Cardio - Physio

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

due to closure of both AV valves

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

• 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

• increase = increase
• decrease = decrease

• increase = decrease
• decrease = increase

• positive inotropic agents (digoxin) = increase
• negative inotropic agents = decrease

decrease

about 7

change in myocardial contractility

change in blood volume

MAP = CO * TPR

baroreceptors in carotid sinus/aortic arch

• 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

J_v = K_f [(P_c - P_i) - (π_c - π_i)]

• J_v = net pressure
• P = hydrostatic
• π = oncotic (protein)
• c = capillary
• i = interstitial

favors filtration vs favors reabsorption

• permeability of capillary wall
• assumed to be 1 unless given

• @ arterial end - favors filtration
• @ venous end - favors reabsorption

• not all fluid is reabsorbed at venous end (about 85%)
• proteins do not move so oncotic pressures remain stable
• lower pressure at venous end

atrial depolarization

ventricular depolarizatioin

ventricular repolarization

• segments are events
• intervals are time periods

AV delay

SA firing to AV firing

ventricular depolarization to repolarization

amount of Ca²⁺ influx

• HR = 60 (seconds) / R-R interval
• R-R interval = 1 cardiac cycle length

>100 bpm and regular

<60 bpm and regular

• prolonged PR interval
• slow conduction through AV node

progressive lengthening of PR interval ending in 1 dropped beat

• no impulses conducted
• atria and ventricles beat independently
• freq of P waves > QRS complexes

• ST segment depression
• T wave inversion

• elevated ST segment
• pathologic Q wave
• inverted T wave

• tall t waves
• long PR interval

pacemaker

AV delay - allows time for ventricular filling

conduct from SAN to AVN

from atria to ventricles

run in R and L ventricles

run in ventricluar muscles, fastest conducting component of all

• 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

enters during plateau phase via vg channels and causes release of additional Ca²⁺ from sarcoplasmic reticulum to generate contraction

• 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

• sympathetic effect on SA node
• NE binds with beta-1 receptors in - increased HR

• sympathetic effect on AV node
• increased conduction in AV node, decreased AV delay

• parasympathetic effect on SA node
• ACh binds w/M2 receptors - decreased HR

• parasympathetic effect on AV node
• decreased velocity of conduction - longer AV delay