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Stroke Volume
Volume of blood ejected by each ventricle in 1 beat.
SV = EDV - ESV ml/beat
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Ejection Fraction
Fraction of EDV ejected in 1 beat.
EF = SV/EDV
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Cardiac Output
Volume of blood ejected by each ventricle per minute.
CO = SV * HR ml/min
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1st Heart Sound
due to closure of both AV valves
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2nd Heart Sound
due to closure of both semilunar valves (mitral and tricuspid)
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Mitral Stenosis
narrowing/obstruction @ opening of mitral valve
diastolic murmur appears
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Mitral Insufficiency
leaky mitral valve, regurgitation from LV to LA during vent. systole
systolic murmur appears
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Aortic Stenosis
narrowing around aortic valve, increased afterload, LV hypertrophy
systolic murmur appears
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Aortic Insufficiency
leaky aortic valve, regurgitation from aorta to LV
diastolic murmur appears
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Isovolumetric Contraction
ventricles full (EDV), QRS, pressure closes AVV = 1st heart sound
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Rapid Ejection
SLV open, max P, V decreases
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Reduced Ejection
P falling, ejection @ lower rate, ESV remains in ventricles @ the end
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Isovolumetric Relaxation
P falls, SLV's close, 2nd heart sound, V remains same as ESV
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Rapid Filling
P falls below that of atria, AV valves open, max filling, V increases, P low as ventricles are relaxing
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Reduced Filling
filling continues, blood flow less, P gradient is low, LONGEST phase (can do w/o)
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Atrial Systole
end of ventricular diastole, P wave - atria contract, small amt of blood into ventricles - EDV - ventricles ready for next systole
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Fick's Principle
cardiac output = (O2 taken up by lungs per minute) / (O2 content of pulm vein - O2 content of pulm artery)
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Frank-Starling Relationship
SV is inversely proportional to EDV
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Frank-Starling Curve
(Cardiac Function Curve)
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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
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Effect of contractility:
Increase?
Decrease?
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Effect of preload on SV?
- increase = increase
- decrease = decrease
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Effect of afterload on SV?
- increase = decrease
- decrease = increase
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Effect of myocardial contractility on SV?
- positive inotropic agents (digoxin) = increase
- negative inotropic agents = decrease
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Effect of loss of myocardial tissue (MI) on SV?
decrease
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Normal mean circulatory filling P
about 7
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Effect of changing total blood vol on vascular function curve?
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What changes the cardiac function curve?
change in myocardial contractility
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What changes the vascular function curve?
change in blood volume
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Effect of increasing contractility on combined curves?
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Effect of changing TBV on combined curves?
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Effect of changing TPR on combined curve?
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Progressive changes in heart failure? (combined curves)
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Mean arterial pressure formula?
MAP = CO * TPR
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Short term control of BP changes?
baroreceptors in carotid sinus/aortic arch
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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
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Starling equation
J v = K f [(P c - P i) - (π c - π i)]
- Jv = net pressure
- P = hydrostatic
- π = oncotic (protein)
- c = capillary
- i = interstitial
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+ Starling P vs - Starling P
favors filtration vs favors reabsorption
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Kf
- permeability of capillary wall
- assumed to be 1 unless given
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Movement of fluid @ arterial end of capillary vs at venous end
- @ arterial end - favors filtration
- @ venous end - favors reabsorption
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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
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P wave
atrial depolarization
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QRS complex
ventricular depolarizatioin
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T wave
ventricular repolarization
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segments vs intervals
- segments are events
- intervals are time periods
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PR interval
SA firing to AV firing
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QT interval
ventricular depolarization to repolarization
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ST segment
amount of Ca2+ influx
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HR and R-R interval
- HR = 60 (seconds) / R-R interval
- R-R interval = 1 cardiac cycle length
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Sinus tachycardia
>100 bpm and regular
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Sinus bradycardia
<60 bpm and regular
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1st degree heart block
- prolonged PR interval
- slow conduction through AV node
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2nd degree heart block
progressive lengthening of PR interval ending in 1 dropped beat
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3rd degree heart block
- no impulses conducted
- atria and ventricles beat independently
- freq of P waves > QRS complexes
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ECG in angina
- ST segment depression
- T wave inversion
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ECG in MI
- elevated ST segment
- pathologic Q wave
- inverted T wave
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ECG in hyperkalemia
- tall t waves
- long PR interval
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AV node
AV delay - allows time for ventricular filling
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Atrial internodal pathways
conduct from SAN to AVN
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Bundle of His
from atria to ventricles
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Bundle branches
run in R and L ventricles
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Purkinje fibers
run in ventricluar muscles, fastest conducting component of all
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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
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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
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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
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Positive chronotropic effect
- sympathetic effect on SA node
- NE binds with beta-1 receptors in - increased HR
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Positive dromotropic effect
- sympathetic effect on AV node
- increased conduction in AV node, decreased AV delay
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Negative chronotropic effect
- parasympathetic effect on SA node
- ACh binds w/M2 receptors - decreased HR
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Negative dromotropic effect
- parasympathetic effect on AV node
- decreased velocity of conduction - longer AV delay
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