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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
What antiarrhythmic class leads to slowed repolarization and consequently increased duration of AP and increased refractory period?
Class III - K+ Channel Blockers
26
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?
Class IV - Ca2+ Channels
27
What Class IA Antiarrhythmic drugs do we need to recognize?
* Quinidine * Procainamide * Disopyramide "The **Qu**een **Proc**laims **Diso**'s **Pyramid**."
28
What Class IB Antiarrhythmic drugs do we need to recognize?
* Lidocaine * Mexilitine * Tocainide (Mexican drugs: Lido, Mexi, Toca)
29
What Class IC Antiarrhythmic drugs do we need to recognize?
* Flecainide * Propafenone * Moricizine ("**Mo**m, **C**an I have **F**ries, **P**lease?")
30
What Class II Antiarrhythmic drugs do we need to recognize?
* Beta-blockers * Propanolol * Acebutolol * Esmolol * Sotalol
31
What Class III Antiarrhythmic drugs do we need to recognize?
* K+ Channel Blockers * Amiodarone * Ibutilide * Dofetilide * Sotalol ("**AIDS"**)
32
What Class IV Antiarrhythmic drugs do we need to recognize?
* Ca2+ Channel Blockers * Dihydropyridines (nifedipine) * Non-dihydropyridines * Verapamil * Diltiazem
33
What Class V Antiarrhythmic drugs do we need to recognize?
* Misfits * Adenosine * Digitalis
34
What are the effects of gravity on cardiovascular function?
* 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
What are the effects of zero-gravity on cardiovascular function?
* 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
What are the basics of vascular smooth muscle contraction?
* Ca2+ + Calmodulin =\> activates MLCK * MLCK + MLC =\> MLC-PO4 * MLC-PO4 + Actin =\> CONTRACTION! * MLC-PO4 + MLCP =\> Myosin-LC =\> RELAXATION!
37
What is the normal range for right ventricular pressure?
25/5
38
What is the normal range for right atrial pressure?
\<5
39
What is the normal range for aortic pressure?
120/80
40
What is the normal range for left atrial pressure?
\<12
41
What is the normal pressure for left ventricular?
120/0
42
What is the normal pressure range for the Pulmonary artery?
25/10
43
What are the basics of vascular smooth muscle contraction?
* 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
How do you calculate Ejection Fraction?
(EDV - ESV) / EDV
45
How do you interpret ejection fraction?
* Left ventricular EF \< 40% =\> systolic dysfunction * normal is \>70%
46
What are the specific variances in arterial pressure regulation and vascular control in the lungs?
* Hypoxia causes vasoconstriction * only well-ventilated areas are perfused
47
What are the specific variances in arterial pressure regulation and vascular control in the Heart?
* Local metabolites (vasodilatory) * CO2 * adenosine * NO
48
What are the specific variances in arterial pressure regulation and vascular control in the Brain?
* Local metabolites (vasodilatory) * CO2 (pH)
49
What are the specific variances in arterial pressure regulation and vascular control in the Kidneys?
* Myogenic and tubuloglomerular feedback * Sympathetic
50
What are the specific variances in arterial pressure regulation and vascular control in the Skeletal Muscle?
* Local metabolites * lactate * adenosine * K+ * H+ * CO2
51
What are the specific variances in arterial pressure regulation and vascular control in the skin?
* Sympathetic stimulation = most important mechanism * temperature control
52
How do you predict the direction of bulk flow in transcapillary fluid movement within a tissue?
* 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
What are the determinants of myocardial oxygen consumption?
* 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
How do Ibutilide and Dofetilide effect the EKG tracing?
* Class III - K+ channel blockers * Increase QT interval
55
How do Procainamide, quinidine, and disopyramide effect EKG tracings?
* Class IA - Na+ channel blockers * increase QRS duration * increase QT interval
56
How do Propranolol and esmolol effect EKG tracings?
* Class II - Beta-blockers * increase PR interval
57
How does Amiodarone effect EKG tracings?
* Class III - K+ channel blocker * also has IA, II, and IV activity * Increase QT interval * Increase PR interval * Increase QRS duration
58
How does Sotalol effect EKG tracings?
* Class III - K+ channel blocker * also has beta-blocker activity * Increase PR interval * Increase QT interval
59
How does Verapamil effect EKG tracings?
* Class IV - Ca2+ channel blocker * Increase PR interval
60
How does Adenosine effect EKG tracings?
Increased PR interval
61
What are the direct processes of the various forms of shock?
* 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
What are the compensatory processes of the various forms of shock?
* 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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