Lecture 7 Test 4 Flashcards
L type calcium channels being phosphorylated…
increases sensitivity to ca channels making them to fire at the wrong time (EAD/DAD)
Phosphorylation of Troponin I
May cause the increase of sensitivity and change the tropomyosin from the actin, active sites are more exposed and produces more force
Causes of arrhythmia’s
- Abnormal pacemaker rhythm
- Pacemaker somewhere else other than SA node
- abnormal or blocks in the transmission pathway
- Spontaneous impulses from any parts of the heart
What can increase Vrm that may cause ectopic impulses?
- Ischemia that cause energy deficiency
- hyperkalemia, acidosis
causes of Sinus tach >100bpm
Normal constant P waves with QRS > 100bpm.
causes: valve issues, hyperthyroid, inc. temp, SNS response, vagal stimulation (reflex tachycardia) , blood loss, toxic conditions (acidosis, nicotine, alcohol)
Sinus Brady <60bpm
Every QRS has a P wave. caused by vagal stimulation. Giving phenylephrine to a healthy person may cause reflex Brady.
Normal: athletes (Large stroke volume), the lower hr = healthier
Paroxysmal atrial tachycardia
Sa node is firing in irregular rate, comes and go. P and T waves overlap
Can be response to Vagal reflex, B-blocker, or Digoxin.
SA Block
Blocked impulses, P waves may be lost, pacemaker is usually the AV node. Purkinjie maybe the pacemaker if both SA and AV nodes are lost (15-30bpm).
If the AV node is generating the APs, the P waves….
If the AP is generated:
- early in the AV node, P waves may look inverted because the AP will be coming from the AV to the SA
- Later in the AV node, P wave may be lost in the QRS
What happens if the depolarization is early or late?
It will cause an AP when the valves are closed l/t turbulence, damaged valves, generates calcifications or clots.
AV block
Blocked impulses d/t ischemia, scar tissue, calcifications, inflammation, excessive vagal stimulation (V & X), excess digitalis/b-blockers
Increased Vrm
More Na in ICF, K efflux d/t digitalis
Bad HF l/t last med to be placed on….
Last Dig resort
1st degree HB
Increase PR interval > 0.2 secs
2nd degree HB Mobitz 1
aka Wenkebach periodicity
irregular PR int >0.25 secs, Constant P waves with a dropped beat
2nd degree HB Mobitz II
More dangerous than type I. Fixed P wave to QRS ratio. Dropped QRS from time to time.
Ratio 2:1, 3:2, 3:1 (P:QRS)
TX: Pacemaker
3rd degree HB
Complete dissociation with P waves to QRS. RR intervals are constant, P waves are all over the place
15-30bpm, low CO, fast atrial rates
A Flutter
- Circular reentry in the atria. Only some are able to penetrate the AV node. Stretched atria can increase the circular re entry. Half of the atria is contracted and the other half is relaxed. High atrial and ventricular rates.
- no p waves
A fib
Uncoordinated, irregular atrial electrical activity, risk for clots and PE
Ectopic pacemakers, circus movements of electrical current that generate into the ventricle, No P waves
Stoke-Adams Syndrome
Fainting/syncope d/t complete AV blocks from time to time, low bp. Purkinjie system taking over (15-30bpm)
Alternans: Incomplete Intraventricular block
Slow conduction in purkinjie system, irregular QRS complex for every other beat. Ischemia and digitalis prevent full resetting of purkinjie system.
Ratio is mainly 1:1 but not absolute
Premature atrial contractions
Ectopic tissue causes early AP d/t ischemia, irritation, calcifications, plaques
Radia pulse deficit: early depolarization in less filling time; low SV
Sound: pulse deficit
Premature (AV nodal) contractions
- Missing P wave; obscured by QRS
- early/inverted P wave high/early AV
-late/inverted P wave low/late AV
Premature Ventricular Contractions
Smaller QRS are the normal
PVCs are tall/large bc ventricular muscle conduction is slower than purkinjie, one ventricle depolarizes before the other
Inverted T waves after PVC
causes; ceffeine, nicotine, stress, lack sleep
Paroxysmal V tach
QRS within ventricles, Prolonged QRS, usually ischemia/infarction and initiates VFib
Ventricular premature depolarization
EAD (early after depolarization)
DAD (Delayed after depolarization)
May look like a long QT interval, very inefficient pumping
Causes: B agonist, m-ACh-R antagonist, Benadryl (anticholinergic)
Ventricular premature depolarization may lead to?
Torsades depointes > Vfib
V-Fib
Low coronary flow > no depolarization > death.
TX: defib
Bundles of Kent
- accessory pathways, abnormal pathways d/t inherited genes.
- 0.2% of people have accessory bundles that give extra pathways between the ventricle and atria
TX: ablation
