Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology Exam 2 > 21 - 24 - Cardiac Arrhythmias > Flashcards

21 - 24 - Cardiac Arrhythmias Flashcards

1
Q

What is excitability?

A

The ability for a cell to respond to an external electrical stimulus (usually in the form of an action potential)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is automaticity?

A

The ability for a cell or region of cells to initiate an action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is conductivity?

A

The ability of a cell or region of cells to receive and transmit an action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is dromotropism?

A

The ability to alter the rate of electrical conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is refractoriness?

A

The inability of a cell to receive and transmit an action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Resting cell - Potassium

A

Potassium (K+) is very high inside the cell and low outside the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Resting cell - Sodium

A

Sodium (Na+) is high outside the cell and low inside the cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Resting cell - Calcium

A

Calcium (Ca++) is low outside the cell and REALLY low inside the cell.

This is advantageous for muscle contraction, which requires calcium for cross bridge cycling at the level of the actin and myosin filaments, and allows for exquisite sensitivity of the muscle to small changes in intracellular calcium concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Five phases of an action potential

A
  • Phase 0 = rapid upstroke, depolarization
  • Phase 1 = early repolarization
  • Phase 2 = plateau phase
  • Phase 3 = rapid repolarization
  • Phase 4 = resting membrane potential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Phase 0

A
  • Rapid influx of sodium
  • Fast phase due to opening of sodium channels
  • Sodium ions and positive charges really want to get inside the cell, so the depolarization occurs rapidly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Phase 1

A

Early repolarization

  • Sodium channels close, but some potassium channels open
  • Repolarization is incomplete
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Phase 2

A

Plateau

  • Membrane potential is approximately ZERO (which is very important for ECGs!!)
  • The plateau occurs due to slow calcium channels (which must be matched by an equal and opposite force by potassium channels - offsets the calcium flow)
  • Requires concurrent movement opposite to calcium
  • Allows blood to be ejected from the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Phase 3

A

Rapid repolarization

  • More calcium channels are closing
  • More potassium channels are opening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Phase 4

A

Resting membrane potential

  • Only potassium channels are open
  • Resting potential is maintained until the next stimulus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where in the heart do we find different types of action potentials?

A

Nodal tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How many phases are there of cardiac action potentials in nodal tissue?

A

Three

  • Phase 0
  • Phase 3
  • Phase 4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe phase 0

A
  • Once threshold potential is met, calcium channels open
  • “No” fast sodium channels
  • Slow response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe phase 3

A

After depolarization, potassium channels open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe phase 4

A

“Funny current” slowly depolarizes the cell

  • Progressive reduction in potassium efflux
  • Progressive increase in calcium influx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In terms of phase 0, what is the main difference between nodal and non-nodal tissues?

A

Nodal tissue
- phase 0 depolarization is due to Ca2+ influx

Non-nodal tissue
- phase 0 depolarization is due to Na+ influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Define ERP

A

Effective refractory period

The duration of the AP during which the cell is not responsive to an additional stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Define APD

A

Action Potential Duration

The entire duration of an action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why is the ERP/APD ratio relevant?

A

Two ways…

Electrophysiologically

  • ERP/APD ratio determines the ability of abnormal impulses to depolarize the tissue
  • The lower the ERP/APD ratio, the easier for the tissue to be depolarized by abnormal impulses

Pharmacologically
- Most antiarrhythmic agents share the ability to prolong refractoriness relative to their effects on action potential duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the two categories (etiologies) of arrhythmias?

A
  • Disorders of impulse formation

- Disorder of impulse conduction

25
Q

What are the different types of disorders of impulse formation?

A
  • No change in original pacemaker site (sinus tachycardia)
  • Change in original pacemaker site (ectopic foci)
  • Triggered activities (early and delayed after-depolarizations)
26
Q

What does a “triggered activity” mean?

A

Abnormal upstrokes only occur after an initial normal, or “triggering” upstroke, and so are termed triggered rhythms

27
Q

What is an EAD or early after depolarization?

A
  • Key abnormality is the prolonged AP
  • This can be caused by a slow HR, hypokalemia, or AP prolonging drugs
  • Phase 3 of the action potential is interrupted by an EAD before the AP is back down to resting membrane potential
28
Q

What type of cells do we typically see EADs in?

A

Purkinje cells

29
Q

If the EAD causes functional reentry in the ventricles, what is the result?

A

EADs triggering functional reentry across the ventricular wall (transmural re-entry) causes torsades de pointes (TdP), a common polymorphic ventricular tachycardia seen commonly as a result of long QT interval (congenital or acquired).

30
Q

What is a DAD or delayed after depolarization?

A
  • An abnormal action potential which occurs in conditions of intracellular Ca++ overload in the sarcoplasmic reticulum
  • A normal action potential will be followed by a mini depolarization hump - a DAD
31
Q

What problems are created by the present of a DAD following a normal action potential?

A
  • If this DAD reaches threshold, a secondary triggered beat or beats may occur.
  • DAD-mediated triggered beats are more frequent when the underlying heart rate is rapid
32
Q

What are the different types of disorders of impulse conduction?

A
  • AV nodal block
  • Ventricular re-entry
  • AV nodal re-entry (PSVT, PAT, WPW)
33
Q

What is an AV nodal block?

A

Recall from cardio…

  • 1st degree = prolonged PR interval
  • 2nd degree = not all p waves lead to a QRS complex (progressive then random)
  • 3rd degree = complete dissociation between p waves and QRS intervals
34
Q

What are reentry disorders?

A
  • reentry represents one of the most common mechanisms of tachycardias
  • the condition for this mechanism is the existence of conduction routes with different conduction velocity
  • This difference may be functional or organic (anatomic)
35
Q

What is AV Nodal Reentrant Tachycardia (AVNRT)?

A
  • Premature atrial impulse finds the fast pathway refractory, allowing conduction only down the slow pathway
  • By the time the impulse reaches the His bundle, the fast pathway may have recovered, allowing retrograde conduction back up to the atria—the resultant “circus movement” gives rise to slow-fast atrioventricular nodal re-entrant tachycardia
36
Q

What are the consequences of arrhythmias?

A
  • Compromise of mechanical performance
  • Proarrhythmic/ arrhymogenic
  • Thrombogenesis
37
Q

Describe the compromise of mechanical performance

A
  • Disorders of cardiac arrhythmia affect ventricular stroke volume directly, leading usually to decreases in cardiac output
  • This may accompany symptoms of congestion.
38
Q

Describe proarrhythmic/arrhythmogenic

A
  • Many arrhythmias, when not corrected, may lead to more severe forms of arrhythmias.
  • For examples, multiple ventricular premature beats/salvos may develop into ventricular tachycardia; or ventricular tachycardia may develop into ventricular fibrillation
39
Q

Describe thrombogenesis

A
  • Arrhythmias, especially chronic, facilitate the formation of thrombi in the heart chambers
  • This is particularly common when there are associated endocardial lesions
  • These thrombi may follow the blood flow to cause vessel occlusion in the periphery
  • Atrial flutter and fibrillation are commonly associated with thrombi
40
Q

What are the four ways in which antiarrhythmic drugs work?

A

Antiarrhythmics work by slowing the automatic rhythm of the heart in one of four ways

  • Decrease phase 4 slope (more time between action potentials due to reaching the threshold for depolarization more slowly)
  • Increase threshold potential
  • Increase maximum diastolic potential (make resting potential more negative - further away from threshold)
  • Increase APD (action potential duration)
41
Q

Other than slowing down the automatic rhythm, what is another way for a drug to be anti-arrhythmic?

A

Decrease sensitivity

The “refractoriness” against abnormal stimuli can be increased by drugs that block Na+ channels or drugs that increase APD

42
Q

What is the Sicilian Gambit?

A
  • This classification system is based on the differential effects of antiarrhythmic drugs on 1) channels, 2) receptors, and 3) transmembrane pumps
  • The grouping is based primarily on the predominant action of drugs but also considers the other ancillary actions that may be clinically relevant
43
Q

What are the names of the drug classes in the Sicilian Gambit?

A
  • Ia, Ib, Ic
  • II
  • III
  • IV
  • Misc
44
Q

Describe Class I drugs

A
  • Drugs having class I action possess “local anesthetic” or “membrane stabilizing” activity.
  • Their predominant action is to block the fast, inward Na+ channel.
  • This produces a decrease in the maximum depolarization rate (Vmax) of the action potential (phase 0) and slows intracardiac conduction.
  • These agents have been further sub-classified as belonging to either class IA, IB, or IC on the basis of their relative effects on specific aspects of intracardiac conduction and refractoriness.
45
Q

Which drugs belong to class Ia?

A
  • Quinidine
  • Procainamide
  • Dysopyramide
46
Q

Describe the general mechanism of action of all class Ia drugs

A
  • Moderate binding to Na+ channels –> moderate effects to slow phase 0 of the AP
  • Block K+ channels –> delayed phase 3, prolonged QRS & QT durations
  • Block Ca2+ at high doses –> depressed phase 2 in myocardial tissue and phase 0 in nodal tissue
47
Q

Which drugs belong to class Ib?

A
  • Lidocain
  • Phenytoin
  • Mexiletin
  • Tocainide
48
Q

Describe the general mechanism of action of all class Ib drugs

A
  • Bind weakly to Na+ channels –> weak effect on phase 0 depolarization
  • Accelerate phase 3 repolarization –> shorten APD and QT.
  • Little effect on PR, QRS or QT intervals at usual doses.
  • Effective in digitalis and MI-induced arrhythmias
49
Q

Which drugs belong to class Ic?

A
  • Propafenone
  • Flecainide
  • Morizicine
50
Q

Describe the general mechanism of actino of all class Ic drugs

A 
- Potent Na+ channel inhibitors
(strongest binders to Na+ channels among class I agents) -->
- Lengthen PR interval, QRS and APD
- Little effect on repolarization –> QT unchanged
51
Q

Which drugs belong to class II?

A

Beta adrenergic antagonists

52
Q

What are the general properties of class II drugs?

A
  • Decrease SA nodal automaticity
  • Decrease AV nodal conduction
  • Decrease ventricular contractility
  • Effective for supraventricular arrhythmias due to excessive sympathetic activity
  • Not very effective in severe arrhythmias such as VT
53
Q

What is very clinically important to remember about class II drugs?

A

THEY ARE THE ONLY ANTI-ARRHYTHMIC DRUGS FOUND TO BE CLEARLY EFFECTIVE IN PREVENTING SUDDEN CARDIAC DEATH IN PATIENTS WITH PRIOR MI

54
Q

Which drugs belong to class III?

A
  • Dronedarone
  • Amiodarone***
  • Sotalol
  • Ibutilide
  • Dofetilide
55
Q

What are the general properties of class III drugs?

A
  • Have multiple effects at K+, Ca2+, Na+ channels and β receptors
  • Main effect: prolong phase 3 repolarization –> increase QT interval
  • Useful for ventricular re-entry/fibrillatory arrhythmia
  • EFFECTIVE IN MANY TYPES OF ARRHYTHMIAS
56
Q

Which drugs belong to class IV?

A

Calcium channel antagonists that preferentially act on cardiac tissue ***

  • Verapamil
  • Diltiazem
57
Q

What are the general properties of class IV drugs?

A
  • Depress SA nodal automaticity, AV nodal conduction
  • Decrease ventricular contractility
  • Similar in utility to class II antiarrhythmic agents with primary effects on nodal phase 0 depolarization (Ca2+ channels)
58
Q

What are the two drugs categorized under “miscellaneous”?

A
  • Adenosine

- Digoxin (in heart failure section - not here)

Pharmacology Exam 2 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions