EKG's made EZ

The NCLEX exam doesn't expect you to be a highly trained cardiologist, and the USMLE on average only asks 2 questions about EKGs, but recognition of important pathological rhythms is a requirement for all future nurses and physicians. One of the most important, yet daunting tasks in the nursing and medical fields is to learn to recognize, both accurately and rapidly, Electrocardiograms (ECGs). Variations from the normal p, QRS, and T waves can be completely harmless to fatal in minutes, and it is up to us in the healthcare field to be able to tell the difference, and act accordingly.

Lets take a look at these variations and see if there is a way to make this a bit easier to understand. We will divide these variations up into three groups: Bradyarrhythmias (abnormal rhythms with rate usually below 60),Tachyarrhythmias (abnormal rhythms with rate usually above 100 bpm), and Dysrhythmias (alterations to the normal sinus rhythm pattern).


Bradyarrhythmias

1.Sinus Bradycardia
–HR less than 60 requires treatment with Atropine only if symptomatic

2.AV Block
A.1st Degree•Key: PR interval above 0.2 seconds; Delay is in AV node
•Usually benign but low HR responds to Atropine


B.2nd Degree type I•Key: Progressive prolongation of PR until a P wave fails to conduct and no QRS follows a P wave; Delay is in AV node
•Usually benign condition seen with normal aging not requiring treatment, but if symptomatic with bradycardia, will respond to Atropine


C.2nd Degree type II
• Key: Normal EKG with a sudden drop of a QRS; Block usually in the His-Purkinje system usually as a result of ischemia
•Can turn into the deadly 3rd degree so temporary transcutaneous pacer may be needed until an implantable pacemaker can be inserted


D.3rd Degree
• AV dissociation often from irreversible damage to the AV node following a MI
• Key: P-P length does not equal R-R length
•Ventricles do not pump fast enough to maintain CO and requires pacemaker



Tachyarrhythmias
•Atrial impulse

A.Sinus Tachycardia•HR 100-140, may occur with exercise or anxiety, but also may be earliest indication of hypovolemia
•Usually not symptomatic until above 140 when diastolic filling time is impaired
•Count the large boxes from top of a QRS to another: 1 box = 300bpm, 2 box = 150bpm, 3 box = 100bpm, 4 box = 75bpm, 5 box = 60bpm
•TX: Eliminate cause (i.e. anemia, stimulant; fluid bolus)



B.SupraVentricular Tachycardia•A conduction signal loops and reenters the atrium causing rapid, atrial driven HR usually above 140bpm
•Atrial tachycardia results in narrow QRS complexes
•TX: Adenosine given rapid IV push



D.Atrial Flutter•One foci in atrium fires rapidly, leading to sawtooth P waves and regular QRS with HR between 75-175
•Occurs most often in COPD, but may be seen with CAD and Atrial septal defects (ASD)
•TX: Identical to AFib



•Atrial Fibrillation•Multiple atrial foci cause lack of P waves and very irregular QRS waves with widely varied HR from 75-175 bpm

•Caused by CAD, MI, HT, PE, Pericarditis, Hyperthyroidism
•Major risk for thrombotic events (CVA) so treat according to protocol
•Treatment Protocol; Determine length/onset of AFib:
• Acute: less than 48hrs
Unstable: (Hypotensive, AMS) Immediate cardioversion
Stable:
»Tachycardic: Control Rate w/ Beta Blocker (Atenolol) then electrical cardioversion
»NSR: Proceed directly to cardioversion (electrical preferred to pharmacologic; If electrical fails or is unfeasible use Amiodarone to convert)
•Acute: greater than 48 hrs or unknown duration
–Before cardioversion: If longer than 2 days must use Warfarin to anticoagulate for 3 weeks before and 4 weeks after
–Avoid the wait: Can obtain an echo to r/o thrombus and load pt with Heparin and proceed to cardioversion; Still require the 4 week Warfarin anticoagulation after
•Chronic: Under 60 with no heart disease or risk factors require no treatment; All others get Warfarin for good


Tachyarrhythmias
•Ventricular impulse

A.Ventricular Tachycardia
•Ventricular foci initiate rapid HR with wide QRS complexes
•Caused by prior MI (most common), active ischemia, hypotension, cardiomyopathy, Drugs, Electrolyte abnormalities•May initially have a pulse, but can rapidly evolve into a deadly pulseless VTach
•TX: VTach with a pulse treated with 150mg Amiodarone
•TX: Pulseless VTach treated identical to VFib with Code being called: CPR, Defibrillation, Epinephrine, Amiodarone, and Lidocaine (Alternate drugs w/ Epi being only drug you can not max out on)



B.Ventricular Fibrillation
•Ventricular foci initiates rapid rhythm which causes heart to fatigue and quiver
•Typically evolves from VTach
•Ischemic heart disease most common cause
•Always pulseless, so initiate a code as above



C.Torsades de Pointe•A polymorphic VTach with varying direction of QRS amplitude (points alternate down to up)
•Often caused by electrolyte problems and long QT, so give a trial of Mag and Calcium



D.Asystole
•Loss of electrical signal initiation so it doesn’t respond to Defibrillation (basically resets rhythm to asystole)
•Epinephrine and Atropine are only hopes



Arrhythmias
•Dysrhythmias

A.Premature Ventricular Contraction (PVC)•Abnormal Foci causes random, wide QRS contractions
•May not progress to any other rhythm and have no symptoms
•Can progress to VTach and VFib, so treat more than 6/min or if symptoms present with BBs



B.ST Elevation
•Usually an ominous sign of actual myocardial infarction
•Treat with ACS protocol including ECG and Enzymes
•If present in all 12 leads may suggest Pericarditis

C.T wave Inversion
•An ominous sign of cardiac ischemia, can precede B
D.Q wave
•If deeper than ½ of QRS, suggests a prior infarction, Follows B

E.U wave
•Suggestive of hypokalemia
F.ST Depression
•Often a sign of ischemia, use MONA, ECG, Enzymes

G.Peaked T wave•Suggestive of hyperkalemia

H.Prolonged QT
•QT width is more than ½ the width of QRS-QRS
•Often caused by low Mg or Ca, as well as many drugs that effect these electrolytes
•TX: Withdrawal medication that caused and check/treat electrolyte abnormalities