Dysrythmias Flashcards
Multifocal atrial tachycardia
(1) irregular P waves (2) atrial rate over 100 (3) ventricular tachycardia
- seen in COPD patients and with digitalis toxicity
- Multiple atria foci are beginning to show entrance block (where they are blocked from being overridden with foci with faster rates) so you get multi atrial foci that all pace at different rates
- “MAT”
Atrial Fibrilation
- (1) No P wave (continuous and chaotic atrial spiked) (2) irregular ventricular rhythm
- multiple atrial foci all suffering from entrance block so all pacing individually and none achieving complete depolarization of the atria which gives you no P wave (just mess) and irregular ventricular rhythmn as only a subset of atrial depolarization make it through the AV node
Stokes Adam Syndrome
When you have a ventricular escape rhythm that is so slow that you don’t get adequate flow to the brain. Need to put in an airway and monitor
Ventricular Escape beat
Parasympathetic activity in the heart acts on the SA node, the atrial foci and the junctional foci but not the ventricular foci so that a burst of transient parasympathetic activity can cause a ventricular escape beat
Ventricular automaticity foci are also very sensitive to O2 content and will fire a beat with low O2
Why do atrial and junctional foci become irritable?
- adrenergics, things that mimic adrenergics, and things that increase the release of adrenergics
1) adrenergic stimulation
2) Sympathetic stimulation
3) B1 stimulators like caffeine and cocaine
4) Digitalis toxicity (other toxins, occasionally ethanol)
5) Hyperthyroidism (directly and makes more sensitive to adrenergic stim)
6) stretch
PAB
Premature atrial beat
- irritable atrial focus gives a overriding beat
- early, differently shaped P wave; often masked by the T wave so can look like an abnormally tall T wave
- if the atrial focus is low down enough, can cause a down to up depolarization which inverts the P wave
- if the depolarization reaches the SA node, it resets it and regular sinus rhythm reoccurs after 1 cycle
- Can cause a widened QRS wave if the premature atrial beat reaches the ventricles before all of the ventricles have repolarized, so part beats with the arrival of the PAB and part on a delay
- Can also have a non-conducted PAB where the whole ventricle is refractory and so you get a early P wave with no QRS, while the PAB does not conduct to the ventricles, it does reset the SA node so you get resumption of rhythm after a cycle as with a normal PAB
Atrial Bigeminy
- PAB couples itself to the end of a normal cycle so you see a double humped P wave, then a normal cycle as the aberrant P wave resets the SA node, then a double P wave, etc. (can can get a widened QRS too for the same reason as a regular PAB
- Atrial Trigeminy occurs when you get this coupling every third wave
Premature Junctional Beat
- PJB usually accompanied with a widened QRS wave due to lack of repolarization of the whole ventricle before the junctional beats reaches the ventricles
- Sometimes a PJB can retrograde depolarize the atria as it depolarizes the ventricles causing an inverted P wave either before the QRS, within the QRS, or just after the QRS
- Can have a junctional bigeminy or trigeminy pattern as well
Why do ventricular foci become irritable?
- Low O2 (primary cause)
- Hypokalemia
- Pathology (mitral valve prolapse, stretch, QT prolonging medications, mycarditis, etc)
(Note: cocaine can cause irritability of ventricular foci by provoking coronary spasm and thus rather severe hypoxia, which induces the automaticity of the ventricular foci)
PVC
- Premature ventricular contraction or complex
- Ventricular automaticity foci are the heart’s hypoxia early warning system
- Represented by a very tall, early QRS complex of opposite polarity to a normal complex and represents the firing of a ventricular automaticity foci
- This is because normally the conduction is moved quickly through the R and L ventricles pretty much simultaneously. When there is a PV beat, the conduction moves more slowly from its point of origin through the rest of the ventricles, and is therefore not dampened by a simultaneous depolarization in the opposite direction, giving a tall and wide QRS
- Corresponds to a ventricular contraction and a weak pulse because the ventricle is less filled when the depolarization occurs
- There is often a P wave that fires on schedule but can’t depolarize the refractory ventricles, producing a pause between the widened QRS and the next normal cycle
- 6 or more PVCs per min = path (usually sign of v. poor oxygenation)
- If the PVCs all look the same they can be assumed to emanate from the same focus = unifocal
Ventricular Parasytole
- Ventricular focus not irritable but suffers from entrance block so is not overdrive suppressed and beats poke up from normal sinus rhythm
Ventricular Tachycardia
- run of more than 3 PVCs
Often due to coronary insufficiency
Can resemble atrial or junctional /svt if in svt you get widened qrs due to a partially refractory ventricle but important to distinguish bc treatment for svt counter-indicated for PVCs
Barlow syndrome
- MV prolapse (mid systolic click and systolic decrescendo murmur)
- benign and common
- Mitral valve moves into LA during systole, chordae pull of papillary muscles causing stretch that initiates the PVC(s)
- most commonly caused by myoxmatous degeneration of the valve (weakening of connective tissue + accumulation of dermatan sulfate (a glycosaminoglycan) w/in the connective tissue matrix
- can be treated with beta blocker (propranalol) or blood thinners if becomes symptomatic
R on T phenomenon
-When a PVC occurs directly at the apex of the T wave or on the beginning of its downward slope it can induce a dangerous run of PVCs
Tachyarrhythmias
Arrhythmias developing from a very irritable focus
- Paroxysmal (150-250); Flutter(250-350); Fibrillation (350-450)
- Sinus tachycardia (tachycardia originating from the SA node), is not rapid in its onset
PAT with AV Block
- Paroxysmal Atrial Tachycardia with an AV Block
- Marked by rapid upstroke P waves and a 2:1 P:QRS ratio
- Often seen with digitalis toxicity or another toxicity where the toxin induces an irritable atrial foci as well as inhibiting the AV node. A P wave depolarizes the atria and is block at the AV node, with the second P wave getting through to induce a ventricular depolarization
- More likely with dig toxicity and low K, giving K can improve the situation as well as dig antibodies
Paroxysmal Supraventricular Tachycardia
- Often the P waves and T waves run together making it hard to distinguish atrial and junctional paroxysmal tachycardia so they can be classified together as supraventricular because the management is pretty much the same
Capture Beat v Fusion Beat
- During VT, the SA node continues to pace the atria normally but dissociated from the AV node
- Capture beat occurs when a depolarizaton from the SA node catches the AV node in a receptive state and the ventricles repolarized and conveys a normal cycle during the PVT
- A Fusion Beat occurs when the SA depolarization catches the AV node receptive and conveys a beat, but part of the ventricles are refractory so you get a normal QRS wave fused with a PVC wave
How can you tell SVT with a wide QRS from PVC runs?
VT- history makes coronary Insufficiency likely; QRS wider than .14 seconds; capture or fusion (AV dissociation), RAD
Tornadoes de pointe
Very rapid ventricular rhythm (250-350) characterized by a series of upright QRS complexes followed by smaller amplitude downward QRS complexes; caused by low k or k channel blocking agents; hypothesized to be the result of two irritable ventricular foci
Atrial Flutter
250-350 bpm
P waves have a “saw tooth” appearance and you see 3 ish p waves for each qrs because the av node is slow so is refractory for many of the fast atrial beats
To better identify a flutter you can turn the tracing upside down or employ a vagal maneuver which can unmask a flutter that had appeared as a 2:1 p:qrs that looked like pat with av block by making the av node more refractory
Ventricular Flutter
250-350 bpm
Appearance of a smooth sine wave
Almost always deteriorates into an ventricular fibrillation
Fibrillation
Multiple foci with entrance block (para systolic) pacing independently
350-450 hypothetically rate bc of independent foci, really more of a twitch not effective for pumping blood
Where does atrial fibrillation usually start from?
Pulm vein osteum of left atrium
What are the three types of cardiac arrest?
Ventricular fibrillation
Cardiac standstill- no electrical activity
PEA- pulse less electrical activity ( some electrical activity in heart but not enough to produce mechanical action in heart)
Wolf parkinson white syndrome
Bundle of Kent gives accessory pathway to ventricles that produces an early depolarization and a delta wave
Can cause paroxysmal tachycardia via 3 routes;
1) supraventricular foci conduct early beat into ventricles via Kent bundle
2) irritable foci in bundle of Kent
3) re-entry from ventricles to atria via bundle of Kent
