Cardiac Rhythm Analysis 2 Flashcards
What are the features of ventricular rhythms?
1) WIDE QRS
Depolarization spreads abnormally along muscle cells and not proper conduction pathways
2) QRS, ST, T look BIZARRE
Conduction is abnormal, repolarization is also abnormal
What do abnormal ST and T waves indicate in ventricular rhythms?
Abnormal conduction, NOT ischemia or infarct
Premature Ventricular Complex: Criteria, types
Early beat, wide and bizarre QRS > 0.12 secs
Unifocal PVC
Multifocal PVC
R-on-T
(The R wave of the PVC falls on the preceding T wave)
Multiple PVCs in a row: 3 or more is a “run of V-Tach”. Paired PVC are “couplets”
Ventricular bigeminy/trigeminy (every 2nd/3rd beat is a PVC)
What is it called when you have more than 3 PVC in a row?
Run of v-tach
Premature Ventricular Complex: Etiology, physiology
Ectopic site in the ventricles, reduces stroke volume by 30-60% due to early depolarization, impaired ventricular contraction and loss of atrial kick
Hypokalemia, dilated ventricles (CHF), myocardial ischemia or infarct
Premature Ventricular Complex: Treatment
Do not require treatment if isolated, treat underlying cause.
If pt symptomatic with increasing PVCs, amio may be given esp if underlying rhythm has a lengthened QT interval
Idioventricular escape rhythm: Criteria, physiology, etiology
QRS wide and bizarre, HR 20-40
Both SA and AV node failed, ventricles initiate impulses to try and sustain life. No atrial activity, very low CO. EMERGENCY
Expected- dying pt
Unexpected- hyperkalemia, severe acid base imbalance
Idioventricular escape rhythm: Treatment
If withdrawing care, no treatment. Otherwise investigate why other pacemakers failed, epinephrine for CO, atropine tried to increase SA node activity, pacing
DO NOT ADMINISTER VENTRICULAR ANTIARRYTHMICS
Can we give amio for Idioventricular escape rhythm?
NO do not administer ventricular antiarrythmics
Accelerated idoventricular escape rhythm: Criteriam, etiology, physiology
QRS wide and bizarre, HR 40-100
Common reperfusion arrythmia, transient, seen after inferior MI with SA/AV node involvement
An ectopic site in ventricles fire at 40-60bpm. Irritable focus usually secondary to ischemia or infarct
Accelerated idoventricular escape rhythm: Treatment
Give O2 if required to reperfuse cardiac tissue. In-between rhythm is hard to treat, usually self-limiting. If sustained HR is LOW and the pt becomes SYMPTOMATIC, then atropine may be trialed to increase SA function
Meds that speed up rhythm may cause more dangerous ventricular arrythmias, ventricular antiarrythmics may further slow down rhythm
Ventricular Tachycardia: Criteria, etiology
QRS wide and bizarre, monomorphic (uniform QRS), polymorphic (QRS shape varies)
Myocardial infarct or ischemia, electrolyte imbalance, acid base imbalance, anything that causes long QT
Ventricular Tachycardia: Physiology
Ectopic sites in the ventricles fire at fast rate, taking over pacemaker functioning. Treatment focuses on suppressing irritable ectopic site.
Torsades de Pointes: Etiology
Meds that lengthen QT interval (Haldol), electrolyte imbalances (hypo-mg, hypo-K)
Ventricular tachycardia: Treatment
Assess pt if stable, unstable, or pulseless
1) Stable (BP normal, pulse strong)
12 lead ECG and consider adenosine if monomorphic and regular for diagnostic purposes
Give antiarrhythmics (amiodarone)!!!
2) Unstable (BP dropping, pulse weak, symptomatic)
Synchronized cardioversion
3) Pulseless (No BP, no pulse)
Defibrillate immediately 120-200J
Continuous CPR with drugs administered during CPR
MD may defibrillate again as needed during session
Epi every 3-5 mins
Amio may be given
Ventricular fibrillation: Criteria, etiology, physiology
Chaotic irregular deflections, no pattern
Myocardial infarction, electrolyte imbalance, acid base imbalance, anything that causes long QT
Ectopic site in the ventricles fire but is not organized or uniform
Ventricular fibrillation: Treatment
Defibrillate immediately 120-200J,
Continuous CPR with drugs administered during CPR
Epi every 3-5 mins
MD may defibrillate again as needed during session
Amio may be given
Asystole: Criteria, etiology, physiology
Flat or wavy line, MAY HAVE P WAVES
Myocardial infarction, hypothermia, massive pulmonary embolism, cardiac tamponade
No electrical activity
Asystole: Treatment
Confirm tracing and leads
CPR
Epinephrine
DO ABOVE WHILE DETERMINING CAUSE
DEFIBRILLATION NOT APPROPRIATE BECAUSE NOTHING TO SHOCK
Pulseless electrical activity (PEA): Criteria, physiology
Electrical activity (excluding VT and VF) with no pulse
Heart has some electrical conduction functioning but little or no contractility and cannot generate cardiac output. May be due to severe hypovolemia due to loss of preload
PEA: Treatment
Prognosis is poor, initiate fluid bolus, investigate other causes while CPR and epinephrine
PEA: Etiologies and most common cause
Loss of preload and severe hypovolemia most common cause
Hypoxia, hypo/hyperthermia, tension pneumothorax, cardiac tamponade
What are the features of junctional rhythms?
Originate in the AV node, and conduction goes down to the ventricles or retrograde up to the SA node therefore resulting in different conduction patterns where P is inverted or absent prior to a narrow QRS:
Absent P before QRS (impulses originate in AV and conduct down to the ventricles. No atrial conduction)
Inverted P before QRS (Conduction first travels retrograde up to the SA node resulting in inverted P wave, then conduct down to ventricles)
Inverted P after QRS (Conduction first goes to ventricles then retrograde up to SA node)
Inverted P during QRS (Conduction goes down to ventricles and retrograde up to SA node at about the same time resulting in inverted P superimposed in the QRS. will make QRS look slightly wide)
Premature Junctional Complex: Criteria, etiology, physiology, treatment
Early beat with inverted or absent P prior to a narrow QRS
Inferior wall MI (affecting SA, AV node), congestive heart failure, electrolyte imbalance
Ectopic focus in the AV junction fires before SA node discharges next impulse
Treatment: Usually none other than to investigate cause
Junctional Escape Beat: Criteria, physiology
Late beat with inverted or absent P prior to a narrow QRS
Occur when SA node periodically fails to fire so AV node initiates beat
Junctional escape rhythm: Criteria, physiology, etiology
Inverted or absent P prior to a narrow QRS, rate 40-60, regular
SA node slows down, AV node tries to take over as pacemaker (40-60)
Severe sinus bradycardia, post cardiac surgery, meds (beta blocker, calcium channel blockers)
Junctional escape rhythm: Treatment
Cardiac output may be reduced. If asymptomatic, monitor and investigate cause
If unstable:
Atropine to increase HR
Dopamine or epinephrine to increase HR
Cardiac pacing
Accelerated Junctional Rhythm: Criteria, etiology, treatment
Inverted or absent P prior to a narrow QRS, HR 60-100, regular
Myocardial infarction, cardiac surgery, valvular heart disease
Irritable focus in AV junction fires impulses at an accelerated rate 60-100. Atrial kick is lost but pts usually asymptomatic due to HR 60-100. Monitor and investigate cause
Junctional Tachycardia: Criteria, physiology
Inverted or absent P prior to narrow QRS, HR > 100, regular
AV junction becomes irritable site and fires off impulses at a rapid rate
Myocardial infarction, cardiac surgery, valvular heart disease
Junctional Tachycardia: Treatment
The higher the HR the more likely pt is symptomatic e.g. HR > 150
Stable:
Vagal maneuvers, adenosine, beta blockers, calcium channel blockers, amiodarone
Unstable: Synchronized cardioversion
What is included in the umbrella term of SVT?
Atrial tachycardia Atrial flutter Atrial fibrillation Multifocal Atrial Tachycardia Junctional tachycardia
What med can be given to diagnose / differentiate the different kinds of SVT?
Adenosine
What are the basis of AV heart blocks?
Blocks in conduction at the level of the AV junction, impulses may move slowly through or be blocked altogether.
1st degree AV block: Criteria, etiology, physiology, treatment
PR > 0.20, one P for every QRS, regular rate
Ischemia or infarct of AV junction nodal area, meds (beta blockers, calcium channel blockers), increased PSNS
Block in conduction of impulses at AV node resulting in longer PR
Pts usually asymptomatic- monitor for progression of block and investigate cause
2nd degree AV block type 1: Criteria, etiology, physiology
Progressively lengthening PR interval until a P wave is not followed by a QRS complex (dropped QRS complex)
Ischemia or infarct of AV junction nodal area, meds (beta blockers, calcium channel blockers), increased PSNS
Delayed conduction in AV junction area above bundle of His
2nd degree AV block type 1: Treatment
CO may be decreased if HR low, e.g. <50
If pt asymptomatic, monitor and assess for progression of block
Symptomatic: Atropine, epinephrine pr dopamine, pacing
2nd degree AV block type 2: Criteria, etiology, physiology
PR interval is a consistent length, dropped QRS complexes, with conduction pattern
Ischemia or infarct of AV junctional area, hyperkalemia, CV surgery
Conduction block is lower in the bundle of His or bundle branches resulting in P waves not being conducted to ventricles. QRS may be slightly long, depending on number of dropped QRS CO may be significantly decreased
2nd degree AV block type 2: Treatment
Pt is likely symptomatic. CO will be low as ventricular rate decreases
Temporary pacemaker is ONLY TREATMENT
Can we give atropine in 2nd degree AV block type 2?
NO
will result in increase in P waves and doesn’t help conduction to ventricles. May increase myocardial O2 demand which is bad
3rd degree AV block: Criteria, etiology, physiology
P regular, QRS regular, no relationship between P and QRS (AV dissociation)
Ischemia or infarct of AV junctional area, cardiac surgery, hyperkalemia
Complete block of conduction at the ventricles despite SA node firing. All impulses blocked at AV node. Therefore AV may initiate escape impulses at 40-60 or ventricles may initiate escape impulses of 20-40
3rd degree AV block: Treatment
Pt is likely symptomatic. CO will be low as ventricular rate decreases
Temporary pacemaker is ONLY TREATMENT
