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cardiac cycle
A complete heartbeat consisting of contraction and relaxation of both atria and both ventricles
Cardiac Cycle: Systole
contraction phase
Cardiac Cycle: Diastole
relaxation phase
when atria contract
atrial systole
-ventricles relax ( ventricular diastole)
when ventricles contract
ventricular systole
-atria relax (atrial diastole)
end of cardiac cycle
atria and ventricles briefly both relax
right atria contracts
-left atria contracts, right ventricle relaxes
right ventricle contracts
-right atria relaxes, left ventricle contracts
atria contract and ventricles relax
when blood is forced into ventricles
atria and ventricles relax
when blood flows passively into the atria and then passively into the ventricles
Pressure during contraction
blood flows from areas of high pressure to low
-controlled by timing of contractions
-directed by one way valves
atrial systole
atrial contraction, AV valves open and blood is ejected into ventricles
ventricular systole and atrial diastole
Atrial systole ends
Atrial diastole begins
Ventricles contain maximum blood volume
Ventricles contract and build pressure
Closing AV valves
Producing isovolumetric contraction
ventricular systole
ventricles contract, opening semilunar valves and blood flows from ventricles to pulmonary trunk and aorta
-semilunar valves then close
ventricular diastole
-isovolumetric relaxation (all valves are closed)
-AV valves open and ventricles fill
isovolumetric relaxation
All heart valves are closed
Ventricular pressure is higher than atrial pressure
Blood cannot flow into ventricles
atrial damage
individuals can survive
ventricular damage
can lead to heart failure
increased heart rate
all phases of cardiac cycle are shorten, especially diastole
BP systole
contraction phase, increases BP
BP diastole
relaxation phase, decreases BP
action potential
cardiomyocytes have a stable resting potential of -90mV, and depolarize only when stimulated
phases of action potential
depolarization, plateau, repolarization
Depolarization
-Na+ gates open and Na+ rushes in, membrane depolarizes quickly.
-action potential peaks at +30mV
-Na+ gates close quickly
Plateau
-200-250ms-sustains contraction
-Ca+ gates open and Ca+ rushes in
-Ca+ binds to troponin on SR, triggering contraction
Repolarization
-Ca+ gates close and K+ channels open
-K+ rushes out of the cell, returning the cell to resting potential
absolute refractory period
cardiac muscles cells cannot respond
-250ms, prevents wave summation and tetanus
relative refractory period
cells respond only to strong stimuli
Summation or treppe
addition of a second twitch, resulting in greater tension, and it results from stimulation the muscles before it has a chance to relax completely
tetany
prolonged contraction without relaxation and results from repeating stimulation before the muscle has had a chance to relax
regulates cardiac cycle
-Potassium - ion concentrations
-calcium - ion concentrations
potassium
affects electrical potential of cell membrane altering its ability to reach threshold for conduction an impulse
Hyperkalemia
decreases rate and force of contraction, may block conduction of cardiac impulses and heart may suddenly stop
Hypokalemia
heart may develop life threatening arrhythmia
calcium
helps initiate muscle contraction
Hypercalcemia
increases heart action and possible danger of heart undergoing prolonged contraction
Hypocalcemia
depresses heart action
heart sounds
due to closing of valves
-detected with a stethoscope
S1
lub-AV valves closing
-occurs during ventricular systole
S2
dup-semilunar valves closing
-occurs during ventricular diastole
murmur
abnormal heart sound, blood leaks back through valves d/t leaky or incompetent closure of heart valves