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Cardiology > Anti-arrhythmics > Flashcards

Anti-arrhythmics Flashcards

1
Q

Beta adrenergic receptors in heart, vascular SM, kidney?

A

B1
B2
B1

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2
Q

B1 receptor agonist effect in heart?

A

increase in contractile force (myocardium), increase in HR (SA, AV nodes) – via inc cAMP and inc intracellular calcium

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3
Q

B2 receptor agonist effect in vasculature?

A

smooth muscle relaxation via inc cAMP and dec intracellular Ca

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4
Q

Epi and NE affinities for B1, B2, and alpha receptors?

A
  • NE void of activity at B2 (high dissociation constant) at therapeutic doses
  • Epi has equal affinity at B1, B2
  • same affinities for alpha receptors
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5
Q

Consequences of vascular alpha1 receptor activation?

A

inc IP3, DAG and inc intracellular calcium = vasoconstriction

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6
Q

How does concentration affect the effects of epinephrine on vascular alpha1 and beta2 receptors?

A
  • low conc = B2 activation (Kd = 800 nm)

- high conc = A1 activation (Kd = 5000 nm)

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7
Q

What reflex responses do drugs that INC and DEC BP have?

A
  • INC: trigger reflex slowing of heart via M2 receptors

- DEC: trigger reflexing increase in HR via B1 receptor

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8
Q

What is oral epi not used?

A

rapid metabolism in gut via MAO

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9
Q

What type of drug is Terazosin?

A
  • Alpha1 blocker in vasculature, prostate

- 2nd line HTN drug

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10
Q

What drug type is phenylephrine? Uses?

A
  • alpha1 agonist = pressor effect
  • raise BP in shock/sepsis/surgery
  • Tx of orthostatic hypotension
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11
Q

What are 3 B1 agonists are used to provide inotropic support in acute Tx of shock and HF?

A
  • milrinone, dopamine, dobutamine

- IV, acute care only

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12
Q

What distinguishes first, second and 3rd gen beta blockers?

A
  • first = B1, B2
  • second = B1 only
  • third = either alpha blocker also or novel effects unrelated to beta blockade
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13
Q

Two AE’s associated with B2 blockade?

A

bronchospasm/inc in airway resistance

exacerbation of PVD

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14
Q

5 uses of B blockers?

A
  • HTN
  • ischemic HD (dec O2 consumption)
  • supraventricular tachyarrhythmias (block of SA/AV B1 receptors)
  • HF
  • following MI (dec O2 consumption)
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15
Q

What are the only two B blockers approved to Tx HF?

A
  • metoprolol
  • carvedilol
  • improve outcomes and dec morb/mort
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16
Q

Proposed mechanisms of B blockers in HF Tx?

A
  • B1R upregulation
  • antagonism of enhanced sum activity
  • blockade of hypertrophic growth/ROS gen
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17
Q

CNS and cardio AE’s of all B blockers?

A

CNS: sedation, fatigue, impairment
CARDIO: hypotension, bradycardia

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18
Q

Which nonselective B blocker has a long 24 h half life?

A

Nadolol (propranolol was 1st useful BB)

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19
Q

Two selective BB widely used?

A

metoprolol and atenolol

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20
Q

Two BB that also block alpha activity?

A

Carvedilol (HF) and Labetalol (HTN)

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21
Q

Novel effects of carvedilol (HF)?

A
  • block alpha
  • block Ca channels
  • inc NO
  • antioxidant
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22
Q

Novel effects of nebivolol?

A
  • inc NO
  • vasodilator
  • good in HTN
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23
Q

What are the consequences of excess stim of beta receptor?

A
  • inactivation of receptor function
  • desensitization via G protein uncoupling from receptor (receptor phosphorylated)
  • down regulation = loss of receptors from cell surface
  • role in HF
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24
Q

Difference between rhythm and rate control?

A

Rhy restores and maintains a completely normal heart beat (more effective, but toxic) - targets voltage-gated Na/K channels

Rate slows ventricles and improves CO (atria still fibrillate - still clot risk) (more modest, but safe) - targets B receptors or L type Ca channels

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25
Q

Difference between mono and poly VTAC? Ex of poly?

A
  • mono has single origin/pathway

- poly = electrical pathways are wandering around ventricles –> Torsades de Points

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26
Q

How are the classes organized? (Vaughn Williams)

A 
I = Na+ block
II = B block
III = K+ block
IV = Ca block
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27
Q

What classes are effective in rate control?

A

affect AV node –> II, IV, digoxin

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28
Q

What drug is effective in AV-RT?

A

adenosine

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29
Q

What classes are effective in rhythm control?

A

I, III

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30
Q

How do rhythm control drugs work? ECG effects?

A
  • Na block slows gen of ventricular AP
  • K block of rapid and slow channels slows depolarization and prolongs cardiac AP (prolonged refractory period, widened QT interval)
  • prolonged PR by II, IV (slowed AV conduction)
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31
Q

Which current is easily blocked by many drugs and can cause cardiac toxicity? Ex?

A
  • rapid K+ depolarizing current

- erythromycin

32
Q

How do rate control drugs work? ECG effects?

A
  • B block reverses acceleration of AV node AP’s by SYM tone
  • Ca channel block slows generation of AV AP’s
  • Prolonged QT (slowed ventricular repolarization)
    - -> IA (intermediate) only because it also blocks K+ channels
  • Widened QRS (slowed V conduction)
33
Q

Cause, consequence and Tx of EAD?

A
  • abnormally long AP (K+ blocker tox)
  • Torsade de pointes (polymorphic VTAC)
  • shorten AP (IV Magnesium, inc HR)
33
Q

Cause, consequence and Tx of DAD?

A
  • toxic cytosolic Ca levels (ischemia, + inotropic drug overstim)
  • PVC, monomorphic VTAC
  • relieve Ca overload
33
Q

Drug of Class IB?

A
  • lidocaine (weakest Na+ channel block)
  • short DOA
  • injection, hepatic elim, local anesthetic
33
Q

Drug of Class IB?

A
  • lidocaine (weakest Na+ channel block, smallest - inotropic effect)
  • short DOA
  • injection, hepatic elim, local anesthetic
34
Q

Cardiac uses of lidocaine?

A

Suppress VTAC once they appear, particularly following MI

34
Q

Cardiac uses of lidocaine?

A

Suppress VTAC once they appear, particularly following MI

35
Q

Preferential effects of Na+ channel blockers on cardiac myocytes?

A
  • preferentially affects rapidly arrhythmic cells
  • drugs bind during AP when channels are open and unbind at rest
  • rapidly firing cells leave less time for drug to unbind increasing the # of blocked channels
35
Q

Preferential effects of Na+ channel blockers on cardiac myocytes?

A
  • preferentially affects rapidly arrhythmic cells
  • drugs bind during AP when channels are open and unbind at rest
  • rapidly firing cells leave less time for drug to unbind increasing the # of blocked channels
36
Q

How do Na+ channel blockers affect reentrant rhythm generation?

A
  • RE currents involves rapidly beating cells
  • inhibits abnormal AP conduction in cells participating in a fast rate of reentry current production = blocker accumulation
37
Q

What is a common AE among Class I drugs?

A

promotion of new monomorphic VTAC = proarrhythmias –> potentially LETHAL

38
Q

How do Na+ channel blockers affect DAD?

A
  • suppress arrhythmias triggered by DAD’s by preventing the generation of unusually rapid AP’s
39
Q

Risks for pro arrhythmia development with Na+ channel blockers?

A
  • damaged, fibrotic, chaotic hearts have multiple reentry circuits that conduct current with variable AP length and timing = dormant circuits
40
Q

How do Na+ channel blockers contribute to activation of dormant circuits and pro-arrhythmias?

A
  • dormant circuits, AP’s are too short and cells are still refractory when depo swings back around
  • drugs slow down AP conduction velocity – since it takes longer for AP to get there, cells are no longer refractory and can depolarize
41
Q

What is the strongest Na+ channel blocker? Class?

A

Flecainide - IC, oral, hepatic elim

42
Q

What causes the negative inotropic effect of Na+ channel blockers?

A

Widened QRS complex due to slowed generation of V AP –> heartbeat spreads through the ventricles slowly so contraction isn’t as synchronous or forceful

43
Q

Flecainide is DOC for what type of patient?

A

low-risk AFIB (prophylaxis or termination) – used as ‘pill in pocket’

44
Q

Intermediate strength Na+ channel blocker + K+ blocker? Class?

A
  • procainamide, IA, injection, renal/hepatic elim
45
Q

Quinidine Class IA can be used additionally for:

A
  • malaria (similar to quinine)

- pseudobulbar affect w/ detromethorphan (uncontrollable laughing/crying in patients with underlying neuro disease)

46
Q

What is procainamide’s primary use? Why so limited?

A
  • life-threatening VTAC

- serious AE’s

47
Q

While Na+ channel blockers can activate a dormant reentry current, K+ blockers can de-activate it. How?

A
  • Na+ blockers slow gen of AP’s so that origin is no longer refractory when the impulse comes back around
  • K+ blockers elongate AP’s/refractory period in the circuit so that the origin is still refractory when the impulse comes back around
48
Q

Additional risks associated with Procainamide (besides Na+ pro arrhythmia, - inotropism)?

A
  • K+ channel block pro-arrhyhmias (Torsades de Pointes can develop due to block of rapid K+ current = abnormally prolonged AP’s yielding EAD’s)
  • Long-term oral: bone marrow suppression, SLE
49
Q

What is unique about Sotalol?

A

both class II (non-selective) and III actions

50
Q

Three ECG effects of Sotalol?

A
  • prolonged QT (K+ channel block)
  • prolonged PR (beta adrenergic block)
  • dec HR (beta adrenergic block)

(B block has both nodal and myocardial effects)

51
Q

Cause of Sotalol’s neg inotropism?

A

Beta block causes inhibitory effects on HR and AV conduction

52
Q

Three AE’s of Sotalol?

A
  • bronchoconstriction/exacerbation of PVD (B2 block)
  • inotropism
  • proarrhythmia (K+ –> EAD –> TDP)
53
Q

Primary use of Sotalol? Two specific patient sub-groups?

A
  • prophylaxis of AFIB/VTAC
  • ischemic disease = beta block useful (dec O2 consumption)
  • implantable defib = lowers defib threshold and dec # of shocks
54
Q

Which Class III drug is available in oral AND IV forms? Use? Off label?

A
  • Amiodarone
  • IV = suppression of VTAC to prevent cardiac arrest
  • Oral = rhythm control in LVH, HF
  • AFIB off-label
55
Q

Why is amiodarone such a good anti-arrhythmic?

A

MULTIPLE targets:

  • rapid and slow K+ channel block
  • weak Ca and Na channel block
  • weak non-competitive antagonist of alpha and beta adrenergic receptors
56
Q

Four long term AE’s?

A
  • LOW risk of pro-arrhythmia
  • pulmonary tox
  • hepatotox
  • skin and corneal micro-deposits
  • neuropathy – peripheral and optic nerves
57
Q

What is unusual about the structure of amiodarone? Potential associated AE’s?

A
  • IODINE
  • Type 1 thyrotoxicosis: inc TH syn
  • Type 2: thy inflamm –> TH release
  • hypothyroidism: most common; inhibits iodinases that convert T4 to T3
58
Q

What is the DOA of amiodarone?

A
  • LONG half life
  • large Vd
  • oral Tx requires high loading dose; highly tissue bound during long-term oral use
59
Q

What are two important drug interactions of amiodarone?

A
  • INC warfarin levels: inhibitor of CYP2C9 and CYP3A4

- INC digoxin levels: inhibitor of P-glycoprotein, a transporter involved in renal and biliary excretion of digoxin

60
Q

What drug class is most often used for rate control and why?

A
  • Class II = beta blockers

- AFIB – rate control lets more blood enter V in diastole = INC CO

61
Q

How do beta blockers function? ECG?

A
  • slow AP conduction across the AV node – some atrial beats will not result in V depolarization
  • prolonged P-R interval
62
Q

Two uses of propanolol?

A
  • AFIB

- V tach (DAD) due to Ca overload from ischemic damage/sympathetic overload = negative inotropic effect

63
Q

What are the Class IV drugs? Two classes?

A
  • dihydropyridine Ca channel blockers = majority

- non-dihydropyridine Ca channel blockers = verapamil, diltiazem

64
Q

Uses of dihydro Ca channel blockers vs non-dihydro?

A
  • Non’s are useful in arrhythmias, but dihydro’s are NOT –> only verapamil and diltiazem directly inhibit the SA/AV nodes and cardiac contractility
  • Both are useful in angina pectoris, HTN = VASODILATORY EFFECTS
65
Q

What are the two prototype Class IV drugs for RATE control of AFIB?

A

verapamil and diltiazem

66
Q

How do the Class IV drugs work?

A
  • block L type Ca channels

- slow the gen of AV nodal AP so each AP takes longer to cross the AV so fewer per min in AFIB

67
Q

What is one non-cardiovascular AE of CCB?

A

relaxation of smooth GI muscle = hypotension

68
Q

Three important drug interactions of CCB?

A
  • co-admin with other AV inhibitors (beta blockers) could cause complete AV block
  • inc DIGOXIN - inhibition of P-glycoprotein (renal and biliary excretion of drug)
  • Inc erythromycin levels via inhibition of CYP3A4 –> erythro blocks cardiac K+ channels!
69
Q

What drug is used specifically for episodic Tx of AV-reentry tachycardia? How does it work?

A
  • adenosine IV bolus
  • hyper polarizes via K+ channel activation and blocks AV node, stopping reentry to resynchronize fast and slow AV nodal pathways
70
Q

Which adenosine receptor subtype is therapeutic? Location? Effects?

A
  • A1 GPCR: SA/AV nodes; slowed HR, slowed AV nodal conduction
71
Q

Three AE’s of adenosine? Why are they usually not a problem?

A
  • cardiac arrest (nodal inhibition)
  • chest pressure (bronchoconstriction via A3 receptor in mast cells = histamine release)
  • flushing (vasodilation via A2 receptor in vasculature)
  • VERY short DOA
72
Q

Specific drug interaction of adenosine?

A

Dipyridamole (anti-platelet drug) inhibits adenosine uptake (potentiates effects of adenosine on platelets) = INC adenosine levels

Cardiology (6 decks)

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