Chapter 36: Dysrhythmias or Arrhythmias part II Flashcards
Questions to ask when looking at an ECG
What is the heart rate?
Is the rhythm regular or irregular? Is there a pattern to the irregularity?
P waves: Present? Regular rhythm? One P wave for EVERY QRS? All look the same?
PR interval: Greater than .2 seconds? All the same length? Any pattern?
QRS: Narrow (.12 sec)? All look the same?
For atrial rate, count the P waves; for ventricular rate, count the R intervals
Regular PQRST cycles
Rate between 60-100 bp
P wave before EACH QRS complex
Narrow QRS complex (
Normal Sinus Rhythm
Can also have sinus brady (c/b vagal stimulation) or sinus tach (c/b SNS stimulation or vagal inhibition)- these can be normal responses to activity or physiologic changes, but they can also be a pathologic response to disease.
C/b Valsalva, gagging, carotid sinus massage, vomiting, suctioning, hypoxia, meds, MI, infection, hypothyroid, increased ICP, beta blockers, calcium channel blockers, digoxin; can be normal (i.e. athletes, sleeping)
ECG-
Sinus Bradycardia
SA node working
C/b exercise, fever, pain, hypovolemia (decreased BP=increased HR), meds, etc.
ECG- 101-200 bpm, regular, everything else is normal (NARROW QRS)
S/S: dizziness (not enough time in diastole=decreased blood to brain), dyspnea, hypotension, decreased urine output, restlessness (decreased CO), chest pain (would be a sx to be concerned about)
Tx: treat the underlying cause (almost always physiologic!)
Sinus tachycardia
Normal phenomenon of mild acceleration (with inspiration) and slowing of the heart rate (with expiration) c/b more blood filling the heart during inspiration causing acceleration
ECG- irregular, everything else normal
S/S: none
Tx: none
Sinus arrhythmia
C/b emotional stress, fatigue, caffeine, tobacco or alcohol, meds (Beta 1 agonist excited cells too much [epi, anything that increases HR])
ECG: can be irregular
S/S: may be asymptomatic or have palpitations, states heart “skipped a beat”
Tx: decrease sources of stimulation (i.e. caffeine, meds)
Quite common, MOST are asymptomatic, most are harmless and require no treatment.
Often hidden in the T wave, usu. followed by a pause
OK (if isolated); be cautious is frequent in pt with heart disease (could be an MI, electrolyte problem, too much atrial stretch)
Can be bigeminy (every other beat) or trigemini (after every two normal beats)
Premature atrial complex
Somewhere in atria, spark (not from SA) fired off, goes to AV, and finishes contraction
Abnormal electrical signal stimulus hits AV, domino affect and finishes contraction (down bundle branches, etc)
NO P WAVE BECAUSE NOT FROM THE SA (P wave means SA had to fire)
> 100 bpm.
Increases work of the heart, increases oxygen need, decreases coronary perfusion time (diastole- increased HR=not enough time to fill the heart=not enough time to feed it)
Initially increases CO and BP, but it will decrease if sustained.
Can cause palpitations, chest pain, restlessness, anxiety, pale/cool skin
Dysrhythmias: aflutter, afib, SVT, VT
Cx: heart failure
Tx: if stable, vagal maneuvers, adenosine (ONLY if regular and monomorphic, can be wide or narrow); if unstable, cardioversion (want electricity to hit on QRS)
Need to rule out electrolyte problems, anemia, dig toxicity
Usually doesn’t cause s/s until >150 bp
Tachydysrhythmias
____ tissue acts as an ectopic pacemaker for 1-2 beats.
P waves don’t all look the same (if a pacemaker other than the SA node fires_
Premature atrial complexes (PAC)
SVT (supraventricular tachycardia)
Atrial flutter
Atrial fibrillation
P WAVE SHAPE CHANGES
Atrial dysrhythmias
Common but rarely in a healthy heart. C/b underlying heart disease, can develop acutely with thyrotoxicosis, alcohol intoxication, caffeine, electrolyte imbalances, transient after cardiac surgery, aging.
ECG: atrial rate of 350-600 bpm; vent rate of 110-140, IRREGULAR, QRS narrow
S/S: 90% are asymptomatic. Decreased CO, thrombi d/t blood stasis, risk of stroke.
Tx: treat like aflutter. Warfarin for 3 weeks before if lasting>48 hrs, may have elective cardioversion, if unstable urgent cardioversion.
Most common dysrhytmia- common with HTN, CAD, obesity
Atrial fibrillation.
Multiple ectopic foci causing everything to be totally disorganized, atria can’t recover between impulses (so no real P waves, just erratic spikes_ so it can’t depolarize causing quivering instead of contraction, unpredictably sends an impulse to the ventricles (irregularly irregular pulse, no pattern); causes loss of atrial kick which is 25-30% of CO
Tx: anticoagulation with coumadin, Plavix or Pradaxa. Control rate with diltiazem (CCB) or metopropolol (BB) or digoxin (if they also have HF). Sometimes use amiodarone (controversial)
Puts pt at risk for clots/stoke d/t blood pooling in the atrium, usually needs to be on anticoags for 6 weeks before cardioversion to prevent a thromboembolic event; cardioversion if drugs are not effective
If recurrent, needs ablation to bundle of Hs (which also requires insertion of a pacemaker)
Rarely occurs in a healthy heart (usu have COPD, HTN, HF, CAD), puts pt at risk for clots/stroke d/t blood stasis in the atrium (needs to be on coumadin), can degenerate to afib. Common after heart surgery.
ECG- recurring, regular, sawtooth-shaped flutter waves, narrow QRS.
AV node can’t respond to all the impulses so it only conducts a few causing ineffective atrial contraction. If the ventricular rate remains normal, may be asymptomatic.
S/S: decreased CO, HF, increased risk of stroke
Tx: coumadin, oxygen, digoxin, CCBs, BBs to slow the ventricular rate; Cardioverson if unstable or electively; radio frequency catheter ablation may be needed.
Atrial flutter.
NOT P WAVES!
Can’t feel a difference in the pulse, can only see on ECG. usually regular rate.
Cardiovert if unstable (showing s/s of low CO), prefer to cardiovert electively if possible to allow time for anticoagulants to stop those emboli in the heart
Abrupt onset and termination of tachycardia followed by a brief period of systole.
ECG: 150-220 bp, regular, P wave may be hidden, narrow QRS
S/S: if prolonged can cause decreased CO (i.e. palpitations, dizziness, chest pain)
Tx: vagal stimulation (i.e. valsalva, coughing), oxygen, IV adenosine, if unstable cardioversion, if recurrent needs radio frequency catheter ablation
Begins or ends abruptly. Impulses originate in the atria or AV junction
Re-entry mechanism recirculating through and restimulating atrial tissue
Supraventricular tachycardia (SVT) or Paroxysmal SVT (PSVT) Can be the same causes as PACs and can happen in healthy people without heart disease.
“If there’s time, _____”- rapid IV push 6 mg over 1 second followed by 20 mL NS and arm elevation, can give 2nd dose of 12 mg
“If they’re about to chill, an electrical pill”- synchronized ____ (50, 100, 200 joules) (unstable, premeditate with sedative if possible”
adenosine
cardioversion
Cause by an ectopic focus (an irritable cell that fires before the next sinus impulse is produced; c/b atrial, junctional, or ventricular tissue).
After there is one there usu a pause before the next normal complex causing irregularity
Can feel “skipping” or “palpitation,” if frequent can cause decreased CO
Can be rhythmic or patterned: couplets (pairs), bigeminy (every other beat), trigemini (every third beat), quadrigemniy (every fourth beat)
Early rhythm complex
Often causes no s/s
Isolated is okay, frequent=warning sign ventricle is getting irritated
Premature complexes
C/b potassium and magnesium imbalance, caffeine, hypoxia, fever, stress, heart disease (anything that shifts O2 supply to demand)
ECG: HR varies, irregular, bizarre shaped QRS without a P wave before it, T wave large and opposite in direction to the QRS
S/S: asymptomatic or feel a “skipped beat,” may cause a pulse deficit, chest pain
Tx: usu don’t have to treat unless it becomes Vtach, treat the cause (K+ bolus, fluids, O2, if long-term may use BBs or lidocaine, amiodarone if unstable VT)
Very common, often harmless and requires no treatment
Unifocal or uniform (same shape) vs. multifocal and multiform (different shapes-more concerning b/c they are coming from different locations)
Often in patterns
Premature ventricular contraction (PVC)
Indicates ventricular irritability so the pts physiologic status needs to be monitored esp if it is causing chest pain or pulse deficit.
Very important to make sure the pt has peripheral perfusion (feel pulses while watching the monitor or listening to apical heart sounds)
OK (if pt has a healthy heart). Bad if frequent or if they have an unhealthy heart or lungs b/v can lead to angina and HF.
3 in a row is Vtach. Can progress to vtach and then vfib.
______ or ____ can be in patterns- bigeminy, trigemini; can also be a couplet
PACs or PVCs
Will lead to wide (>.12 sec) QRS complexes b/c the impulse originates and depolarizes first in one ventricle and then the other.
Usually the atrial rhythm remains regular.
Premature ventricular contraction (PVC)
Ventricular tachycardia
Ventricular fibrillation
Ventricular standstill (asystole)
Pulseless electrical activity (PEA)
More life-threatening than atrial, b/c the left ventricle is so important in terms of getting blood out to the body
Ventricular dysrhythmias
Ominous rhythm
3 or more PVCs. Same causes as PVCs, but often seen with ischemic tissue damage.
Sustained (>30 seconds) or non sustained (
Ventricular tachycardia
Repetitive firing of an irritable ventricular ectopic focus, prevents the heart from filling adequately, can progress to vfib and sudden cardiac death (SCD).
The longer, more sustained, and faster, the more dangerous (b/c the ventricles can’t fill, decreasing CO)
VT has wide QRS complex (SVT has narrow)
Polymorphic more commonly deteriorates to VF
For regular monomorphic use adenosine, if irregular adenosine could cause vfib
Assess first!!! And determine if pt is stable or unstable.
Can progress to vfib.
Tx: treat quickly even if it occurs only briefly, can recur if tx is not started; treat the cause. If stable- give adenosine (rhythm MUST be regular, monomorphic), might give amiodarone, procainamine, or sotalol. If unstable- defibrillation. If pulseless- treat like vfib- CPR! , rapid defib, follow by vasopressors (i.e. epi) and antidysrhythmic (i.e. amiodarone) if needed
Ventricular tachycardia
Runs of vtach- acidotic, electrolyte imbalances, hypoxia- treat the pt
If unstable (pulseless or having chest pain, s/s of low CO), DEFIBRILLATE! Drugs they may give include amiodarone, lidocaine, procainamide, stall
MUST treat if sustained, but even need to treat short bursts. Very unpredictable and likely to recur. Treat the cause and watch closely for PVCs and vfib (frequently deteriorates into vfib)
If recurrent, may need ICD
Associated with AMI, HF, cardiomyopathy, can happen during pacing or after fibrinolytics, also electrical shock, hyperkalemia, hypoxia, acidosis, drug toxicity
ECG- nothing measurable
S/S- unresponsive, pulseless, apneic
Tx- rapid defib, if no conversion give epi or vasopressin, then move to amiodarone
The pt is clinically dead and will become biologically dead unless the rhythm is quickly stopped!
Ventricular fibrillation
Most important rhythm to recognize b/c its lethal and is quickly reversed with defib.
Circulatory arrest occurs within seconds and death within minutes if not immediately corrected- NO cardiac output or perfusion
Most common initial rhythm is cardiac arrests. Firing of multiple ectopic foci in the ventricle causing it to quiver with no contraction and no CO
Pt will be pulseless, apnea, unresponseive- no perfusion, will cause death in minutes b/c the quivering consumes a lot of O2
Defibrillate! Start CPT while waiting for the defibrillator. 200 J then 300, then 360, then CPR and drugs (epi, shock, lidocaine or procainamide or stall, vasopressin, shock, magnesium, shock. Many of these drugs can be given ETT if no IV access)
Coarse vfib is easier to convert than fine vfib because there is more electrical energy
ALWAYS CHECK THE PT! (Artifact can look a lot like this)
Bradydysrhythmias
Can be from disease in the heart’s electrical system, sinus node dysfunction or heart block (Delay of impulses from atria to ventricle)
