Cardio Lec 6 Flashcards
Positive chronotropic agents do what
elevate hr (epi, norepi)
Negative chronotropic agents do what
lower hr (ach)
Heart beats independent of NS
t
At rest _NS dominates
PNS (keeps hr < 100bpm)
During exercise _NS dominates
SNS (hr > 100bpm)
What keeps hr < 100 bpm at rest
Ach
1 heart beat every time __ fires
SA node
Tachycardia factors
stress, drugs, heart disease, fever, caffeine, anemia, hyperthyroidism (very common)
Bradycardia factors
sleep, athletes, hypothermia
Intrinsic rate of SA node
100 bpm (but kept below this at rest by…)
Heart rate controlled by
pacemaker potential (rate of rise to threshold by nodal cells ANS affects this)
SNS makes pacemaker cells depolarize more
quickly
PNS makes pacemaker cells depolarize more
slowly
Main mediator of the PNS
vagus n.
If vagus n. severed & remove parasympathetic influences from the heart, hr would
go up bc PNS is what keeps hr down
How does the PNS affect the pacemaker cells?
Ach closes ca & na channels (doesn’t allow + ions in) -> opens k channels (allow + ions to exit) -> makes nodal cells take VERY LONG to DEPOLARIZE
How does the SNS affect the pacemaker cells?
norepi bind beta1 rs -> incr cAMP -> opens ca & na channels (+ ions enter cell) -> allow cells to DEPOLARIZE to threshold QUICKER
CO peaks at about __ & why
180 bpm bc anything greater -> filling time compromised bc diastole shortens so much & output will start to fall
EDV aka
preload
At rest, most blood is held on __ side
venous (capacitance vessels)
During exercise, venous return goes
up
When EDV/preload incr so too does
SV (Starling’s Law of the heart) HEALTHY HEART
Frank Staling’s Law
SV is directly proportional to EDV/preload
In a healthy heart, EDV is proportional to
SV
In an unhealthy heart, as EDV increases or stretches too much, eventually
SV begins to fall bc some cross-bridges lost -> fibers not aligned -> can’t be used since binding sites on actin not aligned w/ myosin heads
The more cross-bridges (actin & myosin interactions) the more
contractile force
If EDV too low ->
ventricles not stretched enough -> actin filaments overlap one another -> can’t use binding sites -> can’t maximize cross-bridges -> can’t get max contractile force
EDV changes commonly so have to match more blood in w/ more blood out
T
Contractility refers to
greater contractile force at a CONSTANT EDV
Contractility uses excess ___ to get more interactions for a greater force of contraction
calcium
Starling’s Law vs Contractility
IN BOTH: greater contractile force due to more actin & myosin interactions. Starling’s more interactions due to: fibers align properly VENTRICLES MORE STRETCHED; Contractility more interactions due to: EXCESS CALCIUM (calcium moves tropomyosin & allows actin & myosin to interact)
Inotropicity
by flooding more calcium -> more interactions -> bc inhibition relieved
The only thing that can increase contractility is
an increase in intracellular calcium
Starling’s Law relies on
STRETCH
Ejection fraction refers to
% of EDV that is ejected at a given afterload
After load refers to
load heart has to work AGAINST to eject blood
Norm ejection fraction
65%
Ejection fraction calc
EDV / SV
ONLY factor that can increase ejection fraction is
increase in contractility
Only thing that can increase contractility
calcium
Aortic pressure is the
after load
Only way semilunar valve opens
ventricular pressure must exceed aortic pressure
We want after load to be low or high?
low so heart doesn’t have to work as hard
Muscles isometric point
point at which muscle can only generate ISOMETRIC CONTRACTION bc after load is so great - heart cant contact against it
If bp got so high that reached isometric point ->
Co would be 0 -> stay in isovolumetric phase -> wouldn’t enter ejection phase
As you get to a higher EDV, isovolumetric point shifts
out bc heart can generate more forceful contraction bc fibers more aligned
If nothing else changes, why would SV decrease as after load increases?
bc aortic semilunar valve will open LATER. (its spending more time generating PRESSURE, less time for blood to get EJECTED)
Main determinant of after load
total peripheral resistance (TPR)
TPR refers to
sum of all arterial resistance; determines bp & aortic pressure
An increase in tpr result in an increase in
after load
Venous return affects EDV
t
Capacitance vessels
veins (store blood)
Resistance vessels
arteries
Venous side low press low resistance pathway
t
Factors that aid venous return
valves, respiratory pump/breathing (by lowering r. atrial press), skeletal muscle pump, PRESSURE GRADIENT (high->low), exercise/MOVEMENT, sympathetic stimulation
Anything that lowers r. atrial pressure will
improve press gradient -> aid venous return
Anything that increases r. atrial pressure will
lowers press gradient -> retards venous return
We want to keep r. atrial press __ so that __
minimized, blood can go from bottom up (high press -> low)
