CV Week 1 Flashcards
1
Q
Which of the following is not a role or function of the cardiovascular system?
a) dispose of CO2 and other byproducts of metabolism
b) vehicle for hormone transport and regulation of specific functions on target tissues
c) maintenance of body fluid
d) regulation of body temperature
e) provide adequate O2 supply and essential nutrients to select tissues
A
E - ALL TISSUES
2
Q
The heart composed of two pumps organized in ______ and flow is described as ______
A
series, unidirectional
3
Q
Elasticity of arteries has one impact on the intermittent nature of blood flow from heart?
A
reduces the force (attentuates)
4
Q
Elasticity allows for a more _____ flow to tissues due to their ____ during the relaxation phase of the cardiac cycle
A
continuous, recoil
5
Q
How is blood provided to the heart?
A
In systole, aorta and large arterial branches store part of energy by mechanical distension then in diastole energy is released like a rubber band when ventricles are relaxing back to heart.
6
Q
True/False: All blood vessels control their internal diameter via precise control of smooth muscle
A
FALSE - capillaries don’t!
7
Q
Arteries have a thicker wall, are stiffer, and have a strong contractile apparatus due to what two features?
A
presence of elastic fibers and a more prominent smooth muscle layer
8
Q
Why does pressure fall more quickly in the terminal segments of small arteries and arterioles in comparison to large arteries?
A
Increase in frictional resistance and increase in cross sectional area from extensive branching and multiplication
9
Q
What causes dampening of pulsatile arterial flow at capillary level?
A
Distension of large arteries (compliance) and resistance of small arteries and arterioles - non-pulsatile flow
10
Q
As cross-sectional area _______, velocity of blood flow _______
A
area, decreases [watch out!!! increases in respect to diameter tho!]
11
Q
Where is the majority of blood found in CVS and why?
A
Majority of blood found in the veins and venules (67%) because systemic veins and venules act as a large reservoir of blood that can be rapidly mobilized upon demand
12
Q
True/False: In the pulmonary vascular bed, most of the blood is found in the veins
A
FALSE - equally distributed btwn arteries, veins and capillaries
13
Q
Why is the right ventricular wall much thinner and weaker than the left ventricular wall?
A
Left ventricle sustains pressures in the order of 100mmHg at rest whereas right ventricle pressures are around 15mmHg
14
Q
What directly measures blood pressure?
A
pressure in the aorta
15
Q
When is the LUB or S1 produced?
A
When the AV valves close
16
Q
When is the DUB or S2 produced?
A
When the aortic and pulmonary valves close
17
Q
What may produce S3?
A
rapid filling of the ventricles
18
Q
What may produce S4?
A
Contraction of the atrium to get final bits of blood out
19
Q
Where is the SA node located?
A
The SA node is located in the right atrium on the upper lateral side near the superior vena cava
20
Q
The effective pumping of blood into the circulatory system depends on the ______
A
SA node
21
Q
Arrhythmias can compromise mechanical performance and lead to life threatening decreases in ?
A
cardiac output and blood pressure
22
Q
Action potential acts as a trigger for contraction of individual cardiac muscle cells through _______. This is important because it synchronizes contraction of the whole heart.
A
excitation-contraction coupling
23
Q
How are action potentials (and resting membrane potentials in myocytes generated?
A
Via the opening and closing of ion channel proteins - reason why important target for therapeutic drugs
24
Q
Which myocytes are specialized for conduction of electrical impulse? (5)
A
SA node, cells of internal conduction track, AV node cells, Bundle of his, Purkinje Cells
25
Why is SA node considered the primary pacemaker of the cell?
It is SPONTANEOUS
26
The _______ carry electrical impulses that initiate atrial contraction
cells of internal conduction track
27
Describe the pathways of the cells of internal conduction track
Flow through 3 internal pathways and one interatrial conduction tract to activate AV node and left atrium
28
Where is the AV node located?
at the junction between the right atrium and IV septum
29
What is the delay time for AV node activation of ventricles?
120 ms
30
Purkinje fibers run along the _________ surface and penetrate about 1/3 into ventricular tissue
endocardial
31
What happens when there is a left bundle branch block?
Excitation of left ventricle will be slower. The excited right ventricle will propagate its signal to left ventricle (delayed). Pattern of excitation will be shifted rightward.
32
Which electrical impulse cell generates impulses at the fastest rate? The slowest?
a) SA
b) AV
c) His
d) Purkinje
SA is fastest, Purkinje is slowest
33
What are the differences between cardiac muscle and skeletal muscle cells?
Cardiac muscle is interconnected electrically and mechanically - acts as synctium. Cardiac contraction is phasic and cannot summate into tetanus. Skeletal muscles contract individually and need more recruitment of fibers to generate a greater force.
34
Why can't cardiac contraction summate into tetanus?
Action potential duration and refractory period is very long
35
Which cells are considered pacemaker cells?
SA node, AV node, Purkinje
36
Which cells are more depolarized at rest?
a) Purkinje
b) Bundle of His
c) SA node
d) AV node
e) Atrial cells
C,D - exhibit a relatively slower upstroke than atrial, purkinje, ventricular
37
The resting membrane potential is determined by ______
conductance of K+
38
True/False: The RMP in ventricles, atria and AV node is about -80 to -90 mV
FALSE - true for ventricles, atria and PURKINJE SYSTEM
39
The equilibrium potential for K+ is -92mV. Why is the RMP for ventricles, atria and purkinje cells slightly more positive?
Differences in permeability to Na+ - more significant in nodal cells
40
What is the Na+ concentration influenced by?
Na+/K+ pump
41
Describe the ions pumped by the Na+/K+ pump
Pumps in 2K+ for every 3 Na+ pumped out - net loss of a positive charge --> slight hyperpolarization of membrane
42
How much the Na+/K+ pump contributes to the RMP is directly related to what two attributes?
pump activity and membrane resistance - system can contribute as much as -5 to -10 in RMP of ventricular cells
43
K+ channel activity (and thus permeability of K+) is very sensitive to what? This causes PNa/PK ratios calculated via GHK concentration to be higher than expected.
extracellular K+ concentration
44
True/False: Cl- and Ca++ ions contribute significantly to RMP of ventricular, atrial and purkinje cells
FALSE
45
What is the main reason why cardiac cells such as ventricular, atrial and purkinje cells have such long action potentials (about 300 ms)?
large drop in Pk to almost 0 during phase 0 when Na+ channels open. [In neurons, the Pk rises quickly during the action potential.
46
Describe phase 0 in ventricular, atrial and purkinje cells.
Phase 0 is the upstroke caused by an increase in Na+ conductance and depolarization of the membrane.
47
In what membrane potential range are Na+ channels active?
-80mV to -50mV
48
How does extracellular K+ accumulation as a result of ischemia affect RMP? How will this affect Vmax and overshoot?
it becomes more positive (depolarized). decreases Vmax and overshoot.
49
What occurs if Na+ channels when the membrane potential depolarizes?
Na+ channels become less available for activation
50
The slow response caused by Na+ channel inactivation in ventricular, atrial and purkinje cells is analogous to what?
upstroke of action potential in SA node as it involves Ca++ current
51
True/False - The availability of Ca++ channels is influenced by extracellular potassium concentration
FALSE - NOT INFLUENCED
52
How are Ca++ channels regulated
via voltage gated mechanisms - activated at voltage higher than -50mV
53
What happens when Na+ channel inactivation is incomplete in ventricles, atrial, and purkinje cells
Longer action potentials occur which favor the development of early after depolarizations (such as in long QT syndrome)
54
Why are EAD's dangerous?
can lead to severe arrhythmias such as torsades de pointes or v-fibrillation
55
The Vmax (rate of depolarization of the membrane is proportional to ______ and leads to a high _______
number of sodium channels open, conduction velocity
56
Membrane potential reaches a positive value of +20 to +30mV. Time past 0mV is called the ______
overshoot
57
Describe phase 1 of the action potential in ventricles, atrial cells and purkinje cells
Brief period of initial repolarization caused by outward current of K+ ions and decreased Na+ conductance
58
What K+ channels are involved in the phase 1/ initial repolarization phase of action potential in ventricles, atrial cells and purkinje cells?
Kto channels
59
Describe phase 2 of the action potential in ventricles, atrial cells and purkinje cells
Plateau caused by a transient increase in Ca++ conductance but also increase in K+ conductance that cancel each other out
60
What K+ channels are involved in the plateau phase of action potential in ventricles, atrial cells and purkinje cells?
Delayed rectifier K+ channels (Kir)
61
Delayed rectifier K+ channels (Kir) are _____ acting and have an activation threshold of ____
slow, 20mV
62
True/False Delayed rectifier K+ channels activate during a maintained depolarization
false
63
The duration and potential level of the plateau phase determines the amount of _______ developed by cardiac muscle
force
64
Describe phase 3 of action potential in ventricular, atrial and purkinje cells
repolarization phase caused by decrease in Ca++ conductance and increase in K+ conductance which predominantes (Ik current)
65
During phase 3 / repolarization phase what channels are unmasked and at what voltage?
IK1 channels at -20mV. IK1 is time and voltage dependent.
66
Why are IK1 channels not detected at high voltages?
Regulated by internal Mg++ polyamides which block channels at higher voltages
67
Describe phase 4 of action potential in ventricles, atria, and purkinje cells
Resting membrane potential. Inward and outward Ik currents equal
68
The stable membrane potential in phase 4 (RMP) of the action potential in ventricles, atria and purkinje cells is caused by what?
high K+ permeability across IK1 channels
69
The delay in activation of ventricular action potential is important to control _______ and prevent __________
conduction velocity, deleterious conditions favoring abnormal reentrant excitation and ventricular arrhythmias
70
What phases are missing from action potential in the SA node and why?
phase 1 and 2 because the activation of ICa combined with progressive activation of IK leads to rapid repolarization
71
The resting membrane potential in the SA node is unstable and exhibits ______
automacity
72
Intrinsic rate of phase 4 depolarization and heart rate is fastest in the _______ and slowest in the _____
SA node, His-Purkinje
73
In contrast to other heart cells, what is phase 0 in the SA node caused by?
an increase in Ca++ conductance rather than Na
74
Do Na+ channels contribute to phase 0 in SA node action potential?
NO
75
Ca++ current in phase 0 of SA node action potential is dependent on what two factors?
time and voltage
76
Phase 3, repolarization, in SA node ends via the closing of what channels? What channels are activated?
IK channels close, If channels open
77
Describe phase 4 of SA node action potential
Slow depolarization due to Na+ conductance
78
The increase in Na+ current in phase 4 of SA node is called _____
Ifunny
79
What turns on "Ifunny" in phase 4 of the SA node action potential?
Repolarization of the membrane potential during the preceding action potential
80
SA nodal action potential exhibits only a small (if any) overshoot due to slow onset of voltage-activated __________
delayed rectifier K+ (Ik current)
81
______ is the pacemaker channel of th eherat and is stimulated by _____
Ifunny, hyperpolarization below -40mV
82
True/False: Ifunny can be activated by depolarization
FALSE
83
Once Ifunny is activated, it is ______ and allows what two molecules to flow in equally?
non-selective, Na+ and K+. Na+ influx causes rise seen in phase 4.
84
Describe action potential in the AV node.
Upstroke (phase 0) caused by an inward Ca++ current such as in SA node
85
________ reflects the time required for excitation to spread through cardiac tissue
conduction velocity
86
Where is conduction velocity quickest and slowest?
Quickest in Purkinje, slowest in AV node
87
If conduction velocity in the AV node were to be increased, what would this result in?
ventricular filling may be compromised
88
What three characteristics does conduction velocity depend on?
fiber diameter (directly proportional), maximum upstroke of action potential and overshoot of action potential
89
Conduction velocity is inversely proportional to __________
RMP
90
When the membrane is depolarized, RMP increases which ______ Na+ availability and therefore _____ rate of phase 0 in non-pacemaker and AV nodal cells
reduces, reduces
91
________ is a decrease in conduction velocity when conduction spreads
decremental conduction
92
Current is passed between cells via cardiac ________
gap junctions
93
________ is the ability for cardiac cells to initiate action potentials in respond to inward, depolarizing current
excitability
94
__________ are changes in excitability throughout the course of the action potential
refractory periods
95
What is the difference between absolute and effective refractory periods?
Both start at the upstroke of action potential but effective is a slightly longer. Absolute ends after the plateau.
96
Refractory periods depend on what four factors?
sodium conductance, membrane potential, recovery from inactivation and magnitude of outward K+ current during repoarlzation
97
What is excitability in non-pacemaker cells related to? In Pacemaker cells?
increase in Na+ conductance. In pacemaker, would be Ca++
98
What are the three classes of ion channels?
channels activated or suppressed by a ligand, voltage-dependent, or background/leak channels
99
What are the three basic mechanisms to alter pacemaker activity?
change of slope of phase 4 diastolic, change in maximum diastolic potential, change in threshold potential
100
How does vagal output slow down pacemaker activity? [in terms of pressure and slope]
Lowers mean diastolic pressure and decreases slope of phase 4
101
What is the mechanism for how vagal output slows down pacemaker?
Ach binds and activates ligand-gated K+ channels which results in hyperpolarization of SA node cell membrane potential
102
What are the effects of vagal response on the atria?
Reduction in action potential duration by Ach-mediated activation of K+ channels
103
What are the effects of vagal output on ventricles?
little effect, antagonizes the stimulator effects of beta-adrenergic stimulation DOE
104
What are the effects of vagal output on the AV node?
reduces excitability and thereby reduces transmission through ventricles --> ventricular escape in purkinje fibers
105
What are the effects of sympathetic stimulation in SA node?
increases firing rate of pacemaker cells, increases current of all and slope of phase 0, faster upstroke velocity
106
What are the effects of sympathetic stimulation on atria and ventricles?
increased contractibility
107
What are the effects of sympathetic stimulation on AV node?
increased excitability and transmission of impulse --> increased conduction velocity
108
True/False : Sympathetic stimulation lengthens action potential duration
FALSE
109
What happens to cardiac excitability in hyperkalemia in ventricles, atria and purkinje cells?
Hyperkalemia leads to membrane DEPOL in ventricular, atrial and purkinje cells which reduces action potential amplitude (due to inactivation of sodium channels), increases conduction velocity, and increases repolarization activity (IK1 channels) in phase 3
110
What happens to automaticity of SA nodal cells in hyperkalemia?
Decreases
111
What happens to cardiac excitation in hypokalemia in ventricles, atria, and purkinje cells?
Depending on how low K+ is, could lead to instability of resting potential which can lead to ventricular arrhythmias (dangerous)
112
What happens to automacity of AV nodal cells in hypokalemia?
enhanced
113
Variation in PR interval is caused by what?
variation in conduction velocity through AV node (inversely proportional)
114
The negative Q wave represents initial depolarization of the _____ whereas the negative S deflection represents initial depolarization of the _____
septum, base
115
What does the QT interval represent?
Entire period of depolarization of the ventricles
116
What does the ST segment represent?
period when the ventricles are depolarized
117
What does the T wave represent?
ventricular repolarization
118
What does each thick line on the Y axis represent?
0.1 mV
119
The heart can be viewed as a _____ in terms of EKG and a given set of loads will detect the _______
dipole, vectorial sum
120
Where are the positive and negative electrodes found in lead I? Degrees?
Positive is on left arm, negative is on right arm. 0 degrees (horizontal)
121
Where are the positive and negative electrodes found in lead II? Degrees?
Positive is on left foot, negative is on right arm. 60 degrees.
122
Where are the positive and negative electrodes found in lead III? Degrees?
Positive on left foot, negative on left arm. 120 degrees.
123
What are the unipolar leads? The bipolar leads?
Unipolar are AVF, AVL, AVR. Bipolar are I, II, and III
124
Where is the positive electrode on AVF?
left foot, 90 degrees
125
Where is the positive electrode on AVL?
left arm, 330 degrees.
126
Where is the positive electrode on AVR?
right arm, 210 degrees
127
In ________ the voltage is measured relative to a common ground obtained by connecting the three electrodes together
V1-V6 precordial leads
128
What are two types of supraventricular arrythmia?
atrial flutter and atrial fibrillation
129
What are the 4 types of arrhythmias from junctional origin?
AV blocks, premature junctional contractions, junctional escape rhythm, junctional tachycardia
130
What are the four types of ventricular arrhythmias?
PVC's, v tach, v fib, ventricular asystole
131
What may a right axis deviation indicate?
Obstructive lung disease or pulmonary hypertension because of chronic increase in afterload imposed on right ventricle (lungs not letting blood in)
132
What may a left axis deviation indicate?
Can be caused by LVH - LVH can be physiological as seen in athletes or pathological due to increased afterload (aortic stenosis or systemic HTN)
133
How would an impaired artery appear on an EKG?
ST segment will be depressed or elevated; T waves will have variations in amplitude, shape and polarity. In general, axn potentials will be depressed and exhibit a lower RMP and reduced duration
134
An _______ is any disorder of rate, rhythm, origin or conduction of impulses with the heart
arrhythmia
135
Why of the following does not commonly cause arrhythmias?
a) myocardial infarction
b) digitalis
c) running
d) anesthesia
c
136
_______ are abnormal sites of excitation
ectopic foci
137
What are the two general categories of arrhythmias?
abnormal impulse formation and disorders of impulse conduction
138
An _____________ is a delayed repolarization that favors reopening of Ca++ channels with a second phase of depolarization occurring during the relative refractory period
early after depolarization
139
A ___________ is an abnormal Ca++ release event which includes transient membrane depolarization after final phase of repolarization
delayed after depolarization
140
What would cause an early after depolarization?
reduced activity of K+ channels or enhanced acitivity of Na+ or Ca+ channels, long QT syndrome --> Torsades de Pointes
141
What would cause a delayed after depolarization?
seen in conditions favoring Ca++ overload
142
A arrhythmia of impulse conduction without reentry would be classified as a ______
AV block
143
What are the requirements of a slowed conduction arrhythmia with reentry? (3)
a unidirectional block and conduction time around alt pathway must be longer than ERP/ARP
144
What would NOT favor slowed conduction with reentry?
a) long reentrant pathway
b) slow conduction
c) rapid effective refractory period
d) short effective refractory period
C
145
What are the three types of reentry arrhythmias?
reflection, circus movement, phase 2
146
What is an example of an anatomical block for circus movement arrhythmia?
inexcitable valve
147
What is an example of a non-anatomical block for circus movement arrhythmia?
functional block such as a region not being excitable any longer due to severe ischemia --> strong depol of membrane
148
What are the three types of non-anatomical block circus movement arrhythmias?
leading circle, figure of 8, spiral wave
149
The _________ is the temporal change in concentration of free intracellular Ca++ concentration during one cardiac beat
Ca++ transient
150
What does the amplitude of the Ca++ transient regulate?
contractile force
151
What plays a primary role in determining the size of the Ca++ transient?
action potential
152
When the plateau level of the action potential is elevated, what happens to the Ca++ transient?
it increases
153
Describe the positive staircase phenomenon.
When the frequency of stimulations is increased, contraction of the heart increases only progressively before reaching a new steady state.
154
True/False: Most of Ca++ transient is from direct Ca++ entry through voltage and time dependent Ca++ channels
FALSE, only 10% at most
155
Where does the majority of Ca++ influx in the Ca++ transient come from?
Ca++ induced Ca++ release (CICR)
156
Describe the mechanism of CICR.
Ca++ influx triggers Ca++ release from SR. Ca++ channels are juxtaposed with a different class of Ca++ channels in the t-tubules. Ca++ binds and opens these channels.
157
What are the Ca++ channels found on t-tubules called
Ryanodine receptors (RyR)
158
Ca++ binding opens Ryr channels. What closes them?
decreased driving force for Ca++ and intrinsic inactivation
159
______ is the main Ca++ transporter involved in relaxing the Ca++ transient
Ca++ ATPase in the SR membrane
160
Describe the action of Ca++ ATPase in the SR membrane
it drives Ca++ back into the SR
161
______ is a Ca++ transporter found in the t-tubules and sarcolemma that does not require ATP
3Na+/Ca++ transporter, pumps Ca++ out
162
True/False: 3Na+/Ca++ transporter is the major mechanism for balancing Ca++ entry
TRUE
163
How does intracellular Ca++ stimulate contraction?
Free Ca++ binds to troponin C which initiates acto-myosin bridge cycling
164
Myocardial cells are packed with ________ which are regular arrays of filamentous proteins
myofibrils
165
What are myofibrils made up of?
actin, myosin, and structural proteins
166
Myofilaments are surrounded by the _______ which is an extensive intracellular membrane network
sarcoplasmic reticulum
167
_______ surround the myofibrils and make up ___ of muscle cell volume
mitochondria, 35%
168
The plasma surface of cardiac myocytes is called the _______
sarcolemma
169
At fixed intervals, the sarcolemma protrudes into the cell and forms the ________
transverse t-tubules [interior contigious with extracellular space]
170
True/False: Transverse t-tubules are much wider in skeletal muscle cells than cardiac cells
FALSE CARDIAC CELLS
171
The close juxtaposition of _____ with the ____ forms the dyad
portions of the SR and t-tubules
172
What is the portion of the SR involved in the dyad called? What is the rest of the SR called?
In the dyad, it is the subsarcolemmal cisternae. The rest of the SR is the sarcotubular network
173
The ______ are the clear light areas composed of thin filaments, mostly actin
I
174
The _______ is the thin dark line in the middle of the I band
Z line
175
The space between two Z lines is called the _____
sarcomere
176
The _________ is an opaque, dark area consisting of ordered overlap between thick filaments (mainly myosin)
A band
177
How do cardiac glycosides improve mechanical performance of the heart?
Inhibit the Na+/K+ pump. Therefore, increase in intracellular Na+. Na/Ca exchanger does not pump Ca out as a result so Ca++ intracellular increases which is then uptaken by SR and is available for release during an action potential through CICR
178
How does norepinephrine from terminal ending and epi from adrenal gland stimulation increase cardiac contraction?
Stimulates production of AC --> cAMP --> PKA activation - enhances Ca++ channel open probability which increases efficacy as a trigger for CICR
179
How does NE/epi affect Ryr in the SR?
stimulates Ca++ influx to increase Ryr channel activity which improves Ca++ release
180
How does NE/epi affect phospholamban (PLB)?
represses activity of Ca++/ATPase pump and therefore inhibits relaxation of Ca++ transient
181
How does NE/epi affect troponin?
phosphorylation reduces affinity of troponin complex for Ca++ which facilitates relaxation
182
Which sympathetic stimulation mechanism is most important in increasing the size of the Ca++ transient and contraction?
Ca++ influx to increase Ryr channel activity
183
The basic unit structure responsible for contraction of striated muscle is the _________
sarcomere
184
Shortening of muscle results from interaction between ________ and ______ in the sarcomere
thin (actin) and thick (myosin)
185
True/False: Thick filaments are made of actin
FALSE - made of myosin
186
The __________ of myosin reacts with actin
globular region - made up of two heavy chains wound around each other
187
The globular regions of myosin exhibit ________
ATPase activity (cross bridge cycling?!)
188
Myosin filaments are arranged how?
globular regions oriented opposite of each other
189
F-actin polymer composed of two chains wound around each other in a coiled conformation by means of _________ makes up thin filaments of actin
disulfide bonds
190
Each actin chain made up of a monomer called ________
G-actin
191
What are the regulatory proteins bound to actin that couple Ca++ transient to acto-myosin bridge cycling? (4)
tropomyosin, troponin complex - trop C, trop I, trop T
192
Describe the function of tropomyosin
allow or prevent interaction of actin and myosin.
193
The ___________ is found tightly packed on thin filaments, evenly spaced
troponin complex
194
Describe the function of troponin C.
Troponin C binds to Ca++. Two globular regions.
195
Each globular region of troponin C contains two divalent cation binding sites labeled I through IV. Describe actions.
I and II are Ca++ specific, II is acceptor site. III and IV bind both Ca++ and Mg++ and stabilize the troponin complex.
196
Describe the function of troponin I.
Troponin I is located between TnC and TnT and inhibits interaction between myosin and actin (although weaker than tropomyosin)
197
What enhances the inhibitory activity of troponin I?
phosphorylation by PKA - accelerates relaxation - responsible for inhibiting acto-myosin bridge cycling during diastole
198
Describe the function of troponin T
Binds to TnI and Tropomyosin. Maintains structural integrity of complex.
