cardio #2

pathway of conduction

SA → AV → HIS (interventricular septum) → LBB/ RBB → Purkinje fibers

the _ is the pacemaker

SA node

the inter-ventricular septum depolarizes off of branches from the __

LBB

P wave 

atrial myocyte depolarization

QRS complex

ventricular depolarization 
spread of depolarization starting with interventricular septum

T wave 

ventricular myocyte repolarization

q wave is a _ deflection

negative

r wave is a _ deflection

positive

S wave

negative deflection following R wave

QS wave

only negative

the T wave peak is closer to

the end which tends to follow QRS complex

PR segment

end of P wave to beginning of QRS

PR segment represents

spread of depolarization through AV node, bundle of HIS, and bundle branches

ST segment

end of QRS to beginning of T wave

TP segment 

end of T wave to beginning of P wave

electrophysiological property of slope 4

firing rate 

electrophysiological property of slope 0

conduction velocity

electrophysiological property of slope 3

Action potential duration (APD)

important channels of slope 4

HCN/ LTCC

important channels of slope 0

LTCC/ V gated Na+ channels

important channels of slope 3

rapid delayed rectified K+ channel (Kr)

important current in slope 4 

Na+ (in)/ Ca 2+ (in)

important current in slope 0

Ca2+ (in)/ Na+ (in)

important current in slope 3

K+ (out)

clinically relevant location of slope 4

SA node

clinically relevant location of slope 0

AV node
ventricles 

clinically relevant location of slope 3

ventricle 

ECG interval for slope 4

RR

ECG interval for slope 0

PR, QRS

ECG interval for slope 3

QT

bipolar leads

I, II, III

Unipolar lead

aVf, aVl, aVr 

lead I

left arm - right arm

lead II

left leg - right arm

lead III

L leg - L arm

v1

4th intercostal space rt of sternum

v2

4th intercostal space lt of sternum

v4 

mid clavicular line in 4th intercostal space

v3

line midway v2 and v4 

v5

anterior axillary line

v6

mid axillary line

v1 and v2 are

rightward and anterior

v5 and v6 are

most leftward, posterior

interventricular septum forces 

R, A (I)

ventricular free wall - left ventricle

L, P, I

ventricular free wall - right ventricle

R, A, S

in the ventricular freewall, the _ is electrically dominant

LV

small box of EKG represents

0.04sec

1 big box of EKG represents

0.2 sec

calculate BPM

300/ # big boxes RR

Effects of Ne on SA node

B1 Gs receptor → increase cAMP → increase pKA → phosphorylates L type Ca2+ and HCN channels→ increase phase 4 slope → increase SA firing rate (+ chronotropic effect)

Effects of Ach on SA node

M2 Gi receptor → decrease cAMP → decrease pKA → decrease phase 4 slope → decrease SA firing rate (- chronotropic effect)

Effects of Ne on AV node 

B1 Gs receptor → increase cAMP → increase pKA → phosphorylates L type Ca2+ → increase phase 0 slope/ amplitude → increase AV conduction (+ dromotropic effect)

effects of Ach on AV node

M2 Gi receptor → decrease cAMP → decrease pKA → decrease phase 0 slope/ amplitude → decrease AV conduction (- dromotropic effect)

the _ is the first part of the ventricle to depolarize

interventricular septum

depolarization is from

endocardium to epicardium

repolarization is from 

epicardium to endocardium 

lead I + III =

lead II 

depolarization towards + pole of a lead

positive deflection

depolarization towards - pole of a lead

negative deflection

depolarization perpendicular to a lead

biphasic deflection

all position deflections

r/R

initial negative deflections

q/Q

negative deflection following a positive deflection

s/S

all negative

qs/ QS

SA node normal sinus rhythm

upright P wave in lead II
regular
rate 60-100 bpm (3-5 big squares)

sinus tachycardia

sa node is pacemaker but HR >100bpm

sinus bradycardia

sa node is pacemaker but HR <60bpm

sinus arrhythmia

sa node is pacemaker but variability in HR
inspiration → increases HR
expiration → decreases HR

AV node represented by

PR interval

normal PR interval

0.12-0.2 seconds
3-5 small boxes

first degree AV block

increased PR interval, >0.2 seconds

second degree AV block

intermittent block
mobitz type I or type II

mobitz type I (wenckebach)

progressive lengthening of PR interval before dropped QRS complex
P: QRS not 1:1

mobtz type II

P:QRS not 1:1
no progressive lengthening of PR interval

3rd degree AV block is a _ AV block

complete
SA node still paces atria

first type of 3rd degree av block

escape rhythm, pacemaker for ventricle (15-40bpm)

second type of 3rd degree av block

some av node cell in communication → AV node paces ventricle (45-60 bpm), if block low enough to prevent AV node cells from communicating

QRS interval normally

<0.09 seconds

prolonged QRS interval

>0.12 seconds (greater than 3 small boxes)

causes of prolonged QRS interval

1) decreased conduction velocity through ventricle (decreased phase 0 slope)
2) asynchrony of ventricular activation

reasons for decreased phase 0 slope

1) drugs that block v gated Na+ channels
2) hyperkalemia (depolarization blockade)

reasons for asynchrony of ventricular depolarization

1) premature ventricular depolarizations 
2) ventricular tachycardia 
3) ventricular escape rhythm 
4) bundle branch blocks

QT interval depends on

APD, phase 3 slope

QT interval is sensitive to changes in

HR

increase HR

decreases QT interval

decrease HR

increase QT interval

rate corrected QT interval (QTc) =

QT/ square root (RR)

if QT interval is ___, it is prolonged

> ½ RR

reason for prolonged QT interval

block Kr ventricle, decrease phase 3 slope, common pharmacological mechanism

prolonged QTc increases risk for 

Torsade de Pointes

physiological causes of prolonged QTc

hypokalemia
hypocalcemia

mean frontal QRS axis

frontal plane, average, QRS (depolarization of ventricle)

normal mean QRS axis is

-30 to + 90 degrees

right axis deviation of mean frontal qrs is

+90 to -90 degrees

left axis deviation is

-90 to -30 degrees

if both leads & are _ then mean frontal QRS is normal

I and II are both positive

v1 v2 in RBBB

R

v5 v6 in RBBB

ST segment elevation