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Volume of blood ejected by each ventricle in 1 beat.
SV = EDV - ESV ml/beat
Fraction of EDV ejected in 1 beat.
EF = SV/EDV
Volume of blood ejected by each ventricle per minute.
CO = SV * HR ml/min
1st Heart Sound
due to closure of both AV valves
2nd Heart Sound
due to closure of both semilunar valves (mitral and tricuspid)
narrowing/obstruction @ opening of mitral valve
diastolic murmur appears
leaky mitral valve, regurgitation from LV to LA during vent. systole
systolic murmur appears
narrowing around aortic valve, increased afterload, LV hypertrophy
systolic murmur appears
leaky aortic valve, regurgitation from aorta to LV
diastolic murmur appears
ventricles full (EDV), QRS, pressure closes AVV = 1st heart sound
SLV open, max P, V decreases
P falling, ejection @ lower rate, ESV remains in ventricles @ the end
P falls, SLV's close, 2nd heart sound, V remains same as ESV
P falls below that of atria, AV valves open, max filling, V increases, P low as ventricles are relaxing
filling continues, blood flow less, P gradient is low, LONGEST phase (can do w/o)
end of ventricular diastole, P wave - atria contract, small amt of blood into ventricles - EDV - ventricles ready for next systole
cardiac output = (O2 taken up by lungs per minute) / (O2 content of pulm vein - O2 content of pulm artery)
SV is inversely proportional to EDV
(Cardiac Function Curve)
Mech of Starling's Relationship
- 1. increase in venous return
- 2. increase in ventricular filling + EDV
- 3. stretching of ventricular muscle fibers
- 4. increase in initial length of muscle fibers
- 5. more crossbridges during contraction
- 6. increase mycardial tension
- 7. increase in SV and CO
Effect of contractility:
Effect of preload on SV?
- increase = increase
- decrease = decrease
Effect of afterload on SV?
- increase = decrease
- decrease = increase
Effect of myocardial contractility on SV?
- positive inotropic agents (digoxin) = increase
- negative inotropic agents = decrease
Effect of loss of myocardial tissue (MI) on SV?
Normal mean circulatory filling P
Effect of changing total blood vol on vascular function curve?
What changes the cardiac function curve?
change in myocardial contractility
What changes the vascular function curve?
change in blood volume
Effect of increasing contractility on combined curves?
Effect of changing TBV on combined curves?
Effect of changing TPR on combined curve?
Progressive changes in heart failure? (combined curves)
Mean arterial pressure formula?
MAP = CO * TPR
Short term control of BP changes?
baroreceptors in carotid sinus/aortic arch
Long term control of BP changes?
- low BP sensed in kidney - renin secreted - converts angiotensinogen to angiotensin I in plasma - ACE converts angiotensin I to angiotensin II in lungs -
- in kidney stimulates aldosterone secretion - increased Na+ reabsorption
- in hypothalamus stimulates secretion of ADH - increased H2O reabsorption in kidney
- salt + water retention = increased arterial BP
) - (πc
- Jv = net pressure
- P = hydrostatic
- π = oncotic (protein)
- c = capillary
- i = interstitial
+ Starling P vs - Starling P
favors filtration vs favors reabsorption
- permeability of capillary wall
- assumed to be 1 unless given
Movement of fluid @ arterial end of capillary vs at venous end
- @ arterial end - favors filtration
- @ venous end - favors reabsorption
Why does capillary hydrostatic pressure decrease along the length of the capillary?
- not all fluid is reabsorbed at venous end (about 85%)
- proteins do not move so oncotic pressures remain stable
- lower pressure at venous end
segments vs intervals
- segments are events
- intervals are time periods
SA firing to AV firing
ventricular depolarization to repolarization
amount of Ca2+ influx
HR and R-R interval
- HR = 60 (seconds) / R-R interval
- R-R interval = 1 cardiac cycle length
>100 bpm and regular
<60 bpm and regular
1st degree heart block
- prolonged PR interval
- slow conduction through AV node
2nd degree heart block
progressive lengthening of PR interval ending in 1 dropped beat
3rd degree heart block
- no impulses conducted
- atria and ventricles beat independently
- freq of P waves > QRS complexes
ECG in angina
- ST segment depression
- T wave inversion
ECG in MI
- elevated ST segment
- pathologic Q wave
- inverted T wave
ECG in hyperkalemia
- tall t waves
- long PR interval
AV delay - allows time for ventricular filling
Atrial internodal pathways
conduct from SAN to AVN
Bundle of His
from atria to ventricles
run in R and L ventricles
run in ventricluar muscles, fastest conducting component of all
Fast response type action potential
- phase 0 - rapid depolarization, vg Na+phase 1 - initial brief repolarization, vg Na+ close, outward K+ due to high electrochemical gradient
- phase 2 - plateau, vg Ca2+
- phase 3 - rapid repolarization, vg K+
- phase 4 - resting phase
What is the role of Ca2+ in the fast response AP?
enters during plateau phase via vg channels and causes release of additional Ca2+ from sarcoplasmic reticulum to generate contraction
Slow response type AP
- phase 4 - unstable resting phase, gradual depolarization due to:
- 1- inward Na+ channels
- 2- decreased K+ conductance
- phase 0 - vg Ca2+ channels
- phase 3 - vg K+ channels
Positive chronotropic effect
- sympathetic effect on SA node
- NE binds with beta-1 receptors in - increased HR
Positive dromotropic effect
- sympathetic effect on AV node
- increased conduction in AV node, decreased AV delay
Negative chronotropic effect
- parasympathetic effect on SA node
- ACh binds w/M2 receptors - decreased HR
Negative dromotropic effect
- parasympathetic effect on AV node
- decreased velocity of conduction - longer AV delay