

Question 19

Amiodarone drug interactions

Answer 19

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

Question 20

Sotalol (3)

Answer 20

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

Question 21

Dofetilide (tikosyn) (3)

Answer 21

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

Question 22

Verapamil and Dilitazem (4)

Answer 22

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

Question 23

Adenosine

Answer 23

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)

Question 24

PR interval

Answer 24

AV node conduction time

Increased by CA2+ blockers

Question 25

QRS complex

Answer 25

Purkinje fiber/ventricular conduction time | Prolonged by Na+ channel blockers

Question 26

QT interval

Answer 26

ventricular AP | Prolonged by K+ channel blocker (torsades de pointes)

Question 27

CHF treatment

Answer 27

``` Reduce workload of heart Restrict Na+ Give diuretics ACE inhibitors B blockers aldosterone antagonists ```

Question 28

Digoxin

Answer 28

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

Question 29

First line treatments for CHF

Answer 29

Diuretics Ace inhibitors Beta blockers

Question 30

Diuretics

Answer 30

Reduce salt and water retention (decrease BP and afterload and preload) loop diuretics >> K+ diuretics

Question 31

ACE inhibitors

Answer 31

Block conversion of angiotensin I to angiotensin II (active) | reduce preload by decreasing Na+ reaborption = H20 excretion

Question 32

Angiotensin AT1 Receptor antagonist (losartan)

Answer 32

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

Question 33

Mineralocorticoids (aldosterone) blockers

Answer 33

Prevent aldosterone from uptaking Na+ and H20 | act like ACE and AT1

Question 34

Bet blockers

Answer 34

improve mortality by reducing ventricular remodeling | NOT USED IN SEVERE

Question 35

Vasodilators (hydralazine)

Answer 35

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