Cardio Electrophysiology - Part of Ballam Flashcards Preview

Cardio II Midterm > Cardio Electrophysiology - Part of Ballam > Flashcards

Flashcards in Cardio Electrophysiology - Part of Ballam Deck (24)
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P wave

atrial depolarization
o Does not include atrial repolarization – hidden in QRS complex


PR Interval

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


QRS complex

depolarization of the ventricles


QT interval

entire period of depolarization and repolarization of the ventricles


ST segment

isoelectric, period when ventricles are depolarized


T wave

ventricular repolarization


A wave

Venous phase

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


C wave

Venous phase

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


V wave

Venous phase

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


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

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


SA node cardiac AP phases with explanations

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


AV node upstroke of AP

result of inward Ca2+ current


Absolute refractory period

begins with upstroke of the AP, ends after the plateau



end-diastolic volume – related to right atrial pressure
o Increased venous return increases end-diastolic volume, stretches or lengthens ventricular muscle fibers



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


Frank-Starling Relationship

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


Ventricular pressure volume loop

• 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


Increased preload in ventricular pressure-volume loop

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


Increased afterload in ventricular pressure-volume loop

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


Increased contractility in ventricular pressure-volume loop

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


Cardiac and vascular function curves

• 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


Stroke volume

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


Cardiac output

Stroke volume X HR


Ejection fraction

(Stroke volume)/(end-diastolic volume)
• Normal 55%