Cardiac Physiology-03 Flashcards
myocardium
responsible for pumping action, striated involuntary muscle, fibers swirl diagonally around the heart in bundles; the heart wrings blood out of the ventricles
functional syncytium
merging cells performing as a unit; those of the heart are joined electrically
myocytes
form a functional syncytium; in b/w adjacent cells, cardiac cells have branching patterns (Y shapes, Z shapes)
intercalated discs
specialized connections between myocardial cells containing gap junctions and desmosomes
desmosomes
help structurally glue adj. myocytes together; so when one contracts the other contracts + are pulling on e/o to transmit force to blood contained within ventricle
gap junctions
each half of a gap junction is formed in one cell and the other; functions to allow ions to move freely b/w these cells to electrically connect them
- when AP is generated within myocyte in apex, AP spreads like propagated wave through each adjacent myocyte up to base of heart
- wave of contraction occurs from apex to base
SA node
back of right atrium, opening for SVC; where pacemaker cells are found constantly depolarizing, stim. resting HR spontaneously, AP spreads as a wave across all myocytes of atrium to spread across L and R atrium
AV node
base of RA, pacemaker cells depolarize slower, wave slows down when AP reaches this point; fewer gap junctions, gives time to allow atria to contract and send blood to ventricles before electrically stimulating ventricles
AV bundles (bundle of His)
straddles fibrous skeleton, allows an electrical signal to go from atria to ventricles
R and L bundle branches
stim. various regions of ventricle to ensure L and R ventricles contract simultaneously
phases of an AP in a ventricular myocyte
depolarization, plateau, repolarization, refractory period
depolarization phase
AP generated by pacemaker cell makes myocyte reach threshold; opening of voltage-gated sodium channels
plateau phase
voltage-gated potassium and calcium channels open (K+ out, Ca2+ in for stim./regulating contraction)
repolarization
when Ca2+ channels close and K+ channels stay open, depolarization back to RMP occurs; also assisted by sodium-potassium KTPase
refractory period
another cardiac AP cannot be generated; always longer than contraction phase b/c heart needs to relax to allow it to fill up
electrocardiogram
a composite record of APs produced by all the heart muscle fibers, detected at the surface of the body, 3 recognizable waves (P, QRS, and T), electrical event precedes mechanical event (takes time for AP to propagate to stim. myocardiocytes to cause them to release CA2+ to contract)
P wave
atrial depolarization
PQ segment
atrial contraction; slowing of AP conduction at AV node (smaller fibers; less gap junctions)
QRS complex
ventricular depolarization (and atrial repolarization); large amplitude due to amount of muscle in ventricles generating larger electrical signal
ST segment
systolic contraction continues
T wave
ventricular repolarization
after T wave
ventricular diastole (relaxation)
cardiac pressure
BP produced by contraction of heart; only present on arterial side of system and measured w/ sphygmomanometer
dicrotic wave
second wave that occurs when aortic valve closes
S1 sound
AV valve closure; ventricle starts to contract; pressure on AV valves which closes to prevent blood moving from ventricle to atria
S2 sound
SL valve closure; prevent blood from moving back from the aorta/pulm. trunk
isovolumetric contraction
as ventricle contracts, no blood moving anywhere in system, all valves closed, ventricles generate pressure against blood sitting in ventricle, contracts when pressure is greater than the aorta
isovolumetric relaxation
pressure dropping within ventricle, all 4 valves closed, AV valve hasn’t opened on left side until pressure is low enough for it to open
end-diastolic volume
volume left ventricle achieves at end of the diastolic phase
end-systolic volume
at the end of the ventricle undergoing systole
stroke volume
vol. of blood ejected from the LV or RV into the aorta (or pulm. trunk)
what is the formula for stroke volume?
SV = EDV - ESV
cardiac output
volume of blood ejected from the LV (or RV) into the aorta/pulm. trunk each min.
what is the formula for cardiac output?
CO = HR x SV
factors regulating stroke volume
preload, contractility, afterload
preload
degree of stretch on the heart before it contracts
contractility
forcefulness of contraction of individual ventricular muscle fibers; strength of contraction at any given preload and due to changes in cytosystolic calcium lvls (influx from ECF, release from SR)
what increases contractility?
positive inotropic agents
what decreases contractility?
negative inotropic agents
afterload
pressure ventricles must overcome before SL valves open
normal afterload: pressure in aorta approx. 80mmHg, left side of heart needs to generate a lot more pressure before aortic valve opens
factors affecting afterload
blood pressure and vessel structure
heart rate
bpm, regulated by pacemaker cells in SA node
native (resting) HR
75bmp
intrinsic HR
100bpm
factors regulating heart rate
autonomic regulation, chemical regulation, age, body temp.
CV center (medulla oblongata) input
CV center receives input from higher brain regions and from sensory receptors, sends out neural impulses all the time through SNS and PNS (net effect determines if HR goes up or down)
SNS effect on heart
via adrenergic receptors on myocardium & pacemaker cells
parasympathetic effect on heart
via cholinergic receptors on pacemaker cells
