Cardio Electrophysiology - Part of Ballam Flashcards

1
Q

P wave

A

atrial depolarization

o Does not include atrial repolarization – hidden in QRS complex

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2
Q

PR Interval

A

initial depolarization of the ventricle
o Depends on conduction velocity through AV node
• In heart block – PR interval increases
• Sympathetic nervous system stimulation (B1) increases conduction velocity – PR interval decreases
• Parasympathetic (M) decreases conduction velocity – PR interval increases

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3
Q

QRS complex

A

depolarization of the ventricles

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4
Q

QT interval

A

entire period of depolarization and repolarization of the ventricles

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5
Q

ST segment

A

isoelectric, period when ventricles are depolarized

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6
Q

T wave

A

ventricular repolarization

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7
Q

A wave

A

Venous phase

increase in atrial pressure (venous pressure) caused by atrial systole

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8
Q

C wave

A

Venous phase

bulging of the tricuspid valve into right atrium during right ventricular contraction

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9
Q

V wave

A

Venous phase

blood flow into right atrium – rising phase of the wave; from right atrium into right ventricle – falling phase of wave

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10
Q

Phases in Ventricle, atrium and purkinje system cardiac APs and explanation of each

A

o Phase 0
• Upstroke of AP
• Transient increase in Na+ conductance, inward Na+ current depolarizes membrane

o Phase 1
• Brief period of initial repolarization
• Outward current, movement of K+ ions out of cell, decrease in Na+ conductance

o Phase 2
• Plateau of AP
• Transient increase in Ca2+ conductance – inward Ca2+ current, increase in K+ conductance
• Outward and inward currents equal – membrane potential stable at plateau level

o Phase 3
• Repolarization
• Ca2+ conductance decreases, K+ conductance increases and predominates
• Large outward K+ current hyperpolarizes membrane back to K+ equilibrium potential

o Phase 4
• Resting membrane potential
• Inward and outward currents of K+ equal

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11
Q

SA node cardiac AP phases with explanations

A

o Unstable resting potential

o Phase 0
• Upstroke of AP
• Increase in Ca2+ conductance – increase causes inward Ca2+ current drives membrane toward Ca2+ equilibrium potential.

o Phase 3
• Repolarization
• Increased K+ conductance – outward K+ current repolarizes membrane potential

o Phase 4
• Slow depolarization – pacemaker activity of SA node automaticity
• Increase in Na+ conductance – inward Na+ current – turned on by repolarization

o Phases 1 and 2 not present

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12
Q

AV node upstroke of AP

A

result of inward Ca2+ current

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13
Q

Absolute refractory period

A

begins with upstroke of the AP, ends after the plateau

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14
Q

Preload

A

end-diastolic volume – related to right atrial pressure

o Increased venous return increases end-diastolic volume, stretches or lengthens ventricular muscle fibers

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15
Q

Afterload

A

o aortic pressure – Increases in aortic pressure increases afterload on the left ventricle
o pulmonary artery pressure – increases in pulmonary artery pressure causes increase in afterload on the right ventricle

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16
Q

Frank-Starling Relationship

A

o Increases in stroke volume and cardiac output occur in response to an increase in venous return or end-diastolic volume

o Increases in end-diastolic volume cause an increase in ventricular fiber length, which produces an increase in developed tension

o Mechanism that matches cardiac output to venous return – greater venous return = greater cardiac output

o Changes in contractility shifts Frank-Starling curve upward (increases contractility) or downward (decreased contractility)
• Increased contractility cause increase in CO for any level of right atrial pressure or end-diastolic volume
• Decreased contractility cause decrease in CO for any level of right atrial pressure or end-diastolic volume

17
Q

Ventricular pressure volume loop

A

• 1 → 2 Isovolumetric contraction
o normal volume about 140 mL – end-diastolic volume
o All valves are closed, no blood ejected from ventricle

• 2 → 3 ventricular ejection
o Aortic valve opens at 2, blood ejected into aorta (stroke volume), ventricular volume decreases
o Volume remaining at point 3 is end-systolic volume

• 3 → 4 isovolumetric relaxation
o ventricle relaxes at point 3, aortic valve closes
o all valves closed, ventricular volume is constant

• 4 → 1 Ventricular filling
o mitral valve opens, filling of ventricle begins
o Ventricular volume increases to about 140 mL – end diastolic volume

18
Q

Increased preload in ventricular pressure-volume loop

A

o Increased end-diastolic volume due to increased venous return
o Increase in stroke volume – increased width of the pressure-volume loops

19
Q

Increased afterload in ventricular pressure-volume loop

A

o Increased aortic pressure – ventricle must eject blood against a higher pressure → decrease in stroke volume
o Decreased stroke volume reflected in decreased width of the pressure-volume loop.
o Decrease in stroke volume results in an increase in end-systolic volume

20
Q

Increased contractility in ventricular pressure-volume loop

A

o Ventricle develops greater tension, causing increase in stroke volume
o Decrease in end-systolic volume

21
Q

Cardiac and vascular function curves

A
  • Cardiac output as a function of end-diastolic volume
  • Venous function – relationship between blood flow and right atrial pressure

o MAP – point vascular function intercepts x axis
• Point there is no flow in the cardiovascular system
• Altered by an change in blood volume, change in venous capacitance
• Increase shifts curve to the right; decrease shifts to left

o Slope of venous return curve – resistance of arterioles

  • Steeper curve – decrease in total peripheral resistance (TPR)
  • Increased venous return
  • Shallower curve – increase in TPR
  • Decreased venous return

• Intersection – right atrial pressure
o Equilibrium point: CO = venous return

22
Q

Stroke volume

A

(End-diastolic volume) – (End-systolic volume)

23
Q

Cardiac output

A

Stroke volume X HR

24
Q

Ejection fraction

A

(Stroke volume)/(end-diastolic volume)

• Normal 55%