Cardiovascular - Regulation + Electrical Mechanics Flashcards
1
Q
2 major cell types in heart
A
- contracile fibers
- muscle cells/develop tension, and force and do the work of contraction and moving blood
- need electrical signal to tell them to do their job and contract
- not all cardiac muscle cells have nervous input to stimulate - work via gap junctions
- electrical activity gets spread to next muscle cell via gap junctions
- get mechanical stimulation following electrical stimulation
- conducting fibers
- conduct electrical info, AP; specialized muscle cells
- allow electrical info to be passed from cell to cell
- not all fibers are ennervated so electrical signals move from fiber to fiber by special gap junctions called intercalated discs
- connections are important - intercalated discs which link muscle cells since not all muscle cells are connected to nervous system but connected to one another
2
Q
Electrical/Mechanical Relationship in Heart
A
- SA (seno-atrial) node: pacemaker sets up heart rhythm; myogenic: sets own pace
- conducting fibers from SA node relay signal (1m/s)
- this is atrial contraction
- at AV node (btwn atrium and ventricle) conduction velocity slows/electrical activity slows to 0.5 m/s, - allows mechanical activity - atrial contraction to finish
- bundle of His conducts electrical signal to apex (bottom) at 5 m/s
- purkinjee fibers send signal to ventricles (apex to base) which is ventricle contraction
- pushes blood up from apex toward base through semilunars and through aortic and pulmonary valves
- mechanical activity follows electrical activity
3
Q
Cell Death
A
- cells die and release K+ and can have electical activity in small area of heart called circus electrical activity
- these cells are connected and electrical activity can go in reverse or other directions
- get asynchronis mechanical activity so don’t pump any blood and bp falls and you pass out
- if electrical coordination isn’t maintained in sychrony of atrial and ventrical contraction then bag of worms
4
Q
Fibrillation - defibrillation
A
- fibrillation is electrical system out of sync
- defibrillation depolarizes all cells at once
- reboots heart
- and hope SA node restarts heart
- 200V paddles use electrical shock to put all cardiac cells in same electrical state - polarize all at once and get them to repolarize at once so hope SA node pacemaker can restart heart
- electrical shock gets rid of circus electrical mvmt
- EKG developed to look at electrical activity of heart and can be reflective of mechanics but not always
- SA and AV node are ennervated (nervous system connect to heart)
5
Q
Reguation of Cardiac Output - Neural Regulation
A
- parasympathetic - from cranial and sacral region
- vagus nerve at cranial
- sympathetic - thoracic and lumbar
- sympathetic nerves at thoracic
- para and symp make up autonomic NS
6
Q
Parasympathetic via Vagus Nerve
A
- vagus nerve releases Ach to SA node and AV node
- vagus has negative chronotropic effect to < HR
- vagus has negative inotropic effect to < FOC
- so vagus we have < CO
- if cut vagus, > HR to 170 bpm, so pacemaker wants to run fast and vagus slows it down
- really see effect at SA node, some at AV
7
Q
Sympathetic via sympathetic nerves release norepinephrine
A
- sympathetic nervous system nervates the heart and SA and AV node and fibers in ventricle
- NE is from adrenal gland for flight or fight
- symp nerves release norepinephrine to AV node, SA node, and some vent fibers
- positive chronotropic effects - > HR
- positive inotropic effects - > FOC
- this means > HR, > Force Of Contraction, > CO
In exercise need to > CO, so exercise > sympathetic activity and < parasympathetic activity to > CO
8
Q
Blood Pressure
A
- monitored by baroreceptors in aorta and large arteries
- if detect < in bp then signal medulla which > RMV (resp minute vol from respiratory center)
- then medulla also has cardiovascular center brings > HR, > FOC by > symp and < parasymp –> over all this > CO to > bp
- if dectect > bp then medulla (cardiovascular center) will < HR, < FOC and so < CO and < bp
- exercise is exception
- > bp and homeostatic response is overriden since need O2 to tissues so > HR, > FOC and > CO
9
Q
Blood gases/Blood Chemistry
A
- want homeostasis
- monitored by chemoreceptors in medulla (central) and large arteries
- if large arteries see > pCO2, < pO2 and < pH then signal sent to medulla cardiovascular center
- compensatory response is to > CO via > HR and FOV
- do this via > sympathetic actvity and < parasymp activity
•Ex. If increase in pCO2 in arterial blood, then O2 delivery may be compromised so heart will Increase cardiac output to increase gas delivery
10
Q
Heart Rate (ventricle)
A
- to > HR you can shorten/decrease time in diastole but can’t really change systole dramatically
- diastole = filling or at rest
- so to > HR and > FOC we draw on residual volume
- couple change in HR w/our > venous return so we can bring blood back more rapidly
11
Q
Frank Starling Law of the Heart
A
- heart responds approp to amt of blood in it - if > blood in heart then heart > FOC
- heart responds to changes in stretch of cardiac fibers
- force of contraction of heart that you see is proportional to the stretch of myocardial
- as > amt of blood, stroke vol >
- LV EDV is pressure before contraction from ventricle
- stroke vol and CO taper off since can only hold so much blood
- as > EDV, stroke vol > w/out neural input
- change EDV via inhale and > venous return to heart
- family of curves w/diff physiological conditions
- curve depends on symp input
- as symp input on heart you get > stroke vol
- afterloaded situation
- curve depends on symp input
- preloaded situation is what heart sees before contracts which causes second graph where
- heart sees more blood so preloaded and > vol a lot and heart adjusts on its own and returns to normal residual vol
12
Q
Venous Pressure and Flow
A
- cardiac output is dependent on venous return because heart pump can only pump as much blood as you return to it
- venous return is influenced by:
- venous pressure (move blood via pressure gradient)
- > venous pressure means > in venous return which helps generate CO
- venous pressure (move blood via pressure gradient)
13
Q
Cardiac output is influenced by 3 other things
A
- venous return
- systemic resistance
- pulmonary resistance
14
Q
Venous return - influenced by venous pressure
> venous pressure means > venous return and generate CO
what influences venous pressure?
A
- sympathetic veno constriction
- NE released in smooth muscle on venous side causes constriction and > venous pressure
- one-way valves, since < radius which > pressure and blood back to heart
- skeletal muscle pump
- squeezing skeletal muscle > venous pressure since squeeze on blood vessels, which pushes blood back to heart
- this helps > venous pressure when exercising which > venous return and CO
- coordinated w/> CO since symp activity > and parasym < which means more blood flow to heart
veno = venous
vaso = arterial (a)
15
Q
Hemodynamics and Viscosity
A
- how blood flows through vessels
- blood in middle of vessel moves fastests since no friction
- increase radius means faster flow
- viscosity takes into account thickness, internal friction; if viscosity >, resistance to flow >
- viscosity influenced by:
- water content - if < water content of blood, viscosity >
- hematocrit (% rbc) if >, then > viscosity since more internal friction
- >blood lipids, then > viscosity
- if > protein content then > viscosity
16
Q
Blood
A
- heterogenous mix
- non-Newtonian fluid - does not keep a constant velocity
- capillaries have decrease in functional viscosity
- as vessel radius < then viscosity will decrease tons!!
- “sigma effect” or Fahres-Linquist
- blood goes through tiny vessles, rbc line up and go thru one at a time –> functional decrease in viscosity in smal vessels
17
Q
Poiseulle’s Law - addresses blood flow
A
- change in pressure is driving pressure since goes from high to low pressure
- arterial pressure is what you see at high end and venous at low end
- change PE to KE is driving pressure
- get delta P via bp and arterial pressure
- pi/8L is geometry of cylinder
- viscosity doesn’t chagne in moment-to-moment basis
- just look @ flow = driving pressure and radius 4
- small change in radius makes big diff in flow
- change in driving pressure is determined by cardiac output which influence bp which is upper side of pressure differential
- and diastolic reboud in arterial tree can influence driving pressure
18
Q
Poisuelle’s Law cont.
A
- we can adjust radius to change flow
- increase radius, means < resistance and > flow or vice versa
- Flow = driving pressure/resistance
- partition CO by changing radius - blood follows path of least resistance
- relate to Ohm’s Law V = IR
- flow is difficult to measure so we measure delta P as blood pressure to get handle on upper end of pressure gradient
- total peripheral resistance = TPR = bp aorta - bp vena cava/cardiac output
- for pressure differential, if low CO then higher TPR
- lower TPR if higher/good CO for pressure diff
19
Q
Blood FLow and Pressure
A
- generate CO from heart; worry about flow and generate pressure
- elastin nature of arteries w/smooth muscles- CO partitioned at arterioles
- bounce of arteries help driving pressure “rebound”
- take blood flow and partition to get GI tract or skeletal muscle and take arterioles and change radius which changes resistance and blood flow follows path of least resistance - blood flow goes in larger radius
- pressure begins as wave - moves to constant flow when reaches capillaries
- arterioles - control distribution of blood flow
- at capillaries - one continuous pressure and flow - PE to KE
20
Q
Morphology of vasculature reflects jobs
A
- arteries have lots of elastic and some muscle
- arterioles lots of smooth muscle where do partitioning
- capillaries where exchange so keep simple w/endothelial cells
- small veins hold stuff together w/fibous tissue
- larger veins some elastin so comply and enlarge but smooth muscle to help w/venous return and restriction
21
Q
Arteries as pressure reservoir
A
Because of their elasticity, arteries act as a pressure reservoir.
9a) The elastic arteries distend during cardiac systole as more blood is ejected into them than drains off into the narrow, high resistance arterioles downstream.
(b) The elastic recoil of arteries during cardiac diastole continues driving the blood forward when the heart is not pumping.
22
Q
Pressure changes throughout Vasculature
A
- L ventricle has high pressure for ventricular systole
- Blood in arteries have systolic and diastolic pressure which is oscillation – see mean pressure
- On arterial side what is happening?
- Conduit to the capillaries
- We partition cardiac output by changing the radius and thereby changing the level of resistance – we decrease the radius we increase resistance; we change radius by sympathetic vasoconstriction – sympathetic nervous system at work and it enervates the smooth muscle on the arterioles and by changing the radius of the vessel via smooth muscle contraction, or relaxation, we can change the radius
- Pressure reservoir
- Dampen oscillations in pressure and flow - At end of arterioles we no longer have pressure oscillations – one steady flow which helps exchange
24
Q
Sympathetic Ennervation of Vessel Diameter
A
- Sympathetic enervation to do this – sympathetic neuron enervating our arteriole and it releases norepinephrine from sympathetic neuron
- There is always a sympathetic tone which we release, if want to decrease radius then we release more neurotransmitter (norepinephrine) and get contraction and radius goes down
- If change radius to get bigger then release less sympathetic tone (less norepinephrine) to relax and bigger radius
- Sympathetic enervation w/constant sympathetic tone we can drive up or down to < or > radius; sympathetic tone is amount of sympathetic activity resulting in certain amount of neurotransmitter
- Arterial side is pressure reservoir
- At end of arterial system – dampen oscillation in pressure and flow
- Vaso means arterial side and veno means venous side
25
Q
Capillaries and Area and Velocity
A
- Into capillaries: equation of continuity
- A1V1 = A2V2
- Art = capillaries
- Capillaries are the swamp
- Cross sectional area and velocity of flow has to match but what happens is in capillaries cross sectional area is huge and velocity drops here
- Numerous capillaries in parallel to each other here in pic so resistance in parallel – resistance in each one of them and total resistance is actually a lot less than what may expect
27
Q
Cross Sectional Area and Velocity Changes
A
•Total cross sectional area of all capillaries for ex which is huge in terms of cross sectional area so have to drop the velocity since A1V1 = A2V2 which is what we see
•Gas exchange in capillaries – exchange of nutrients
•Capillaries Decrease velocity which is good since allows time for exchange and with flow of velocity decreased then this yields increase in lateral pressure which facilitates increased exchange
- Bernoulli – w/slower velocity then increase in lateral pressure on sides of capillaries which helps with exchange
- Decrease in functional viscosity (sigma effect when rbc line up in capillary and move through orderly fashion)
•Resistance in parallel – 1/RT = 1/R1 + 1/R2 + 1/R3…. Which is lower resistance than would assume
- Resistance in series then would add them like R1+R2+R3 would be tons of resistance and too much
- Help blood flow through vessels at small radius
28
Q
Blood Flow in Circulatory system
A
- see pressure gradient and changes
- see area changes - highest in capillaries
- velocity changes w/lowest at capillaries and tends to get into viens
