The cardiac skeleton consists of 4 bands of
dense collagenous tissue - fibrous rings
central fibrous body/trigone - function
supports 4 valves + insulator that prevents contact bw myocardial cells and stops n impulses
layers of pericardium
fibrous (outermost) and serous (visceral and parietal)
pericarditis vs pericardial effusion
inflammation of the pericardium, reducing pericardial fluid (friction)
fluid accumulation, increased p, tamponade (wall collapse)
Myocytes arranged in
myofibrils - striated and branched
Myocytes in myocardium are connected by ________ that help them adhere to desmosomes
intercalated discs
Pores in myocardium that allow electric conductivity?
gap jxns of connexin proteins bw myocytes
layers of cells of endocardium
outer - n, v, purkinje fibers
middle - connective tissue
inner - endothelial cells
Which conducting tissue is normally suppressed instead of performing spontaneous action potentials
SA node
Electrophysiological cardiac cycle steps (3)
action potential in SA node
action potential thru atria then av bundle then ventricles (delay)
signal to bundle of His then Purkinje fibers to ventricular myocytes
How does action potential carry out
myocardium made of sarcomeres that contract if Ca+2 released from sarcoplasmic reticulum
What happens after action potential causes inward Ca+2 current?
triggers release more Ca2+ in sarcoplasmic reticulum, binds to troponin C, tropomyosin moves out and actin + myosin make cross-bridges
Relaxation of action potential occurs when
ca2+ reaccumulated in sarcoplasmic reticulum by Ca2+ ATPase
Ventricular diastole begins when
cardiac valves closed + ventricles relax
ventricular systole begins after
atrial systole, valves close
What happens in ventricular diastole
ventricles relax + p falls
valves open + blood flows from atria to ventricles
v + p rises, atria contract (systole)
What happens in ventricular systole
ventricular p rises, closing valves
isovolumic contraction until aortic + pul valves open and blood ejected into circ
Stroke volume
The amount of blood ejected from the ventricle in one contraction
EJection fraction
the fraction of the end-diastolic volume ejected from the heart, measures ventricular efficiency/ contractility
cardiac output
the total volume of blood ejected from the ventricle per minute
Cardiac output depends on
stroke volume (v ejected on 1 beat) and heart rate (# beats/min)
Stressed volume
The volume of blood contained in the arteries
Smooth muscles in walls of arterioles are always
contracted (tonically active)
sympathetic adrenergic nerve fibers of arteriole's smooth muscle walls
a1 - in arterioles of vascular beds, vasoconstrictor
b2 - in arterioles of skeletal m, vasodilator
Lipid vs water-soluble substances thru capillary walls
lipid - cross by dissolving in and diffusing across
water - cross by clefts or pores of fenestrated caps
Blood flow thru vessel is determined by
pressure diff bw ends of vessel and resistance of vessel to blood flow
Total Peripheral Resistance (TPR)
the resistance to the flow of blood through the entire systemic circulation
Poiseuille's equation - resistance to flow is :
proportional to viscosity + length
inversely to r 4 of vessel
Series vs. Parallel resistance
series - total resistance equal to sum of individual resistances
parallel - resistance in parallel way less than individuals, no loss p in big a.
Korotkoff sounds
series of sounds that correspond to changes in blood flow through an artery as pressure is released (turbulent flow)
positive vs neg inotropy
pos - increase contractility, SV, CO
Pulse pressure
difference between systolic and diastolic pressure, reflects stroke volume
pulse pressure depends on
stroke volume and arterial compliance
Mean Arterial Pressure (MAP) (def + dependent on)
pressure forcing blood into tissues
peripheral resistance and cardiac output
in the steady state, cardiac output from the heart equals
venous return to the heart
3 types of cardiac muscle + their levels of contractability
Atrial
Ventricular
Excitatory & conductive (low)
What do myocytes do with synaptic input from autonomic neurons?
use synapses to modulate (not initiate) electrical activity + contractile force of cardiac muscle
Myocytes are surrounded by __________ which delimits the __________
sarcolemma
sarcoplasm/cytoplasm
A vs I bands of myofibrils
dark regions (anisotropic)
light regions (isotropic)
I bands are divided in the middle by darker lines called
Z lines
Protein aggregates of sarcomere
contractile (actin and myosin), regulatory and structural proteins
structure of myosin
2 heavy chains in helix and 4 lights chains
2 types of myosin
a (higher atpase activity) and b (higher velocity contraction)
cross-bridges of myosin
protruding arms and heads, that bind to actin
3 isoenzymes of heavy chains
V1 - 2 a chains
V2 - a and b chains
V3 - 2 b chains
Which isoenzyme of heavy chains is dominant in atrial myocardium vs ventricular myocardium
V1 in atrial
all 3 in ventricular
2 types of actin (thin filaments)
globular (G, monomer) and fibrillar (F, in vivo)
Constitution of an actin molecule
2 G actins that make F actin - 2 F actins in helix
The main regulatory proteins of the sarcomere are represented by
tropomyosin and troponin (only in actin)
Where is tropomyosin bound when resting?
rest - active sites of actin (blocks interaction bw actin and myosin, no contraction)
protein subunits of troponin + roles
troponin C - binds Ca2+
troponin T - structural, binds troponin w/ tropomyosin
troponin I - inhibitory
What do the regulatory proteins do during contraction?
Ca+2 binds to troponin C, tropomyosin moves deeper into grooves bw actins, myosin sites uncovered
Function of titin
anchors thick myosin to Z line w/ its extensible part
power stroke
action of myosin pulling actin inward (toward the M line), when Ca2+ levels high
sliding filament mechanism
Myosin binds to actin when it breaks down atp (closer to backbone) . The myosin then alters its configuration, resulting in a "stroke" that pulls on the actin filament and causes it to slide across the myosin filament, sarcomere shortens
Sympathetic stimulation _________ activity of Ca+2 channels
increase
Activity of Ca2+ ATPase
energy from atp cleavage expels ca2+ from cell (against gradient), stimulated by calmodulin
Na+/Ca2+ exchanger
sarcolemmal protein w/ Transverse tubules that expulses ca2+
the passive release of Ca+2 from sarcoplasmic reticulum occurs thru
ryanodine-receptor channels in jxnal region of sarcoplasmic reticulum
What does Ca2+-dependent ATPase transport?
performs ca2+ reuptake into sarcoplasmic reticulum
phospholamban
regulatory protein in contractile myocardium that inhibits Ca2+ ATPase in the sarcoplasmic reticulum
Ca2+ storage in sarcoplasmic reticulum relies on binding to _________, a protein in jxnal region of SR
calsequestrin
____________ of myocyte plays a buffer role of intra/extracell Ca2+ concs
mitochondria
Action potential is caused by opening of 2 channels
voltage-activated fast sodium channels (same as skeletal)
L-type calcium channels (slow)
After the onset of action potential, what decreases in cardiac m membrane
permeability for K+ ions (less outflux)
At the end of plateau of cardiac action potential, what happens?
Ca+2 influx stops and they are pumped back out into SR and T tubule extracell space, sodium transported out
Phase 1: initial repolarization
-Na+ channels close
-K+ leave thru open K+ channels
Phase 2: plateau
Ca+2 channels open + influx, fast K+ channels close (efflux)
(+ brief repolarization)
Phase 3: Rapid Repolarization
Ca+2 channels close, slow K+ channels open
How is the T tubule system in cardiac muscle different from skeletal muscle?
T-tubules @ Z lines - part of extracell, helps in Ca+2 diffusion from extracell
Ca2+ induced Ca2+ release (CICR)
most important trigger for Ca+2 rise, increased Ca2+ in SR causes further release
Action potential is conducted via
T tubules in myocyte
_________ stimulation is the main physiological factor that modulates electro-mechanical coupling, related w/ β1-adrenergic receptors stimulation to induce ____________
sympathetic
phosphorylation (of channels, increase Ca2+)
absolute refractory period of heart
time during which normal cardiac impulse can't re-excite an already excite area, longer in ventricles