Normal Sinus Rhythm
Sinus Arrhythmia
Variable rates. Usually asymptomatic
Sinus Bradycardia
Normal in athletes
Beta blockers, Decreased function of SA Node
Generally asymptomatic unless pathologic condition exists (may be in the presence of 2nd or 3rd degree
block
May c/o dizziness, syncope, angina
Sinus Tachycardia
Generally benign (SA node automaticity increased and pts asymptomatic
Fear, anxiety, caffeine, nicotine, amphetamines, or demands of O2 are higher (exercise, infection, MI,
hemorrhage
T-wave might blend into P wave in tachycardia
Sinus exit block
block in conduction of impulse from SA node to atria
Sinus Exit Block: pause equal to two complete cardiac cycles; overall heart rate, 70.
Premature Atrial Contraction
Ectopic focus in either atria initiates an impulse before the next impulse initiated by the SA node
Causes: emotional stress, nicotine, caffeine, alcohol, infection, hypoxemia, MI, atrial damage
Asymptomatic and if frequency is low, no treatment required, and pt should be able to participate in
activity
When frequency increased, atrial tachy or a-fib may result
P wave comes earlier than usual. P wave is usually a little bit larger.
Atrial Tachycardia
HR may be 100-200bpm
Same causes as PAC but also includes pulmonary HTN, altered pH, and COPD
Q (cardiac output) compromised if prolonged
Dizziness, fatigue and SOB
Atrial Flutter
Caused by pathologic conditions: mitral valve disease, CAD, infarction, stress, renal failure, pericarditis,
rheumatic heart disease, MI
Rapid rate d/t the firing of an ectopic source in the atria
AV-node is crucial- blocks the signal from getting to ventricles
Unless ventricular rate becomes too high, Q is not compromised
Asymptomatic
Atrial flutter-1-2 areas causing atria to contract but signal is not getting thru to QRS. QRS is on normal
rhythm
Atrial Fibrillation
Erratic quivering of atria
Multiple ectopic foci emit electrical impulses
No true depolarization of the atria
AV Node acts to control ventricles
Causes: Advanced age, CHF, ischemia or infarction, cardiomyopathy, digoxin toxicity, drug use,
stress/pain, renal failure
QRS are not regular rhythm either; AV node tries to pace ventricles. Compromised response to exercise
Problems associated with a-fib
No atrial “kick”
Responsible for forcing out the last amount of volume from atria to ventricles
Accounts for 30% of Q
If ventricular rate is less than 100bpm at rest, should monitor with exercise for Q compensation
If ventricular rate is greater than 100bpm at rest, monitoring should be assessed during all activities and
engaged in with caution (a-fib with RVR)
Likely to have Q compensation
Missing p-wave then SA node in not pacing the heart; av node initiated rhythm but not p-wave . Look at
5th QRS complex. Asymptomatic if infrequent
Faster; inverted p wave or retrograde p wave depolarization. SOB and not feeling well, possible
fluttering in chest, losing atrial kick; wide qrs comple
They look the same and coming from same place.
They look different. Diminished cardiac output due to decreased systolic filling time.
AV node is like a police officer sometimes not letting signal conduct through resulting in block.
V-tach is likely from this point. Stop all activity. Decreased stroke volume, and cardiac output. PVC
bigemony is every other beat a PVC.
Flat line or agonal rhythm is next step
Looks similar to v tach. Unclear if it is from a single site or multiple sites. Unlike v tachy the wave
amplitude of torsaes begins close to the baseline, gradually increasing and decreasing in a repeating
pattern. Resembles a twisting and turning mpotion along the baseline . Need to differentiate because
treated differently. Starts suddenly, frequently preceded by a prolonged QT interval. Might be caused
by low Potassium. Translated as “Twisting of Points”
Coming from ventricle, 20-40 bpm, wide qrs, ventricle is pacing. Very slow rhythm. Cardiac output is
severely compromised
Beginning p-wave to beginning of r wave or longer pr interval longer than 0.2 seconds
Has p wave and normal qrs, rate will be a little slower
2nd degree block, 1st type is Wenckebach and 2nd type. Wenckebach PR interval is getting longer each
beat then drops QRS.
Pr interval but missing qrs
LAE can be caused by mitral valve stenosis
Right bundle block the right side is conducting slower typically seen in V1
Left bundle block more prominent in R-wave in V5-6