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Vertebrate Physiology > Exam 2 > Flashcards

Exam 2 Flashcards

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

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2
Q

Postextrasystolic potentiation

A

when an extra beat is generated, the tension developed for the next beat is greater than normal

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3
Q

Cardiac glycosides

A

drugs that produce the positive inotropic agents

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4
Q

Effect of cardiac glycosides (steps)

A
  1. The Na-K ATPase is inhibited at the extracellular K binding site
  2. Less Na is pumped out of the cell and the Na concentration inside the cell is increased
  3. The function of the Ca-Na exchanger is altered
  4. Less Ca is pumped out of the cell by the Ca-Na exchanger and intracellular Ca concentration increases
  5. Continue to increase tension
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5
Q

Use of cardiac glycosides

A

treatment of congestive heart failure

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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

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7
Q

Preload (Frank Starling Relationship)

A

left ventricular end-diastolic volume

resting length from which the muscle contracts

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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

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9
Q

Function of ventricles

A
  1. stroke volume is the volume of blood ejected by the ventricle on each beat
  2. Ejection fraction is the fraction of the end-diastolic volume ejected in each stroke volume which is a measure of ventricular efficiency
  3. cardiac output is the total volume ejected by the ventricle per unit time
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10
Q

Stroke volume

A

the volume of blood ejected on one ventricular contraction

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11
Q

Stroke volume (equation)

A

Stroke volume = end-diastolic volume - end-systolic volume

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12
Q

End-diastolic volume

A

volume in the ventricle before ejection (mL)

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13
Q

End-systolic volume

A

Volume in the ventricle after ejection (mL)

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14
Q

Ejection fraction

A

the effectiveness of the ventricles in ejecting blood

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15
Q

Ejection fraction (equation)

A

Ejection fraction = stroke volume/end-diastolic volume

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16
Q

Cardiac output

A

total volume of blood ejected per unit time

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17
Q

Cardiac output (equation)

A

Cardiac output = Stroke volume (volume ejected per minute mL/min) X Heart rate (beats/min)

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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

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19
Q

Negative inotropic effect (Frank Starling Relationship)

A

produce decreases in stroke volume and cardiac output for a given end-diastolic volume

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20
Q

Fick principle

A

there is conservation of mass

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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
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22
Q

Isovolumetric ventricular contraction (B)

A
  • ventricles contract
  • ventricular pressure increases
  • Ventricular pressure is constant
  • QRS complex
  • mitral valve closes
  • 1st heart sound
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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
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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
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25
Q

Isovolumetric ventricular relaxation (E)

A
  • Ventricles relaxed
  • ventricular pressure decreases
  • ventricular volume is constant
  • aortic valve closes
  • second heart sound
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26
Q

Rapid ventricular filling (F)

A
  • Ventricles relaxed
  • Ventricles fill passively with blood from atria
  • ventricular volume increases
  • ventricular pressure low and constant
  • mitral valve opens
  • third heart sound
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27
Q

Reduced ventricular filling or diastasis (G)

A
  • ventricles relaxed

- final phase of ventricular filling

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28
Q

Cardiac and vascular function curves

A

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

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29
Q

Unstressed volume

A

volume of blood that produces no pressure (in veins)

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30
Q

Stressed volume

A

volume in blood that produces pressure by stretching vessel walls (arteries)

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31
Q

Blood volume 0-4L

A

all volume unstressed

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32
Q

Blood volume >4

A

some blood in stressed volume and pressure increases

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33
Q

Increased blood volume about 4L

A

No change in unstressed volume but changes in stressed volume

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34
Q

Mean systemic pressure

A

Value for pRA when VR=0
increases when BV increases
decreases when BV decreases

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35
Q

Positive inotropic effect (CV function curve)

A

Cardiac function curve has a higher slope so steady point moves up and left
increased contractility

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36
Q

Negative inotropic effect (CV function curve)

A

Cardiac function curve has a lower slope so it shifts down

decreased contractility

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37
Q

Increased blood volume (CV function curve)

A

Vascular function increases so line shifts up

increased systemic pressure

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38
Q

Decreased blood volume (CV function curve)

A

Vascular function decreases so line shifts down

decreased systemic pressure

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39
Q

Increased TPR (total peripheral resistance)

A

Vascular and Cardiac function decreases so both curves shift down

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40
Q

Decreased TPR (CV function curve)

A

Vascular and cardiac function so both curves shift up

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41
Q

Mean arterial pressure (Pa)

A

driving force for blood flow and it must be maintained at a high constant level of approximately 100 mm Hg

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42
Q

Mean arterial pressure (equation)

A

Pa = cardiac output (mL/min) X TPR (mmHg/mL/min)

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43
Q

Pa regulation

A

regulated by the neural system (high-pressure baroreceptors) and hormonal (renin/Angiotensin/aldosterone)

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44
Q

Baroreceptors

A

pressure sensors located within the walls of the carotid sinus and the aortic arch and relay information about blood pressure to cardiovascular vasomotor centers

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45
Q

Increases vs decreases in arterial pressure (baroreceptors)

A

stretch the baroreceptors and increase the firing rate in the afferent nerves
decreases do the opposite

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46
Q

Microcirculation

A

functions of the smallest blood vessels, the capillaries and the neighboring lymphatic vessels

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47
Q

How are solutes and gases exchanged across the capillary wall?

A

simple diffusion

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48
Q

How do lipid soluble molecules pass through the capillary wall?

A

endothelial cells (o2, CO2, steroid hormones, fatty acids)

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49
Q

How do water soluble molecules pass through the capillary wall?

A

between the cells (H2O, glucose, ions, amino acids, small peptides)

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50
Q

Fluid exchange

A

Osmotic pressure and hydrostatic pressure

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51
Q

osmotic pressure

A

solute gradient influences direction and magnitude of water molecule movement

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52
Q

Hydrostatic pressure

A

pressure exerted by a fluid when gravity is acting on it

fluid can exert a pressure on fluid around it

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53
Q

Starling equation

A

fluid movement across a capillary wall is determined by the net pressure across the wall

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54
Q

Starling equation (equation)

A 
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)
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55
Q

Net filtration pressure

A

pressure that promotes filtration - pressure that promotes reabsorption

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56
Q

filtration

A

when the net fluid movement is out of the capillary into the interstitial fluid

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57
Q

absorption

A

when net fluid movement is from the interstitium into the capillary

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58
Q

Hydraulic conductance

A

water permeability of the capillary wall

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59
Q

capillary hydrostatic pressire

A

force favoring filtration out of the capillary

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60
Q

Interstitial hydrostatic pressure

A

force opposing filtration, nearly 0 or slightly negative

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61
Q

capillary oncotic pressure

A

force opposing filtration

determined by the protein concentration

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62
Q

interstitial oncotic pressure

A

force favoring filtration that is determined by the interstitial fluid protein concentration

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63
Q

Lymphatic system (purpose)

A

responsible for returning interstitial fluid and proteins to the vascular compartment

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64
Q

lymphatic capillaries

A

possess one-way flap valves which permit interstitial fluid and protein to enter but not leave the capillaries

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65
Q

thoracic duct

A

empties lymph into the large veins

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66
Q

Edema

A

Increase in interstitial fluid volume

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67
Q

Causes of edema

A
  • can form when there is increased filtration

- when lymphatic drainage is impaired (can happen when lymph nodes are surgically removed or irritated

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68
Q

local control

A

primary mechanism utilized for matching blood flow to the metabolic needs of a tissue

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69
Q

Neural or hormonal control

A

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

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70
Q

Autoregulation

A

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
Q

Active hypremia

A

blood flow to an organ is proportional to its metabolic activity

72
Q

Reactive hyperemia

A

increase in blood glow in response to a prior period of decreased blood flow

73
Q

Myogenic hypothesis

A

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
Q

Metabolic hypothesis

A

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
Q

Neurological control

A

sympathetic innervation of vascular smooth muscle
whether to vasodilate or vasoconstrict depends on the type of receptors (alpha 1 = vasoconstriction)
(beta 2 = vasodilation)

76
Q

Hormonal control

A

many locally produced molecules can act as vasoconstrictors or vasodilators

77
Q

Coronary control

A

Primarily local metabolites and small contribution of sympathetic innervation
Stimulus is chemoreceptive; low O2

78
Q

Cerebral control

A

Primarily local metabolites and small contribution of sympathetic innervation
Stimulus is chemoreceptive; high CO2

79
Q

Pulmonary control

A

Stimulus is chemoreceptive; low O2
Hypoxia = vasoconstriction
Shunts blood from regions of low ventilation to regions of higher ventilation

80
Q

Renal control

A

Combination of local and sympathetic

81
Q

Skeletal muscle

A

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
Q

skin

A

Sympathetic to regulate temperature control

Local hormones released during trauma (histamine produces inflammatory response symptoms)

83
Q

Temperature Regulation

A

set point is 98.6 F or 37 C

hypothalamus

84
Q

Thyroid hormones (temp)

A

increased metabolic rate which increases heat

85
Q

Autonomic regulation (temp)

A

sympathetic neurons inhibit cutaneous blood flow)

86
Q

Sympathetic regulation of brown fat metabolism

A

Brown fat packed with mitochondria, can generate heat by using energy for metabolism
Brown fat content low in adults, high in babies

87
Q

shivering

A

skeletal muscle contractions

88
Q

Stimulant for fever

A

pyrogen a pathogenic fever-causing agent that targets the hypothalmus

89
Q

Metabolic change for fever

A

for every 1 F above ~7% increase in metabolic rate

90
Q

Atrioventricular valves

A

designed so that blood can only flow in one direction from the atrium to the ventricle

91
Q

systemic circulation

A

pumps blood into the lungs

92
Q

cardiac output

A

rate at which blood is pumped from either ventricle

93
Q

venous return

A

rate at which blood is returned to the atria from the veins is the venous return

94
Q

hemodynamics

A

the principles that govern blood flow in the cardiovascular system

95
Q

Arteries

A
  • 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
Q

Arterioles

A
  • smallest branches of the arteries
  • made up of smooth muscle
  • site of highest resistance and where resistance can be changed
97
Q

alpha 1 adrenergic receptors

A

cause contraction or constriction of smooth muscle

increase contraction decrease unstressed volume

98
Q

beta 2 adrenergic receptors

A

cause relaxation of smooth vascular muscle

increase diameter and lower resistance

99
Q

Capillaries

A
  • 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
Q

Venules and Veins

A
  • 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
Q

Velocity of blood flow

A

V=Q/A
v= velocity of blood flow (cm/s)
Q = flow (mL/sec)
A= cross-sectional area (cm2) pir2

102
Q

Blood flow is determined by (2)

A

pressure difference between the two ends of the vessel

pressure is the driving force, the ristance is the impediment to flow

103
Q

Magnitude of blood flow (equation)

A

Q=deltaP/R
q = flow (mL/min)
delta P = pressure difference (mmHg)
R = resistance (mmg/mL/min)

104
Q

Magnitude of blood flow relationship to delta P

A

directly proportional

105
Q

Direction of blood flow

A

determined by the direction of the pressure gradient and is always high to low

106
Q

Blood flow relationship to resistance

A

increasing resistance decreases flow and vice versa

107
Q

Total peripheral resistance

A

resistance of the entire system vasculature

108
Q

Poiseuille equation

A

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
Q

Series resistance

A

Arrangement of all blood vessels within an organ

110
Q

Series resistance (equation)

A

Rtotal = Rartery + Rarterioles + Rcapillaries + Rvenules +Rveins

111
Q

Where does the greatest decrease in pressure occur in series resistance and why?

A

Arterioles because the contribute to the largest portion of the resistance

112
Q

Parallel resistance

A

distribution of blood flow
total resistance is less than any of the individual resistances
no loss of pressure

113
Q

What happens when you add resistance to a parallel circuit?

A

the total resistance decreases not increases

114
Q

Laminar flow

A

streamlined flow

velocity of flow is the highest int he center of the vessel and lowest towards the vessel walls

115
Q

Turbulent flow

A

the fluid streams do not remain in parabolic profile; mix radially and axially

116
Q

Reynolds #

A

predicts either laminar or turbulent

117
Q

Reynolds # (equation)

A 
N=pdv/n
p = density
d = diameter
v = velocity
n=viscocity
118
Q

Reynolds number results

A

<2000 then the blood is laminar
20003000 then the flow is probably turbulent
>3000 then it is turbulent

119
Q

Anemia

A

decreased hematocrit (red blood cells)
due to turbulent blood flow murmers occur
high cardiac output

120
Q

Thrombi

A

blood clots in the lumen of a vessel narrows the diameter of the vessel

121
Q

Shear

A

occurs when blood travels at different velocity in the same vessel
highest at vessel wall
lowest at center
decreases blood viscosity

122
Q

Compliance of blood vessels

A 
C= V/P
C= compliance or capacitance (mL/mmHg)
V = volume (mL)
P = pressure (mmHg)
greater in veins than arteries
123
Q

Compliance and volume relationship

A

increased compliance means increased volume

124
Q

Where is the highest pressure?

125
Q

What effect does aging have on arteries?

A

makes them stiffer, less distensible and complacent

126
Q

Mean pressures high to low

A 
aorta (100)
large arteries
arterioles
capillaries
venules
veins
127
Q

Arterial pressure

A

pulsations in the arteries reflect the pulsate activity of the heart

128
Q

Diastolic pressure

A

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
Q

Systolic pressure

A

highest arterial pressure; pressure in arteries after blood has been ejected from the left ventricle

130
Q

pulse

A

systolic - diastolic

131
Q

Mean arterial pressure average

A

mean = diastolic + 1/3 pulse pressure

132
Q

Pulsations in arteries vs aorta

A

larger arteries have greater pulsations due to pressure waves pushed backwards into artery branches

133
Q

Ateriosclerosis

A

plaque deposits in the arterial walls decreasing the diameter of arteries
systolic, pulse, and mean pressure to increase

134
Q

Aortic stenosis

A

aortic valve is narrowed, less blood enters the aorta

systolic, pulse, and mean pressure decrease

135
Q

Aortic regurgitation

A

aortic valve is incompetent, one way flow of blood is ruined and flow goes backwards into the ventricle

136
Q

Pulmonary vs systemic resistance

A

pulmonary resistance is much lower than systemic resistance

137
Q

contractile cells

A

constitute the majority of atrial and ventricle tissues and are working cells of the heart

138
Q

Conducting cells

A

constitute the tissues of the SA note, atrial internodal tracts, the AV node, the bundle of His, and the Purkinje system

139
Q

SA node

A

action potential initiated here

pacemaker

140
Q

Atrial internodal tracts and atria

A

action potential moves from SA node through these to the atria

141
Q

AV node

A

receives action potential

slow conduction ensures that the ventricle has sufficient time to fill before they contract

142
Q

Bundle of His, Purkinje system, and ventricles

A

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
Q

Action potential in His-Purkinje system

A

extremely fast which is efficient for contraction and ejection of blood

144
Q

Spread of action potential

A

SA node-atrial internodal tracts - av node - bundle of His - purkinje system

145
Q

normal sinus rythm

A

the pattern and timing of the electrical activation of the heart are normal

146
Q

Qualifications for normal sinus rythm

A

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
Q

Long duration of action potential

A

-150 msec in atria to 250 msec in ventricles to 300 msec in purkinje fibers
long refractory periods

148
Q

Action potential in His-Purkinje system (Phase 0)

A

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
Q

Action potential in His-Purkinje system (Phase 1)

A

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
Q

Action potential in His-Purkinje system (Phase 2)

A

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
Q

Action potential in His-Purkinje system (Phase 3)

A

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
Q

Action potential in His-Purkinje system (Phase 4)

A

electrical diastole

-inward and outward currents are =

153
Q

Action potential in SA node (phase 0)

A

upstroke

  • increase in Na current
  • result of an inward Ca current
154
Q

Action potential in SA node (phase 1-2)

155
Q

Action potential in SA node (phase 3)

A

repolarization

-increase in K outward current

156
Q

Action potential in SA node (phase 4)

A

spontaneous depolarization

  • automacity of SA node
  • -65 mV
  • slow depolarization due to inward Na current
  • sets heart rate
157
Q

Latent pacemakers

A

includes cells of the AV node bundle of His, purkinje fibers

suppressed when SA node drives the heart rate(overdrive suppression)

158
Q

ectopic pacemaker

A

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
Q

Conduction velocity

A

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
Q

Excitability

A

the capacity of myocardial cells to generate action potentials in response to inward depolarizing current

161
Q

Absolute refractory period

A

most of the duration of the action potential
no second impulse can be conducted no matter how strong
-50mV

162
Q

Effective refractory period

A

longer than absolute

can generate another action potential but needs a really strong stimulus

163
Q

supranormal period

A

begins when the membrane potential is -70 mV and continues until the membrane repolarizes to -85 mV

164
Q

chronotropic

A

sympathetic stimulation increase heart rate

parasympathetic stimulation decreases the heart rate

165
Q

positive chronotropic

A

norenephrine

166
Q

negative chronotropic

A

acetylcholine

167
Q

dromotropic effects

A

increase in conduction velocity is positive due to SNS

decreasse is due to PNS and is negative

168
Q

P wave

A

depolarization of aorta

169
Q

PR interval

A

160 ms

depolarization of atria to depolarization of ventricles

170
Q

QRS complex

A

depolarization of ventricles

171
Q

T wave

A

repolarization of ventricles

172
Q

Heart rate

A

Measured by counting the number of QRS complexes there are per minute

173
Q

excitation-contraction coupling

A 
cardiac action potential
-inward Ca flow
increase in Ca concentration (inward)
Ca binds to tropnin C
Cross bridge cycling
- tension or relaxation

Vertebrate Physiology (1 decks)

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