Circulation 4 Flashcards
cardiac cycle (2)
- pumping action of the heart
- contains two phases: systole and diastole
cardiac cycle: systole (2)
- contraction/pressure-generating
- blood is forced out into the circulation
cardiac cycle: diastole (2)
- relaxation
- blood enters the heart
fish cardiac cycle (2)
- serial contractions of chambers
- valves are passive
fish cardiac cycle: valves (2)
- valves open and close according to pressure differences
- assure unidirectional flow of blood
fish cardiac cycle: bulbus arteriosus
- in teleosts, noncontractile bulbus arteriosus serves as volume and pressure reservoir
mammal cardiac cycle (2)
- atria and ventricles alternate systole and diastole
- maximizes stroke volume and therefore, cardiac output
mammal cardiac cycle steps (4)
- two atria contract simultaneously
- there is a slight pause
- two ventricles contract simultaneously
- atria and ventricles relax while the heart fills with blood
mammal cardiac cycle simplified (5)
- ventricular diastole 1
- atrial systole
- ventricular systole 1
- ventricular systole 2
- ventricular diastole 2
mammal cardiac cycle: ventricular diastole 1 (3)
- pressure in atria exceeds ventricular pressure
- AV valves open and the ventricles passively fill
- atria is in diastole
mammal cardiac cycle: atrial systole (2)
- atrial contraction forces additional blood into ventricles
- ventricles are in diastole
mammal cardiac cycle: ventricular systole 1 (3)
- isovolumetric contraction (volume remains the same)
- ventricular contraction pushes AV valves closed and increases pressure inside the ventricle
- atria are in diastole
mammal cardiac cycle: ventricular systole 2 (3)
- ventricular ejection
- increased ventricular pressure forces the semilunar valves open and blood is ejected
- atria are in diastole
mammal cardiac cycle: ventricular diastole 2 (3)
- as ventricles relax, pressure in arteries exceeds ventricular pressure
- semilunar valves close
- atria in diastole
birds/mammals: ventricular filling (2)
- fill passively during diastole due to venous pressure
- atrial contraction adds a little blood to the ventricles
fish/some amphibians: ventricular filling (2)
- ventricles actively filled by contraction of atrium
- they generate little passive ventricular filling due to low venous pressure after going through two capillary beds
left ventricular pressure
- contracts more forcefully and develops higher pressure to pump blood to body/systemic system
right ventricular pressure
- contracts less forcefully as less pressure is needed to pump blood through the lungs
characteristics of the pulmonary circuit system (2)
- resistance is low due to high capillary density in parallel
- large cross-sectional area
why is the pulmonary circuit a low pressure system (2)
- protects delicate blood vessels of lungs
- prevents edema that would be caused by fluids exiting the blood into the lungs
circuit blood flow
- systemic and pulmonary circuits have the same total blood flow
control of cardiac contraction (3)
- neurogenic pacemakers
- myogenic pacemakers
- artificial pacemakers
neurogenic pacemakers (2)
- rhythm generated in neurons
- present in some invertebrates
myogenic pacemakers (2)
- rhythm generated in myocytes
- present in vertebrates and some invertebrates
artificial pacemakers
- rhythm generated by a device
control of cardiac contraction: vertebrates (3)
- hearts are myogenic
- electrically coupled cardiomyocytes produce spontaneous rhythmic depolarizations
- does not require nerve signal
how are cardiomyocytes electrically coupled (2)
- via gap junctions to ensure coordinated contractions
- allows action potentials to pass direction from cell to cell
vertebrate pacemaker location (2)
- in sinus venosus of fish
- in right atrium at the sino-atrial (SA) node of tetrapods (amphibians, reptiles, birds, mammals)
cell membrane state (3)
- polarized
- the resting (stable) membrane potential is negative relative to the outside
- -60mV to -110mV inside
what creates the resting membrane potential (2)
- created by ATPases working against selectively permeable ion channels
- results in ionic gradients across the cell membrane
why are electrochemical gradients important in cell membranes
- create the ‘battery’ for life by providing electrical potential energy for many cell activities
what cells are excitable (2)
- cells that become ‘excited’ due to brief changes in ion channel permeabilities
- eg. neurons and muscles
muscle cell action potentials (2)
- voltage-gated ion channels can open in muscles cells to create an action potential
- action potential will trigger muscle contraction
pacemaker cells (3)
- derived from cardiomyocytes
- small, with few myofibrils, mitochondria, or other organelles
- do not contract; lack contractile tissues
pacemaker cells: resting membrane potential (2)
- have unstable resting membrane potential (pacemaker potential)
- this potential depolarizes until it reaches threshold and initiates an action potential
vertebrate pacemaker action potential (4)
- cell gradually depolarizes to threshold (-60mV to -40 mV)
- voltage-gated channels open
- initiates “spike”, or the action potential
- cell repolarizes
what causes the unstable resting membrane potentials in pacemaker cells (2)
- slow decrease in K+ permeability
- opening of “funny” channels (Na+ channels), increasing Na+ permeability
what causes the action potential/spike in pacemaker cells
- voltage-gated Ca2+ channels open, increasing Ca2+ permeability
what initiates repolarization in pacemaker cells
- K+ channels open, increasing K+ permeability
what support repolarization in pacemaker cells
- “funny” channels (Na+ channels) close, decreasing Na+ permeability
what are the major differences between action potentials and pacemaker action potentials (2)
- pacemaker cells are never resting; they continue to create action potentials regardless if stimulus is present
- stimulus is what alters the membrane potential to trigger an action potential in other cells, and cells rest in-between stimulus
nervous system modulation of pacemakers (3)
- no modulation
- sympathetic stimulation
- parasympathetic stimulation
nervous system modulation of pacemakers: no modulation
- no hormonal influence, so rate of depolarization is “normal”
nervous system modulation of pacemakers: sympathetic nervous system stimulation
- increases rate of pacemaker potentials
nervous system modulation of pacemakers: parasympathetic nervous system stimulation
- decreases rate of pacemaker potentials
control of pacemaker potentials: increasing heart rate (3)
- hormones and origin
- voltage-gated channels affected
- result
- norepinephrine released from sympathetic neurons and epinephrine released from the adrenal medulla
- more Na+ and Ca2+ channels open
- rate of depolarization and frequency of action potentials increase
increasing heart rate: pathway (6)
- cardiovascular control center (medulla) stimulates sympathetic neurons
- neurons release norepinephrine and stimulate the adrenal medulla to release epinephrine
- norepinephrine and epinephrine bind to beta-receptors of autorhythmic cells
- signaling cascade occurs, resulting in release of cAMP and activation of protein kinases
- funny and Ca2+ channels open, resulting in an influx of Na+ and Ca2+
- rate of depolarization increases, resulting in increased heart rate
control of pacemaker potentials: decreasing heart rate (4)
- hormones and origin
- voltage-gated channels
- results (2)
- acetylcholine released from parasympathetic neurons
- more K+ channels open
- pacemaker cells hyperpolarize
- time for depolarization takes longer, causing frequency of action potentials to decrease
decreasing heart rate: pathway (4)
- cardiovascular control center (medulla) stimulates parasympathetic neurons to release acetylcholine
- acetylcholine binds muscarinic receptors of autorhythmic cells
- signaling cascade results in closing of funny channels and opening of K+ channels so that Ca2+ cannot enter and K+ can leave
- cell hyperpolarizes, increasing time for depolarization and decreasing heart rate
