Week 1 etc. Flashcards
Firing rate of: SA node AV node Bundle of His Purkinje fibers
70-80 (ipm)
40-60
40
15-20
Absolute refractory
Relative refractory
Supranormal period
No repolarization can occur because most Na+ channels are closed.
Cell is almost repolarized, but can fire an AP with a large enough impulse.
During hyperpolarization.
Chronotropic
Changes the HR.
Dromotropic
Changes the speed of conduction.
Iontropic
Changes the strength of contraction.
Lusitropic
Changes rate of relaxation.
Sympathetic stimulation of the heart
Stimulus carried via cardiac splanchnic ns. to SA/AV nodes and cardiac tissue.
Receptor is B-1.
PSNS stimulation of the heart
Stimulus is carried via vagus n. to SA/AV nodes and cardia tissue. ACh is NT and receptor is muscarinic.
Lead I placement
RA to LA
Lead II placement
RA to LL
Lead III placement
LA to LL
Draw the axis of standard and augmented leads
Draw
Inferior region and RCA are seen best in which leads? (3)
Leads II, III, aVF
Septal region and LAD are seen best in which leads? (2)
V1, V2
Anterior region and LAD are seen best in which leads (3)
V2, V3, V4
Lateral region and circumflex a. are seen best in which leads? (5)
I, aVL, V4, V5, V6
P wave is upright in:
Inverted in:
I, II, aVF, V4-6
aVR
T wave is upright in:
Inverted in:
I, II, V3-6
aVR
Normal duration of PR interval
0.12 to 0.20 sec.
Longer than 0.20 could suggest AV block.
Normal duration of QRS complex
0.05 to 0.10 sec.
Longer than 0.12 could suggest bundle branch block or hypertrophy.
ST segment morphology
Should be baseline, but should not be elevated over 1 mm in standard leads and 2 mm in chest leads. Should not be depressed more than 0.2 mm (indicative of ischemia or transmural injury).
T wave height
Up to 5 mm in standard leads and 10 mm in chest leads.
Inverted T waves are associated with:
Ischemia
U waves can be associated with:
Hypokalemia
QT interval duration
Avg is 0.35 sec., but no longer than 0.45 sec.
Draw the cardiac axis
Draw
What happens to the cardiac axis in a patient with ventricular hypertrophy?
The axis moves to the side of hypertrophy.
What happens to the cardiac axis in an MI?
Axis deviates from the side of the infarct.
Excitation-coupling mechanism
Depolarization causes Ca to flow into the cell via L-type channels. Ca binds to ryanodine receptors causing the SR to leak more Ca.
Ca binds to troponin C, causing tropomyosin to move away and allows myosin to bind actin and contraction occurs.
Relaxation can occur by:
Ca ATPase
CNX
a wave
c wave
v wave
Increase in atrial pressure.
Due to increasing ventricular pressure.
Pressure while the atrium fills with blood.
S1
S2
S3
S4
Closing of the AV valves.
Closing of the SL valves.
Rapid ventricular filling.
Atrial contraction.
Receptor and NT setup for Sympathetic NS
Draw
Receptor and NT setup for PSNS
Draw
Sympathetic activation of SA/AV node
NE binds B1 causing an increase in Na (f) channels which increases phase 4 and HR.
Sympathetic activation of cardiac myocytes
NE binds B1 receptor that stimulates L-type Ca channels to stay open longer which increases contractility and SV.
Sinus arrhythmia
Initiated by the SA node.
Wave morphology is normal, but time between each cycle varies.
Junctional rhythm
Initiated by the AV node.
P waves are absent or trail the QRS complex.
Rate is about 40-60.
Premature atrial contraction (PAC)
P waves come earlier than expected based on previous cycle. Normal.
Multifocal atrial tachycardia (MAT)
3 different P waves caused by different atrial foci causing a depolarization.
Rate is tachycardic.
AFib
Continuous atrial spikes with no discernable P or T waves.
Spacing in QRS is variable.
Supraventricular tachycardia (SVT)
P and T waves are indistinguishable from QRS. Can be in alteration.
PVC
P wave is absent before a QRS complex that is long and wide.
Vtach
Big, wide QRS complex in rapid succession w/ no identifiable P waves. Rate is tachy.
VFib
Peaks/waves are not distinguishable.
Caused by multiple ventricular foci firing without synchronicity.
AV block
PR interval is longer than 0.2 s.
