Cardiac Flashcards
Atrial action potentials compared to ventricular
shorter plateau due to larger K+ outflow current than Ca2+ current
Do not have Na+ channels, must target the Ca2+ channels
Arrythmia
Timing or path of electrical depolarization is altered:
- abnormal initiation of cardiac action potential (site or timing)
- abnormal conduction pathway
Ectopic pacemaker
tissue that does not have automaticity spontaneously generates an AP
Usually following ischemia (O2 is out for K+/ATPase)
After-depolarization
multiple APs initiated by single incoming AP
- Early depolarization - AP rise off plateau (prolonged AP from K+ channel blocker)
- Delayed after depolarization (Ca2+ overload)
Early depolarization
K+ channel blocker
Torsade de pointes
Delayed after depolarization
Digoxin
Ca2+ overload (rise from RP)
Abnormal conduction pathway
- Non-conductive tissue in the center
- Unidirectional block so anterograde impulse is extinguished by retrograde is transmitted
- Retrograde impulse do not enter refractory tissue
Treat re-entry arrythmias
Increase the refractory period (K+ channel blocker)
Types of arrythmias
- Premature ventricular beat
- Atrial or ventricular tacchycardia (HR 100-200bpm)
- Supraventricular tachycardia
- Paroxysmal tachycardia
- Flutter (rapid regular contractions 200-350bpm)
Atrial flutter
Treat with Ca2+ Channel blocker
Vaughan williams classification
- Na+ channel blocker (fast tissue)
- Beta-blocker (slow tissue)
- K+ channel blocker (re-entry arrythmia)
- Ca2+ channel blocker
Quinidine (1a)
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
Procainamide (1a)
Na+ channel blocker
K+ channel
Lidocaine (1b)
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
Flecainide (1c)
Potent Na+ channel blocker
His purkinje system, supraventricular arrythmias
ONLY use short-term because increased death do to proarrythmic
Propanolol (2)
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
Amiodarone (3)
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
Amiodarone side effects
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)
Amiodarone drug interactions
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
Sotalol (3)
B-blocker
L-isomer NON-selective B- blocker
D-isomer blocks K+ channels (torsade de pointes)
Dofetilide (tikosyn) (3)
Selective blocker of ONLY CARDIAC K+ channels
Adverse: torsades de pointes
FEW extracardiac effects
only in clinics with special training
Verapamil and Dilitazem (4)
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
Adenosine
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)
PR interval
AV node conduction time
Increased by CA2+ blockers
QRS complex
Purkinje fiber/ventricular conduction time
Prolonged by Na+ channel blockers
QT interval
ventricular AP
Prolonged by K+ channel blocker (torsades de pointes)
CHF treatment
Reduce workload of heart Restrict Na+ Give diuretics ACE inhibitors B blockers aldosterone antagonists
Digoxin
Cardiac glycoside
BOTH direct effects on heart and indirect on autonomic nervous system
Direct»_space; CHF
Ionotropic effect inhibit Na+/K+/ATPase, and parasympathomimetic
NARROW TOXIC RANGE
Not first line
First line treatments for CHF
Diuretics
Ace inhibitors
Beta blockers
Diuretics
Reduce salt and water retention (decrease BP and afterload and preload)
loop diuretics»_space; K+ diuretics
ACE inhibitors
Block conversion of angiotensin I to angiotensin II (active)
reduce preload by decreasing Na+ reaborption = H20 excretion
Angiotensin AT1 Receptor antagonist (losartan)
Block AT1 receptor before angiotensin II effects
Same as ACE inhibitor effects
only for patients that do not tolerate ACE
Mineralocorticoids (aldosterone) blockers
Prevent aldosterone from uptaking Na+ and H20
act like ACE and AT1
Bet blockers
improve mortality by reducing ventricular remodeling
NOT USED IN SEVERE
Vasodilators (hydralazine)
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
