Cardiac Physiology/Biochem Flashcards
Is energy required to set a cardiac membrane back to baseline during the process of contraction?
Yes; ATP is required for ATP pumps to reset cardiac muscle cells
What are the different types of cardiac muscle?
atrial + ventricular muscle (contract like skeletal muscle with longer duration)
specializied muscle fibers (excitatory and conductive) - automatic rhytmical electrical d/c in form of APs, controls rhythmic beating of heart
Describe the histology of cardiac muscle
striated muscle fibers in lattice (in series, parallel)
myofibrils w/ actin + myosin that slide during contraction
intercalated discs that separate individual cardiac cells; at each disc, cell membranes fuse to form permeable communicating gap junctions
what are gap junctions? what is their purpose?
intercellular channels that allow cell to cell transfer of ions and small molecules
they allow for rapid diffusion of ions
the gap junctions allow for cardiac muscle to be a _______. what does this mean?
synctium; when one cell excites, the AP spreds rapidly to all and do a synchronized contraction
there are two synctiums; atrial and ventricular; to allow for atria to contract before ventricles
where does the cardiac AP occur?
in all cardiac myocytes except SA and AV nodes, which have their own system
what are the steps (without description) of the cardiac muscle AP?
phase 0 - rapid depolarization
phase 1 - initial repolarization
phase 2 - plateau
phase 3 - rapid repolarization
phase 4 - return to resting membrane potential
explain phase 0 of cardiac muscle conduction
rapid depolarization
fast VG sodium channels open, sodium flows rapidly into cell (+1) > quickly depolarizes cell membrane
in background, slow VG calcium channels open (2+), making it even more pos
explain phase 1 of cardiac muscle conduction
initial repolarization
fast VF sodium channels close
fast VG potassium channels open > +1 leaving cell > cell begins to repolarize, but does not fully repolarize bc slow VG calcium channels are still open (+2)
explain phase 2 of cardiac muscle conduction
plateau
fast VG potassium channels close
slow VG calcium channels still open and the concentration of calcium is now high enough to trigger:
- Ca release from SR
- myocyte contraction via excitation contraction coupling
explain phase 3 of cardiac muscle conduction
rapid repolarization
slow VG calcium channels close
slow VG potassium channels open > +1 charge leaving cell
what phase of cardiac muscle contraction is the main difference from other muscle types contraction/APs?
phase 2 - plateau
explain phase 4 of cardiac muscle conduction
resting membrane potential
high permeability of potassium through potassium channels
about -80/-90 mV
explain how excitation-contraction coupling works
cardiac AP spreads to inferior membrane along t-tubules >
t tubules use L type Ca channels to act on membranes of longitudial sarcoplasmic tubules which triggers release of Ca ions from SR > myofibrils + promote sliding
= contraction
after plateau, Ca influx stops, Ca pumped back into SR and t tubule ECS via:
- calcium ATPase pump
- Na-Ca exhanger (ca taken out, na comes in)
-Na-K ATPase pump (na taken out, k comes in)
main differences between cardiac and skeletal muscle
Cardiac muscle has all of the below and skeletal does not:
the myocytes are coupled electrically by gap junctions and intercalated discs (synchronized contraction)
AP has plateau (due to ca influx, k efflux)
requires Ca influx from ECF to induce Ca release from SR
what are the two main phases of the cardiac cycle and what occurs during each?
systole - contraction/ejection
diastole - relaxation/filling
what generates the cardiac cycle?
spontaneous generation of AP in sinus node
what is the relationship between the heart rate and the cardiac cycle?
cardiac cycle is reciprical of HR
faster HR = shorter duration of cardiac cycle = shorter diastole (systole does not shorten)
what aoccurs during diastole? what begins diastole?
ventricles fill with blood
allows passive flow of blood from A > V
begins with opening of AV valves
what are the subphases of diastole?
rapid inflow
diastole
atrial systole (contraction of atria to give extra 20% of filling to ventricles)
what aoccurs during systole? what begins systole?
ventricles ejecting blood to either lungs or systemic circulation
allows active ejection
starts with closure of AV valves
what are the subphases of systole?
isovolumic contraction (contraction without emptying, inc pressure before atria opens)
ejection
isovolumic relaxation
what are the right sided heart valves?
tricuspid
pulmonary
what are the left sided heart valves?
mitral
aortic
what is the relationship of the semilunar valves to the cardiac cycle?
open to start ejection (systole), close to start diastole
what is the relationship of the AV valves to the cardiac cycle?
open to start rapid inflow in disastole, close to start systole
where do we see papillary muscles? what is their purpose?
papillary muscles attach AV valves via chordae tendinae, stabilize the valves - do NOT close/open valves
is the opening of valves active or passive?
passive; due to pressure gradient pushing blood forward or backward
describe the aortic pressure curve
how does this compare to the RV/PA pressure curve?
pressure dec during diastole, becasue the aortic valve is closer
at the end of isovolumic contraction, aortic valve opens
during ejection, aortic pressure rises to equal that of ventricles (~120mmHg), then dec back to baseline (~80mmHg) after closure of aortic valve
a similar action occuring in RV and PA but pressure numbers are much smaller
describe the atrial pressure curve
initial (a) wave occurs during atrial sysole, due to atrial contraction
secondary (c) wave occurs during isovolumic contraction due to back bulging of AV valves from ventricular pressure inc
last (v) wave occurs during isovolumic relaxation due to filling of atria wihtout AV valve being open yet (this sets up the body for rapid filling of ventricles)
what are the phase of the ventricular pressure/volume curves
phase 1 - filling
phase 2 - isovolumic contraction
phase 3 - ejection (systole)
phase 4 - isovolumic relaxation
phase 1 of ventricular pressure/volume curve
period of filling (diastole)
volume:
- starts at ESV, ends at EDV
pressure:
- mild pressure increase
phase 2 of ventricular pressure/volume curve
isovolumic contraction
volume:
- NO volume change (still at EDV)
pressure:
- increases due to contraction without valve opening
phase 3 of ventricular pressure/volume curve
period of ejection (systole)
volume:
- decreases due to ejection through the aorta
pressure:
- increased pressure at initial contraction/ejection, then starts to decrease
phase 4 of ventricular pressure/volume curve
isovolumic relaxation
volume:
- NO volume change (still at ESV)
pressure:
- pressure returns to diastolic pressure level due to aortic valve closing
EKG components
P wave
- due to depolarization through atria
- followed by (causes) > atrial contraction
QRS complex
- due to depolarization through ventricles
- followed by (causes) > ventricular contraction
T wave
- due to repolarization of ventricles
- happens slightly before isovolumic relaxation
where is the repolarization of the atria on an EKG?
you can’t see it; happens somewhere behind QRS complex
on abnormal EKG, at times can be seen as a U wave
the S1 heart sound happens when
closure of AV valves (near isovolumic contraction)
the S2 heart sound happens when
closure of semilunar valves (near isovolumic relaxation)
by what mechanisms is the cardiac cycle regulated?
- intrinsic cardiac pumping regulartion in response to changes in volume of blood flowing though heart (frank starling mechanism)
- control of HR and heart strength by ANS
how does the frank starling mechanism regulate the cardiac cycle?
the frank starling mechanism is the hearts ability to adapt to increased volumes of blood ;
the more the heart msucle is stretched during filling > the greater force of contraction (actin + myosin brought to max overlap) > the greater quantity of blood pumped to aorta > arteries
what comes in (venous return) must go out
how does the ANS regulate the cardiac cycle?
sympathetic stimulation > increased CO, inc HR + force of contraction > inc vol of blood pumped + ejection pressure
parasympathetic stimulation > dec CO, minor dec strength of contraction, MAJOR dec HR
why does parasympathetic stimulation only minorly dec contraction strength but majorly decreases HR?
vagal n fibers are distributed more to the atria than the ventricles; atria house SA node whereas ventricles have more musculature/contractile function
how do irregular levels of potassium ions affect the heart? why?
excess extracellular potassium >
dilated, flaccid heart > slowed HR
block conduction from A >V
this happens bc potassium:
dec resting membrane potential (less neg)
dec intensity of AP
dec heart contraction
how do irregular levels of calcium ions affect the heart? why?
excess intracellular calcium ions have opposite effect of increased EC pottasium:
> spastic contraction BC calcium initiates the cardiac contractile process
dec intracellular calcium > cardiac weakness (similar to effects of high EC potassium)
what effect does temperature have on HR? why?
inc body temp > inc HR
heat inc permeability of cardiac muscle membrane to ions that control HR > this inc the self-excitation process
what are the changes in temp and HR during exercise?
during exercise the hearts strength of contraction is temporarily inc with a moderate temp inc
delayed moderate temp inc will eventually > temporary weakness of contraction due to metabolic needs
summarize the pathway of conduction throughout the heart
SA node > internodal pathways in atria > AV node > AV bundle > to ventricles via purkinje fibers > R and L bundle branches
where along the conduction pathway is the impulse delayed? why?
impulse is delayed at the AV node/AV bundle to allow time for atria to empty blood into ventricles and allow atrial contraction to occur
happens bc there is a fibrous insulating barrier everywhere along the A/V separation except for the A/V node and bundle
AND in this area there are fewer gap junctions b/w cells > slows transmission of AP due to slower ion permeability
what is the SA node? where is it located?
small, flat strip of cardiac muscle cells with NO contractile muscle filaments
located on superior, posterolateral wall of RA below and lateral to opening of SVC; contacts with atrial muscle fibers directly, controls beat of heart
what are the differences between the AP of the SA node versus that of a ventricular muscle fiber?
SA node fibers have:
a less neg RMP > fast sodium channels blocked from opening
longer waiting period before depolarization caused by leaky Na and Ca ions
> slower AP overall
what causes self excitation of the SA node?
a high concentration of sodium in the ECF encourages sodium to leak inside the cell through inward “funny” channels, down its concentration gradient (ca also slowly influxing)
b/w heartbeats, influx of Na ions > slow rise in resting MP
once MP reaches -40 mV (orig -60), L type ca channels open > trigger AP
where is the AV node located?
posterior wall of RA behind tricuspid valve
how do purkinje fibers compare to ventricular muscle fibers?
larger and therefore transmit AP faster
where are the purkinje fibers located? what is their purpose?
beneath endocardium and spread over entire ventricle, eventually becoming continuous with ventricular muscle fibers
this allows for instantaneous transmission of cardiac impurlse through ALL of ventricular muscle and allows a synchronous + strong contraction of ventricles
what is the pacemaker of the heart, and why?
what is the HR from this pacemaker? what would it be if other impulses took over?
SA node; the d/c rarte is faster than that of AV or purkinje so they recieve the SA impulse before they can generate their own
SA HR: 70-80 bpm
Ectopic Pacemaker rates:
AV: 40-60
Purkinje: 15-40
how does the parasympathetic system affect the rhymicity and conduction of the heart?
vagal n stimulation (mainly at SA and AV nodes, minimally innervated to A+V muscle)
release of Ach at vagal n endings > Ach inc permeability of membrane to potassium > inc membrane negativity (hyperpolarization) > tissue is less excitable
=
dec rate of SA node > dec HR
dec excitability of AV junctional fibers between atrial muscle and AV node > slowed transmission of impulse to ventricles > dec HR
how does the sympathetic system affect the rhymicity and conduction of the heart?
sympathetic nerves are distributed to all parts of the heart, w a strong showing in ventricualr muscle
NE released at nerve endings > stimulates beta-1 adrenergic receptors > inc cardiac rhymicity and conduction (unknown mechanism)
=
inc rate SA node d/c
inc rate of conduction and level of excitability
inc force of contraction of muscles (esp ventricles)
what does the R-R interval on an EKG represent?
rate of one single cardiac cycle or heartbeat
what does the P-Q/P-R interval on an EKG represent?
depolarization of atria through the start of ventricular contraction
what does the Q-T interval on an EKG represent?
depolarization and repolarization of ventricles
