Lecture 4 (Electrolytes and MIs) Flashcards

1
Q

The heart is reliant on what four ions for proper function?

A
  • calcium, sodium, and potassium for proper depolarization/repolarization.
  • magnesium.
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2
Q

In the heart, potassium is responsible for:

A
  • repolarization of all cardiac cells (pacemakers and plateaus).
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3
Q

In an ECG of a person with a severe potassium imbalance (hyper- or hypokalemia), you will see:

A
  • abnormal T waves (ventricular repolarization).
    • hyperkalemia = tented T waves.
    • hypokalemia = T wave flattening/inversion.
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4
Q

In the heart, calcium is responsible for:

A
  • slow and rapid depolarization of pacemaker cells and in the
  • plateau phase of myocyte depolarization.
  • Cross-bridge cycling and cardiac myocyte contraction.
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5
Q

In an ECG of a person with a severe calcium imbalance (hyper- or hypocalcemia), you will see:

A
  • abnormal QT segment.
    • hypercalcemia = short QT complex.
    • hypocalcemia = long QT complex.
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6
Q

What is this ECG suggesting?

A

hypocalcemia

  • Prolonged QT interval
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7
Q

How does hypocalcemia lead to a prolonged QT interval?

A
  1. Type L calcium channels (plateau phase) are regulated by both voltage and extracellular calcium levels.
  2. Low extracellular calcium levels: Type L channels open and stay open for a much longer time than normal.
  3. Lengthened plateau phase, repolarization (T wave) occurs later.
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8
Q

How does hypercalcemia lead to shortened QT intervals?

A
  1. Type L calcium channels (plateau phase) are regulated by both voltage and extracellular calcium levels.
  2. High extracellular calcium levels: Type L channels close faster than normal.
  3. Shortened plateau phase, repolarization (T wave) occurs faster.
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9
Q

Antiaarhythmic medications function by (3):

A
  • inhibiting cardiac SNS activity (beta-blockers)
  • delaying depolarization
  • prolonging repolarization
    • (lengthens time spent in APs)
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10
Q

How does delaying depolarization and prolonging repolarization (antiarrythmic medications) treat arrhythmias?

A
  • By prolonging events of one AP in surrounding cells, the odds of one of the aberrant pacemakers hitting a tissue when it is responsive is less likely.
  • Cells spend more time in APs.
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11
Q

Possible antiarrhythmic medications for plateau potentials (myocytes):

A
  • Sodium channel blockers:
    • blocking sodium channels will prolong depolarization
  • Potassium channel blockers:
    • blocking potassium channels will prolong repolarization.
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12
Q

Possible antiarrhythmic medications for Pacemaker potentials:

A
  • Beta-blockers:
    • anti-SNS prolongs phase 4 (slow depolarization), which prolongs
    • reaching threshold for rapid depolarization.
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13
Q

Cause of supraventricular tachycardia:

A
  • ventricular tachycardia being driven by abnormal atrial impulses (ectopic pacemakers) above the AV node.
  • A-Fib can lead to supraventricular tachycardia.
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14
Q

Why would exercise help someone experiencing A-Fib feel better?

A
  • Exercise increases SNS activity, which increases inotropy.
  • Increased contractile force will make up for the lessened atrial contribution to diastole.
  • Atrial contribution to diastole is 20%.
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15
Q

The atrial contribution to diastole is roughly:

A
  • 20%.
  • 80% is passive.
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16
Q

Cardizem mechanism and outcome:

A
  • type L Ca2+ channel blocker.
  • will slow the rapid depolarization stage of pacemaker potentials in the AV node.
    • increases AV nodal delay.
  • ventricles will contract at a slower rate, diastole increases.
17
Q

Digoxin/digitalis mechanism and outcome:

A
  • blocks Na+/K+ ATPase, blocking NCX and increasing intracellular calcium levels.
  • inotropy/contractile force increases, cardiac output increases.
  • increases AV nodal delay.
18
Q

The two functions of digitalis/digoxin:

A
  • increases positive inotropy, thereby increasing cardiac output.
  • increases AV nodal delay, thereby decreasing HR.
19
Q

How does digitalis/digoxin increase AV nodal delay?

A
  • parasympathomimetic effect by increased acetylcholine release and increase of the sensitivity of CM2 receptors.
  • HR slows.
20
Q

Why is this part of the ECG important for reentrant arrhythmias?

A
  • relative refraction occurs mid-end T wave.
  • myocyte can now be prematurely depolarized by a reentrant rhythm.
21
Q

Basic physiology of a myocardial infarction:

A
  1. blood vessel to myocardium occluded.
  2. oxygen supply to myocardium cut off, myocardium dies.
  3. depolarization/repolarization properties of dead/ischemic myocardium altered.
22
Q

Myocardial infarction ECG manifestations (3):

A
  1. ST elevation.
  2. peaked and then inverted T waves.
  3. new Q waves.
23
Q

What ECG finding indicates that myocardial injury has occurred?

A

ST elevation.

24
Q

What ECG finding indicates irreversible myocardial death has occurred?

A
  • new Q waves.
  • represent misdirection of current away from dead region.
25
Q

What is this ECG showing/indicative for?

A

inverted T waves

myocardium ischemia, possibly MI

26
Q

What is this ECG showing?

A
  1. ST elevation (red)
    • myocardium injury
  2. new Q waves (blue)
    • irreversible myocardium death
27
Q

Which ECG leads would best represent the areas shown?

A
28
Q

On an ECG, a myocardial infarction (MI) that occurs in the posterior regions of the heart will be reflected as (2):

A
  1. prominent R wave in V1.
29
Q

The inferior and posterior regions of the heart are supplied by which artery, and which ECG leads would indicate a MI due to occlusion of this artery?

A
  • right coronary artery.
  • inferior leads (II, III, and aVF).
30
Q

The left lateral myocardium of the heart is supplied by which artery, and which ECG leads would indicate a MI due to occlusion of this artery?

A
  • left circumflex artery
  • left lateral leads (I, aVL, V5, and V6)
31
Q

The anterior myocardium of the heart is supplied by which artery, and which ECG leads would indicate a MI due to occlusion of this artery?

A
  • anterior interventricular artery (LAD)
  • precordial leads (V1-V6)
32
Q

Draw anterior view of heart with arteries by region:

A