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CRRAB Week 5 - WLB > Nordgren's Final Exam Study > Flashcards

Nordgren's Final Exam Study Flashcards

1
Q

What is the concept of state-dependency?

A
  • Therapeutically useful channel-blocking drugs:
    • Bind readily to activated (phase 0) or inactivated (phase 2) channels
    • Bind poorly or not at all to rested channels
      • prevents drug binding in this state and/or promotes drug-dissociation from receptors when channels become rested
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2
Q

Why is state-dependency useful in antiarrhythmics?

A
  • State-dependency drugs block electrical activity when:
    • Fast tachycardia
      • Many channel activations and inactivations per unit time
    • Significant loss of resting potential
      • Many inactivated channels during rest
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3
Q

What are the important toxicities associated with Procainamide (Class IA)?

A
  • torsades de pointes
  • syndrome resembling lupus erythematosus
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4
Q

What are the important toxicities associated with Quinidine (Class IA)?

A

torsades de pointes

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5
Q

What are the important pharmacokinetics associated with Disopyramide (Class IA)?

A

Loading doses NOT recommended

(because of risk of precipitating heart failure)

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6
Q

What are the important toxicities associated with Lidocaine (Class IB)?

A

Prophylactic use may actually increase total mortality => therapeutic use not advised!

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7
Q

What are the important extracardiac effects associated with Mexiletine (Class IB)?

A

Significant efficacy in relieving chronic pain, especially due to diabetic neuropathy and nerve injury (off-label use).

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8
Q

What are the important cardiac effects associated with Flecainide (Class IC)?

A

Potent blocker of Na+ and K+ channels with slow unblocking kinetics (but does not prolong the AP or QT-interval).

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9
Q

What are the important cardiac effects associated with Propafenone (Class IC)?

A

Weak beta-blocking activity

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10
Q

What are the important toxicities associated with Amiodarone (Class III)?

A
  • Bradycardia
  • Heart block
    • in pts with preexisting SA/AV node disease
  • Drug accumulates in tissues
    • dose related pulmonary toxicity
    • abnormal liver fxn, hypersensitivity hepatitis
    • photodermatitis, gray-blue skin discoloration
    • corneal microdeposits (nearly ALL pts)
    • Hypo/Hyperthyroidism
  • Blocks peripheral conversion of T4 → T3 (source of inorganic iodine)
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11
Q

What are the important contraindications associated with Dofetilide (Class III)?

A
  • DO NOT USE IF:
    • long QT
    • bradycardia
    • hyopkalemia
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12
Q

What are the important cardiac effects associated with Ibutilide (Class III)?

A
  • Also slow inward Na+ activator
    • delays repolarization
      • inhibits Na+ channel inactivation → increases ERP
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13
Q

What are the important contraindications associated with Verapamil (Class IV)?

A
  • DO NOT USE IF:
    • Wolff-Parkinson-White
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14
Q

What are the important contraindications associated with Adenosine (Class V)?

A
  • DO NOT USE IF:
    • 2° or 3° AV Block
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15
Q

What are the important toxicities associated with Digitalis (Class V)?

A
  • GI distress
  • Hyperkalemia
  • Life-threatening arrhythmias (every type except a-fib & a-flutter)
    • increased automaticity
    • decreased AV conduction/AV nodal blockade
  • Narrow therapeutic index
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16
Q

What are the important drug interactions associated with Nitroglycerine (Antianginal)?

A
  • Synergistic hypotension with phosphodiesterase type 5 inhibitors such as Vardenafil
    • Viagra
    • Cialis
    • Levitra
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17
Q

What are the three traditional classes of Antianginal drugs?

A
  • Organic Nitrates
    • Nitro, Isosorbide dinitrate/mononitrate
  • Ca2+ Channel Blockers
    • Very Nice Drugs
    • Verapamil, Nifedipine, Diltiazem
  • Beta-Adrenoceptor Blockers
    • Atenolol, Metoprolol, Propanolol
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18
Q

What is the gross mechanism of action of Nitrates/Nitrites for treating angina?

A
  • Releases NO in smooth muscle → activates guanylyl cyclase → increases cGMP
    • venous dilation
      • decrease preload
      • decrease pulmonary vascular resistance
      • decrease LV end-diastolic pressure
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19
Q

What is the gross mechanism of action of Ca2+ Channel Blockers for treating angina?

A
  • Nonselective block of L-type Ca2+ channels in vessels and heart
    • Reduced vascular resistance
    • Decreased HR
    • Decreased contractility
    • Decreased aortic diastolic pressure
    • Increase total coronary blood flow (during diastole)
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20
Q

What is the gross mechanism of action of β-Adrenoceptor Blockers for treating angina?

A
  • Nonselective (Propanolol) or β1-selective (Atenolol, Metoprolol) competitive antagonist at β-adrenoceptors
    • Decrease HR, CO, BP
      • decreases myocardial oxygen demand
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21
Q

What antiarrhythmic class leads to reduced rate and magnitude of depolarization, prolonged action potential, increased effective refractory period, and increased QT interval?

A

Class IA - Na+ Blockers

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22
Q

What antiarrhythmic class leads to a reduced rate and magnitude of depolarization, decreased duration of action potential, and shortened refractory period?

A

Class IB - Na+ Blockers

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23
Q

What antiarrhythmic class leads to a reduced rate and magnitude of depolarization, prolonged refractory period, and minimal effect on AP duration?

A

Class IC - Na+ Channel Blockers

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24
Q

What antiarrhythmic class leads to decreased AV node conduction velocity and increased AV node refractory period?

A

Class II: Beta-Adrenoceptor Blockers

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25
Q

What antiarrhythmic class leads to slowed repolarization and consequently increased duration of AP and increased refractory period?

A

Class III - K+ Channel Blockers

26
Q

What antiarrhythmic class leads to shortened plateau phase of fast response AP (consequently reducing the force of contraction), reduced rate of depolarization/slow rise of AP and consequent prolonged repolarization in slow response APs?

A

Class IV - Ca2+ Channels

27
Q

What Class IA Antiarrhythmic drugs do we need to recognize?

A
  • Quinidine
  • Procainamide
  • Disopyramide

“The Queen Proclaims Diso’s Pyramid.”

28
Q

What Class IB Antiarrhythmic drugs do we need to recognize?

A
  • Lidocaine
  • Mexilitine
  • Tocainide

(Mexican drugs: Lido, Mexi, Toca)

29
Q

What Class IC Antiarrhythmic drugs do we need to recognize?

A
  • Flecainide
  • Propafenone
  • Moricizine

(“Mom, Can I have Fries, Please?”)

30
Q

What Class II Antiarrhythmic drugs do we need to recognize?

A
  • Beta-blockers
    • Propanolol
    • Acebutolol
    • Esmolol
    • Sotalol
31
Q

What Class III Antiarrhythmic drugs do we need to recognize?

A
  • K+ Channel Blockers
    • Amiodarone
    • Ibutilide
    • Dofetilide
    • Sotalol

(“AIDS”)

32
Q

What Class IV Antiarrhythmic drugs do we need to recognize?

A
  • Ca2+ Channel Blockers
    • Dihydropyridines (nifedipine)
    • Non-dihydropyridines
      • Verapamil
      • Diltiazem
33
Q

What Class V Antiarrhythmic drugs do we need to recognize?

A
  • Misfits
    • Adenosine
    • Digitalis
34
Q

What are the effects of gravity on cardiovascular function?

A
  • Stand up (GRAVITY)
    • blood volume shift (legs & feet)
    • increased peripheral pressure
    • increase filtration
  • Decrease SV => CO => MAP
    • decrease baroreceptor firing => medulla
  • Sympathetic stimulation (vasoconstriction)
  • Skeletal muscle contracts
    • compression of vessels
  • After skeletal muscle contraction, veins & lymphatics relatively empty
    • NET = increased HR and TPR
  • If no compensatory mechanisms => vasovagal syncope
35
Q

What are the effects of zero-gravity on cardiovascular function?

A
  • Immediate = fluid shift from lower to upper body
    • distended head/neck veins, facial edema, nasal congestion, decreased leg volume
    • stimulates cardiopulmonary mechanoreceptors => influences renal fxn
  • Delayed = reduced renal sympathetic drive
    • promotes fluid loss => weight loss => within a few days become hypovolemic
    • compenstory mechanisms to gravity not good => orthostatic hypotension
36
Q

What are the basics of vascular smooth muscle contraction?

A
  • Ca2+ + Calmodulin => activates MLCK
  • MLCK + MLC => MLC-PO4
  • MLC-PO4 + Actin => CONTRACTION!
  • MLC-PO4 + MLCP => Myosin-LC => RELAXATION!
37
Q

What is the normal range for right ventricular pressure?

A

25/5

38
Q

What is the normal range for right atrial pressure?

A

<5

39
Q

What is the normal range for aortic pressure?

A

120/80

40
Q

What is the normal range for left atrial pressure?

A

<12

41
Q

What is the normal pressure for left ventricular?

A

120/0

42
Q

What is the normal pressure range for the Pulmonary artery?

A

25/10

43
Q

What are the basics of vascular smooth muscle contraction?

A
  • Ca2+ complexes with calmodulin
    • complex activates Myosin light-chain kinase
  • MLC kinase allows ATP to phosphorylate MLC protein
  • MLC phosphorylation enables cross-bridge formation & cycling
    • CONTRACTION
    • depends on NET STATE of MLC phosphorylation
44
Q

How do you calculate Ejection Fraction?

A

(EDV - ESV) / EDV

45
Q

How do you interpret ejection fraction?

A
  • Left ventricular EF < 40% => systolic dysfunction
    • normal is >70%
46
Q

What are the specific variances in arterial pressure regulation and vascular control in the lungs?

A
  • Hypoxia causes vasoconstriction
    • only well-ventilated areas are perfused
47
Q

What are the specific variances in arterial pressure regulation and vascular control in the Heart?

A
  • Local metabolites (vasodilatory)
    • CO2
    • adenosine
    • NO
48
Q

What are the specific variances in arterial pressure regulation and vascular control in the Brain?

A
  • Local metabolites (vasodilatory)
    • CO2 (pH)
49
Q

What are the specific variances in arterial pressure regulation and vascular control in the Kidneys?

A
  • Myogenic and tubuloglomerular feedback
  • Sympathetic
50
Q

What are the specific variances in arterial pressure regulation and vascular control in the Skeletal Muscle?

A
  • Local metabolites
    • lactate
    • adenosine
    • K+
    • H+
    • CO2
51
Q

What are the specific variances in arterial pressure regulation and vascular control in the skin?

A
  • Sympathetic stimulation = most important mechanism
    • temperature control
52
Q

How do you predict the direction of bulk flow in transcapillary fluid movement within a tissue?

A
  • Starling forces: Net filtration rate =

K(Pcapillary–Pinterstitial) – (πcapillary–πinterstitial)

  • P : hydrostatic pressure
  • π : oncotic pressure
  • K : constant

+Net filtration = filtration

–Net filtration = reabsorption

53
Q

What are the determinants of myocardial oxygen consumption?

A
  • Myocyte contraction
    • increased tension => increase O2 demand
  • Heart rate
    • increased HR => more cycles of tension
  • Inotropy
    • increased inotropy => increased rate & magnitude of tension
  • Aortic pressure/Afterload
    • increased afterload => requires overcoming more tension
54
Q

How do Ibutilide and Dofetilide effect the EKG tracing?

A
  • Class III - K+ channel blockers
  • Increase QT interval
55
Q

How do Procainamide, quinidine, and disopyramide effect EKG tracings?

A
  • Class IA - Na+ channel blockers
  • increase QRS duration
  • increase QT interval
56
Q

How do Propranolol and esmolol effect EKG tracings?

A
  • Class II - Beta-blockers
  • increase PR interval
57
Q

How does Amiodarone effect EKG tracings?

A
  • Class III - K+ channel blocker
    • also has IA, II, and IV activity
  • Increase QT interval
  • Increase PR interval
  • Increase QRS duration
58
Q

How does Sotalol effect EKG tracings?

A
  • Class III - K+ channel blocker
    • also has beta-blocker activity
  • Increase PR interval
  • Increase QT interval
59
Q

How does Verapamil effect EKG tracings?

A
  • Class IV - Ca2+ channel blocker
  • Increase PR interval
60
Q

How does Adenosine effect EKG tracings?

A

Increased PR interval

61
Q

What are the direct processes of the various forms of shock?

A
  • Cardiogenic shock
    • myocardial failure → decreased cardiac contractility → dec CO → dec MAP → dec baroreceptor activity
  • Anaphylactic/Septic shock
    • vasodilator release → dec venous/arterial tone → dec filling pressure → dec central venous pressure → dec cardiac filling → dec CO (dec TPR) → dec baroreceptor activity
  • Neurogenic shock
    • dec sympathetics → dec arteriolar tone → dec TPR → dec mean arterial pressure → dec baroreceptor activity
62
Q

What are the compensatory processes of the various forms of shock?

A
  • FOR ALL TYPES (Cardiogenic, Hypovolemic, Anaphylactic/Septic, Neurogenic):
    • decreased parasympathetics → inc HR/inc contractility → inc CO
    • Increased Sympathetics → inc arteriolar/venous tone → dec capillary pressure → fluid absorption → inc TPR → inc CO → inc MAP

CRRAB Week 5 - WLB (5 decks)

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