Part 1: EKG's Flashcards
Intrinsic Rhythmicity
Sinus (SA) node-natural pacemaker
60-100 BPM
AV node
40-60 BPM
Ventricular or Purkinje Fibers
40 or less BPM
Common Causes of Dysrhythmias
Electrolyte imbalances (especially K+, Ca++, Na+ and Mg++)
Hypovolemia (dehydration causes tachycardia)
Electric shocks (e.g. lightning)
Medications (e.g. beta blockers)
Illegal drugs (e.g.cocaine causes tachycardia, heroin causes bradycardia)
Poisons
Temperature extremes
Sympathetic/parasympathetic stimulation
Stimulants (e.g.caffeine, amphetamines)
**Electrolytes are most commonly disturbed with arrhythmias.
Bradycardic episode from standing up too fast, bowel movement (Parasympathetic)
Best method of calculating heart rate:
Count the number of TINY boxes between the R waves
Divide this number into 1500 (there are 1500 tiny squares in a minute)
1500 ÷ 22 = 68 bpm
Sinus Bradycardia
Regular rhythm, P wave is before each QRS, identical.
PR Interval: 0.12-0.20 seconds
QRS: < .12 seconds
Mild Sinus Bradycardia (HR 50 -59) Often produces no symptoms. Bradycardia without symptoms is called asymptomatic.
Marked Sinus Bradycardia (HR 35 - 50) Clinical symptoms may occur.
Cardiac Symptoms: Hypotension and reduced cardiac output, congestive heart failure, chest pain, dyspnea
Sinus Bradycardia Cont.d
Neuro Symptoms: Decreased perfusion to the brain causes lightheadedness, dizziness and syncope.
Treatment
No serious signs & symptoms: Observe the patient!
Serious signs & symptoms present:
Prepare for Transcutaneous pacing
Atropine 0.5mg IVP Epinephrine 2 - 10 mcg/min (IV)
Sinus Tachycardia
Supraventricular Tachycardia (SVT) – impulse emanates somewhere above the AV node/ Bundle of HIS, usually unable to determine specific focus due to the very fast rate Rate = 150 to 300, may be regular or irregular
Paroxysmal Supraventricular Tachycardia- (PSVT)- same as above, abrupt onset & termination after short periods
Junctional Tachycardia- emanates from the AV node, characterized by the absence of the P-wave
Rate = 60 to 100 bpm
Why is Tachycardia bad?
Think about the cardiac cycle. The heart fills with blood during diastole (the resting phase) just before it gets ready to contract again. When the heart rate speeds up, it is this diastolic time that gets cut short, giving the heart less time to fill.
The coronary arteries fill passively during diastole. Therefore, decreased diastolic time means decreased blood supply to the myocardium
A sub-optimally filled heart has less volume and contracts poorly, therefore delivering less oxygenated blood to the tissues, including the myocardium.
The heart has to work harder when it is tachycardic—increased myocardial O2 demands but less supply available—ischemia develops—-chest pain, MI. Ischemic myocardium can lead to lethal arrhythmias.
Tachycardia cont.d
Rhythm = Regular Rate = 100 to 150 bpm P waves = Normal and precedes each QRS P - R interval = 0.12 - .20 seconds QRS duration = 0.10 seconds or less Clinical Significance : Stable or Unstable
Treatment:
Look for and treat cause.
Eliminate or treat the underlying cause, i.e. treat the fever, medicate for pain, check hemoglobin, give IV fluids, administer oxygen, etc.
Vagal stimulation (rarely done now)
Adenosine
CCBs
Beta blockers
Atrial Fibrillation
Irregular rhythm, P wave is fibrillary, PR interval = N/A, QRS is < 0.12 seconds
*Narrow QRS complex
Why is A fib bad?
Approx. 30% of our cardiac output comes from the atrial contraction that helps blood to flow down into the ventricles. When the atria are fibrillating, this 30% is lost.
Some people can tolerate this without symptoms but others may become very hypotensive.
When blood does not flow smoothly through the heart, clots are likely to form. These can break loose and travel into the circulation causing pulmonary embolism or stroke.
A fib treatment
New onset (within 24 hours)—can try to convert chemically or electrically. Clots have not had time to form yet.
**Effective drugs to try: Amiodarone, Diltiazem, beta blockers to slow the ventricular response.
If the patient is symptomatic (low BP, altered mentation, chest pain etc)—synchronized cardioversion ASAP. Can convert the heart back to sinus rhythm quickly.
If onset > 24hours, or unknown, patient MUST BE ANTI-COAGULATED before we try to convert the rhythm to normal. If we don’t do this, any clots that have formed in the atria will move forward in the bloodstream when the atria stop fibrillating and contract normally.
A fib. treatment: Cardioversion
Risks of cardioversion
Risks with sedation
Risk of thromboembolism (<1% with anticoagulation)
Postcardioversion arrhythmias
Many people have chronic A. Fib that is unresponsive to drugs or cardioversion. The goal is to keep the ventricular rate < 100 and keep them anti-coagulated with Warfarin.
Atrial Flutter
Atria are fluttering instead of contracting. Rate = variable (slow, normal or fast)
Atrial rate = usually 250 – 200 bpm
Ventricular rate = variable
Regularity = depends on conduction ratio
i.e. 3:1 = 3 flutter waves to each QRS
2:1 = 2 flutter waves to each QRS
May have irregular number of flutter waves for each QRS
QRS = normal configuration, interval
PR = not measurable
QT = not measurable
Treatment: correct the cause, usually not lethal rhythm
SAWTOOTHED APPEARANCE
Premature Atrial Contractions
PACs are extra beats generated by the atria. Sometimes an ectopic focus (“hot spot”) fires off an electrical impulse from somewhere other than the SA node.
Most of us have extra beats, especially after taking a stimulant such as caffeine.
PACs, AKA atrial ectopics, have a narrow QRS complex and occur EARLIER than the expected sinus beat.
Atrioventricular (AV) Blocks
An atrial impulse is blocked from normal conduction through the AV node to trigger the ventricular contraction.
***Three types of AV blocks
First degree- prolonged PR interval. Longer Longer drop (> 0.2 sec)
Second degree
Mobitz I – increasing PR interval until blocked
Mobitz II- sudden block of impulse, normal PR
Third degree- complete heart block
AV dissociation.
Independent atrial and ventricular rates
Life threatening…needs transvenous pacemaker
