Lecture 4 (Electrolytes and MIs) Flashcards
The heart is reliant on what four ions for proper function?
- calcium, sodium, and potassium for proper depolarization/repolarization.
- magnesium.
In the heart, potassium is responsible for:
- repolarization of all cardiac cells (pacemakers and plateaus).
In an ECG of a person with a severe potassium imbalance (hyper- or hypokalemia), you will see:
- abnormal T waves (ventricular repolarization).
- hyperkalemia = tented T waves.
- hypokalemia = T wave flattening/inversion.
In the heart, calcium is responsible for:
- slow and rapid depolarization of pacemaker cells and in the
- plateau phase of myocyte depolarization.
- Cross-bridge cycling and cardiac myocyte contraction.
In an ECG of a person with a severe calcium imbalance (hyper- or hypocalcemia), you will see:
- abnormal QT segment.
- hypercalcemia = short QT complex.
- hypocalcemia = long QT complex.
What is this ECG suggesting?
hypocalcemia
- Prolonged QT interval
How does hypocalcemia lead to a prolonged QT interval?
- Type L calcium channels (plateau phase) are regulated by both voltage and extracellular calcium levels.
- Low extracellular calcium levels: Type L channels open and stay open for a much longer time than normal.
- Lengthened plateau phase, repolarization (T wave) occurs later.
How does hypercalcemia lead to shortened QT intervals?
- Type L calcium channels (plateau phase) are regulated by both voltage and extracellular calcium levels.
- High extracellular calcium levels: Type L channels close faster than normal.
- Shortened plateau phase, repolarization (T wave) occurs faster.
Antiaarhythmic medications function by (3):
- inhibiting cardiac SNS activity (beta-blockers)
- delaying depolarization
- prolonging repolarization
- (lengthens time spent in APs)
How does delaying depolarization and prolonging repolarization (antiarrythmic medications) treat arrhythmias?
- 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.
Possible antiarrhythmic medications for plateau potentials (myocytes):
-
Sodium channel blockers:
- blocking sodium channels will prolong depolarization
-
Potassium channel blockers:
- blocking potassium channels will prolong repolarization.
Possible antiarrhythmic medications for Pacemaker potentials:
-
Beta-blockers:
- anti-SNS prolongs phase 4 (slow depolarization), which prolongs
- reaching threshold for rapid depolarization.
Cause of supraventricular tachycardia:
- ventricular tachycardia being driven by abnormal atrial impulses (ectopic pacemakers) above the AV node.
- A-Fib can lead to supraventricular tachycardia.
Why would exercise help someone experiencing A-Fib feel better?
- 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%.
The atrial contribution to diastole is roughly:
- 20%.
- 80% is passive.
Cardizem mechanism and outcome:
- 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.
Digoxin/digitalis mechanism and outcome:
- blocks Na+/K+ ATPase, blocking NCX and increasing intracellular calcium levels.
- inotropy/contractile force increases, cardiac output increases.
- increases AV nodal delay.
The two functions of digitalis/digoxin:
- increases positive inotropy, thereby increasing cardiac output.
- increases AV nodal delay, thereby decreasing HR.
How does digitalis/digoxin increase AV nodal delay?
- parasympathomimetic effect by increased acetylcholine release and increase of the sensitivity of CM2 receptors.
- HR slows.
Why is this part of the ECG important for reentrant arrhythmias?
- relative refraction occurs mid-end T wave.
- myocyte can now be prematurely depolarized by a reentrant rhythm.
Basic physiology of a myocardial infarction:
- blood vessel to myocardium occluded.
- oxygen supply to myocardium cut off, myocardium dies.
- depolarization/repolarization properties of dead/ischemic myocardium altered.
Myocardial infarction ECG manifestations (3):
- ST elevation.
- peaked and then inverted T waves.
- new Q waves.
What ECG finding indicates that myocardial injury has occurred?
ST elevation.
What ECG finding indicates irreversible myocardial death has occurred?
- new Q waves.
- represent misdirection of current away from dead region.
What is this ECG showing/indicative for?
inverted T waves
myocardium ischemia, possibly MI
What is this ECG showing?
- ST elevation (red)
- myocardium injury
- new Q waves (blue)
- irreversible myocardium death
Which ECG leads would best represent the areas shown?
On an ECG, a myocardial infarction (MI) that occurs in the posterior regions of the heart will be reflected as (2):
- prominent R wave in V1.
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?
- right coronary artery.
- inferior leads (II, III, and aVF).
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?
- left circumflex artery
- left lateral leads (I, aVL, V5, and V6)
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?
- anterior interventricular artery (LAD)
- precordial leads (V1-V6)
Draw anterior view of heart with arteries by region:
