Glossary of Cardiology part I

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LV contraction
LV relaxation
systolic pressure
max pressure in systole
diastolic pressure
min pressure in diastole
dicrotic notch
marks end of systole and beginning of diastole
dicrotic wave
pressure changes in diastole
central venous pressure is equal to what?
RAP (right atrial pressure)
describe how the cardiac action potential (AP) initiates contraction
(1) electrical impulse arises in sino-atrial node (SAN)
(2) electrical impulse first activates the atria
(3) then spreads via the atrioventricular node (AVN) to the His-Purkinje system and then to the ventricles
smallest branches of arteries, undergo vasoconstriction and vasodilation to regulate the blood flow by changing resistance to flow to an organ or through the entire circulation
what regulates arteriole diameter?
autonomics, circulating vasoactive hormones, and local metabolites
total peripheral resistance

the resistance to blood flow for the systemic circulation as a whole
- P wave
atrial depolarization
- QRS complex
ventricular depolarization
- T wave
ventricular repolarization
Describe how the events in the cardiac cycle are based on the LV

before systole:
- ventricular P is lower than arterial P and lower than atrial P
- semilunar valves are closed and the AV valves are open

- as blood rushes into ventricles, increasing P causes AV valves to snap shut (S1 -- "lubb")
- at this point all valves are closed and P builds up as the ventricles contract
- P increases until it reaches Paortic, then the semilunar valves open

- as contraction ends, LV P begins to fall; when falls to below Paortic the aortic valve snaps shut
- the pulmonic valve closes after the aortic valve
- closing of the semilunar valves causes second heart sound (S2 - "dup")


- first an isovolumetric relaxation
- then LV pressure falls to below atrial pressure and AV valves open
- ventricles are passively filled until the very end: atrial contraction
cardiac sarcomere:
- thin filaments
f-actin, troponin, tropomyosin
cardiac sarcomere:
- thick filaments
compare #'s b/t cardiac & skeletal muscle:
- myofibrils
- SR
- mitochondria
- T-tubules
- cardiac muscle has less myofibrils, a smaller SR volume, but a greater # of mitochondria than does skeletal muscle
- T-tubules are found at each Z-line in the ventricle and are much wider than in skeletal muscle
How does the junction of the SR and sarcolemma differ in heart and skeletal muscle?
In heart the SR forms diads with limited SR-T-Tubule contact. In skeletal muscle triads envelope the T-tubules
How does Ca2+ interact with troponin-C?
- when Ca2+ rushes into intracellular environment, it binds to troponin C (TnC) which causes tropomyosin to shift on the thin filament
- this unblocks the myosin binding site and allows weak binding of actin to myosin
- weak A-M complexes become strong A-M complexes (cross-bridges) that rapidly split ATP and generate force
- formation of strong A-M's increases the Ca2+ affinity of TnC
compare and contrast the Na+/Ca2+ exchanger and the Sarcolemmal Ca2+ pump
- both push Ca2+ from intracellular to the extracellular environment

- Na+/Ca2+ exchanger is a high capacity, low affinity transporter, which means that it can transmit LOTS of Ca2+ when the concentration is high

- sarcolemmal Ca2+ pump is a low capacity / high affinity pump, which means that it transmits a lot less Ca2+, but that it works well even at low [Ca2+]i
by what means does the SR push Ca2+ inside?
Ca-ATPase pump
What is the siginificance of the fact that mitochondria can accumulate Ca2+?
Mitochondria CAN accumulate Ca2+, but this process is not important with regards to muscle contraction because the uptake is slow. Rather, the accumulation is more important in regulating ATP production
electrical syncytium of heart
every fiber is activated (no recruitment)
by what mechanism does the heart prevent stimulation at a high enough rate?
refractory period
the intrinsic ability of the muscle to generate force independent of muscle length
the number of cycling cross-bridges depends on two factors. What are they?
- the number of strong A-M complexes (a fxn of length)

- the fraction of TnC bound to Ca (which depends on [Ca2+]i and TnC Ca2+ affinity
what are three factors that alter contractility?
(1) ANS
(2) drugs and ions
(3) Heart Rate
what effect does SNS have on contractility?
sympathetic NS via norepinephrine -- positive inotropy
what effect does PSNS have on contractility?
parasympathetic NS via acetylcholine -- negative inotropy
ascending staircase model of contractility
- why are several contractions necessary to obtain a new steady-state?
due to the time required for Ca2+ accumulation by the SR
- rest potentiation
after a longer than normal interval between beats, the first beat will exhibit greater than normal (potentiated) contractile F
post-extrasystolic potentiation
an early extrasystole (i.e. extra beat) has a reduced contractile force -- but the next beat exhibits greater than normal contractile force
active tension
active tension = total tension - resting tension
length at which max developed tension is generated
T/F -- Skeletal muscle is "stiffer" than cardiac muscle

Resting tension increases more rapidly with increasing muscle length in heart than in skeletal M
what accounts for the difference between resting stiffness of cardiac and skeletal M?
different titin isoforms
force-velocity relationship
- max velocity of shortening is where?
at zero load
force-velocity relationship
- zero velocity is where?
when load is equal to the isometic tension
force-velocity relationship
- shifted upward and to the right by?
- increased initial length
- increased contractility
- increased heart rate
what are the four major factors that determine the viscosity of blood?
temperature, hematocrit, tube diameter, and shear rate
stroke volume (SV)
amount of blood ejected during systole (ml/beat)
end diastolic volume (EDV)
volume of blood in ventricle the instant before systole begins
end systolic volume (ESV)
volume of blood in ventricle at completion of systole as marked by closure of the aortic and pulmonic valves
ejection fraction
cardiac index
CO/body surface area
cardiac fxn curve
relates right atrial P (RAP), factor controlling blood flow into the heart, to cardiac output, the blood flow out of the heart
what represents the preload on the intact heart?
atrial P
what represents the afterload on the intact heart?
arterial (aortic) P
pressure-volume loop
cycle of contraction, ejection, relaxation, and refilling
what factors cause the cardiac fxn curve to plateau?
increasing afterload, inelastic pericardium
positive inotropic intervention does what?
increases SV and CO
which has a higher compliance: veins or arteries?
why doesn't the pressure in the arteries and veins fall to zero?
because there is still an enclosed volume
mean circulatory pressure
the pressure in the system at zero flow
What is the "knee" of the vascular fxn curve due to?
negative pressures in the thoracic cavity -- veins collapse like straws when sucked on too hard
two ways to change the stressed volume
(1) change the blood volume
(2) change the amount of blood subjected to stress
capacitance eqn
Ca = dV/dP
what are the two most common ways to change the mean circulatory pressure (Pmc)?
change blood volume

venous contraction
what is the rate of cardiac oxygen consumption proportional to?
amount of ATP synthesized & the amount utilized
what is the primary source of energy (metabolic) of cardiac muscle?
fatty acids
Fick Principle
The amount of oxygen consumed by an organ per unit time must equal the difference between the amount entering the organ via the arterial supply and the amount leaving via the veins.
which is more costly (in terms of oxygen consumption) -- work done to increase pressure in the ventricle or work done to increase the volume?
work done to increase the pressure
a beta adrenergic blocker, inhibits the positive inotropic and chronotropic effects of the symp NS
a vasodilator -- reduces O2 demand by reducing tension development
positive inotropic agent, increases SV and consequently decreases end diastolic volume and radius
Vascular Fxn Curve
- Pms
- Cv/Ca & TPR
- Intrathoracic pressure
- Pms determines the zero intercept
- Cv/Ca and TPR determine slope
- Intrathoracic P determines "knee"
inc contractility
inc contractility --> inc SV & CO --> dec RAP (more blood pumped out of the heart) --> inc VR (decreased pressure gradient back to heart is inc). New state state CO = VR, higher than before.
inc blood volume
inc VR --> inc RAP (more blood going to heart) --> inc CO (Frank-Starling). New steady state: CO = VR, higher than before.
inc VR --> inc RAP --> inc CO (Frank-Starling). New steady state: CO = VR, higher than before.
(1) inc afterload --> dec CO --> inc RAP

(2) dec VR --> dec RAP

two RAPs kind of cancel (we wouldn't be responsible to know exactly how)

New steady state: CO = VR, lower than before
Dec contractility
dec SV & CO --> inc RAP --> dec VR. New steady state: CO = VR, lower than before
Is the highest P at the end of systole?
No, it is slighly before the dicrotic notch
what is central venous pressure essentially equal to?
right atrial pressure (RAP)
where do the electric impulses the inititiate cardiac muscle contraction arise?
what is the approximate duration of the cardiac contraction?
350 ms
what are the three main important fxns of the CV system?
- moves material
- moves heat
- transmits force (erectile)
transmural P for a vessel
intravascular P - extravascular P
what is the typical CO for a 70 kg individual?
5 L/min
For a cardiac function curve, which values are held constant?
contractility, TPR, HR
what two factors lead to the upper plateau of the cardiac function curve?
(1) increasing afterload

(2) inelastic pericardium
cardiac fxn curve
- above which HR is diastole too brief for complete filling?
above HR > 100
cardiac fxn curve
- HR x SV peak at what HR?
125 beat / min
which has a higher compliance: arteries or veins?
mean circulatory P

aka mean systems pressure

pressure in the system at zero flow
what is the driving force for venous return?
Pven - Pms
Venous Return
(Pms-Pven) x [(Cv/Ca) + 1]
= --------------------------
what are the two ways to change the stressed volume?
(1) change the blood volume

(2) change the amount of blood subjected to stress
how does the body maintain the arteries and veins always partially constricted?
NE from the symp NS
what is a continuously released vasodilator?
what maintains the BP during the 2/3 of cardiac cycle when the heart is not actually ejecting blood?
elastic recoil of the arteries
Pp = Ps - Pd
pulse pressure
- eqn relating Pp, SV, Ca
Pp ~= ----
how can you use Fick Principle to calculate Cardiac Output?
CO = -------------------
[O2]PV - [O2]PA

q-total = O2 consumption
atherosclerosis therapy:
- prapranolol
- beta adrenergic blocker

- inhibits positive inotropic effects of symp NS
atherosclerosis therapy:
- nitroglycerin
- vasodilator

- reduces tension development
atherosclerosis therapy:
- digitalis
- inc contractility --> dec RAP --> dec EDV --> dec tension --> less MV O2 consumption (more efficient)
what are the three observable changes the symp NS has on the cardiac output / venous return graph?
NE binds to alpha-1 receptors on smooth muscle of vascular system

(1) in arterioles this means inc TPR, which decreases the slope of the vascular fxn curve

(2) in veins this decreases the unstressed volume, inc Pms, and shifts the vascular fxn curve x-intercept to the right

(3) NE also binds to beta receptors of the heart to produce a positive inotropic effect (inc contractility), which rotates the cardiac fxn curve to the left (counterclockwise)

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