Cardio Electrophysiology - Part of Ballam Flashcards
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
Preload
end-diastolic volume – related to right atrial pressure
o Increased venous return increases end-diastolic volume, stretches or lengthens ventricular muscle fibers
Afterload
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%
