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action potential in pacemaker cells
voltage starts at -60mv , where funnny channels open and allow slow influx of Na+ til reaching threshold of -40mv resulting in depolorization known as
at threshold calcium channels open, Ca+ flow into the cell further depolorizing the membrane, resulting in the rising phase (depolarizing) of the AP
at the peak of depolorization, K+ channels open and Ca channels inactivate, K+ ions leave the cell and voltage returns to -60mV, this is the falling (repolorization) phase of action potential
action potential in contractile myocytes
resting at -90mv, depolorize when stimulated by a neighbouring myocyte and bring the membrane voltage up to the threshold of -70mv
at threshold fast Na+ channels open creating rapid influx in Na+ and a sharp rise in voltage (depolorisation phase)
L-type, or slowm Ca+ channels also open at -40mv causing slow but steady influx
when the membrane reaches a peak, K+ channels open allowing K+ to exit, leading to early repolarization, calcium channels remain open and Ca and K end up being balanced keeping the membrane potential steady and making a platuea known as the action potential plateau phase. After the plateau phase, K+ continues to leave the cell, which leads to a full repolarization back to the resting potential of -90mV.
then calcium induced calcium release sets off muscles contraction via the sliding filament
Ca+ channels slowing closed and then
the platuea phase leads to longer contraction in the heart and longer refractory period allowing
types of blood vessels (arterial system)
elastic artery - thick walled near heart
muscular artery - thick wall, less elastin - deliver blood to tissue
arterioles - resistance vessels - regulate blood flow to capillaries
capillaries - thin walled, small lumen diameter
types of blood vessels (venous system)
venule - connection between capillaries and veins
veins - lack significant muscle layer - highly compliant - little recoil
endothelium
produces substances that change smooth muscle contraction
nitic oxide
endothelin
prostaglandins
mediates the actions of circulating substance s
angiotensin
thrombin
histamine
bradykinin
systolic bp
max pressure exerted in arteries when blood is ejected into them during systole (heart contracting phase)
diasstolic bp
MIN PRESSURE WITHIN THE ARTERIES WHEN BLOOD DRAINING off into the remaineder of the vessels during diastole (heart relaxing/ fillinfg phase)
pulse pressure
a measure of strength of pressure wave ( = difference between SBP and DBP)
mean arterial pressure MAP
average pressure responsiple for driving blood forward into tissues throughout cardiac cycle
MAP = diastolic BP + 1/3 pulse pressure
frank-starling mechanism - stroke volume
increased volume of blood in ventricle leads to increased stretch on muscle wall
increased muscle stretch leads to increased force contraction
increased force contraction leads to increases stroke volume
preload
the initial stretching of the cardiac muscle prior to contraction, determined by the volume of blood in the ventricles at the end of diastole.
can also be measured by EDP which is used clinically
afterload
the hydraulic load imposed on the ventricle during ejection
measures include;
aortic pressure'
total peripheral resistance
arterial impedance
myocardial peak wall stress