CVS Flashcards
(424 cards)
1
Q
What is the primary function of the CVS?
A
To deliver blood to tissues, providing essential nutrient transport to cells for metabolism and removes waste from cells.
2
Q
What homeostatic functions is the CVS involved in? (4)
A
- regulation of arterial pressure 2. deliver regulatory hormones 3. Participates in thermoregulation 4. Adjusts to altered physiologic sates (hemorrhages, exercise, postural changes)
3
Q
What is the pathway of blood through the heart in relation to the blood vessels?
A
Heart -> Arteries -> arterioles -> Capillary body -> venules -> veins -> Heart
4
Q
What occurs in the capillaries?
A
Nutrient, waste, fluid exchange
5
Q
What percentage of circulation is systemic?
A
84%
6
Q
What percentage of circulation is pulmonary?
A
9%
7
Q
What percentage of circulation is of the heart?
A
7%
8
Q
How much of the circulation goes to the venous system?
A
64%
9
Q
How much of the circulation goes to the arterial system?
A
13%
10
Q
How much of the circulation goes to the arterioles and capillaries?
A
7%
11
Q
Which organs receive 25% of the cardiac output?
A
Renal, GI, Skeletal Muscles
12
Q
Which organs receive 15% of the cardiac output?
A
cerebral
13
Q
Which organs receive 5% of the cardiac output?
A
Coronary, Skin
14
Q
What can change the percentages of cardiac output to organs?
A
Tissue demand
15
Q
The left side of the heart composes which portion of the CVS?
A
Systemic
16
Q
The right side of the heart composes which portion of the CVS?
A
Pulmonary
17
Q
What structure connects the two sides of the heart relative to their atria and ventricles?
A
Arterioventricular valves
18
Q
What direction is the flow of blood through the AV valves?
A
Unidirectional
19
Q
True/False: The left and right side function simultaneously to pump blood.
A
False, they function in series (Left side -> systemic circulation -> right side -> pulmonary circulation)
20
Q
What is the term given to the rate at which blood is pumped from either ventricle?
A
Cardiac output
21
Q
What term is given to the rate at which blood is returned to the atria from the veins?
A
Venous return
22
Q
True/False: Increasing venous return decreases cardiac output in steady state.
A
False, they are equal so an increase in one leads to an increase in the other.
23
Q
What structure(s) delivers blood to and from the tissues?
A
Blood vessels
24
Q
True/false: Blood vessels are a closed system of active conduits.
A
False, Passive conduits
25
True/False: Resistance of BVs have no effect on blood flow.
False, When resistance is altered, flow is altered.
26
What are the blood vessel types?
Arteries, Arterioles, Venules, Veins, capillaries
27
Which blood vessel type is the largest?
Arteries
28
Which blood vessel type delivers oxygenated blood to the organs?
Arteries
29
Which blood vessel type is the site for nutrient, gas, water, and solute exchange?
Capillaries
30
Which blood vessel type have walls innervated by alpha-adrenergic receptors that allow for contraction?
Arterioles and venules
31
What do the beta-adrenergic receptors that innervate arterioles and venules allow?
Dilation
32
Which blood vessel type is the least elastic?
Venous
33
What are the walls of veins composed of?
Endothelium and modest amount of elastin, smooth muscle, and connective tissue
34
Which blood vessel type receives the highest pressure (stressed volume)?
Arteries
35
Which blood vessel type receives the unstressed volume?
Veins
36
True/False: Veins have the largest capacitance.
True.
37
Where does blood from the lungs travel to?
LA
38
Where does blood go next from the LA?
LV
39
Through what structure does blood pass through to get to the LA?
Pulmonary veins
40
Through what structure does blood flow through to get from the LA to LV?
Mitral valve
41
Where is blood transported following the fill of the LV?
Aorta
42
Through what structure does blood need to pass through to get to the aorta from the LV?
Aortic Valve
43
Where does blood flow from the aorta?
Arterial system
44
Through what structure(s) does the cardiac output distribute blood to the organs?
Parallel arteries
45
Where does blood go travel through to return to the heart?
Veins
46
Venous return pumps blood into what structure?
RA
47
Where does blood travel to following the fill of the RA?
RV
48
Through what structure must blood flow through to go from the RA to RV?
Tricuspid Valve
49
Where does the blood flow go following fill of the RV?
Pulmonary arteries
50
Through what structure must blood flow through to get to the pulmonary arteries from the RV?
Pulmonary valve
51
Where does blood travel after its release from pulmonary valves?
Lungs
52
Where does the blood flow from the lungs next?
Back to the heart via pulmonary veins for new cycle to begin
53
What are the three mechanisms for achieving blood flow change?
1. CO remains constant but blood flow is redistributed 2. CO increases or decreases but distribution percentage is constant. 3. Both are altered (strenuous activity)
54
What are the principles that govern blood flow?
Hemodynamics
55
What is the velocity of blood flow?
The rate of displacement of blood per unit
56
What is the primary determinant of velocity of blood flow?
The size of the diameter
57
What is the normal cardiac output?
5L/min
58
What is cross sectional area formula?
pi x r^2
59
What is the formula for velocity of blood flow through a vessel?
Velocity = Flow/Cross sectional area
60
Would a small or large blood vessel at a given flow have a greater velocity?
Small
61
What two factors determine blood flow?
Pressure difference and vascular resistance
62
What gives rise to the determining of the relationship between voltage, resistance, and current?
Ohm's law
63
What is the formula for flow in relation to pressure and resistance?
Pressure Difference/Resistance
64
How would you rearrange the flow formula to find the resistance of a blood vessel?
Resistance = Pressure difference/ Flow
65
What is the term given to the resistance of the entire systemic vasculature?
Total Peripheral Resistance
66
How do you determine total peripheral resistance?
TPR = Change in pressure/CO
67
What is the name of the equation to determine the relationship between resistance, diameter, and viscosity?
Poiseuille equation
68
What is the poiseuille equation?
Total resistance (R) = 8 x viscosity X length / pi x r^4
69
If a radius decreased by half, how much would resistance increase?
16-fold (2^4)
70
Does greater or lower viscosity have higher resistance?
greater viscosity
71
What determines viscosity?
Hematocrit
72
Describe series resistance.
BVs within a given organ is supplied by a major artery and drained by a major vein so resistance builds: Total = Rartery+Rarterioles+Rcapillaries+Rvenules+Rvein
73
Describe parallel resistance.
Blood flow among the various major arteries branching off the aorta is a fraction of the total blood flow: = 1/Rtotal = 1/R1 +1/R2+ 1/R3....
74
What is laminar flow?
Smooth, parabolic profile of velocity of blood flow and center of the stream.
75
What does an irregularity in blood flow due to a defective valve or clot cause?
Turbulent flow
76
What is used to predict whether blood flow will be laminar or turbulent?
Reynolds number
77
What is the formula for Reynolds number?
Nr= density of blood x diameter of BV x velocity of BV / viscosity
78
What value indicated laminar flow? turbulent?
<2000, >3000
79
Turbulent flow causes what to occur in blood pressure?
Korotkoff sounds
80
What can stenosis of BVs causing turbulent flow cause?
Audible vibrations = murmur
81
Ultimately, what happens when narrowing of a BV occurs?
decrease diameter = increase velocity = increase Reynolds number
82
What condition can result in functional murmurs?
Anemia (decrease hematocrit)
83
What does thrombus in a BV cause?
(Blood clot in lumen) = narrow diameter = increase velocity = increase reynolds number = turbulence
84
What does polycthemia do to reynolds number?
(increased hematocrit) = increase viscosity = increase resistance (=CO) will be less turbulent
85
What is the consequence of blood traveling at different velocities within a blood vessels adjacent to others?
Shear
86
Where is shear highest? Lowest?
At BV wall, at center of BV
87
What is the term given for the volume capable of being held at a given pressure?
Compliance (capacitance)
88
What is compliance related to?
The distensibility
89
What is the formula for compliance?
C= volume/Pressure
90
Ultimately, does a higher or lower volume have a greater compliance at a given pressure?
Higher
91
What does changes in compliance result in?
Redistribution of blood between the veins and arteries (unstressed and stressed blood)
92
If compliance decreases, what happens to the ratio of unstressed to stressed volume?
Decreases volume = Decreases unstressed volume and increases stressed volume
93
If compliance increases, what happens to the ratio of unstressed to stressed volume?
increases volume = increases unstressed volume and decreases stressed volume
94
What affects does aging have on BVs?
Become stiffer and less distensible, therefore, less compliant
95
True/False: Blood pressures are equal.
False, blood pressures aren't equal, creating a driving force for blood flow
96
What is the mean pressure measured in?
mm Hg
97
What are the pressures in the systemic circulation?
Aorta, Large arteries, Arterioles, Capillaries, Vena Cava, Right Atrium
98
What are the pressures in the pulmonary circulation?
Pulmonary artery, capillaries, pulmonary vein, left atrium.
99
Does systemic circulation or pulmonary circulation have higher pressures?
Systemic
100
What is the mean pressure of the aorta?
100 mm Hg
101
What is the mean pressure of the large arteries?
100 mm Hg (systole 120, diastole 80)
102
What is the mean pressure of the arterioles?
50 mm Hg
103
What is the mean pressure of the capillaries of the systemic circulation?
20 mm Hg
104
What is the mean pressure of the vena cava?
4 mm Hg
105
What is the mean pressure of the Right atrium?
0-2 mm Hg
106
What is the mean pressure of the pulmonary artery?
15 mm Hg (systole 25, diastole 8)
107
What is the mean pressure of the capillaries of the pulmonary circulation?
10 mm Hg
108
What is the mean pressure of the of the pulmonary vein?
8 mm Hg
109
What is the mean pressure of the Left atrium?
2-5 mm Hg
110
What exists in the arterial pressure that reflect the activity of the heart?
Pulsations/oscillations
111
What is the lowest arterial pressure measured during a cardiac cycle when no blood is being ejected and ventricles relax?
Diastolic pressure
112
What is the highest arterial pressure measured during a cardiac cycle when the blood is being ejected from the left ventricle?
Systolic pressure
113
What is the blip in the arterial pressure curve produced when the aortic valve closes?
Dicrotic notch
114
Where is the greatest pressure drop and why?
Capillaries because of the resistance provided
115
What is the difference between the systolic pressure and diastolic pressure?
Pulse pressure
116
What are the factors that affect pulse pressure?
Stroke volume, arterial compliance
117
What is stroke volume?
the volume of blood ejected from the left ventricle on a single beat
118
True/False: If all other factors are equal, the magnitude of pulse pressure reflects the stroke volume.
True
119
What is the average pressure completed in a complete cardiac cycle?
Mean arterial pressure
120
What is the formula for finding mean arterial pressure?
Diastolic pressure + 1/3 Pulse pressure
121
Why does damping (decrease of amplitude) of the oscillations other than the large large arteries occur?
resistance of blood vessel makes it difficult to transmit pulse pressure and compliance , the more complianr the more volume can be added to it without causing an increase in pressure
122
What effect does arteriosclerosis have on pressure?
Decreases diameter = decreases compliance therefore increasing systolic pressure, pulse pressure, and mean arterial pressure
123
What affect does aortic stenosis have on pressure?
narrows Valve and size of opening = decreases blood ejection = decreased systolic pressure, pulse pressure, and mean arterial pressure
124
What affect does aortic regurgitation have on pressure?
incompetent valve causes back flow and pressure can drop close to zero
125
What affect does PDA (patient ductus arteriosus) have on pressure?
1/2 of blood volume pumped back into aorta causing a decrease in diastolic blood pressure
126
For the heart to serve as a pump what must be electrically activated and contract?
Ventricles
127
Where does an action potential in the heart generate?
SA node
128
What is the ability of the heart to self excitation?
Automaticity
129
What is the ability of APs to propagate the electrical impulses from one cell to another?
Conductivity
130
What are the two types of cardiac muscle cells?
Contractile and conducting
131
What type of cells make up the atrial and ventricular tissue, functioning as the working cells of the heart?
Contractile cells
132
What type of cells make up the tissues of the SA node, Atrial internodal tracts, AV node, bundle of His, and purkinje system that can spontaneously generate action potentials and generate them over the myocardium?
Conducting cells
133
What structure initiates the action potential?
SA node, serving as the pacemaker
134
Where does the action potential go after leaving the SA node?
Atria via atrial internodal tracts to the AV node
135
What happens to the AP when it arrives the the AV node?
Conduction velocity slows to ensure ventricles have sufficient time to fill before activation and contraction
136
Where does the AP go from the AV node?
Rapidly enters the bundle of His to the purkinje system then rapidly to one ventricular muscle cell to the next via low resistance pathways
137
Where does the AP end?
Ventricle
138
What is normal sinus rhythm?
AP generates from the SA node at rate of 60-100 impulses per minute for activation of myocardium to occur in the correct sequence with correct timing and delays
139
What determines the membrane potential?
Conductance/permeability to ions and the concentration gradients for those ions
140
What will occur if the cardiac muscle has a high conductance/permeability to an ion?
That ion will flow down its gradient and will attempt to drive MP toward equilibrium potential
141
How is the membrane potential expressed in terms of measure and polarity?
mVs and intracellular potential expressed relative to extracellular (-85 mV = 85 mV w/ negative cell interior)
142
What type of ions does the resting membrane potential of cardiac cells favor?
K+
143
Do cardiac cells utilize Na+ K+ ATPase?
Yes, to maintain the concentrations
144
What causes changes in membrane potential?
Flow of ions in or out of the cell due to a change in conductance or in electrochemical gradient
145
What is the potential difference at which there is a net inward current, where upstroke occurs?
Threshold potential
146
What are the characteristics of action potentials on the ventricles, atria, and purkinje system?
Have a long duration ( ~150 ms in atria, ~250 ms in ventricles, ~ 350 ms in Purkinje system), Have a stable RMP, and have a plateau (sustained period of depolarization)
147
What occurs during phase 0 of the action potential in VAPs?
Upstroke - rapid depolarization from Na+ influx
148
What occurs during phase 1 of the action potential in VAPs?
Initial repolarization - brief period of repolarization, Na+ inactivation gates close and K+ efflux occurs.
149
What occurs during phase 2 of the action potential in VAPs?
Plateau - long period (150-200 ms) of stable, depolarized MP by a balance of currents due to efflux of Ca2+ (slow inward current)
150
What occurs during phase 3 of the action potential in VAPs?
Repolarization - gradually at the end of phase 2, speeds up here to RMP by decrease of conductance of K+ and Ca2+
151
What is the final phase of the action potential in VAPs?
RMP/Electrical diastole = MP returns to resting levels of ~ -85 mV. MP is stable again and currents are equal.
152
Describe the major difference in an AP in the SA node vs VAPs?
SA node does not have phase 1 (initial repolarization) or 2 (plateau)
153
What occurs during phase 0 of an AP in SA node?
Upstroke, by increase in conductance and inward current of Ca2+ carried by L-type Ca2+ channels
154
What occurs during phase 3 of an AP in SA node?
Repolarization due to an increase in K+ conductance due to electrochemical driving forces = outward current of K+, which depolarizes the membrane
155
What occurs during phase 4 of an AP in SA node?
Spontaneous depolarization/pacemaker potential - ~65 mV, slow depolarization produced by the opening of Na+ channels and inward current occurs. Once brought back to threshold, Ca2+ channels open for upstroke.
156
What is the firing rate of the SA node?
70-80 impulses/min
157
What is the firing rate of the AV node?
40-60 impulses/min
158
What is the firing rate of the Bundle of His?
40 impulses/min
159
What is the firing rate of purkinje fibers?
15-20 impulses/min
160
What does the rate of the spontaneous depolarization help determine?
The heart rate
161
What effect does ischemia have on cardiac APs?
Heart cannot extract O2, so ATP production decrease, decreasing Na+K+ATPase which increases ECF [K+] and ICF [Na+] so the RMP becomes less negative and Na+ channels remain inactivated and lose phase 0 so AP is slower
162
How do Ca2+ channel blockers affect the AP?
L-type channels are inhibited so Ca2+ prevent the release of Ca2+ so inhibits plateau period
163
What do calcium channel blockers do to blood pressure?
Decrease it
164
What are the examples of calcium channel blockers?
Nifedipine, diltiazem, verapamil, amlodipine
165
What is a latent pacemaker?
Other cells have the capacity to take over the spontaneous phase 4 depolarization
166
What is the term given for the latent pacemakers being suppressed when the SA node controls the HR?
Overdrive suppression
167
Will the heart beat slower or faster when driven by a latent pacemaker?
Slower
168
What is the term given when the latent pacemaker becomes THE pacemaker?
Ectopic pacemaker/ectopic focus
169
What is the speed at which APs are propagated?
Conduction velocity
170
What is the CV of the atria?
1 m/s
171
What is the CV of the AV node?
0.01-0.05 m/s
172
What is the CV of His-Purkinje?
2-4 m/s
173
What is the CV of Ventricle?
1 m/s
174
What is the total time it takes for an action potential to spread through the heart?
220 ms
175
In what part of the action potential is there a time delay?
Through the AV node
176
In normal rhythm, what is the approximate time it takes the AP to get from the SA node (time zero) to the AV node?
~60 ms
177
In normal rhythm, what is the approximate time it takes the AP to get through the AV node to the bundle of His?
~100 ms = 160 ms
178
In normal rhythm, what is the approximate time it takes the AP to get from the bundle of his to the bundle branches?
~10 ms = 170 ms
179
In normal rhythm, what is the approximate time it takes the AP to get from the bundle branches to the Purkinje fibers?
~20 ms = 190 ms
180
In normal rhythm, what is the approximate time it takes the AP to get from the purkinje fibers to the ends of the ventricles?
~LV: 20 ms = 210 ms, ~RV: 30 ms = 220 ms.
181
What does conduction velocity depend on most?
The size of local currents
182
What refractory period is the majority of the duration of AP in which another AP cannot be generated?
Absolute
183
What refractory period includes and extends the coverage of the absolute refractory period?
Effective Refractory Period
184
What occurs at the end of the ERP?
Na+ channels start to recover
185
Can another AP generate during the ERP?
It COULD but it would not conduct, meaning there is not enough inward current to move the AP to the next site
186
What refractory period begins at the end of the ERP and continues until the cell membrane has almost fully repolarized?
Relative Refractory Period
187
What occurs in the RRP?
Na+ channels have recovered to the closed but available state
188
Could a second AP generate in the RRP?
It could but it would require a greater-than-normal stimulus
189
What would happen to the second AP if it were to generate in the RRP?
will be abnormal in configuration and shortened plateau phase
190
What refractory period follows the RRP while the MP is at ~-75 until it returns back to normal ~-85 mV?
Supranormal period
191
Could a second AP generate during the supranormal period?
Yes, The cell's excitability prior to MP makes it easier to fire an AP than if it were at RMP.
192
What parts of the heart receive sympathetic innervation?
All parts
193
What parts of the heart receive parasympathetic innervation?
Via Vagus nerve stimulated SA and AV nodes, and slight atria
194
What is the term given to the effects of the ANS on heart rate?
Chronotropic effects
195
What type of chronotropic effects increase heart rate?
Positive chronotropic effects
196
What type of chronotropic effects decrease heart rate?
Negative chronotropic effects
197
What type of stimulation mostly effects the increase in heart rate?
sympathetic stimulation
198
What type of stimulation mostly effects decreases in heart rate?
parasympathetic stimulation
199
Describe the mechanism behind increasing heart rate by sympathetic stimulation.
Norepinephrine released by beta1 receptors at the SA node couple with adenylyl cyclase through Gs protein which produces an increase in spontaneous depolarization which increases Heart rate
200
Describe the mechanism behind decreasing heart rate by parasympathetic stimulation.
Ach released from PNS fibers activated muscarnic (M2) receptors in SA node couple with Gk which inhibits adenylyl cyclase which decreases the rate of spontaneous depolarization and increases the conductance K-ACH Channels producing outward current of K+ leading to hyperpolarization therefore decreasing heart rate
201
What autonomic effects effect conduction velocity?
Dromotropic effects
202
In what part of the heart are dromtropic effects more important?
AV nodes which alter the rate at which APs are conducted
203
Which ANS system increases conduction velocity?
SNS
204
How does the SNS work to increase conduction velocity?
Increases the Ica, which causes upstroke in the AV node which directly increases inward current and CV
205
Which ANS system decreases conduction velocity?
PNS
206
How does the PNS work to decrease conduction velocity?
Decreases the Ica and increases Ik-ach which decreases the rate of AP conduction
207
What can occur if no production can be conducted at all from overstimulation of the PNS?
Heart block
208
What are the effects that alter contractility?
Inotropic effects
209
Which inotropic effects increase contractility?
Positive
210
Which inotropic effects decrease contractility?
Negative
211
What ion is primarily responsible for the changes in contractility?
Ca2+, more release = larger inward current = more contractility
212
What type of ANS stimulation have a positive inotropic effect on the myocardium?
SNS
213
How does the SNS increase contractility?
Beta1 receptors, coupled w/ Gs protein to adenylyl cyclase which leads to the production of cAMP and protein kinase A, and phosphorylates Sarcolemmal Ca2+ channels and Phospholamban (regulates SERCA) to increase contractility.
214
What type of SNS stimulation have a negative inotropic effect on the atria?
PNS
215
How does the PNS decrease contractility?
Muscarinic receptors coupled with Gk to adenylyl cyclase which is inhibits by Ach decreasing the inward current of Ca2+ during the plateau phase and increasing the Ik-ach shortening the duration of AP and indirectly decreasing the Ca2+ current which produces a decrease in contractility
216
What substances also act as positive inotropic agents?
Cardiac glycosides
217
Name a few examples of cardiac glycosides.
Digoxin, digitoxin, oubain
218
What are the functions of cardiac glycosides?
To treat CHF
219
How do cardiac glycosides increase contractility?
By inhibiting the Na+ K+ Pump, increasing the intracellular [Na+] which alters the Na+ gradient the and Ca2+ Na+ exchanger decreasing the amount of Ca2+ released so intracellular [Ca2+] increases producing an increase in tension which increases contractility
220
True/False: As heart rate increases or decreases, contractility increases or decreases the opposite way.
False, a decrease in one leads to a decrease in the other and same for increase
221
How would increasing HR increase contractility?
Increasing HR increases the AP propagation which will increase the total amount of Ca2+ that enters the cell during the plateau phases which increases tension therefore increasing contractility
222
What type of effect best shows the HR and tension relationship?
Staircase Effect/Bowditch staircase/Treppe Staircase
223
What is a measurement of tiny potential differences on the surface of the body that reflect the electrical activity of the heart?
Electrocardiogram
224
On an EKG, what does the P wave represent?
The depolarization of the atria
225
On an EKG, what does the QRS complex represent?
Collectively, Depolarization of the ventricles
226
On an EKG, what does the T wave represent?
Repolarization of the ventricles
227
On an EKG, what does the QT interval represent?
the time of the first ventricular depolarization to the last
228
On an EKG, what does the ST segment represent?
Isoelectric portion of the QT interval that corresponds with the plateau period of ventricular AP
229
How is HR measured?
Counting the number of QRS complexes per minute
230
what can occur because of the relationship between HR and refractory periods?
Arryhthmias
231
What is bradycardia?
Decreased HR
232
What is tachycardia?
Increased HR
233
True/False: overall, myocardial contractile machinery is similar to skeletal muscle.
True, composed of actin/myosin, sarcomeres, t tubules, etc
234
What does the excitation-contraction coupling in cardiac muscle translate the AP into?
Tension
235
Describe the mechanism behind ECC in cardiac muscle.
1. Ap is initiated and depolarization spreads to the cell interior via T-tubules. Plateau period results in an increase in Gca and an inward current flows through dihydropyridine receptors from ECF to ICF. 2. Entry of Ca2+triggers CICR from ryanodine receptors. 3/4. Ca2+ bind to troponin c, tropomyosin moves and actin and myosin cross bridge cycling occurs, producing tension. This continues until Ca2+ levels drop below levels for it to unbind from troponin c. (the magnitude of tension developed is proportional to intracellular [Ca2+], 5. Relaxation occurs when Ca2+ is reaccumulated in SR by SERCA. [Ca2+] falls to resting levels and it dissociated from troponin, actin-myosin interaction is blocked and relaxation occurs.
236
What is the basis for the length-tension relationship?
Degree of overlap of thick and thin filaments and the number of possible sites for it to cross bridge
237
In myocardial cells where does maximal tension occur? (Lmax)
2.2 microunits
238
What other two things (aside from degree of overlap) alter tension development?
Increasing muscle length increases Ca2+ sensitivity of Troponin C AND it increases Ca2+ release from SR.
239
What component of the length-tension relationship corresponds with the LV end-diastolic volume?
Length (the length of a muscle fiber just prior to contraction
240
What component of the length-tension relationship corresponds with the pressure developed by the entire LV?
Tension
241
Check out ventricular pressure curve ppt!
Check out ventricular pressure curve ppt!
242
What is preload for the left ventricular end-diastolic volume?
the resting length from which the muscle contracts
243
What is afterload for the left ventricle?
Aortic pressure.
244
The velocity of shortening of cardiac muscle is maximal when afterload is _ and velocity of shortening _ as afterload _.
zero, decreases, increases
245
What is stroke volume?
The amount of blood ejected by the ventricle on each beat.
246
What is the "formula" for stroke voluma?
End-diastolic volume - end-systolic volume
247
What is ejection fraction?
a fraction of the end-diastolic volume ejected in each stroke volume
248
What is cardiac output?
The total volume ejected by ventricle per time unit
249
What is the normal stroke volume?
~70 mL
250
What is the normal ejection fraction?
55%
251
What is the "formula" for ejection fraction?
SV/ End diastolic volume
252
What is the formula for cardiac output?
CO = SV + HR
253
What is the normal cardiac output?
5000 mL/min in a 70 kg man
254
What is the Frank-Starling Relationship?
The volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole (CO=VR)
255
What occurs during isovolumetric contraction?
LV has filled with blood from LA and its volume is the end-diastolic volume, 140 mL. Ventricle is activated, it contracts, and ventricular pressure increases dramatically. Valves are closed
256
What occurs during ventricular ejection?
Ventricular pressure is higher than aortic so aortic valve opens and blood rapidly ejects from LV. LV pressure remains high due to ventricular contraction but volume decreases to ~70 mL (=SV)
257
What occurs during isovolumetric relaxation?
systole ends and ventricle relaxes. Ventricular pressure decreases below aortic pressure so aortic valve closes so volume remains constant at ~70 mL.
258
What occurs during ventricular filling?
Ventricular pressure has fallen to a level that is now less than left atrial pressure causing the mitral valve to open and blood flows into LV. LV vol increases back to 140 mL and is relaxed and there is only a slight pressure increase, waiting for the next cycle.
259
What affect does increased preload have on the ventricular cycle?
VR increased = increase preload = increase SV due to increased VR but contractility remains constant
260
What affect does increases afterload have on the VC cycle?
(or, increased aortic pressure) LV must eject blood against greater than normal pressure so ventricular pressure must rise to compensate. Less blood is ejected, decreasing SV so more blood stays in LV increasing end-systolic volume.
261
What affect does increasing contractility have on the ventricular cycle?
Increased contractility = greater tension and pressure and can eject a larger volume so, SV increases so less blood remains in LV at the end of systole thus end-systolic volume decreases
262
What two components alter SV?
End-diastolic volume, end systolic volume
263
What factors alter end diastolic volume?
Filling pressure, filling time, ventricular compliance
264
What factors alter the end systolic volume?
HR, Preload, afterload, contractility
265
What two components alter HR?
Intrinsic and extrinsic regulation
266
What factors alter intrinsic regulation?
Threshold potential, max diastolic potential, slope of diastolic depolarization
267
What factors alter extrinsic regulation?
ANS, Humoral Factors
268
What is work defined as?
Force x distance
269
What is stroke work defined as?
The work the heart performs on each beat
270
What is cardiac minute work?
cardiac output x aortic pressure
271
What are the two components of cardiac minute work?
Pressure work and volume work
272
What correlates directly with cardiac minute work?
Myocardial O2 consumption
273
Which work is more costly for O2 consumption?
Pressure work
274
What affect does aortic stenosis have on O2 consumption?
Greatly increased because the LV must develop extremely high pressures to pump blood
275
Does O2 consumption increase or decrease in conditions when a larger-than-normal percentage of total cardiac work being pressure work?
Increases
276
When CO is very high and volume work contributes a greater-than-normal percentage of total cardiac work what happens to O2 consumption?
O2 consumption will increase just a little
277
What affect does systemic hypertension on cardiac work?
Requires LV to perform more pressure work than normally so LV wall will hypertrophy as compensation for increased workflow
278
What is the Law of Laplace?
for a sphere, pressure correlates directly with tension and wall thickness and inversely with radius
279
What is the formula for pressure regarding the law of laplace?
P = 2 x thickness x tension / radius
280
Ultimately, the _the thickness of the wall, the _ the pressure that can be developed.
greater, greater
281
What will happen as a compensatory mechanism that happens when wall thickness increases?
Ventricle has to pump harder so atrial pressure is increased
282
Pulmonary hypertension can cause what to happen?
RV Hypertrophy
283
What can be used to measure CO?
Fick principle
284
What does the fick principle state regarding the heart?
in steady state, CO of LV and RV are equal
285
How is the fick principle applied to O2 consumption?
In steady state, O2 consumption rate must equal the amount of air leaving the lungs in the pulmonary vein minus the amount of O2 returning to the lungs in the pulmonary artery
286
What is the "equation" for O2 consumption?
(CO x [O2] pulm vein) - (CO x [O2] pulm artery)
287
How would you solve for cardiac output in relation to O2 consumption?
CO = O2 consumption/ ([O2]pulm vein - [O2]pulm artery)
288
What is the typical total O2 consumption?
~250 mL/min in a 70 kg man
289
What is the first phase of the cardiac cycle?
Atrial systole
290
What part on an EKG indicates atrial systole?
P wave, PR interval
291
What are the major events of atrial systole?
Atrial contraction marks the depolarization of the atria. Final phase of ventricular filling, Mitral valve is open so ventricle fills with blood from atrium.
292
What heart sound is made during atrial systole?
Fourth (S4) not audible in normal adults
293
What is phase two of the cardiac cycle?
Isovolumetric Ventricular Contraction
294
What part on an EKG indicates isovolumetric ventricular contraction?
QRS complex
295
What are the major events of isovolumetric ventricular contraction?
Electrical activation of ventricles, ventricle pressure increases but volume is constant, mitral vvalve closes
296
What heart sound is made during isovolumetric ventricular contraction?
First (s1)
297
What occurs during the third phase of the cardiac cycle?
Rapid ventricular ejection
298
What part on an EKG indicates the rapid ventricular ejection?
ST segment
299
What are the major events of Rapid ventricular ejection?
Ventricle continues to contract, ventricle pressure reaches highest value, blood is ejected rapidly into aorta, atrial pressure increases due to large volume, aortic valve opens
300
What is the fourth phase of the cardiac cycle?
Reduced Ventricular Ejection
301
What part on an EKG indicated the reduced ventricular ejection phase?
T wave
302
What major events occur during reduced ventricular ejection?
Ventricles begin to repolarize, ventricular pressure falls, blood continues to eject into aorta (at a reduced rate), aortic pressure falls, L arterial pressure continues to increase as blood returns to the left heart from the lungs
303
What is the fifth phase of the cardiac cycle?
Isovolumetric ventricular relaxation
304
What part on an EKG indicates the isovolumetric ventricular relaxation phase?
end of T wave
305
What majors events occur during the isovolumetric ventricular relaxation phase?
Ventricles are fully repolarized, LV pressure decreases below aortic pressure, ventricular volume is constant ,aortic valve closes
306
What heart sound is made during isovolumetric ventricular relaxation phase?
Second (S2)
307
What is the sixth phase of the cardiac cycle?
Rapid ventricular filling
308
What major events occur during Rapid ventricular filling?
Ventricular pressure is minimal so mitral valve opens and ventricles fill and volume increases, ventricular pressure remains low, aortic pressure decreases
309
What heart sound is made during Rapid ventricular filling?
Third (S3)
310
What is the seventh and final phase of the cardiac cycle?
Reduced ventricular filling (Diastasis)
311
What are the major events that occur during reduced ventricular filling?
Final portion of ventricular filling but at a slower rate, atrial systole marks the end of diastole, ventricular volume is end diastolic volume.
312
What does changes in HR alter the time available for?
Diastasis
313
What can be used to plot the relationship between CO of the LV and the right atrial presure?
Cardiac Function Curve
314
What can be used to plot the relationship between VR and right atrial pressure?
Vascular function curve
315
What determines the slop of the VF Curve?
TPR
316
What will a decrease in TPR do to the VF Curve?
causes a clockwise rotation of it
317
What will an increase in TPR do to the VF Curve?
Causes a counterclockwise rotation of it
318
What is the mean systemic pressure?
the pressure that would be measured throughout the CVS if the heart stopped
319
When VR is zero and Pa is maximal, what would the MSP look like?
Equal to the pressure through the vasculature, so no blood will flow
320
What is the volume that the veins can hold (under no pressure)?
Unstressed volume
321
What is the volume in the arteries (produces BP by stretching of walls)?
Stressed volume
322
If the blood volume is 0-4 L, what does the distribution of the blood volume look like?
All unstressed
323
If the blood volume rises above 4 L, what does the distribution of blood volume look like?
some of the blood will move to stressed volume
324
what will happen to the MSP if stressed volume is added?
Quick increase
325
What effect does decreasing compliance have on the blood volume distribution?
decreases the amount of blood it can hold = Decreases the unstressed volume to stressed volume, so MSP increases
326
What effect does increasing compliance have on the blood volume distribution?
veins can hold more blood = unstressed vol will increase and stressed will decrease = decrease MSP
327
Combining the cardiac function curve and vascular curve causes an intersection which indicates what?
Steady state - Where CO and VR are equal
328
What effect will a positive inotropic effect have on the CVF Curve?
will increase contractility, SV, and CO for a given R atrial pressure so the Cardiac Curve will have an upward shift and the new steady state will be at a higher CO but lower atrial pressure
329
What effect will a negative inotropic effect have on the CVF Curve?
A negative inotropic effect decreases contractility, which decreases CO for any given atrial pressure. CF Curve shifts downward, VF Curve remains constant and a new steady state = CO decrease and atrial pressure increased.
330
What effect does a increasing blood volume have on the CV-F Curve?
Increasing the blood volume increases stressed volume therefore increases Mean Systemic Pressure (MSP) [where VR=0]. This shifts the intersection point to the right so the shift is parallel in manner. New steady state = CO increased and R atrial pressure increased.
331
What effect does decreasing blood volume have on the CVF Curve?
Decreasing the blood volume decreases stressed volume therefore decreases Mean Systemic Pressure (MSP) [where VR=0]. This shifts the intersection point to the left, parallel in manner. New steady state = CO decreased and R atrial pressure decreased.
332
What effect does increasing TPR have on the CVF Curve?
Increasing TPR constricts the arterioles so increases atrial pressure. This increases afterload which decreases CO. The CF Curve shifts downward and VF Curve rotates counterclockwise. New steady state = both CO and VR are decreased.
333
What effect does increasing TPR have on the CVF curve?
Decreasing TPR dilates the arterioles so decreases atrial pressure. This decreases afterload which increases CO. The CF Curve shifts upward and VF Curve rotates clockwise. New steady state = both CO and VR are increased.
334
When changes in TPR occur, why does it appear as if Pa is unaffected?
Because the effect of changing TPR can not be easily predicted, as magnitude of effects can either increase, decrease, or unchange the Atrial pressure
335
What is Mean Arterial Pressure (Pa)?
driving force from difference in arterial and venous pressures ~100 mm Hg.
336
True/False: The Pressure in the major artery serving each organ is equal to Pa due to the parallel arrangement of the arteries off the aorta.
True
337
What is the formula for Pa?
Pa = CO x TPR
338
What change will occur to Pa if TPR doubles?
It will also double (and CO will 1/2 to compensate)
339
What change will occur to Pa if CO halves?
A compensatory increase in TPR will decrease Pa only slightly.
340
What two major systems regulate Pa?
Baroreceptor reflex and Renin-Angiotensin-Aldosterone System (RAAS)
341
What does the baroreceptor reflex attempt to do?
restore Pa to set pint value in a matter of seconds
342
What does the RAAS attempt to do?
regulated Pa but more slowly, primarily by its effect on blood volume
343
Where are baroreceptors located?
in the walls of the carotid sinus and aoritc arch
344
Where do baroreceptors relay information about blood pressure changes to?
Cardiovascular vasomotor centers in the brain stem (medulla)
345
What stimulates a baroreceptor?
Stretch/pressure
346
What does the stretch on baroreceptors cause to happen?
increase the firing rate of afferent nerves
347
What cranial nerve sends the information from the baroreceptor on the carotid sinus nerve to the brain stem?
CN IX (Glossopharyngeal)
348
What cranial nerve sends the information from the baroreceptor on the aortic arch nerve to the brain stem?
CN X (Vagus nerve)
349
Afferent serves send the information to what structure for directing the changes in activity of the CVS centers?
Nucleus tractus solitarius
350
What effects does PNS outflow have?
effect of vagus nerve on SA node to decrease HR
351
What effects does SNS outflow have?
increase HR, contractility, and SV; arterioles vasoconstrict and increases TPR, veins venoconstrict and decreased unstressed volume.
352
An increase in Pa will cause a(n) _ in SNS activity and a(n) _ in PNS activity.
decrease, increase
353
An decrease in Pa will cause a(n) _ in SNS activity and a(n) _ in PNS activity.
increase, decrease
354
So describe the baroreceptor reflex as an compensatory mechanism for an increase in Pa.
Baroreceptor is stretched by the added pressure and this information is sent to the brain centers via the nucleus tractus solitarius which sends the integration for change: increase PNS = decrease HR. decreases SNS = decreased contractility, CO, TPR (which increased unstressed volume) = Pa back to set point
355
What is the baroreceptor reflex like during the valsalva maneuver?
VM increases intrathoracic pressure which decreases VR, therefore reducing CO, causing a decrease in Pa. so baroreceptors have a decreased stretch which is sent to the brain center which causes decreased PNS to decrease HR and increased SNS outflow = to increase CO, VR, and Pa to decrease HR.
356
What substance(S) are responsible for regulating blood volume by the RAAS?
Hormones
357
In RAAS, what is stimulated by a change in pressure?
mechanoreceptors
358
What does a decrease in Pa cause to [first] happen during the RAAS?
Prorenin to convert to renin in the juxtaglomerular cells.
359
What increases renin secretion? What decreases it?
Beta-agonists (isoproterenol), B-antagonists (Propanolol)
360
Renin catalyzes what conversion?
angiotensinogen to angiotension I
361
Where does the conversion of angiotensin I to angiotensin II occur?
lungs and kidneys
362
What enzyme catalyzes the conversion of angiotensin I to II?
ACE
363
What does the production of AGTII cause? [4 things]
1. acts on zona glomerulosa cells of the adrenal cortex to stimulate the synthesis and secretion of Aldosterone which increases Na+ reabsorption to increase ECF and blood volume
2. stimulates Na+H+ exchange in the renal proximal tubule to increase the reabsorption of Na+ and HCO3-
3. acts on hypothalamus to increase thirst and water intake therefore stimulating the secretion of ADH which increases water reabsorption, complementing the increase in Na+ absorption
4. bind to AT1 receptors to activate IP3/Ca2+ second messenger system to cause vasoconstriction and increase TPR which leads to an increase in Pa.
364
Why is the RAAS mechanism a slower response?
Synthesis of aldosterone requires transcription which can tale hours-days
365
What two substances can block the actions of AGTII?
ACE inhibitor (captopril) and AT1 receptor inhibitor (losartan)
366
Renal artey stenosis causes an early rise in MAP due to what three things?
vasoconstriction, renin secretion normalized, second rise in MAP due to Na+, H2O retention of the RAAS system
367
What compensatory mechanism is in place for decreases in O2 (increasing CO2, and decreashing pH)?
Peripheral chemoreceptors
368
Peripheral chemoreceptors sense the decrease in Po2 and cause what to occur?
increase firing rate of afferent nerves to activate sympathetic vasoconstriction centers to cause arteriolar vasoconstriction AND increase PNS outflow to decrease HR, this decrease in Po2 causes increase in ventilation to counter the PNS decrease in HR
369
What compensatory mechanism is in place for changes in Pco2 and pH?
Central Chemoreceptors
370
What happens if the brain becomes cerebral ischemic?
cerebral Pco2 increases and pH decreases
371
How do central chemoreceptors work to counter cerebral ischemia?
increases SNS outflow = intense arteriolar vasoconstriction and increase TPR so blood flow is redirected to the brain to maintain its perfusion.
372
What is a consequence of the vasoconstriction by central chemoreceptors?
dramatic increase in Pa, even to life threatening levels
373
What illustrates the role of the cerebral chemoreceptors?
Cushing reaction
374
What role does ADH play in regulation?
regulated body fluid osmolarity and participates in the regulation of arterial blood pressure
375
How does ADH work to regulate?
When activated, vasoconstriction of arterioles occurs which increases TPR
376
Where are low pressure baroreceptors located?
veins, atria, and pulmonary arteries
377
What are low pressure baroreceptors sensitive to?
changes in blood volume
378
Primarily, How do low pressure baroreceptors regulate an increase in blood volume?
by excretion of Na+ and water
379
What are the four responses to incresing blood volume by low pressure baroreceptors?
1. increased secretion of ANP which binds to ANP receptors to cause vasodilation and decreased TPR. This vasodilation increases Na+ and H20 excretion which decreases total body Na+ content, ECF volumes, and blood volume.
2. Decreased secretion of ADH = decreased water reabsorption = increased water excretion.
3. inhibition of SNS vasoconstriction in renal arteries which leads to dilation and increased Na+ and H2o excretion
4. bainbridge reflex- the baroreceptors send info to the brain and it works to increase venous low-pressure receptors to increase heart rate, increasing CO leading to increased renal profusion and increased excretion
380
In what ways may obesity contribute to HTN?
increase CO, decreasing baroreceptor activity which increases SNS activity and RAAS activity; impairment of renal pressure natriuresis; adipocyte dysfunction = increase inflammatory mediators and vascular remodeling and endothelial dysfunction
381
What are the three types of capillaries? describe them.
continuous - endothelial cells closely joined together by intracellular junctions w/ tiny coated pits
Fenestrated - endothelial cells contain fenestra (pores) that allow the passage of some solutes
Discontinuous(sinusoidal) - endothelial cells contain large fenestrations and gaps = very leaky
382
What are the most predominant type of capillaries?
Continuous
383
Which type can you find in skeltal muscle tissue and brain? Liver? Small intestine?
continuous, discontinuous, fenestrated
384
What affects the blood flow through the capillaries?
Degree of constriction or relaxation
385
What structure function to open and close to allow blood flow?
Precapillary sphincters
386
Gases/solutes exchange occurs across the capillary wall by what type of transport?
Simple diffusion
387
What substances can pass through the capillary wall?
Lipid-soluble (O2, CO2)
388
What substances can pass between endothelial cells by clefts?
Water soluble (H2O, ions, glucose, amino acids)
389
How could protein cross the capillary wall?
Vesicles
390
What is the most important mechanism for fluid transfer?
osmosis
391
What forces drive fluid movement in the capillaries?
hydrostatic and osmotic pressures (Starling forces)
392
What is the Starling equation?
Jv (fluid movement) = Hydraulic conductance[(Capillary-interstitial hydrostatic pressure) - (capillary - interstitial oncotic pressure)]
393
What is hydraulic conductance? (Kf)
the water permeability of the capillary wall
394
What is capillary hydrostatic pressure? (Pc)
force favoring filtration out of the capillary, determined by arterial and venous pressures ~17 mm Hg
395
What is interstitial hydrostatic pressure? (Pi)
force opposing filtration, normally ~0 or may be slightly negative
396
What is capillary oncotic pressure? (PIc)
Force opposing filtration determined by protein concentration
397
Does increasing or decreasing protein concentration increase filtration?
Decreasing
398
What is interstitial oncotic pressure? (PIi)
Force favoring absorption determined by protein concentration, usually quite low due to low loss of protein from capillaries
399
What are the primary two proteins to affect oncotic pressure?
Albumin and Globulins
400
What is the function of the lymphatic system?
returns interstitial fluid and proteins to vasculature
401
Describe the flow of lymph.
IF and proteins flow to lymphatic capillaries via one way flap valves. then to lymphatic vessels to the thoracic ducts to large veins
402
What type of muscle makes up the walls of lymph vessels and what is the benefit?
Smooth muscle to aid in intrinsic contractile activity (propel substances)
403
What is the amount of total daily lymph?
2-3L
404
What effect does edema have on circulation of lymph?
increases interstitial fluid by increased filtration or impaired drainage
405
What is left sided edema called? Right sided?
pulmonary, peripheral
406
If pressure increases, what will happen to lymph flow?
It will plateau ~2 mm Hg due to excess pressure compressing the outside surfaces of the larger lymphatics and impedes flow
407
What happens to lymph flow during exercise?
increases 10-30 fold
408
What alters to change blood flow to an organ?
Arteriolar resistance
409
What are the two mechanisms that regulate blood flow to various organs?
Local control and neural/hormonal regulation
410
What occurs during local control?
Direct action of local metabolites on arteriolar resistance (autoregulation)
411
What occurs during active hyperemia?
blood flow is proportional to its metabolic activity = increase in one increases the other
412
What occurs during reactive hyperemia?
an increase in blood flow occurs in response to a prior period of decreased blood flow
413
What are the two mechanisms that explain local control?
Myogenic hypothesis, metabolic
414
Which hypothesis states that when vascular smooth muscle is stretched, it contracts?
Myogenic
415
Which hypothesis states that 02 delivery can be matched by its consumption by altering resistance of the arterioles to alter blood flow?
Metabolic hypothesis
416
Describe how myogenic hypothesis acts on regulation.
If Pa is suddenly increased, arterioles are stretched anc contract hich leads to constriction which increases resistance to maintain a constant flow. (If decrease Pa = relaxation = decrease resistance)
417
Describe how metabolic hypothesis acts on regulation.
As a result of metabolic activity, tissues produce vasodilator metabolites = vasodilation of arterioles which decreases resistance and increases flow to meet demand.
418
Describe the extrinsic mechanism for regulation.
(Neural/hormonal control) Increases of decreases SNS innervation to either vasodilate or vasocontrict
419
In which two circulations is sympathetic control the most important and how do they work?
Skin (vasoconstriction by alpha1 receptors) and skeletal muscle (vasconstrict by alpha1 receptors or vasodilate by beta2 receptors)
420
What are some other vasoactive substances that control regulation and how do they work?
Histamine, Bradykinin (both released in response to trauma which produces dilation of arterioles and constriction of venules to increase filtration and local swelling), serotonin (release in response to BV damage - local vasoconstriction attempts to reduce blood flow and loss), and prostoglandins (Vasodilators = Prostacyclin and Prostaglandin E series; vasoconstrictors = Thromboxane A2 and porstoglandin F series; AGTII and vasosupressin = potent vasoconstrictors that increase TPR; ANP = vasodilator hormone secreted by atria in response to increases in Pa)
421
What are the overall CVS responses to exercise?
Exercise stimulates local responses to increase vasodilator metabolites which decreases TPR. It also increases SNS outflow to increase contractility, CO, constriction of arterioles, and constriction of veins to decrease unstressed volume to increase VR and decreases PNS outflow to increase heart rate to increase blood flow to skeletal muscle
422
What are the overall CVS responses to Hemorrhage?
Hemorrhage decreases Pa which stimulates the barorecptor reflex to increase SNS outflow to increase HR, contractility, and CO and constriction of arterioles which increases TPR, and constriction of veins which decreases unstressed volume to increase VR. It also stimulated the RAAS system to increase AGTII secretion to increase TPR and secrete aldosterone which increases Na+ reabsorption to increase blood volume. It also stimulates the capillaries to decrease capillary hydrostatic pressure to increase fluid absorption to increase blood volume. all to increase Pa back toward normal
423
What are the overall CVS responses to moving from supine to standing?
Stand = blood pooling in veins = decrease Pa so baroreceptor reflex to increase SNS outflow to increase HR, contractility, and CO, constriction of arterioles to increase TPR and constriction of veins to decrease stressed volume to increase VR, all to increase Pa back toward normal
424
What is orthostatic hyoptension?
a decrease in arterial blood pressure upon standing which may cause lightheadesness and possibly fainting
