Cardiac Muscle Physiology Flashcards
describe the functional organization of the cardiovascular system
- details about pressue and flow from a basic physics perspective?
- a pump (heart) of pressure system that is regulated by electrical impulses
- this pump obtains molecules (O2 from the lungs and nutrients from the GI) & releases them (through the skin and the kidneys)
- how are the pressures? high pressure Left and aterial system pumps blood through the arteries to the capillaries
- in order to decreases resistance to the flow of pressure–> multiple capillaries(multiple avenues) of the blood decrease the resistance –> allow to flow
- the pressure decreases but remains high enough to travel back to the heart through the venous system (just a lower pressure pathway)
thinking about the principles of intergration:
- cardiac output?
- arterial pressure?
- blood flow to each tissue is determined by the NEED of the tissue
- cardiac output: determined by the SUM of all tissue flow
-
arterial pressure: 2 control mechanisms
– cardiac output (if you decrease total output— youre getting nothing)
– arterial blood local control (peripheral resistance of dilation/constriction)
explain the meaining behind….
Q = changeP/R
MAP = CO x TPR
CO = HR x SV
Q = “bulk flow”
change P = pressure gradient (from high to low) – determined by muslces in the heart and their ability to force
R = resistance
– **flow is determined by the pressure changes and by the (inversley) resistance (increase resistance will decrease flow)
MAP = mean arterial pressure
CO: cardiac output
TPR: resistance
mean arterial pressure is dependent on the cardiac output and the amoutn of resistnace
CO= cardiac output
HR: heart rate
SV: stroke volume
compensatory mechanism –> if you have a decreased stroke volume, youll try to beat harder to get blood to where it needs to be
so why do we need a pump at all for the cardiovascular system?
relative pressures of the heart once blood has been pumped?
pressure is lost in the form of resistance as the flow interacts with the vessel walls – overtime there will be so much resistance that the flow will eventually become 0
so our LV pumps 100mg of pressure in systole & 0 in diastole
differ in pressures from left to right but always same amount of volume
Aorta: 120/80
LV: 120/0
LA: 5
Pulm. art: 25/8
RV: 25/0
RA: 2
Cardiac Anatomy
- pericardium
- mycardium
- endocardium
pericardium: dense connective tissue covering heart (fiberour) with cavity to allow for decrease in friction upon movement (30-50mL of fluid in there)
myocardium: the muscle cells of the heart which are fiberous, condcutive tissues within function in syncytium
endocardium: the innermost lining of the heart (2 membranes) which lines the ventricles and the insides!!
- endothelium : the elastic connective tissue, irregular connectve tissue & vasculature
contraction of the heart & the roles of the valves (& names)
when the ventricels contract: they squeeze (constrict) inwards, the chambers shorten and eject their contents (ejection fracture)
when the atria contract: the short “free” wall shortens and the atria move up and down to contract and force blood into the ventricles
Atrioventrucular valves 2 leaflets: tricuspid & mitral
- tricuspid (right) 3 leafs
- mitral (left)
Semilunar valves 3 leaflets: pulmonary and aortic
Walk through the basics of myocyete cell contraction
- functional unit of the myocyte & relative role of calcium in how it triggers
- types of myocytes
- general overview of when the contraction occurs what is happening on a cellular level (dont talk about voltages yet)
the myocyte: has striated muscle with sarcomeres –> made of myofibrils –> made of individaul myofilaments –> made of myosin!
Nodal & myocytes
myosin is the trigger for the contraction process
- CALCIUM influx triggers myosin binds to actin – forms a bridge
- myosin pulls toward the center – contracting the actin-myosin unit
- when CALCIUM is reduced this triggers relaxtion & release of myosin from actin
- there is a voltage: triggers L-type calcium channels to open –> flood of calcium inside the cell
- this triggers calcim to be released from the sarcoplasmic reticulum –> further flooding the cell with calcium
- calcium bings to troponin –> interacts with tropomyocin to trigger the above steps of contraction SYSTOLE
- calcium is reuptaken by the sarcomere and released from the cell via Na/Ca+ channels or by Ca+/ ATP mediated pumps
any process which increases Ca+ into the cell will increase contractilty –> increase inotropy
- think about Epi and NE –> increase Ca+ into cell
- think about Ach –> decrease Ca+ into the cell
define
- Automaticity
- Rhythmicity
- Excitability
- Conductivity
Automaticity: the ability of the heart to set its own electrical rhythm
- this is APs generated by the heart itself
- modified by the autonomic (Sympa or parasympa) system
Rhythmicity: the sequence of electrical events that coordiantes constrction
Excitibility: the myocardium can respond to electrical stimulation
Conductivity: the myocytes have the ability to spread this electrical signal from one cell to another (vai special fibers)
Electrical impulse stimulation: the electrical conduction pathway
- what pump maintains negative resting cell membrane
- what pump “loads” the cell to maintain its concentration gradient
describe the resting potential of a non-pacemake cell
the myocyte wants to maintain a negative resting membrane potential (-85/-90 mV)
- this resting potential: due to a contant ATP use of pumping Potassium INSIDE the cell (against its gradient)
and pumping Na+ OUTSIDE the cell (against its gradient)
** there is alwasy a slow leak of potassium INSIDE – maintaining this membran potential**
- the Na+/Ca+ * ATP/Ca+ pump maintian the “loading” concentration of calcium inside
in sum
- rests at -90 mV because of the ATP forcing K+ inside the cell and the slow leak of K outside
- this is phase 4
how is the electrical signal propogated to ajacent cells & what happens after the signal has spread
describe phase 0
- neighbor cell is depolarized
- or nodal cell triggers
- the cell gets to threshold –slow leak from sister cell through gap junctions
- triggers FAST voltage gated Na+ channels to open up
- this RAPIDLY depolarizes the cell (to approx. +10 mV) & then these fast Na+ close
describe phase 1&2 of electrical conduction in a myocyte
Phase 1: the fast Na+ closed and now triggered K+ open –> release the K+ from inside to outside in attempts to offset this high postivity
- this K+ out triggers L-type Ca+ channels to open and begin to flow in
Phase 2: slow increase of Ca+ via L type channels
once the Ca+ has been slowly leaking in –> at 0 mV it triggers MORE Ca+ to leak in
- but this is a plateau (becuase K+ is continuously slowly leaking out)
- this leak of Ca+ in triggers more Ca+ from the sarcoplasmic reticulum to go into the cell & muscle contraction happens
describe phase 3 of myocyte contraction
phase 3: repolarization
- the Ca+ L type begin to close –> so now K+ is flowing out unopposed
- this repolarizes the cell back to its Phase 4 membrane potential
describe phase 3 of myocyte contraction
phase 3: repolarization
- the Ca+ L type begin to close –> so now K+ is flowing out unopposed
- this repolarizes the cell back to its Phase 4 membrane potential
any leftover Ca+ pumped out via atp channels & Na+ pumped out by Na+/K+ channels
when are the absolute refractory periods
relative?
absloute?
phase 0, 1, & 2 & 3
relative
end of 3 (could repolarize if it had to)
4 (when its back to baseline)
if its gonna fire –> needs a bigger trigger of Na+ to flood in
describe phase 0&3&4 of nodal cell excitiment
phase 0: depolarization via L-type Ca+ (open at -40)
phase 3: the L Ca+ channels close & K+ open to leave the cell (repolarize it – delayed rxn from Ca+)
phase 4: the “resting” membrane of a nodal cell –> funny-type Na+ cells slow leak in until -55 then
T-type Ca+ channels open and let Ca+ in
once the T-type Ca+ and funny Na+ channels allow threshold — cycel starts with the opening of the L-type
