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
1st Degree AV Block
The normal PR interval is 0.12 - 0.20 sec. 1st degree AV block is defined by a PR interval > 0.2 second. This may be caused by drugs, such as digoxin; excessive vagal tone (parasympathetic); ischemia; or intrinsic disease in the AV junction or bundle branch system. Not usually dangerous, does not require treatment. What is the PR interval below?
AV Block- 2nd degree-Type 1“Wenckebach”
Conduction through the AV node gets progressively slower until one P wave is not conducted. The cycle then repeats itself.
AV Block- 2nd degree- Mobitz II
PR interval stays the same. Without warning, the block occurs and a P wave is non-conducted. Sometimes this occurs in a pattern, e.g. 2:1 AV block, meaning that every other beat is non-conducted, but often it is random.
Needs treatment—if not corrected, will progress to complete heart block. Usually needs pacemaker.
Atrial rate is regular but some of the P waves are not conducted so no QRS
AV Block- 3nd degree- Complete Heart Block
There is complete dissociation between the atria and ventricles.
The atrial impulses are “completely blocked” from the AV node & therefore cannot initiate ventricular contraction.
Atrial rate is constant at 60-100 bpm and regular (P to P interval)
Ventricular rate is regular at 30-60 bpm & is generated from the ventricles, but not associated with the atrial impulse.
Ventricular rate is constant (R to R interval)
Dangerous arrhythmia—can progress to asystole
AV Block- 3nd degree- Complete Heart Block Cont.d
QRS duration :
Normal - if blocked at Bundle of HIS
Wide - if blocked at bundle branches or lower
Clinical Significance: Life Threatening…
Excessively slow heart rates are the same as those in symptomatic sinus bradycardia.
Can be very serious, especially when associated with a wide QRS, leading to ventricular asystole
This may result in syncope,, seizures and apnea (Stokes-Adams Syndrome) and death if an escape pacemaker does not respond or asystole not treated.
Treatment : Stable or Unstable?
Asymptomatic Bradycardia: StableAtropine 0.5 -1 mg IVP (may be helpful)
Symptomatic Bradycardia: Unstable
Transcutaneous pacing, until transvenous pacing is available Dopamine 5-20 mcg/kg/min Epinephrine 2-10 mcg/min
Bundle Blocks in General
A bundle branch block IS NOT an AV block. When myocardial tissue is damaged, impulses may be unable to travel down one or more of the three bundle branches. The impulse then tries to get around the blockage by depolarizing nearby undamaged cells. This leads to a widened complex.
Premature Ventricular Contractions (PVCs)
Ectopic focus (“hot spot”) somewhere in the ventricles fires off an electrical impulse, causing ventricular depolarization.
Complex is wide (QRS > 0.12sec), bizarre-looking.
We all have them!
Can be a problem if they occur frequently and can progress to V.tach or V. Fib
Often caused by hypoxia, ischemic myocardium, electrolyte imbalances, irritation from misplaced central lines
Unifocal PVCs
Unifocal means that the extra beats came from the same hot spot so
they look the same—identical twins.
Multifocal PVCs
PVCs look different—more than
one hot spot firing off extra beats
Ventricular tachycardia
Life-threatening arrhythmia!
Can be with or without a pulse (check the patient—may need CPR)
Ventricles beating very fast (150-300 bpm)
Cardiac output falls rapidly.
Can progress to ventricular fibrillation
Caused by electrolyte imbalances, myocardial irritation (MI, reperfusion arrhythmias, post cardiac surgery, central line placement), digitalis toxicity, amphetamines, cocaine
*Fast, regular, wide QRS, no P waves seen
Ventricular Tachycardia Treatment
CHECK THE PATIENT!!!!!
Does the patient have a pulse?
If no, call a code and start CPR
Defibrillate ASAP!!!
If the patient has a pulse: Check the BP Notify physician immediately Antiarrhythmic medications—***Amiodarone, Lidocaine If BP low, prepare for cardioversion
Ventricular Fibrillation
Code Blue situation!
The ventricles are quivering instead of contracting.
No cardiac output, no BP, no perfusion to brain or other organs. Patient is pulseless and requires CPR followed by RAPID defibrillation for best chance of survival.
*When normal rhythm restored, start anti-arrhythmic medications IV (Amiodarone, Lidocaine, Esmolol)
Cardioversion
Cardioversion is done when the PATIENT IS ALIVE AND HAS A PULSE! We want to deliver the shock at a precise spot in the cardiac cycle. When we cardiovert, we SYNCHRONIZE the shock to the R wave (middle of ventricular contraction). The machine does this for us.
If we don’t synchronize, the shock might randomly hit the T wave, which will result in ventricular fibrillation (no pulse). More problems!
Defibrilation
We DEFIBRILLATE when the patient is DEAD!!!!
The patient is in V Tach without a pulse or V-fib. No need to synchronize—just go ahead and deliver the shock. Usually need more joules to defibrillate than cardiovert (200 to 360J for defibrillation, 50-200J for cardioversion)
Asystole
NO ELECTRICAL ACTIVITY in the heart
Flat line
Patient is pulseless
Immediate CPR
Give epinephrine 1mg IV to try and stimulate electrical activity.
THIS RHYTHM CANNOT BE TREATED BY DEFIBRILLATION-there is no electrical activity to convert.
Pulseless Electrical Activity (PEA)
ECG could show any organized electrical complexes, but there is no pulse
Electrical conduction system is working but the heart cannot physically contract.
There is no contraction of the atria or ventricles!
Electrical depolarization continues with no contraction, no mechanical activity.
Treatment is same as for ASYSTOLE
TREAT THE CAUSE
PEA Causes
Hypovolemia, hypoxia, hypotension, hypothermia
Cardiac Tamponade
Tension Pneumothorax, Tamponade, Thrombosis, Toxins
Cardiac muscle is too damaged to contract (MI)
Myocardial rupture
Chest trauma
Several others
REMEMBER- check for a pulse with all dysrhythmias.
