CV 1 Flashcards
Inotropy definition
Strength of contraction
Chronotropy definition
rate of contraction
Lusitropy definition
Relaxation
Dromotropy definition
Conduction
Bathmotropy definition
Excitability
The heart pumps how much blood
6 L/min
8640 L/day
2282. Gallons/day
CO =
CO = HR x SV
SV =
SV = EDV - ESV
MAP =
MAP = CO x TPR
MAP = 2x DBP + SBP / 3
F ( Tissue Blood flow ) =
F = MAP / VR
of Nucleus in cardiac myocytes
1 per myocyte
Titin
~ Giant Protein
~ Bungee cord of the heart
~ molecular spring that functions as passive elasticity for the muscle (striated muscle)
What are Titans made of
Immunoglobulins
Intercalated disks are comprised of:
Fascia Adherens
Desmosomes
Gap Junctions
What do Fascia Adherens do
~ Anchoring sites for myocyte
~ Connect to the closest myocyte
What do Desmosomes do
~ Specialized for cell to cell adhesion
~ Resist searing forces
What do Gap Junctions do
~ Think electrical
~ Allow Ads to spread between cardiac cells - permits ion passages
~ Connexons: specialized tunnels
What separates the Atrial syncytium and Ventricular syncytium?
Thick fibrous connective tissues
What is the Cardiac Muscle controlled by
ANS
length of cardiac action potential
200 msec
Resting membrane potential of cardiomyocyte is
-90 mV
What maintains -90mV of the cardiiomyocyte?
constant outward leak of K+ through - inward rectifier channels
Phase 0
Depolarization
~ Threshold is reached at -70 mV activating fast Na+ channels
~ Rapid depolarization
~ L-type Ca+ channels open at -40 mV
~ Overshoot to +30
Phase 1
Early repolarization
~ Some K+ channels open briefly and outward flow of K+ returns TMP to 0 mV
Phase 2
Plateau phase
~ L-type Ca2+ channels are still open - small constant influx of Ca2+. Becomes significant in the *** excitation contraction coupling process
~ K+ leaks out - delayed rectifier K+ channels
~ K+ permeability decreases x5
~ Two currents are electrically balanced at 0 mV
Phase 3
Repolarization
~ Ca2+ channels gradually inactivate
~ K+ outflow exceeds Ca2+ inflow.
~ Membrane ionic concentrations are restored by
- Na+ - Ca2+ exchanger,
- Ca2+ ATPase
- Na+ - K+ Atpase
Phase 4
Resting membrane potential
Number of cardiac T-tubules
1 tubule to 1 SR ( Diad )
( Triad in skeletal )
DHP receptor differences
Electrochemical in cardiac
Electromechanical in skeletal
Cardiac T tubules
5x diameter in skeletal
What does phospholamban do
inhibits re-uptake of calcium into the SR
What happens when phospholamban is phosphorylated
When phosphorylated it becomes inactive (disinhibition) increasing Ca++ uptake by the SR (enhances lusitropy)
Normal mitral annulus
3 - 3.5 cm
Normal aortic annulus
1.8 - 2.3 cm
AV valve properties
~ Thin, flimsy, low pressure valves
~ Papillary muscles
~ Chordae Tendinae
prevents bulging into atria during contraction
Semilunar valve properties
~ Strong yet pliable fibrous tissue
~ Smaller diameter compare to AV valves
~ More rapid ejection and valve closure
~ Prone to mechanical abrasions
Total duration of cardiac cycle
70 bpm; 1/70 = 0.014 min/beat or 0.84 sec
What is the delay between atria and ventricular contraction? Why?
~ 0.1 seconds
~ To allow for ventricular filling
Atria contract ______ second ahead of the ventricles
1/6
Resting membrane potential of SA nodal fibers
-55 to -60 mV
Why isn’t the SA node depolarized all the time?
Ca++ channels become inactive after about 150ms of opening
Atrial muscle velocity
0.3m/sec
Specialized conduction fiber velocity
1m/sec
What 4 Specialized conduction fibers are in the Atria
~ Anterior Interatrial band (Bachman’s Bundle) Right atrium to Left Atrium
~ Anterior Internodal Pathway
~ Middle Internodal Pathway
~ Posterior Internodal pathway
AV node delay
0.09 sec delay in node
AV node location
Posterior wall of right atrium behind tricuspid valve
AV bundle delay
0.04 sec delay
Conduction travels through the AV node then through the AV bundle what are the associated delays?
~ AV node - 0.09 sec
~ AV bundle - 0.04 sec
What causes delay at the AV node and AV bundle
reduction in number of gap junctions between the AV node and the AV bundle (resistance to conduction = slow excitation)
Purkinje conduction velocity
1.5 - 4 m/sec ( 6x ventricular muscle conduction velocity)
Purkinje fibers are
Large fibers ( larger than ventricular muscle fibers )
Conduction velocity from bundle branches to terminating purkinje fibers
0.03 seconds
Conduction velocity from endocardium to epicardium
0.03 seconds
Conduction velocity from bundle branches to contraction
0.06 seconds
What happens with PNS stimulation
ACh is released which increases membrane permeability to K+
This causes hyper-polarization = less excitability ( SA node -65 to -75mV )
What happens with SNS stimulation
Release of NE stimulates B1 adrenergic receptors
increased membrane permeability of Na+ and CA++ ions ( closer to threshold - decreasing conduction times )
~ increases nodal discharge
~ increases chronotropy
~ increases isotropy
~increases overall heart activity
At rest, O2 consumption by beating heart =
9mL / 100g / min