Heart Rhythms Flashcards
Explain Augmented Leads
Using the same placement of three-electrode pads and a little fancy math, we can get different views of the electrical activity in the heart. Known as augmented limb leads, unipolar limb leads, or just unipolar leads, an electrocardiogram can create an augmented theoretical null point in the center of Einthoven’s triangle allowing a view of the absolute potential in each electrode (My.EKG, 2021).
Sound a little esoteric? Well, it is all about the angle, or vector, from which you are looking at the heart. Think about standing at the end of an extremity, right arm, left arm, or the feet, lying side by side. Now squint up at the heart along that axis. Electric waves moving away from your position will have a positive amplitude on the ECG strip. The waves moving toward you, a negative deflection. At the same time, electrical events doing neither will just be minimized or even merge with the baseline (Bernard.Health, 2021).
The augmented leads are named aVR, aVL, and aVF. “A” for “augmented,” “V” for “voltage,” then “Right,” “Left,” and “Foot.” The leading “A” can be lower case or capitalized, though the lower case is correct.
Lead aVR:
The augmented unipolar right arm lead is oriented toward the cavity of the heart.
Electrical current from the heart is traveling towards the right arm.
All deflections of the ECG, P, QRS, and T should be negative in this lead.
Lead aVL:
The augmented unipolar left arm lead oriented toward the heart facing the anterolateral aspect of the left ventricle.
Electrical current from the heart is traveling towards the left arm.
Lead aVF:
The augmented unipolar left leg lead (feet). It is oriented toward the inferior surface of the heart.
Electrical current from the heart is traveling toward the feet.
Sinus Tachycardia
There are various types of tachycardia. Sinus tachycardia is a regular cardiac rhythm that meets normal sinus rhythm standards, apart from being too fast. Greater than 100 bpm (beats per minute) in a resting adult, faster than 150 bpm in infants to around six years old.
Do not be misled. Too quick a heart rate, even with a normal conduction mechanism, can be problematic. Strokes, heart failure, and the risk of heart attack from increased cardiac demands can accompany sinus tachycardia.
Sinus tachycardia may result from stress, exercise, pain, fever, pump failure, hyperthyroidism, caffeine, nitrates, atropine, epinephrine, and isoproterenol, nicotine, electrolyte imbalances, fatigue, blood loss, and other situations which places stress on the body.
Sinus Arrythmia
Have you ever heard that there is a healthy arrhythmia?
Well, this is it. When your cardiac system is vigorous enough that, guided by the vagal nerve, there is a slight slowing in the resting heart rate after a big breath followed by a slight speeding up during exhalation. Now that is a healthy sinus arrhythmia!
Sinus arrhythmia is most common among children and frequent among adults. It is not pathogenic and requires no treatment.
If there is any danger from sinus arrhythmia, it is misdiagnosed as a more serious arrhythmia. The rate is usually 60-100 beats/min but may be transiently faster or slower. Should the rate be problematic, consider a rate-specific treatment. The rhythm itself is not an issue.
A distinct P wave will be associated with each QRS complex. Be sure to look at your client’s overall condition and, if in doubt, a 12-lead ECG should clarify the situation.
Sinus Arrest or Sinus Pause
A sinus pause is not your friendly neighborhood sinus arrhythmia.
Sinus arrest or sinus pause is an indication of a dysfunction in the SA node. This arrest or pause leads to the dropping or pausing of electrical conduction in the normal sense. The electrical depolarization cycle is initiated yet somehow blocked before the impulse can leave the SA node. These missed beats may cause little to significant symptoms yet should never be taken lightly. Whatever mechanism may be blocking a beat here and there could easily manifest into a significant and potentially deadly sinus heart block.
Interestingly our older clients are where sinus arrest is most often seen. This sinus arrest has led to the hypothesis that it is due to accumulative deterioration or damage to the SA node, which may hold, though it is difficult to do a blind study. When found in younger adults or children, sinus arrest can often be directly correlated with a specific cardiac event or a severe electrolyte imbalance. Possible symptoms accompanying sinus arrest include feeling an occasional missed beat, fatigue, dizziness, or angina.
Sinus Exit Block (Sinoatrial Block)
Sinus exit blocks are when a depolarization wave leaves the SA node yet fails to be conducted to the atria and therefore fails to stimulate the ventricles. Delays of the SA depolarization wave before they can kick start the muscular compression wave of the heartbeat also occur as atrioventricular (AV) blocks. There are three main types. We will get to the three major AV blocks a little later.
Failure of SA node conduction is a crisis. It may lead to the creation of an abnormal P wave and a following normal-looking QRS complex. Or a complete blocking of P wave generation leading to a condition known as sinus arrest, where secondary escape pacemaker cells are called upon to replace the missing SA conduction impulse.
Sinus arrest leads to symptoms such as bradycardia (remember, the firing of escape beats is always slower than the genuine impulse generator), dizziness, syncope, or palpitations.
Premature Atrial Complexes (PACs)
Expanding out into the heart atrium, we begin to see some common arrhythmias that present challenges to us as health professionals. Premature beats of any type are problematic, and clients who report the feeling of skipped heartbeats need to be assessed for premature heartbeats.
Let us start in the atrium, however, outside of the SA node, which is the official timekeeper and pacesetter of our heart. Premature atrial contractions (PACs) come from early depolarization somewhere in the atrium outside of the SA node leading to an interruption or replacement of the SA node-derived beat. Conduction initiation comes from areas of irritation, inflammation, or spots just firing off early for no discernable reason. These early depolarizations take off like wildfire and initiate an untimely contraction that flows through the atrium and then down into the ventricles, creating an early beat with a malformed P wave, though relatively normal QRS complex.
Ask about the client’s clinical history. Of particular interest are any previous cardiac disorders or structural heart disease. Reviewing medication for any proarrhythmic drug use is important and for the presence of stress, fatigue, caffeine, alcohol, tobacco, and such conditions as hypertension or hyperthyroidism. An electrolyte study focusing on sodium or magnesium levels is also handy.
Symptoms of dizziness, syncope, and of course, the perception of a skipped heartbeat may accompany PACs. Be aware that when a PAC occurs, the early triggering of the ventricles will mean a contraction carrying less than a full volume of blood, so the feeling of skipping is an accurate perception by the client.
Keep in mind that premature beats are identified by their site of origin (atrial, junctional, and ventricular). PACs occur when an irritable site within the atria discharges before the next SA node is due to discharge.
PACs with a wide complex are referred to as aberrantly conducted PACs, acknowledging the conduction wave’s eccentric route. PACs and other early beats may occur in pairs (couplet), bursts (premature atrial tachycardia) (PAT), or even every other beat (bigeminy).
In the absence of other pathology, the heart rate tends to stay normal, from 60-100 when there are only occasional premature atrial contractions. Be aware that the presence of a sinus tachycardia may serve to promote more frequent PACs, depending on the overall client condition prompting a fast heart rate.
The rhythm will be irregular due to the early PACs. The presence of the early atrial impulse will throw the rhythm into the irregular category.
The P wave of the early beat differs from SA node P waves and is early, premature. The aberrant P waves may be flattened or notched. They may even be lost in the preceding T wave, which is where a 12-lead ECG shines as it allows detection by changing up the vector of observation.
The PR interval, sometimes abbreviated to PRI, may vary from .12- .20 depending on how near the pacemaker site is to the SA node. A longer PRI means the initiation site is higher up in the atrium, e.g., closer to the SA node, while a shorter PRI indicates the pacemaker site is nearer the AV node.
The QRS complex will usually <.10 but may be prolonged.
Supraventricular Tachycardia
Tachycardia means fast. Supraventricular means the origin of the impulses is from above the cardiac ventricles. These high and fast aberrant rhythms tend to be clustered together due to their shared diagnostics.
Supraventricular tachycardia (SVT) is a group of regular fast rhythms characterized by narrow QRS complexes and high heart rates. Please note that while atrial fibrillation and atrial flutter share a high conduction origin point and fast rate, they are typically irregular rhythms and will be discussed later.
Women are twice as likely to experience SVT as men at any age. In general, about 2.25 Americans out of 1000 fit the diagnosis of SVT (Hahn, 2020).
Be aware that SVT symptoms are often misdiagnosed as a panic attack. So, when in doubt, slide on some ECG patches and get to the truth of the matter. An unusual accompanying symptom of SVT is drumroll, please, polyuria.
SVT can be a spontaneous occurrence with no known trigger. More commonly, mechanisms such as too many energy drinks, cocaine, sepsis, dehydration, or increased intracardiac pressures contribute to this arrhythmia. Cardiac structural changes may also prompt an SVT response, such as congestive heart failure, myocardial infarction, pulmonary embolus, or valvular regurgitation or stenosis.
Vagal maneuvers up to and including carotid massage, Valsalva maneuver, even cold immersion have been used as a treatment to break the SVT cycle. Pharmacologic agents that tone down AV node sensitivity and help to end the SVT reentry pattern include adenosine, verapamil, esmolol, and diltiazem (Hahn, 2020).
Definition: Frog Sign
An interesting diagnostic indicator referred to as the “frog sign” may occur during atrioventricular nodal reentry tachycardia (AVNRT). AVNRT is where the atria fire against a closed tricuspid valve causing strong rebound pressure waves referred to as “cannon waves,” which pound retrograde into the jugular vein.
This gives the appearance of a billowing neck, hence the name “frog sign.”
While this is not an ECG wave, diagnosis is a compilation of available data, and yes, cannon waves can be noted in baseline polarization deviations of a 12-lead.
Cannon waves, and to a lesser extent, the frog sign may also occur in ventricular tachycardia. However, the ECG would demonstrate a wide QRS complex which lowers the back pressure and diminishes the frog sign.
(Hahn, 2020)
Junctional Tachycardia
Note the P wave immediately before the Q as seen on lead II. This P wave is common for all junctional rhythms as the depolarization pacing point are in the AV node, and the depolarization wave must travel upwards into the atria simultaneously, or the closest thing to concurrent, as the same aberrant firing wave heads to the His bundle and ventricles (Knapp, 2020).
Junctional Rhythm Types
Rhythms sourced from the AV node are characterized by rate.
Junctional bradycardia rate is <40 bpm.
Junctional rhythm runs 40-60 bpm.
Accelerated junctional rhythm runs from 60-100 bpm.
Junctional tachycardia > 100 bpm.
Junctional rhythms will have a regular RR interval, and as a signature sign, one of the following P wave variations:
Absent P waves
A sign that the AV node is sending depolarization impulses simultaneously to the atria and ventricles
Inverted P waves
When the AV depolarization reaches the atria before the ventricles
Post QRS P waves
When the AV depolarization reaches the ventricles first
Ventricular Tachycardia
Ventricular tachycardia (V-Tach, VT) is a regular fast heart rate originating from an area of ventricular irritation. Short bursts of rapid ventricular contractions may not endanger a person. However, the less efficient circulation of blood from prolonged bouts can be life-endangering.
Characteristic findings indicating VT are tachycardia at >100 bpm, wide QRS complexes >.12, and AV dissociation. VT can be monomorphic, originating from one electrical excitation where all QRS complexes look alike. Or polymorphic, where multiple spots of electric stimulation are firing within the ventricles. Polymorphic VT is seen when each QRS shows a different morphology.
Bursts of VT lasting under 30 seconds are referred to as non-sustained V-Tach, while stretches longer than 30 seconds are referred to as sustained V-Tach.
Symptoms of ventricular tachycardia fall along the lines of reduced cardiac output and include hypotension, dizziness, syncope, cardiogenic shock, cardiac arrest.
Rate: Ventricular rate 100-250 beats/minute; atrial tends not to be discernible.
Rhythm: Atrial not discernible, ventricular essentially regular.
P Waves: May or may not be present. If present, they have no set relationship to the QRS complexes. P waves may appear between the QRS complexes at a rate different from that of the VT.
P-R Interval: None.
QRS Complex: Wide, >.12 ms (or 3 small ECG squares). Often difficult to differentiate between QRS and T wave. Three or more PVCs in a row at a rate of 100 per minute are referred to as a “run” of VT. There may be a long or a short run. A client may or may not have a pulse. If it is unclear whether a regular, wide QRS tachycardia is VT or Supraventricular Tachycardia, treat the rhythm as VT until proven otherwise.
Note: Ventricular tachycardia can occur in the absence of apparent heart disease.
T Wave: Difficult to separate from QRS.
QT Interval: Should be 390-450 ms. If longer be on alert for Torsades de Pointes.
Other Components: ≥ 3 consecutive wide QRS complexes at a frequency ≥ 100/minute and signs of AV dissociation confirm VT diagnosis. Should the rapid QRS complexes appear identical to the client’s NSR QRSs, suspect a supraventricular tachycardia is occurring.
It may be due to: An early or a late complication of a heart attack, or during cardiomyopathy, alveolar heart disease, myocarditis, electrolyte imbalance, or following heart surgery.
Torsades de Pointes
Torsades de pointes (TdP) is a type of polymorphic VT signified by a prolonged QT interval. The characteristic that makes TdP distinctive is how the QRS complexes twist around the isoelectric baseline during self-limiting bursts.
Around 50% of clients discovered with intervals of TdP are not symptomatic. However, 10% of those presenting with TdP will experience cardiac death (Cohagan, 2020).
The R on T phenomenon plays a significant role in TdP due to the prolonged QT interval that is associated with it. For example, as a PVC, stomps on the tail of an extended T wave torsades de pointes or polymorphic VT may be triggered. This occurrence magnifies the need for a thorough review of client medications as drug-induced long QT syndrome is, unfortunately, common (Cohagan, 2020).
Rate: Generally, >100 bpm
Rhythm: Irregular with an oscillating or spindle looking twist around the baseline
P Waves: Absent, yet if by chance you see some, they will not be related to the QRS complexes
P-R Interval: Chaotic
QRS Complex: Each differs from its neighbor. There will be an overall effect of tall QRSs, which shorten then regain height. This complex goes with the spindle or torsade’s effect.
T Wave: In the QRS complexes just before the torsades effect triggers, look for long prominent T waves. Also, keep an eye out for the R on T phenomenon, which can trigger VT or VF.
QT Interval: Prolonged QT intervals may be congenital, or more commonly, an unwanted effect of some prescription and over-the-counter medications.
Other Components: TdP is a significant adverse arrhythmia. However, the great concern when present increases in rate and degenerates into an even deadlier arrhythmia, ventricular fibrillation.
It may be due to: R on T trigger, antiarrhythmics, antipsychotics, antiemetics, antifungals, antimicrobials, basically any pharmaceutical with the adverse effect of prolonging the cardiac QT interval. Also, beware of substances that slow the hepatic metabolism. Slower liver breakdown of complex chemicals can turn a previously tolerated QT-prolonging substance into a landmine trigger, just waiting for an early R wave to activate the torsades effect (Cohagan, 2020).
Ventricular Fibrillation
Ventricular fibrillation (V-fib or VF) is where the lower heart chambers quiver rather than constrict. Too many electrical polarization signals, arriving much too rapidly, reduce the strong rhythmic myocardial contractions to chaotic spasms. V-fib is a lethal arrhythmia resulting in rapid loss of consciousness, no pulse, and cardiac death in the absence of treatment.
Nearly 70% of cardiac arrest victims experience ventricular fibrillation. Without treatment, clinical death comes within minutes when V-fib is the prominent rhythm. Even when rescue efforts succeed, residual damage from the anoxic brain and neurologic damage requires follow-up and perhaps long-term treatment (Ludhwani, 2020).
V-Fib tends to accompany damage to the structure of the heart. Anything that can irritate or inflame the Purkinje cells of the ventricles has the potential to initiate the fast and multiple stimuli sites leading toward VF. Myocardial infarction, for example, shows V-Fib incidence of from 3 to 12% during the acute phase of myocardial damage. Many common conditions are associated with the chaotic irritability of V-Fib, including electrolyte abnormalities (hypokalemia, hyperkalemia, hypomagnesemia), acidosis, hypothermia, hypoxia, cardiomyopathies, family history of sudden cardiac death, congenital QT abnormalities, and alcohol use (Ludhwani, 2020).
Image 52:
ventricular fibrillation
9K+Save
Rate: Rapid and disorganized
Rhythm: Irregular and chaotic
P Waves: Absent but may be recognized among the chaos
P-R Interval: Not measurable
QRS Complex: Composed of fibrillatory waves, wide irregular oscillations of the baseline
T Wave: Not measurable
QT Interval: Not measurable
Other Components: Coarse VF is where most waveforms are 3mm or wider. Fine VF is where most waveforms are less than 3mm
Electronic Pacemaker Spikes
The natural electrical sources produce heart rhythms within the heart. When those natural pacemaker sites fail by producing too fast, too slow, or an absence of depolarization signals, another source of control is warranted. Enter the artificial cardiac pacemaker.
An implantable cardiac pacemaker is the most common type used. There are also external pacemakers that introduce a rhythmic electronic pulse that is used mostly during emergencies. Internal pacemakers are used in cases requiring long-term availability to override a dangerous heart rhythm or replace an absence of functional heart rhythm.
Implantable pacemakers can pace on-demand or continuously. They tend to stimulate just one heart chamber, or sometimes two. The small pacemaker unit is implanted under the skin with output leads connected directly to the heart muscle. Small batteries provide power to recognize the heart’s electrical activity and provide needed electrical pulses to the heart muscle.
Types of Artificial Implantable Cardiac Pacemakers
Fixed-rate pacemaker
They are used primarily on clients with significant or complete heart blocks. The rate is pre-set to a rate such as 70 bpm, though rate changes can be made using external magnetic control (most commonly).
Demand pacemaker
Only fires when the R-R interval of the client’s natural rhythm meets or exceeds a preset limit.
R Triggered Pacemaker
When dealing with heart blocks possessing occasional sinus rhythm, the ventricular synchronized demand-type pacemaker, the R wave triggered pacer, looks for the absence of R waves and stimulates the heart ventricles should they not appear after a short delay.
R Blocked Pacemaker
For clients with sinus rhythm and only an occasional heart block, the R wave blocked pacemaker stops firing when it detects a natural R wave produced by the client.
Atrial Triggered Pacemaker
When detecting natural atrial depolarization, the pacemaker stimulates the ventricles after a reasonable delay. This pacemaker provides the best cardiac output while following the normal atrial rate fluctuations.
Ventricular Paced or Ventricular Paced
Dual Chamber Pacemaker
Treats most sino-atrial conditions by providing both atrial and ventricular stimulation whenever it is needed.
Pacemaker Terminology
Firing refers to the pacemaker’s generation of electrical stimuli. This impulse is seen as a narrow vertical pacemaker spike on the ECG.
Capture refers to the presence of a P, a QRS, or both after a pacemaker spike. This capture indicates that the tissue in the heart chamber being paced has been depolarized. The term is that the pacemaker has “captured” the chamber being paced. Paced QRS is wide, bizarre, and resembles PVCs.
Sensing refers to the pacemaker’s ability to recognize the client’s intrinsic rhythm to determine if it needs to fire. Most pacemakers function in the demand mode and fire when needed.
Pacemaker Malfunctions
Our heart is an exquisitely crafted pumping machine whose myocardial muscle cells move upwards of six thousand liters of blood every day. These wonderful engines are controlled by rhythmic electrical pulsations originating from natural pacemaker cells located in the apex of the heart itself. So well designed are our hearts’ that redundant backup pacemaker points exist to take over should our primary pacing points fail. Ironically, this problem is one reason we need a consistent method of examining the heart’s electrical activity to see what in our heart is happening.
Electrocardiography is the science of recording and examining the activity of the heart. From how the sinus node’s pacemaker cells polarize then depolarize, sending a spark of life in a wave of depolarization down through electric sensitive tissue pathways. This depolarization wave creates myocardial muscle contracture of the near atrial chambers and quickly after the large muscular ventricles of the heart, creating a bellows that pushes blood into an eager body. Each step the electrical conduction wave takes through the heart creates a different waveform on the isoelectric baseline of an ECG monitor strip.
The atrial depolarization from the sinus node is the P wave. The movement of the electric pulse through the atrial tissue to the AV node and the His-Purkinje fibers causes atrial constriction. This constriction is the PR Interval. As the depolarization enters and spreads widely into the cardiac ventricles, a QRS complex is projected onto the ECG. The short period of recovery occurring between ventricular cell depolarization and repolarization is seen as the ST segment, with the T wave signaling full repolarization. Always one for a bit of mystery, our heart can throw up a wave we call U, which follows the T and precedes the P. We have no idea why, yet life contains plenty of mysteries to pique our curiosity (Amboss, 2021).
We place the positive and negative cardiac monitor to give us special angles for viewing the hearts’ electrical activity. Twelve special lead placements compose a cardiac 12-lead ECG, the diagnostic standard for electrocardiograms. How we evaluate what is going on in the heart using an ECG strip requires a system. Some of the steps of a winning system include looking at the heart rhythm, heart rate, P waves, PR Intervals, QRS complexes, ST segment, T wave, QT duration, and then anything special such as Delta or U waves.
Using a systematic approach, we can determine where the rhythm originates from the atria, junction, or ventricles if it is normal, fast, or slow; If there are unusual beats; If the entire rhythm is unusual and perhaps unwanted, an arrhythmia; if unusual spots of excitement, electrical blockage, chaotic electrical fibrillation, or lack of electrical activity are present.
Not only can we see and diagnosis natural cardiac functions, but we can also look at the functioning of implanted cardiac pacemaker devices to determine if their function is appropriate or failing. A failing artificial pacemaker can show as under sense, failure to capture, or output failure.
When you want to see to the heart of health issues, remember, ECG!
Conclusion
Our heart is an exquisitely crafted pumping machine whose myocardial muscle cells move upwards of six thousand liters of blood every day. These wonderful engines are controlled by rhythmic electrical pulsations originating from natural pacemaker cells located in the apex of the heart itself. So well designed are our hearts’ that redundant backup pacemaker points exist to take over should our primary pacing points fail. Ironically, this problem is one reason we need a consistent method of examining the heart’s electrical activity to see what in our heart is happening.
Electrocardiography is the science of recording and examining the activity of the heart. From how the sinus node’s pacemaker cells polarize then depolarize, sending a spark of life in a wave of depolarization down through electric sensitive tissue pathways. This depolarization wave creates myocardial muscle contracture of the near atrial chambers and quickly after the large muscular ventricles of the heart, creating a bellows that pushes blood into an eager body. Each step the electrical conduction wave takes through the heart creates a different waveform on the isoelectric baseline of an ECG monitor strip.
The atrial depolarization from the sinus node is the P wave. The movement of the electric pulse through the atrial tissue to the AV node and the His-Purkinje fibers causes atrial constriction. This constriction is the PR Interval. As the depolarization enters and spreads widely into the cardiac ventricles, a QRS complex is projected onto the ECG. The short period of recovery occurring between ventricular cell depolarization and repolarization is seen as the ST segment, with the T wave signaling full repolarization. Always one for a bit of mystery, our heart can throw up a wave we call U, which follows the T and precedes the P. We have no idea why, yet life contains plenty of mysteries to pique our curiosity (Amboss, 2021).
We place the positive and negative cardiac monitor to give us special angles for viewing the hearts’ electrical activity. Twelve special lead placements compose a cardiac 12-lead ECG, the diagnostic standard for electrocardiograms. How we evaluate what is going on in the heart using an ECG strip requires a system. Some of the steps of a winning system include looking at the heart rhythm, heart rate, P waves, PR Intervals, QRS complexes, ST segment, T wave, QT duration, and then anything special such as Delta or U waves.
Using a systematic approach, we can determine where the rhythm originates from the atria, junction, or ventricles if it is normal, fast, or slow; If there are unusual beats; If the entire rhythm is unusual and perhaps unwanted, an arrhythmia; if unusual spots of excitement, electrical blockage, chaotic electrical fibrillation, or lack of electrical activity are present.
Not only can we see and diagnosis natural cardiac functions, but we can also look at the functioning of implanted cardiac pacemaker devices to determine if their function is appropriate or failing. A failing artificial pacemaker can show as under sense, failure to capture, or output failure.
When you want to see to the heart of health issues, remember, ECG!
