Heart Flashcards
Elements of contraction
Actin, myosin, SEC (attached to actin + myosin), PEC (attached to actin + myosin + SEC), collagen (rich fiber system => overexpansion is prevented)
- Isometric phase: only SEC are stretched
- Isotonic phase: when stretch in balance with weight => shortening
- Max filling: collagen fibers -> max resistance (prevent rupture)
Single working fibers
In short sarcomeric length: low performance, increased length: increased performance. In heart muscle entry of Ca into sarcomeric space is length dependent.
Total working musculature
“Law of the heart”- Starling and Frank:
Heart m adapt itself to higher requirements automatically (increased stretch => increased contraction)
Volume fractions
- EDV: blood in the heart- end of diastole (ventricles max filled)
- ESV: ————” “——— systole (ventricles mostly empty)
- SV: EDV - ESV, -> aorta (~80)
CO
V of blood -> aorta by the LV per unit time
Fick’s principle (Law of Conservation of Mass)
CO = total O2 consumption divided by the arterio-venous [O2] difference
CO = SV X fr
SV = EDV - ESV
=> CO = (EDV - ESV) X fr
Starling’s experiment
- Increases venous return (EDV, ESV) => SV + CO increase
- Chenge the peripheral resistance => CO + SV unchanged
=> hart can increase its diastolic reserves => increase stretch + performance
Work of the heart
Outer (mechanical) + inner (heat production): Wt = Wo + Wi
Kinetic component = 4%
Wo = SV X ΔP (P diff bw aorta and v.c)
Wt = O2 consumption X equivalent energy of O2
E (efficiency): Wo / Wt
Rushmer diagram: work of the heart during cardiac cycle
- Mitral valve closes => Isovolumetric conduction
- Aortic valve opens => ejection phase
- Semilunar valves close => isovolumetric relaxation
- Mitral valve opens => filling
Stewart’s principle
Injecting Evans-blue i.v -> plot curve and before recirculation do extrapolation
Area under the extrapolated curve = CO.
Factors influencing CO
- EDV: diastolic filling time, ventricular compliance, maintained by CVP (v.c + atrial P)
- ESV: contractility- depends on isometric max tension
In constant metabolic state: increasing preload => increases isometric tension, Vmax does not change
In altered: Sm + Vmax change
Contractility increases by S + decreases by PS activity - Frequency: S effect: artificial increase -> decreased duration of diastole => Starling’s effect doesn’t work => CO decreases, normal increase: remaining diastolic time (Starling works) => SV + CO increase
PS effect: const firing of vagus n => freq decreases => contractility decreases
Excitable tissues
- Working fibers: elongated AP, prevent the heart from early secondary contraction.
An AP closer to the base + endocardium has a longer plateau phase than that closer to the apex + epicardium - Pacemakers: NO permanent RMP, but const depolarization
- Conductive system: rapid spreading of stimuli => synchronized contraction bw atria + ventricles
AP of working fibers
▪️Average of RMP = -90mV
▪️Electr impulse -> stimulation => RMP -> threshold potential
▪️=> Na channels open -> Na influx from EC (1 enters the 0-phase)
0-phase - depolarization: cont influx, MP ~ +25mV => inactivation of channels
1-phase - overshoot: => repolarization: Cl influx, K efflux
2-phase - plateau: Ca channels open => Ca influx, K channels open => K efflux. Balance => elongation => prevention of a premature AP
3-phase - full repolarization: late K channels open => K rapidly flows out while Ca channels close => electrochemical gradient
“Absolute refractory period”: stimulus -> after 0-phase + before the end of 2-phase => cannot elicit new AP
“Relative refractory period”: stimulus -> after the end of 2-phase, but before reaching threshold potential => if strong -> new AP
“Supernormal Period”: bw threshold + RMP, even a slight stimulus => new AP
Electromechanical coupling
🔹DIAD (skeletal m: triad): T-tubules + SR are in contact.
L-type Ca (tubular) + Ca dependent (SR) + membrane Ca dependent (EC) channels open => HUGE amount of Ca around sarcomeres => contraction
ATP-dependent pump: Ca -> SR
Na/Cl antiport: Ca -> EC space
IC Ca => relaxation
Cardiac cycle
Systole (contraction) + Diastole (relaxation).
Total length (Ca) = 800msec
- Ventricular Systole (270msec):
Ventricles are filled with blood => tension closes the cuspidal valves (to the atria). Tension keeps increasing => CC shorten + SEC stretch, no V change => “isovolumetric contraction”: when P in ventr > P found in aorta + pulmo a => semilunar valves open (50 msec)
Increasing tension => heart: ovoid -> spherical shape
Auxotonic contraction: blood -> large aa (220msec)- fast ejection (80% of SV = 90msec) + slow ejection (tension drops = 130msec)
- Ventricular Diastole (530msec):
Isovolumetric relaxation: P in ventricles < P in atria -> passive opening of cuspidal valves => filling phase (120msec).
Isotonic relaxation: Isotonic filling (410msec)- fast filling (60% = 110msec), reduced filling (NA node => new AP => depolarization + contraction of atria commences = 190msec), atrial systole (110msec)
Parameters of cardiac cycle
- P: determines the position of valves + flow of blood, changes
- V: Isovolumetric stage = const, Systole (early ejection) = decreased, Diastole: rapid filling and then reduced
- Valves: semilunar = closed during diastole/ opened during systole, cuspid = the opposite
- Heart sounds: 1st: systolic heart sound (closure of cuspid valves) + vibration of m contraction (weak) + turbulence of blood due to closure of valves (pronounced) + due to fast ejection (weak)
2nd: diastolic heart sound (closure of semilunar valves- 1st aortic)
3rd: filling of ventricles
4th: turbulent flow by atrial contraction (may lack) - Jugular P: sudden cardiac relaxation (heart -> cran => increases P in jugular v)
