Exam 1 lecture 4 Flashcards
re-entry
when depolarization that does not die out, but keeps going along various branching or circular pathways within the myocardium, generated by wave of depolarization hitting areas that have already been repolarized, results in continuous wave of depolarization that encircles a region of heart.
conditions that favor re-entry
long pathway, reduced conduction velocity which has same effect as long pathway, shortened refractory period which accelerates muscle repolarization
ventricular or atrial fibrillation
many small waves spreading through micro-loops in different directions over the myocardial surface
re-entry can cause
ventricular tachycardia or atrial flutter
Long pathways
dilated atria and ventricles
variable conduction rates and regions of excitability
during normal repolarization, ischemia and injury which slows conduction and repolarization, hyperkalemia and cocaine can slow the conduction velocity
altered repolarization rates (short refractory period)
catecholamines
aberrant pathways or accessory anatomical pathways
AV nodal re-entry
ventricular tachycardia
current from an ectopic beat re-enters the focus, travels slowly through it and again emerges to find surrounding myocardium repolarized and vulnerable-> series of ectopic beats can be initiated .
aberrant pathways (AV nodal re-entry)
2 pathways develop in AV node. Slowly conducting pathway with a short refractory period, and a preferred alternate rapidly conducting pathway with a long refractory period
re-entrant supraventricular tachycardia
rapid heart rhythms at or above AV node
Wolff-parkinson white syndrome
short P-R and pre-excitation wave slurring the upstroke and the QRS. Aberrant muscular bridge (bundle of Kent) connects atria with ventricles and bypasses AV node. Can suddenly cause tachycardia at a rate that impairs ventricular filling, cardiac output drops, fall in mean arterial pressure, leading to dizziness, fainting and angina pectorsis due to inadequate perfusion of the coronary arteries
delta or pre-excitation wave
from WPW, rapid activation of some regions of the ventricle directly through the bypass before slower activation of other regions through the atrioventricular node produces delta wave on upstroke of QRS
paroxysmal supraventricular tachycardia
premature atrial depolarization occurs while accessory pathway is still in refractory period but AFTER AV node has recovered-> impulse passes anterogradly through excitable AV node into ventricles-> in meantime accessory pathway has recovered its excitabilty and impulse conducts retrogradely from ventricles back to atria. Causes inverted P wave after QRS, and if impulse arrives at atria at time when AV node has again recovered its excitability, whole circuit can repeat.
WPW
impulse conducts rapidly down Bundle of Kent directly into ventricular myocardium, and will see short P-R interval, pre-excitation wave (delta wave) and slurred QRS upstroke
Lown-Ganong-Levine (LGL) syndrome
short P-R interval and NORMAL WIDTH QRS. AV node re-entry involving fast and slow pathways or an AV node by pass are possible mechanisms
Triggered activity
premature ectopic foci occuring in atria or ventricles are sometimes “triggered events”, abnormal depolarization that are ALWAYS coupled to a preceding action potential
EAD (early after depolarization)
depolarizations that occur before the cell is fully repolarized , occur in congenital or acquired LQTS where repolarization has been slowed, (can be because of mutation or drug effects of Ikr)
what produces the EAD
when repolarization is prolonged, L-type calcium channels become reactivated again to produce an EAD
transmural dispersion of repolarization
slow repolarization favors increased TDR. increased TDR creates functiona substrate for transmural reentry, how EAD’s can trigger a ventricular arrhythmia
torsades de pointes
“twisting of the points”, ventricular tachycardia seen in long QT syndrome
Delayed after depolarization (DAD)
depolarizations that occur after the cell is fully repolarized. Associated with intracellular calcium overload
what causes high intracellular calcium levels
rapid heart rate, digitalis toxicity, high extracellular calcium ion concentration, or prolonged action of NE or E
what does high intracellular calcium cause?
will activate the calcium/sodium exchange antiport (pump), which pumps calcium ions out of the cell in exchange for sodium ions passing into the cell. These sodium ions tend to depolarize the membrane by moving the Em in direction of sodium, if threshold reached, DAD triggered
treatment of DAD
relieving intracellular calcium with calcium channel blockers, beta-blockers or ryanodine
abnormal voltage in ECG, increased voltage caused by
hypertrophy of ventricle or ventricles increased their height of R wave. Hypertrophy of left ventricle can be caused by elevated MAP (from hypertension or aortic stenosis), or hypertrophy of right ventricle from secondarily to pulmonary hypertension
abnormal voltage in ECG, decreased voltage caused by
decreased muscle mass, shunting out of current (fluid accumulation in pericardial space) other alterations in intrathoarcic electrical resistance (increased air in lungs)
Q wave myocardial infarction
larger Q wave than normal
genesis of T wave
represents ventricular repolarization, but in same direction as R wave (which represent ventricular depolarization).
why is T wave same direction as R wave
outer epicardial and apical surfaces of myocardium repolarize before the inner endocardial and basal surfaces. Maybe because high pressure in ventricles reduces coronary flow to the endocardium and delays repolarization in endocardial areas
net positive QRS means
axis is directed toward the positive pole of that lead
net negative QRS means
axis is directed away from the positive pole of that lead
net zero QRS
means axis is at right angles to lead
easy way to pick axis
look for lead with zero or isoelectric QRS, axis i oriented at right angles to this lead and just inspect orientation in another lead to determine correct axis
abnormal right axis deviations RAD
90 to 180
normal axis
-30 to 120
abnormal left axis deviation LAD
-30 to -90
LAD signifies
COPD, extreme obesity (both resulting in physical shifts of heart), left anterior hemiblock (left anterior fascicular block) and pathologic Q waves from MI
RAD signifies
right ventricular hypertrophy (pulmonic valve stenosis or pulmonary hypertension), or left anterolateral myocardial infarction (axis shifts away from site of infarction).
vectors associated with depolarization
are of anterior and septal regions that lie within the transverse plane, right angles to frontal plane, and therefore will only affect precordial leads V1-V4
Lateral represented by
I, aVL, V5 V6, supplied by left circumflex and diagonal branch of left anterior descending coronary artery (LAD). Reciprocal ST, depression in II, III and aVF
Septum represented by
V1, V2, no reciprocal ST depression
Anterior represented by
V2, V3 and V4 no reciprocal ST depression
Inferior represented by
reciprocal ST depression in I and aVL, supplied by right coronary artery
St elevation in inferior leads
II, II and aVF indicates an inferior wall infarction
