Lecture 7 - Cardiac Rhythm

Question 1

Sinus rhythm maintained by?

Answer 1

entrainment and suppression of lower pacemakers, co-ordinated excitation, existence of prolonged refractory period in endothelium

Question 2

Arrhythmia - disorders of impulse formation?

Answer 2

early discharge of pacemaker or activity triggered by unstable resting membrane potential, leading to extrasystoles

Question 3

Arrhythmia - disorders of impulse conduction?

Answer 3

partial or complete AV block (leading to bradycardia), left and right bundle branch block and reentry (alternates ventricular activation sequence); arise due to spatial or temporal dispersion of repolarisation

Question 4

Types of reentrant arrhythmia?

Answer 4

atrial flutter (fast regular), AF (rapid disorganised), VT (rapid, risk of VF developent), VF (chaotic, leads to death)

Question 5

Atrial flutter?

Answer 5

fast regular atrial rate, sawtooth appearance, heart block may develop

Question 6

Wavelength of reentry activation?

Answer 6

wavelength = effective refractory period x cardiac volume; vulnerability increases with decreased RP and CV

Question 7

Reentrant activation requirements?

Answer 7

a circuit. slow conduction and/or ERP, unidirectional block, a trigger; slow conduction and unidirectional block can occur when repolarisation is not spatially homogenous

Question 8

Rate of propagation of ectopic beat - during vulnerable period (T wave)?

Answer 8

NaC dont fully reset so reduced Na current -> slower propagation; or non-uniform repolarisation increases probability of local conduction block

Question 9

Myocardial Ischemia - potential for arrhythmia?

Answer 9

slow conduction, reduced AP duration (both reducing wavelength), non-uniform repolarisations (increased prob. local depol. block), ectopic activations (DADs) (trigger)

Question 10

Causes of slow conduction in MI?

Answer 10

decreased ATP, Na/K ATPase and therefore gradients, causing a partial membrane depolarisation, deactivating NA channels, gap junctions also reduced due to metabolic acidosis

Question 11

ECG signs of WPW syndrome?

Answer 11

short PR, delta wave , wide QRS

Question 12

AP changes in MI

Answer 12

shortens: decreased Na/K ATPase increases Na(i) and K(o), hyperkalemia outside of cell means more rapid repolarisation (ATP reduction also shortens AP)

Question 13

Delayed-after-depolarisation in MI?

Answer 13

impaired Ca homeostasis increases intracellular Ca, spontaneous Ca release from SR, increaseing Ca efflux through channel and causing abnormal depol and activation

Question 14

VT complications?

Answer 14

+ve feedback loop of: rapid rate, poor contraction, increased O2 demand w decreased supply, more severe ischemia ALL -> VF

Question 15

Cardiac rhythm of healed MI?

Answer 15

monomorphic VT due to infarct border zone complex

Question 16

Heart failures effect on cardiac rhythm?

Answer 16

structural and cellular changes, atria dilation (re-entrant risk), pressure increase (stretch activated ion channels) and fibrosis (conduction slowing), altered NCX (DADs), ANS input remodelling, VT/VF risk

Question 17

Long Qt syndrome physiology?

Answer 17

prolonged action potentials causing Ca influx leads to early after depolarisation

Question 18

Causes of increased AP (long QT)?

Answer 18

amiodarone, extracellular hypokalaemia (decreased influx), K and Na ion channel mutations

Question 19

Long Qt ECG?

Answer 19

polymorphic VT, Torsade de Pointes, reseolves or forms VF