cardiac rhythm Flashcards

1
Q

what is sinus rhythm maintained by

A
  • entrainment and suppression of lower pacemaker
  • coordinated excitation via specialised conduction system
  • existence of prolonged refractory period in the myocardium
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2
Q

what are arrhythmias due to

A

disorders of impulse formation
- e.g. DAD, EAD

disorders of impulse conduction
- e.g. AV block, LBBB, reentry, dispersion of repolarization

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3
Q

types of reentrant arrhythmia

A
  • atrial flutter
  • atrial fibrillation
  • ventricular tachycardia
  • ventricular fibrillation
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4
Q

describe atrial flutter

A
  • fast regular atrial rate
  • p wave = sawtoothed appearance
  • ignores SA node
  • don’t all get through to the ventricular due to the AV node
  • all the same shape P wave due to the circuit in the atria being the same over and over again
  • normal QRS as when it gets through normal system
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5
Q

describe atrial fibrillation (AF)

A
  • rapid disorganised atrial activation
  • not all impulsed conducted to ventricles
  • QRS still normal due to fast conduction system
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6
Q

describe ventricular tachycardia

A
  • rapid ventricular activation
  • impaired mechanical function and risk of VF
  • wide QRS complexes as its not using the conduction system
  • p wave absent
  • rapid regular rhythm
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7
Q

the inactivation of Na+ channels are important in which phase of the cardiac action potential

A

refractory period

- longer as sodium channel takes time to repolarise back

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8
Q

re-entrant circuit model

A
  • region of block e.g. scar tissue, inactive area
  • usually impulse travels either side of region of block (collide & continues)
  • if activation blocked down one side (unidirectional block) → spreads around & can re-enter
  • vulnerability to re-entry increases w/ ↓CV or ERP
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9
Q

describe wavelength equation

A

wavelength = ERP * CV

  • more likely to get a re-enttrant activation with decreased conduction velocity (CV) or decreased refractory period
    gives the cell more time to repolarise
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10
Q

what does re-entrant activation require

A
  • a ‘circuit’
  • slow conduction and/or short ERP
  • unidirectional block
  • a trigger
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11
Q

describe wolf-parkinson white syndrome

A
  • ventricles activated through accessory pathway
  • wide QRS as its not using the fast conduction system
  • delta wave, short P-R interval
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12
Q

rate of propagation of electrical activation determined by:

A
  • electrical properties of myocytes
    (increased coupling between increases propagation. Rate > in larger cells)
  • inward current during excitation
    (density and status of Na+ channels)
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13
Q

describe how and when ectopic beats occurs

A
  • occurs during vulnerable period (T wave)
  • Na+ channels not fully reset so reduce Na+ current (slower propagation)
  • repolarization non-uniform giving greater chance of local conduction block
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14
Q

myocardial ischaemia results in:

A
  • slow conduction
  • reduced AP duration
  • non-uniform repolarization
  • ectopic activations (DADs)
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15
Q

why does slow conduction occur in myocardial ischaemia

A

low ATP → ↓Na/K ATPase & reduction of gradients → partial membrane depolarisation →
(partial) inactivation of Na channels → ↓INa → ↓ rate of spread

↓ pH due to regional metabolic acidosis → ↓ gap junction coupling

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16
Q

describe the action potential changes in myocardial ischaemia

A

low ATP → ↓Na/K ATPase & reduction of gradients → hyperkalaemia shortens AP duration (IKr)

low ATP also activates IK, ATP → shortens AP duration

as this only occurs in ischemic regions, gives differences in electrical properties (AP duration, conduction velocities) = non-uniform repolarisation

17
Q

describe delayed after depolarisations (DADs)

A

trigger for myocardial ischaemia

  • impaired Ca homeostasis (due to↓Ca ATPase activity) → ↑Ca conc in SR
  • may lead to episodic Ca-induced Ca release from SR → efflux of Ca via NCX
  • NCX is electrogenic → activation
18
Q

describe the ways in which myocardial ischaemia can result in re-entry

A
  • slow conduction and reduced AP duration = reduced wavelength
  • ectopic activations (DADs) = trigger
  • nonuniform depolarisation = ↑ probability of local conduction block
19
Q

consequences of VT in acute MI

A

VT means their rate has increased but still poor conduction. As a result, theres an increased demand for O2 but a reduced O2 supply. Causing more severe ischaemia
- positive feedback cycle
risk for VF

20
Q

rhythm changes in HF

A
  • atria dilate → increases re-entrant path lengths & promote AF
  • ↑ atrial P → stimulates stretch-activated channels = currents at the wrong time
  • atrial fibrosis → regional slowing of conduction
  • altered expression & function of NCX (can cause DADs → re-entrant arrhythmia)
  • remodeling of autonomic nervous system (influences electrical properties)
21
Q

describe early after depolarizations (EADs)

A
  • caused by prolonged action potential which enable Ica(L) to re-activate
22
Q

what causes an increased AP duration

A
  • drugs (amiodarone)
  • reduced extracellular K conc (hypokalaemia)
  • K+ ion channel mutations, changing current through
  • Na+ ion channel mutations