Cardiac Rhythm Analysis Flashcards
What are the standard limb leads?
Lead 1 –> RA Neg, LA Pos
Lead 2 –> RA Neg, LL Pos
Lead 3 –> LA Neg, LL Pos
What are bipolar and unipolar leads?
Three standard leads are bipolar, chest leads are unipolar
What does P wave represent?
Atrial depolarization. Normal is smooth, rounded, upright, no more than 2.5mm high
What does PR interval represent?
Time taken from atrial depolarization and delay in conduction at the AV node.
Normal is 0.12 - 0.20 seconds
What does QRS complex represent?
Ventricular depolarization. Normal is 0.06 - 0.10 secs
What do Q waves represent?
Ventricular septum depolarization.
Should be less than 1 box wide and less than 1/4 height of the following R wave, or it is pathological.
What does ST segment represent?
End of ventricular depolarization and beginning of ventricular repolarization. Starts at J point, depression or elevation is anything +- 1mm from the isoelectric line
What does ST elevation represent?
Myocardial injury, pericarditis (Global ST), ventricular aneurysm, electrolyte imbalances
What does ST depression represent?
Myocardial ischemia, NSTEMI, electrolyte imbalance
What does T wave represent?
Ventricular repolarization.
In first 1/2, cells are in absolute refractory.
Normal T wave is upright, rounded, less than 5 boxes in height and larger than P waves.
What does a peaked T wave represent?
Myocardial infarction or hyperkalemia
What does a negative / inverted T wave represent?
Myocardial ischemia, subarachnoid bleed
What does a flattened T wave represent?
Hypokalemia
What is the QT interval?
Duration of ventricular depolarization and repolarization, in NSR should not exceed 0.44 secs. Should be 1/2 of RR.
What does lengthened QT interval represent?
Longer refractory period, caused by electrolyte imbalances, hypothermia, meds (amiodarone, haloperidol, antibiotics, antidepressants)
Normal Sinus Rhythm: Criteria?
HR 60-100, regular, PR normal, QRS normal
Sinus Bradycardia: Criteria, physiology, significance?
HR < 60, regular, PR normal, QRS normal
Caused by PSNS dominance, electro-conduction is normal but just slower
CO might be low, hypotension, decrease LOC, shock, ischemic chest discomfort. If HR is low an escape rhythm may take over
Sinus Bradycardia: Etiology and treatment?
Myocardial infarction, meds (Ca channel blockers, beta blockers), increased ICP
Treatment if symptomatic: Atropine 0.5mg IV push (can repeat every 3-5 mins max 3mg). If ineffective consider dopamine, epinephrine, cardiac pacing
Sinus tachycardia: Criteria, physiology, significance?
HR 100-150, regular, PR normal, QRS normal
Faster electro-conduction, SNS dominance
Diastolic filling time decreases as HR increases, decreased perfusion to coronary arteries, potential loss CO
Sinus Tachycardia: Etiology and treatment?
Anxiety, pain, shock states, stimulants
Treat underlying cause
Sinus arrhythmia: Criteria, physiology, significance?
Irregular rhythm, PR normal, QRS normal
SA node influenced by variation in PSNS, causes increase in rate during inspiration and decrease in rate during expiration.
Normal variation due to changes in intrathoracic pressure
Sinoatrial block vs Sinus arrest: Criteria, physiology?
Sinus block: Missing PQRST(s), pause length is exact multiple of the underlying R-R (maps out)
SA node generates an impulse on time but is blocked from exiting, atrial cells do not depolarize.
Sinus arrest: Missing PQRST(s), pause length is not an exact multiple of underlying rhythm
SA node fails to initiate an impulse, loss of automaticity, when SA node fires again it can begin at any time
Sinus block + arrest: Etiology and treatment?
Ischemia of SA node, inferior wall MI, sick sinus syndrome, meds (beta blockers, calcium channel blockers)
Review meds, if symptomatic may use atropine / pacing
What is altered atrial automaticity?
Cells other than the nodal cells can abnormally initiate an impulse (ectopic impulse). If it occurs at a fast rate, it will take over the SA impulses
What is re-entry?
Abnormal path of conduction where impulses from the ventricle travel back up to the atria usually through a secondary pathway and cause early atrial depolarization. Can happen several times in a circular pattern
How does thrombus formation occur with atrial rhythms?
Loss of atrial kick or abnormal contraction causes blood stagnating in the atria. 48-72 hrs later a thrombus forms.
RA thrombus –> Goes into lungs, pulmonary embolus
LA thrombus –> Goes into brain, causes stroke, or elsewhere in body
Premature atrial complex: Criteria, physiology, etiology?
Early beat, upright P, different shape than P waves in underlying rhythm
Cells with enhanced automaticity fire a premature ectopic beat which produces abnormal P wave. Sometimes this can depolarize the ventricle but sometimes ventricles in absolute refractory (non-conducted PAC)
Caused by excess SNS / Sympathomimetics, atrial enlargement (CHF), valvular heart disease
Atrial tachycardia: Criteria, physiology, etiology?
HR 150-250, regular rhythm, normal QRS, (PR may be unable to measure)
Re-entry circuit or enhanced automaticity, ectopic site with fast rate becomes pacemaker
Caused by excess SNS / Sympathomimetics, atrial enlargement (CHF), valvular heart disease
Atrial tachycardia: Significance?
1) Increases workload of the heart, increases myocardial O2 demand
2) Decreases diastolic filling time, decrease CAD blood supply
Eventually lead to myocardial ischemia and infarction
Atrial tachycardia: Treatment?
If asymptomatic: Vagal manoeuvres (bearing down, carotid sinus massage), adenosine, beta / Ca blockers, amio
If symptomatic: Synchronized cardioversion
What is synchronized cardioversion?
Indicated for atrial tach and other tachycardias where pts are hemodynamically unstable. Works best for re-entry rhythms, charge stops all electrical activity allowing SA node to regain firing.
Shock is synchronized with pt R wave to prevent delivering shock during the relative refractory period
What are the joules for synchronized cardioversion?
Regular rhythms 50-100J
Irregular rhythms 120-200J
Atrial flutter: Criteria, physiology, etiology?
Atrial rate > 250, saw tooth atrial pattern (F waves)
Predominant re-entry rhythm, ventricular response is dependent on number of atrial impulses conducted through AV node
Caused by lung + heart disease: chronic lung disease, valvular heart disease, myocardial infarction / ischemia, post cardiac surgery
Atrial flutter: Paroxysmal vs peristent?
Paroxysmal –> Self terminate in less than 7 days
Persistent –> >7 days
Atrial flutter: Treatment?
Goal of rate and rhythm control.
Rate control: Metoprolol, diltiazem. Target to lower HR to < 100, anticoagulants recommended if > 48hrs
Rhythm control: Amiodarone or synchronized cardioversion if unstable (only if < 48hrs)
Atrial fibrillation: Criteria, physiology, etiology?
Irregular rhythm, f waves
Enhanced automaticity or re-entry pathway, AV node is bombarded with impulses
Caused by lung + heart disease: chronic lung disease, valvular heart disease, myocardial infarction / ischemia, post cardiac surgery
Atrial fibrillation: Treatment?
Goal of rate and rhythm control.
Rate control: Metoprolol, diltiazem. Target to lower HR to < 100, anticoagulants recommended if > 48hrs
Rhythm control: Amiodarone or synchronized cardioversion if unstable (only if < 48hrs)
Multifocal atrial tachycardia: Criteria, physiology, etiology?
HR > 100, irregular, changing P waves, at least 3 different P shapes, normal QRS
Many ectopic sites in the atria depolarizing atrial tissue. Pacemaker “wanders” (if HR < 100, called wandering pacemaker )
Caused by lung + heart disease: chronic lung disease, valvular heart disease, myocardial infarction / ischemia, post cardiac surgery
Multifocal atrial tachycardia: Treatment?
Same as A flutter and A fib, but occasionally adenosine may be given for diagnostic purposes
