Physiology Flashcards
1
Q
Systole
A
Ventricular contraction
2
Q
Systolic pressure
A
Pressure on systemic arteries when the heart contracts
3
Q
Diastole
A
Ventricular relaxation, filling stage
4
Q
Diastolic pressure
A
Pressure in systemic arteries when the heart is in relaxation
5
Q
S1
A
Sound associated with the mitral valve closing and beginning of systole
6
Q
S2
A
Sound of the aortic valve closing
Associated with the end of systole and beginning of diastole
7
Q
EDV
A
Volume in the LV after filling during diastole, right at the end of diastole
8
Q
ESV
A
Volume of blood in the LV right after systole
9
Q
Stroke volume
A
Volume of blood that was ejected from the heart during systole
SV=EDV-ESV
10
Q
Ejection fraction
A
% of blood that was pumped out from the LV during systole
EF= SV/EDVx100
11
Q
Cardiac output
A
Volume of blood the heart pumps out per minute
CO= SV x HR
12
Q
Preload
A
The tension put on the heart when LV is full of blood and ready to contract, end of diastole
This is the EDV or pressure
The greater the stretch of fibers the stronger the muscle contracts
13
Q
If you increase preload
A
Increase volume of blood
Slower HR (Increase filling time), constrict veins (symp innerv)
14
Q
Decrease preload
A
Lower volume
Increase HR
Dilate veins
15
Q
Afterload
A
Load the heart must eject blood against, thought of as aortic pressure
Pressure the heart must overcome to eject blood during systole (use SBP or MAP to determine)
Ventricular wall tension during contraction shows how much force is needed to eject
16
Q
Increase afterload
A
Decrease in SV
17
Q
Cause of increase afterload
A
Raised MAP, obstruct outflow, increase TPR
18
Q
Decrease afterload
A
Increase SV
19
Q
Cause of decrease afterload
A
Lower MAP, relieve obstruction, decrease TPR
20
Q
Phases of the cardiac cycle
A
Ventricular filling, atrial systole, isovolumetric contraction, ejection, isovolumetric relaxation
21
Q
Isovolumetric contraction
A
When all of the heart valves are closed, the mitral valve closes because pressure in LV is greater than LA and the LV is pressurized and preparing to eject, building pressure to overcome aortic pressure
There is no volume change, only pressure change
22
Q
Ventricular ejection
A
When the pressure in the LV exceeds that of the aorta so aortic valve opens and blood is pumped out of the heart
23
Q
Isovolumetric relaxation
A
The blood has just been pumped from the heart, aorta is at higher pressure again so aortic valve closes. LV still at greater pressure than LA so all valves are closed and there is no volume change
24
Q
Ventricular filling
A
Pressure in the LA is greater than LV so mitral valve opens and blood fills the LA
25
Atrial systole (contraction)
At the end of diastole the atria push a contraction to get all of the blood into the LV
26
Phases of the cardiac cycle that are systole
Isovolumetric contraction, ejection
27
Phases of the cardiac cycle that are diastole
Isovolumetric relaxation, ventricular filling, atrial systole
28
P-wave
Depolarization signal right before atrial contraction
29
QRS wave
Depolarization signal right before ventricle contraction
30
T wave
The repolarization of the ventricles
31
Label the diagram
32
33
Stroke work
Work of LV to eject a volume of blood (eject SV)
Represented by area inside the PV loop
34
Pacemaker cardiac muscle cell
Specialized cell that sends the electrical signal throughout the heart that allows for contractile muscle cells to contract the heart
35
Characteristics of pacemaker cells
Make up little muscle mass
No RMP, automaticity
AP phases are 0,3,4
Doesn't show up on EKG
36
Contractile muscle cells
Cells that are responsible for making actin and myosin contract and the heart beat
37
Characteristics of contractile cells
Make up 99% of mass
RMP at -80mV and need an AP to activate
Phases are 0,1,2,3,4
Show up on EKG
38
Intercalated disks
The mechanical linkage between heart cells
39
Gap junction
The electrical linkage between heart cells, allows the AP to travel from one cell to the next
40
Sinoatrial node
The origination of the Ap traveling through the heart
Pacemaker cell that has automaticity
60-100 bpm
41
42
Atrioventricular node
Receives the signal from the SA node and slows it down, allows for atria to fully contract before ventricles contract
Rests in-between the RA and RV and is electrical link between atria and ventricles
Can take over if SA fails, 40-60bpm
43
Bundle of his
Receives the signal from the AV node, rapidly sends down the IV septum and then through right and left bundle branches
20-40bpm
44
Purkinje fibers
At the apex of the heart and receives signals from left and right bundle branches
Sends the signal back up through the rest of the heart so ventricles can contract (hits papillary muscles first so valves can contract before the ventricle does)
45
46
Stage 4 of SA node AP
Funny sodium channels are open and the amount of Na in the cell is slowly increasing until it reaches a specific threshold (-60mV to -40mV)
47
Stage 0 of SA node AP
Once enough Na has entered the cell and the threshold has been met (-40mV), Na channels close and L-type Ca channels open causing depolarization of the cell
48
Stage 3 of SA node AP
Once the cell has depolarized, Ca channels close and K+ channels open. As K+ exits the cell it becomes more negative allowing for repolarization
At -60mV K+ channels close and funny Na channels open again
49
50
Phase 0 myocardial AP
When the Ap travels through gap junction to cell causes a depolarization, Na+ channels open rapidly causing large influx and depolarization signal
-80mV to +20mV
Once at the peak upstroke Na+ channels become inactivated
51
Phase 1myocardial AP
Transient K+ channels (fast voltage gated) open allowing for beginning of repolarization, initial sharp downstroke
52
Phase 2 myocardial Ap
Transient K+ channels close and K+ channels open as well as L-type Ca channels triggering contraction of the cell
Cell continues to repolarize
Influx of Ca and efflux of K is balanced so around 0mV causing plateau
53
Phase 3 myocardial Ap
L-type Ca channels close leaving just K+ channels open causing the final repolarization of the cell
54
Phase 4 myocardial AP
K+ channels close and cell is back at -80mV (RMP)
Na+ channels are no longer inactive
RMP stabilized by K1 ion channels that are leak channels
55
56
57
EC-coupling anatomy of components
Sarcolemma is the cell membrane, T-tubule is the dip within the membrane that contains the L-type Ca channels (DHP)
Inside of the membrane is the RyR receptor on the sarcoplamsic reticular that is a ligand gated Ca channel and causes release of Ca from the SR
Ca then attaches to myosin and actin to contract
58
EC coupling physiology
AP propagates down sarcolemma and T-tubule, opens voltage gated L-type channels and Ca influx that then binds to Ryr channel
SR releases Ca+ into cytoplasm and activates contractile proteins
Need to now decrease Ca in cytoplasm, use SERCA into SR, NaCaX to exchange Na and Ca, and Ca pump for ATP initiated pumping
59
60
Tunica externa
Outer part of the blood vessel that is composed of connective tissue
61
Tunica media
Middle part of the blood vessel that contains smooth muscle, receives innervation from symp and parasymp to constrict or dilate
62
Tunica intima
Inner most layer that is composed of endothelium
Single layer of simple squamous cells, allows for diffusion and absorption
63
Components of circulatory system
Arteries
Arterioles
Capillaries
Veins
64
Arteries
Carries blood away from the heart, because of the large BP have thicker cell walls with more smooth muscle
65
Arterioles
Comprise the arterioles further along in the body
Create the most resistance for the systemic vascular system because of length and radius (smallest of the arteries)
66
Capillaries
Single stream of RBC, site of fluid exchange, diffusion, etc... Single layer of epithelium with no smooth muscle
67
Veins
Return blood back to the heart, not pressurized and use muscle movement to return
Can create pooling before return to lessen cardiac load
68
Pressure
Driving flow created by ventricular contraction that is transferred to the blood
69
Factors that impact pressure
Vasoconstriction (increase)
Vasodilation (decrease)
Resistance up (increase)
Volume up (decrease)
70
How the aorta is intermediate pump
Can lessen the outward pressure on the rest of the body because of its elasticity
Elasticity allows for increase stretch, therefore increase volume means decrease in pressure
71
Aorta impact on DBP
Recoil in the aorta after ejection and closing of the aortic valve, elasticity allows the aorta to snap back and push in to the heart momentarily increase pressure during diastole
72
Compliance in veins
Are able to change in volume related to change in distending pressure
Can expand and collapse for different pressures
73
Pulse pressure
The difference between systolic and diastolic pressure
The force that the heart generates each time it contracts
74
MAP (Mean arterial pressure)
Average blood pressure in the arteries
How much pressure is needed to push blood into the capillaries (drives blood flow)
75
Main determinants of MAP
CO and SVR
76
Calculating MAP
2/3DP +1/3SP = MAP
77
Ohm's law of blood flow
Flow= change in pressure gradient/resistance
78
Determinants of blood flow
Pressure gradient (P1 pressure of a vessel to P2 pressure): Increase gradient increase flow
Resistance of vessel: Increase resistance decrease flow
79
Relationship between volume and pressure
Indirect, more volume then less pressure
80
Resistance
Opposition to flow, mostly due to friction between blood and vessel wall
81
Laminar flow
Streamline flow of blood, each layer is same distance from wall
Velocity inside is highest and velocity close to the vessel is more turbulent due to friction
82
Turbulent flow
Causes murmurs or bruits
High velocity flow with sharp turns, hitting rough surfaces, rapid narrowing, etc...
83
Poiseuille's law equation
Resistance = Ln /r^4
84
Poiseuille's law
Showing that the biggest influence of resistance is radius of the blood vessel
85
Factors determining resistance
Directly proportional to length (Increase L increase R)
Inversely proportional to radius (Increase radius decrease R)
86
Systemic vascular resistance
Resistance to blood flow offered by all systemic vasculature (total peripheral resistance)
87
Systemic vascular resistance equation
MAP/CO
88
Determinants of SVR
If SVR increases than CO decreases
If MAP increases, SVR increases
89
If SVR increases then
LV needs to pump harder to get blood out into the body
This results in decrease SV and drop in cardiac output
It's harder to pump blood out of the heart
90
Baroreceptor reflex
Primary pathway of homeostatic control of MAP
Sends signals of BP to the brain to influence pressure
91
Location of baroreceptors
Carotid sinus in the internal carotid artery
92
Baroreceptors: Increase in BP
Baroreceptors detect increase in pressure and start firing faster sending signals to the brain to decrease pressure and HR
Decreases symp response, decreases NE, decrease BP and HR, vasodilation, decrease TPR
Increase parasymp, increase ACh, decrease BP
93
Baroreceptors: Decrease in BP
Detect low pressure and aren't firing as rapidly
Increase symp, NE and vasocontriction, increase BP and HR as well as TPR
Decrease parasymp, decrease ACh, increase HR and BP
94
Stroke Volume
Amount of blood that is pumped out the LV during systole
95
Stroke volume equation
SV= EDV - ESV
96
Cardiac output
How much blood the heart pumps out in one minute
97
Cardiac output equation
CO = SV x HR
98
Ejection fraction
% of blood that the heart pumps out of the LV during systole
99
Ejection fraction equation
EF= SV/EDV x 100
100
Frank-Starling Law
Heart has built in mechanism that allows it to pump automatically whatever amount of blood that flows into the right atrium from the veins
If increase stretch during filling, greater the force to pump it all out (greater stretch of actin and myosin leads to greater force generation)
101
Contractility
Strength of contraction independent of preload and afterload
102
Increase in contractility
Reduce ESV, squeezing harder so more blood out, increase in SV
103
Decrease in contractility
Decrease SV
104
Innervation to increase contractility
Symp beta 1 receptors
105
Innervation to decrease contractility
Beta 1 receptor antagonists
106
Venous return
Quantify of blood flowing from veins to RA/min
107
To increase venous return
Decrease RA pressure (want to flow down a pressure gradient)
Decrease TPR (decreases the pressure against veins when returning, decrease pressure increases flow)
108
Right atrial pressure
Equal to central venous pressure, no valves impede flow into atrium
109
Decrease right atrial pressure
Intravascular volume depletion
110
Increase right atrial pressure
Increases with intravascular volume overload, RV failure
111
Resistance to venous return determined by
Venous resistance and small amount due to arteriolar and small artery resistance
