Cardiac Exam Lecture 3 Flashcards
All cardiac dysrhthmias result from disturbances in __________ or _________ or __________
All cardiac dysrhytmias result from disturbances in IMPULSE FORMATION or IMPULSE CONDUCTION or from a combination of BOTH.
What are the three general mechamisms of cardiac dysrhytmias?
General Mechanisms of Cardiac Dysrhytmia’s:
- Altered Automaticity
- Re-entry of Excitation
- Triggered Activity
Explain what Altered Automaticity is
Altered Automaticity is essentially problems with the pacemaker… there are alterations in the pacemaker rate that are mediated through changes in the pacemaker mechanisms that normally exist in pacemaker cells (located within the special conduction system)
What HR is defined as Tacycardia?
What HR is defined as Bradycardia?
Tachycardia is any HR > 100 bpm
Bradycardia is defined as any HR < 60 bpm
List the possible causes of TACY-dysrhythmias
Possible Causes of Tacy-Dysrhythmias:
- NE (sympathetic nervous activity)
- Stimulants - amphetamines
- Stretching- ventricular aneurysm
- Electrolytes - hypokelemia
- Sick Sinus Syndrome (where the location of the pacemaker is changing)
- Fever
- Hypothyroidism (symptoms of high sympathetic NS activity, you increase the expression of adrenergic receptors)
What are the possible EKG manifestations of enhanced automaticity? (increase pacemaker rate)
Some EKG manifestations of enhanced automaticity:
- sinus tachycardia
- premature atrial contraction (PAC)
- Premature Ventricular Contraction (PVC)
- Atrial or Ventricular Tachycardia (AT, VT)
- Supraventricular Tachycardia (SVT)
What are the possible causes of BRADY-dysrhytmia’s? What are the possible EKG manifestations of brady dysrhthymia’s?
Brady-dysrhytmia causes:
- Drugs - anti arrhythmics, Beta blockers, Ca antagonists, Digatalis, Barbiturates, Anethesia
- Ischemia or Infart
- Sick Sinus Syndrome
- Aging - fibrosis
Some EKG Manifestations:
a) sinus bradycardia
b) atrial or ventricular premature beats - these occur due to the loss of overdrive suppresion
Where can Re-entry of Excitation occur in the heart?
What are the three general requirements for re-entry of excitation?
Re-entry of Excitation can occur anywhere in the heart!
Most common cause of dysrhytmias seen clinically.
Three general requirements for re-entry of excitation:
- Geometry for a Conduction Loop
- Slow or delayed conduction
- Unidirectional Concuction Block
What are some of the causes of Re-entry of Excitation?
Causes of Re-entry of Excitation:
a) ischemia
b) infarction
c) congenital bypass tracts (example Wolf Parkinson White aka “WPW” where there are little connections between atria and ventricles)
What are the manifestations of Re-entry of Excitation on an EKG?
EKG Manifestations of Re-entry:
- Premature atrial or ventricular beats
- Atrial or Ventricular Tachycardia
- SVT
- Atrial Flutter
- Atrial or Ventricular Fibrillation
Where can Triggered Activity occur in the heart?
Triggered Activity can occur in atrial or ventricular tissues
Explain the mechanism of a DAD.
Elevated calcium is taken up by the SR. When the SR becomes overloaded with calcium, and AP can trigger an abnormal release of Ca AFTER an action potential had ended. This released Ca is extruded from the cell via Na/Ca exchanger, causing depolarization and thus causing a Delayed Afterdepolarization.
What is a DAD due to essentially?
What are the possible causes for DAD?
What are the possible EKG manifestations of a DAD?
DAD is due to abnormally high intracellular calcium
Clinically documented in dysrhythmias resulting from digitalis toxicity
Possible Causes:
a) digatalis toxicity
b) elevated catecholamines
c) rapid HR
d) all of those combined
Possible EKG manifestations: premature atrial or ventricular contractions (PAC or PVC)
Explain DADs and PVCs
DAD can result in PAC or PVCs. For Premature Ventricular Contractions, they might occur spontaneously and then not recur, or they may lead to ventricular tachycardia and VF.
Explain what an EAD is.
What are the possible causes
Possible EKG manifestations?
EAD: (more dangerous than DAD)
a) related to prolongation of action potential duration
b) mechanism is still not certain but believed to be due to abnormal reactivation of slow inward L type Ca channel
c) also may contribute to prolonged Q-T syndrome by extending duration of the action potential
Possible causes: acidosis (as in ischemia), hypokalemia, quinidine, slow heart rates (ALL OF THESE CAUSE LENGTHENED AP DURATION, leads to triggered activity)
Possible EKG manifestations: PAC or PVC, atrial or ventricular tachycarida (torsades)