Bradyarrythmias: Disorders of the Sinoatrial Node Flashcards
Autonomic Nervous System
Regulates the rate of phase 4 diastolic depolarization and thus the firing rate of both primary (SA node) and subsidiary pacemaker.
2 most common causes of pathologic bradycardia
SA node dysfunction
AV conduction block
Only reliable therapy for symptomatic bradycardia in the absence of extrinsic and reversible etiologies (inc vagal tone, hypoxia, Hypothermia)
Permanent pacemaking
Where is the SA node?
Sulcus terminalis on the epicardial surface at the right atrial superior vena cava junction
Where does the SA nodal artery arise from?
right coronary artery (55-60%)
left circumflex artery (40-45%)
Slow conduction within SA node explained by
Absence of I(Na) and poor electrical coupling
Most common causes of extrinsic SA node dysfunction
Drugs and autonomic nervous system influences
Other extrinsic causes of SA node dysfunction
Hypothyroidism, sleep apnea, Hypothermia, Hypoxia, and increased intracranial pressure (cushing’s response) and endotracheal suctioning via activation of the vagus nerve
Inflammatory disorders that are associated with SA nodal disease ( sinus bradycardia, sinus arrest and exit block)
Pericarditis, Myocarditis, Rheumatic Heart Disease
Infiltritative disorder in patients typically in the ninth decade of life
Deposition of amyloid protein in the atrial myocardium
Senile amyloidosis
Ophthalmoplegia
Pigmentary degeneration of the retina
Cardiomyopathy
Kearns-Sayre Syndrome
Coexisting diseases that may hasten deposition of fibrous tissue in SA node
CAD DIabetes Mellitus Hypertension Valvular diseases Cardiomyopathies
Incidence of persistent atrial fibrillation or atrial flutter in SA node dysfunction increases in the ff condition
Advanced age Hypertension Diabetes mellitus Left Ventricular Dilation Valvular Heart Disease Ventricular Pacing
ECG manifestation of SA node dysfunctin
sinus bradycardia Sinus pauses sinus arrest sinus exit block tachycardia (in SSS) Chronotropic incompetence
Chronotropic incompetence
inability to increase the heart rate in response to exercise