1
Q
Positive staircase effect
A
Also known as the bowditch effect
As the heart rate doubles, the tension increases stepwise
with each beat more Ca is accumulated by the SR until a maximum storage level is reached
2
Q
Postextrasystolic potentiation
A
when an extra beat is generated, the tension developed for the next beat is greater than normal
3
Q
Cardiac glycosides
A
drugs that produce the positive inotropic agents
4
Q
Effect of cardiac glycosides (steps)
A
- The Na-K ATPase is inhibited at the extracellular K binding site
- Less Na is pumped out of the cell and the Na concentration inside the cell is increased
- The function of the Ca-Na exchanger is altered
- Less Ca is pumped out of the cell by the Ca-Na exchanger and intracellular Ca concentration increases
- Continue to increase tension
5
Q
Use of cardiac glycosides
A
treatment of congestive heart failure
6
Q
Frank Starling Relationship
A
ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return
7
Q
Preload (Frank Starling Relationship)
A
left ventricular end-diastolic volume
resting length from which the muscle contracts
8
Q
Afterload(Frank Starling Relationship)
A
aortic pressure
velocity of shortening of cardiac muscle is maximum when afterload is zero
velocity of shortening decreases as afterload increases
9
Q
Function of ventricles
A
- stroke volume is the volume of blood ejected by the ventricle on each beat
- Ejection fraction is the fraction of the end-diastolic volume ejected in each stroke volume which is a measure of ventricular efficiency
- cardiac output is the total volume ejected by the ventricle per unit time
10
Q
Stroke volume
A
the volume of blood ejected on one ventricular contraction
11
Q
Stroke volume (equation)
A
Stroke volume = end-diastolic volume - end-systolic volume
12
Q
End-diastolic volume
A
volume in the ventricle before ejection (mL)
13
Q
End-systolic volume
A
Volume in the ventricle after ejection (mL)
14
Q
Ejection fraction
A
the effectiveness of the ventricles in ejecting blood
15
Q
Ejection fraction (equation)
A
Ejection fraction = stroke volume/end-diastolic volume
16
Q
Cardiac output
A
total volume of blood ejected per unit time
17
Q
Cardiac output (equation)
A
Cardiac output = Stroke volume (volume ejected per minute mL/min) X Heart rate (beats/min)
18
Q
Positive inotropic effect (Frank Starling Relationship)
A
uppermost curve, produce increases in stroke volume and cardiac output for a given end-diastolic volume
19
Q
Negative inotropic effect (Frank Starling Relationship)
A
produce decreases in stroke volume and cardiac output for a given end-diastolic volume
20
Q
Fick principle
A
there is conservation of mass
21
Q
Atrial Systole (A)
A
- atrial contraction
- preceded by the p wave
- contraction of the left atrium causes an increase in left atrial pressure
- left ventricle is relaxed during this phase
- ventricular blood volume increases
22
Q
Isovolumetric ventricular contraction (B)
A
- ventricles contract
- ventricular pressure increases
- Ventricular pressure is constant
- QRS complex
- mitral valve closes
- 1st heart sound
23
Q
Rapid ventricular ejection (C)
A
- ventricles contract
- ventricular pressure increases and reaches maximum
- ventricles eject blood into arteries
- ventricular volume decreases
- aortic pressure increases and reaches maxium
- ST segment
- Aortic valve opens
24
Q
Reduced ventricular ejection (D)
A
- Ventricles eject blood into arteries
- ventricular volume reaches minimum
- aortic pressure starts to fall as blood runs off into arteries
- T wave
25
Isovolumetric ventricular relaxation (E)
- Ventricles relaxed
- ventricular pressure decreases
- ventricular volume is constant
- aortic valve closes
- second heart sound
26
Rapid ventricular filling (F)
- Ventricles relaxed
- Ventricles fill passively with blood from atria
- ventricular volume increases
- ventricular pressure low and constant
- mitral valve opens
- third heart sound
27
Reduced ventricular filling or diastasis (G)
- ventricles relaxed
| - final phase of ventricular filling
28
Cardiac and vascular function curves
the cardiac function curve is cardiac output as a function of right atrial pressure
the vascular function curve is venous return as a function of right atrial pressure
29
Unstressed volume
volume of blood that produces no pressure (in veins)
30
Stressed volume
volume in blood that produces pressure by stretching vessel walls (arteries)
31
Blood volume 0-4L
all volume unstressed
32
Blood volume >4
some blood in stressed volume and pressure increases
33
Increased blood volume about 4L
No change in unstressed volume but changes in stressed volume
34
Mean systemic pressure
Value for pRA when VR=0
increases when BV increases
decreases when BV decreases
35
Positive inotropic effect (CV function curve)
Cardiac function curve has a higher slope so steady point moves up and left
increased contractility
36
Negative inotropic effect (CV function curve)
Cardiac function curve has a lower slope so it shifts down
| decreased contractility
37
Increased blood volume (CV function curve)
Vascular function increases so line shifts up
| increased systemic pressure
38
Decreased blood volume (CV function curve)
Vascular function decreases so line shifts down
| decreased systemic pressure
39
Increased TPR (total peripheral resistance)
Vascular and Cardiac function decreases so both curves shift down
40
Decreased TPR (CV function curve)
Vascular and cardiac function so both curves shift up
41
Mean arterial pressure (Pa)
driving force for blood flow and it must be maintained at a high constant level of approximately 100 mm Hg
42
Mean arterial pressure (equation)
Pa = cardiac output (mL/min) X TPR (mmHg/mL/min)
43
Pa regulation
regulated by the neural system (high-pressure baroreceptors) and hormonal (renin/Angiotensin/aldosterone)
44
Baroreceptors
pressure sensors located within the walls of the carotid sinus and the aortic arch and relay information about blood pressure to cardiovascular vasomotor centers
45
Increases vs decreases in arterial pressure (baroreceptors)
stretch the baroreceptors and increase the firing rate in the afferent nerves
decreases do the opposite
46
Microcirculation
functions of the smallest blood vessels, the capillaries and the neighboring lymphatic vessels
47
How are solutes and gases exchanged across the capillary wall?
simple diffusion
48
How do lipid soluble molecules pass through the capillary wall?
endothelial cells (o2, CO2, steroid hormones, fatty acids)
49
How do water soluble molecules pass through the capillary wall?
between the cells (H2O, glucose, ions, amino acids, small peptides)
50
Fluid exchange
Osmotic pressure and hydrostatic pressure
51
osmotic pressure
solute gradient influences direction and magnitude of water molecule movement
52
Hydrostatic pressure
pressure exerted by a fluid when gravity is acting on it
| fluid can exert a pressure on fluid around it
53
Starling equation
fluid movement across a capillary wall is determined by the net pressure across the wall
54
Starling equation (equation)
```
J= K[(Pc-Pi)-(Pic-Pii)]
K = hydraulic conductance (mL/min X mm Hg)
Pc = capillary hydrostatic pressure (mmHg)
Pi = interstitial hydrostatic pressure (mmHg)
Pic = capillary oncotic pressure (mmHg)
Pii = interstitial oncotic pressure (mmHg)
```
55
Net filtration pressure
pressure that promotes filtration - pressure that promotes reabsorption
56
filtration
when the net fluid movement is out of the capillary into the interstitial fluid
57
absorption
when net fluid movement is from the interstitium into the capillary
58
Hydraulic conductance
water permeability of the capillary wall
59
capillary hydrostatic pressire
force favoring filtration out of the capillary
60
Interstitial hydrostatic pressure
force opposing filtration, nearly 0 or slightly negative
61
capillary oncotic pressure
force opposing filtration
| determined by the protein concentration
62
interstitial oncotic pressure
force favoring filtration that is determined by the interstitial fluid protein concentration
63
Lymphatic system (purpose)
responsible for returning interstitial fluid and proteins to the vascular compartment
64
lymphatic capillaries
possess one-way flap valves which permit interstitial fluid and protein to enter but not leave the capillaries
65
thoracic duct
empties lymph into the large veins
66
Edema
Increase in interstitial fluid volume
67
Causes of edema
- can form when there is increased filtration
| - when lymphatic drainage is impaired (can happen when lymph nodes are surgically removed or irritated
68
local control
primary mechanism utilized for matching blood flow to the metabolic needs of a tissue
69
Neural or hormonal control
mechanisms as the action of the sympathetic nervous system on vascular smooth muscle and the action sof vasoactive substances such as histamine, bradykinin, and prostaglandins
70
Autoregulation
the maintenance of a constant blood flow to an organ in the face of changing arterial pressure. If pressure increases the radius must increase
71
Active hypremia
blood flow to an organ is proportional to its metabolic activity
72
Reactive hyperemia
increase in blood glow in response to a prior period of decreased blood flow
73
Myogenic hypothesis
stretching smooth muscle in arteriolar vessel wall occurs with increased pressure - stimulates smooth muscle contraction
increased Pressure = increased stretching = vasoconstriction = increased resistance = decreased blood flow = decreased pressure
74
Metabolic hypothesis
O2 consumption = O2 delivery
metabolism produces metabolites which act as vasodilators
increased metab = increased metabolites = vasodilation = decreased resistance = increased blood flow = increased O2 delivery
75
Neurological control
sympathetic innervation of vascular smooth muscle
whether to vasodilate or vasoconstrict depends on the type of receptors (alpha 1 = vasoconstriction)
(beta 2 = vasodilation)
76
Hormonal control
many locally produced molecules can act as vasoconstrictors or vasodilators
77
Coronary control
Primarily local metabolites and small contribution of sympathetic innervation
Stimulus is chemoreceptive; low O2
78
Cerebral control
Primarily local metabolites and small contribution of sympathetic innervation
Stimulus is chemoreceptive; high CO2
79
Pulmonary control
Stimulus is chemoreceptive; low O2
Hypoxia = vasoconstriction
Shunts blood from regions of low ventilation to regions of higher ventilation
80
Renal control
Combination of local and sympathetic
81
Skeletal muscle
Combination of local and sympathetic
At rest: primarily sympathetic
During exercise: primarily local metabolites
Increased O2 consumption (metabolic hypoth)
Build up of lactate (metabolic hypoth)
82
skin
Sympathetic to regulate temperature control
| Local hormones released during trauma (histamine produces inflammatory response symptoms)
83
Temperature Regulation
set point is 98.6 F or 37 C
| hypothalamus
84
Thyroid hormones (temp)
increased metabolic rate which increases heat
85
Autonomic regulation (temp)
sympathetic neurons inhibit cutaneous blood flow)
86
Sympathetic regulation of brown fat metabolism
Brown fat packed with mitochondria, can generate heat by using energy for metabolism
Brown fat content low in adults, high in babies
87
shivering
skeletal muscle contractions
88
Stimulant for fever
pyrogen a pathogenic fever-causing agent that targets the hypothalmus
89
Metabolic change for fever
for every 1 F above ~7% increase in metabolic rate
90
Atrioventricular valves
designed so that blood can only flow in one direction from the atrium to the ventricle
91
systemic circulation
pumps blood into the lungs
92
cardiac output
rate at which blood is pumped from either ventricle
93
venous return
rate at which blood is returned to the atria from the veins is the venous return
94
hemodynamics
the principles that govern blood flow in the cardiovascular system
95
Arteries
- aorta is largest
- function is to deliver oxygenated blood to the organs
- thick walled with elastic tissue, smooth muscle and connective tissue
- volume of blood is called stressed volume
96
Arterioles
- smallest branches of the arteries
- made up of smooth muscle
- site of highest resistance and where resistance can be changed
97
alpha 1 adrenergic receptors
cause contraction or constriction of smooth muscle
| increase contraction decrease unstressed volume
98
beta 2 adrenergic receptors
cause relaxation of smooth vascular muscle
| increase diameter and lower resistance
99
Capillaries
- thin walled, lined with a single layer of endothelial cells
- site where nutrients, gasses, water, and solutes are exchanged between the blood and the tissues
100
Venules and Veins
- thin walled with endothelial cell layer, elastic tissue, smooth muscle, and connective tissue
- have large capacity to hold blood
- largest percentage of blood in the cardio vascular system (unstressed)
101
Velocity of blood flow
V=Q/A
v= velocity of blood flow (cm/s)
Q = flow (mL/sec)
A= cross-sectional area (cm2) pir2
102
Blood flow is determined by (2)
pressure difference between the two ends of the vessel
| pressure is the driving force, the ristance is the impediment to flow
103
Magnitude of blood flow (equation)
Q=deltaP/R
q = flow (mL/min)
delta P = pressure difference (mmHg)
R = resistance (mmg/mL/min)
104
Magnitude of blood flow relationship to delta P
directly proportional
105
Direction of blood flow
determined by the direction of the pressure gradient and is always high to low
106
Blood flow relationship to resistance
increasing resistance decreases flow and vice versa
107
Total peripheral resistance
resistance of the entire system vasculature
108
Poiseuille equation
R=8nl/pir^4
R = resistance
n = viscosity of blood (proportional to resistance)
l = length of blood vessel (proportional to resistance)
r4 = radius ^4 (inversely proportional to resistance)
109
Series resistance
Arrangement of all blood vessels within an organ
110
Series resistance (equation)
Rtotal = Rartery + Rarterioles + Rcapillaries + Rvenules +Rveins
111
Where does the greatest decrease in pressure occur in series resistance and why?
Arterioles because the contribute to the largest portion of the resistance
112
Parallel resistance
distribution of blood flow
total resistance is less than any of the individual resistances
no loss of pressure
113
What happens when you add resistance to a parallel circuit?
the total resistance decreases not increases
114
Laminar flow
streamlined flow
| velocity of flow is the highest int he center of the vessel and lowest towards the vessel walls
115
Turbulent flow
the fluid streams do not remain in parabolic profile; mix radially and axially
116
Reynolds #
predicts either laminar or turbulent
117
Reynolds # (equation)
```
N=pdv/n
p = density
d = diameter
v = velocity
n=viscocity
```
118
Reynolds number results
<2000 then the blood is laminar
20003000 then the flow is probably turbulent
>3000 then it is turbulent
119
Anemia
decreased hematocrit (red blood cells)
due to turbulent blood flow murmers occur
high cardiac output
120
Thrombi
blood clots in the lumen of a vessel narrows the diameter of the vessel
121
Shear
occurs when blood travels at different velocity in the same vessel
highest at vessel wall
lowest at center
decreases blood viscosity
122
Compliance of blood vessels
```
C= V/P
C= compliance or capacitance (mL/mmHg)
V = volume (mL)
P = pressure (mmHg)
greater in veins than arteries
```
123
Compliance and volume relationship
increased compliance means increased volume
124
Where is the highest pressure?
arteries
125
What effect does aging have on arteries?
makes them stiffer, less distensible and complacent
126
Mean pressures high to low
```
aorta (100)
large arteries
arterioles
capillaries
venules
veins
```
127
Arterial pressure
pulsations in the arteries reflect the pulsate activity of the heart
128
Diastolic pressure
lowest arterial pressure during a cardiac cycle and is the pressure in the arteries during ventricular relaxation when no blood being ejected from the left ventricle
129
Systolic pressure
highest arterial pressure; pressure in arteries after blood has been ejected from the left ventricle
130
pulse
systolic - diastolic
131
Mean arterial pressure average
mean = diastolic + 1/3 pulse pressure
132
Pulsations in arteries vs aorta
larger arteries have greater pulsations due to pressure waves pushed backwards into artery branches
133
Ateriosclerosis
plaque deposits in the arterial walls decreasing the diameter of arteries
systolic, pulse, and mean pressure to increase
134
Aortic stenosis
aortic valve is narrowed, less blood enters the aorta
| systolic, pulse, and mean pressure decrease
135
Aortic regurgitation
aortic valve is incompetent, one way flow of blood is ruined and flow goes backwards into the ventricle
136
Pulmonary vs systemic resistance
pulmonary resistance is much lower than systemic resistance
137
contractile cells
constitute the majority of atrial and ventricle tissues and are working cells of the heart
138
Conducting cells
constitute the tissues of the SA note, atrial internodal tracts, the AV node, the bundle of His, and the Purkinje system
139
SA node
action potential initiated here
| pacemaker
140
Atrial internodal tracts and atria
action potential moves from SA node through these to the atria
141
AV node
receives action potential
| slow conduction ensures that the ventricle has sufficient time to fill before they contract
142
Bundle of His, Purkinje system, and ventricles
Action potential leaves the AV node and enters the bundle of His then the left and right bundle branches and then smaller bundles of the purkinje system
143
Action potential in His-Purkinje system
extremely fast which is efficient for contraction and ejection of blood
144
Spread of action potential
SA node-atrial internodal tracts - av node - bundle of His - purkinje system
145
normal sinus rythm
the pattern and timing of the electrical activation of the heart are normal
146
Qualifications for normal sinus rythm
The action potential must originate in the SA node
The SA nodal impulses must occur regularly at a rate of 30 - 100 impulses per minute
the activation of the myocardium must occur in the correct sequence with correct timing and delays
147
Long duration of action potential
-150 msec in atria to 250 msec in ventricles to 300 msec in purkinje fibers
long refractory periods
148
Action potential in His-Purkinje system (Phase 0)
rapid depolarization (upstroke)
- opening of Na channels with inward Na current
- potential reaches +20mV
- called dV/dT: rate of change of the membrane potential
149
Action potential in His-Purkinje system (Phase 1)
initial repolarization (net outward current)
- Na channels close due to repolarization
- inward Na current ceases
- outward K current due to K moving out of the cell during the upstroke
150
Action potential in His-Purkinje system (Phase 2)
Plateau (stable, depolarized membrane potential)
- increase in Ca due to current inward (slow)
- L-type channels are inhibited by Ca channel blockers
- outward k current to balance Ca invlux
- net current is 0
- Ca induced Ca release
151
Action potential in His-Purkinje system (Phase 3)
repolarization
- decrease in Ca (inward)
- increase in k (outward)
- at the end the outward current is reduced because repolarization brings the membrane potential closer to the K eq. potential
152
Action potential in His-Purkinje system (Phase 4)
electrical diastole
| -inward and outward currents are =
153
Action potential in SA node (phase 0)
upstroke
- increase in Na current
- result of an inward Ca current
154
Action potential in SA node (phase 1-2)
absent
155
Action potential in SA node (phase 3)
repolarization
| -increase in K outward current
156
Action potential in SA node (phase 4)
spontaneous depolarization
- automacity of SA node
- -65 mV
- slow depolarization due to inward Na current
- sets heart rate
157
Latent pacemakers
includes cells of the AV node bundle of His, purkinje fibers
| suppressed when SA node drives the heart rate(overdrive suppression)
158
ectopic pacemaker
SA node firing rate decreases or stop completely
intrinsic rate of firing of one of the latent pacemakers should become faster than that of the SAnode
Conduction of action potentials from the sa node to the rest of the heart is blocked due to disease
159
Conduction velocity
speed at which action potentials are propagated within tissue (m/sec)
determines how long it takes for the action potentials to spread to various locations in myocardium
160
Excitability
the capacity of myocardial cells to generate action potentials in response to inward depolarizing current
161
Absolute refractory period
most of the duration of the action potential
no second impulse can be conducted no matter how strong
-50mV
162
Effective refractory period
longer than absolute
| can generate another action potential but needs a really strong stimulus
163
supranormal period
begins when the membrane potential is -70 mV and continues until the membrane repolarizes to -85 mV
164
chronotropic
sympathetic stimulation increase heart rate
| parasympathetic stimulation decreases the heart rate
165
positive chronotropic
norenephrine
166
negative chronotropic
acetylcholine
167
dromotropic effects
increase in conduction velocity is positive due to SNS
| decreasse is due to PNS and is negative
168
P wave
depolarization of aorta
169
PR interval
160 ms
| depolarization of atria to depolarization of ventricles
170
QRS complex
depolarization of ventricles
171
T wave
repolarization of ventricles
172
Heart rate
Measured by counting the number of QRS complexes there are per minute
173
excitation-contraction coupling
```
cardiac action potential
-inward Ca flow
increase in Ca concentration (inward)
Ca binds to tropnin C
Cross bridge cycling
- tension or relaxation
```
Vertebrate Physiology
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