CV Week 1 Flashcards
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
E - ALL TISSUES
The heart composed of two pumps organized in ______ and flow is described as ______
series, unidirectional
Elasticity of arteries has one impact on the intermittent nature of blood flow from heart?
reduces the force (attentuates)
Elasticity allows for a more _____ flow to tissues due to their ____ during the relaxation phase of the cardiac cycle
continuous, recoil
How is blood provided to the heart?
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.
True/False: All blood vessels control their internal diameter via precise control of smooth muscle
FALSE - capillaries don’t!
Arteries have a thicker wall, are stiffer, and have a strong contractile apparatus due to what two features?
presence of elastic fibers and a more prominent smooth muscle layer
Why does pressure fall more quickly in the terminal segments of small arteries and arterioles in comparison to large arteries?
Increase in frictional resistance and increase in cross sectional area from extensive branching and multiplication
What causes dampening of pulsatile arterial flow at capillary level?
Distension of large arteries (compliance) and resistance of small arteries and arterioles - non-pulsatile flow
As cross-sectional area _______, velocity of blood flow _______
area, decreases [watch out!!! increases in respect to diameter tho!]
Where is the majority of blood found in CVS and why?
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
True/False: In the pulmonary vascular bed, most of the blood is found in the veins
FALSE - equally distributed btwn arteries, veins and capillaries
Why is the right ventricular wall much thinner and weaker than the left ventricular wall?
Left ventricle sustains pressures in the order of 100mmHg at rest whereas right ventricle pressures are around 15mmHg
What directly measures blood pressure?
pressure in the aorta
When is the LUB or S1 produced?
When the AV valves close
When is the DUB or S2 produced?
When the aortic and pulmonary valves close
What may produce S3?
rapid filling of the ventricles
What may produce S4?
Contraction of the atrium to get final bits of blood out
Where is the SA node located?
The SA node is located in the right atrium on the upper lateral side near the superior vena cava
The effective pumping of blood into the circulatory system depends on the ______
SA node
Arrhythmias can compromise mechanical performance and lead to life threatening decreases in ?
cardiac output and blood pressure
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.
excitation-contraction coupling
How are action potentials (and resting membrane potentials in myocytes generated?
Via the opening and closing of ion channel proteins - reason why important target for therapeutic drugs
Which myocytes are specialized for conduction of electrical impulse? (5)
SA node, cells of internal conduction track, AV node cells, Bundle of his, Purkinje Cells
Why is SA node considered the primary pacemaker of the cell?
It is SPONTANEOUS
The _______ carry electrical impulses that initiate atrial contraction
cells of internal conduction track
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
Where is the AV node located?
at the junction between the right atrium and IV septum
What is the delay time for AV node activation of ventricles?
120 ms
Purkinje fibers run along the _________ surface and penetrate about 1/3 into ventricular tissue
endocardial
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.
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
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.
Why can’t cardiac contraction summate into tetanus?
Action potential duration and refractory period is very long
Which cells are considered pacemaker cells?
SA node, AV node, Purkinje
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
The resting membrane potential is determined by ______
conductance of K+
True/False: The RMP in ventricles, atria and AV node is about -80 to -90 mV
FALSE - true for ventricles, atria and PURKINJE SYSTEM
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
What is the Na+ concentration influenced by?
Na+/K+ pump
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
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
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
True/False: Cl- and Ca++ ions contribute significantly to RMP of ventricular, atrial and purkinje cells
FALSE
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.
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.
In what membrane potential range are Na+ channels active?
-80mV to -50mV
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.
What occurs if Na+ channels when the membrane potential depolarizes?
Na+ channels become less available for activation
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
True/False - The availability of Ca++ channels is influenced by extracellular potassium concentration
FALSE - NOT INFLUENCED
How are Ca++ channels regulated
via voltage gated mechanisms - activated at voltage higher than -50mV
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)
Why are EAD’s dangerous?
can lead to severe arrhythmias such as torsades de pointes or v-fibrillation
The Vmax (rate of depolarization of the membrane is proportional to ______ and leads to a high _______
number of sodium channels open, conduction velocity
Membrane potential reaches a positive value of +20 to +30mV. Time past 0mV is called the ______
overshoot
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
What K+ channels are involved in the phase 1/ initial repolarization phase of action potential in ventricles, atrial cells and purkinje cells?
Kto channels
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
What K+ channels are involved in the plateau phase of action potential in ventricles, atrial cells and purkinje cells?
Delayed rectifier K+ channels (Kir)
Delayed rectifier K+ channels (Kir) are _____ acting and have an activation threshold of ____
slow, 20mV
True/False Delayed rectifier K+ channels activate during a maintained depolarization
false
The duration and potential level of the plateau phase determines the amount of _______ developed by cardiac muscle
force
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)
During phase 3 / repolarization phase what channels are unmasked and at what voltage?
IK1 channels at -20mV. IK1 is time and voltage dependent.
Why are IK1 channels not detected at high voltages?
Regulated by internal Mg++ polyamides which block channels at higher voltages
Describe phase 4 of action potential in ventricles, atria, and purkinje cells
Resting membrane potential. Inward and outward Ik currents equal
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
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
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
The resting membrane potential in the SA node is unstable and exhibits ______
automacity
Intrinsic rate of phase 4 depolarization and heart rate is fastest in the _______ and slowest in the _____
SA node, His-Purkinje
In contrast to other heart cells, what is phase 0 in the SA node caused by?
an increase in Ca++ conductance rather than Na
Do Na+ channels contribute to phase 0 in SA node action potential?
NO
Ca++ current in phase 0 of SA node action potential is dependent on what two factors?
time and voltage
Phase 3, repolarization, in SA node ends via the closing of what channels? What channels are activated?
IK channels close, If channels open
Describe phase 4 of SA node action potential
Slow depolarization due to Na+ conductance
The increase in Na+ current in phase 4 of SA node is called _____
Ifunny
What turns on “Ifunny” in phase 4 of the SA node action potential?
Repolarization of the membrane potential during the preceding action potential
SA nodal action potential exhibits only a small (if any) overshoot due to slow onset of voltage-activated __________
delayed rectifier K+ (Ik current)
______ is the pacemaker channel of th eherat and is stimulated by _____
Ifunny, hyperpolarization below -40mV
True/False: Ifunny can be activated by depolarization
FALSE
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.
Describe action potential in the AV node.
Upstroke (phase 0) caused by an inward Ca++ current such as in SA node
________ reflects the time required for excitation to spread through cardiac tissue
conduction velocity
Where is conduction velocity quickest and slowest?
Quickest in Purkinje, slowest in AV node
If conduction velocity in the AV node were to be increased, what would this result in?
ventricular filling may be compromised
What three characteristics does conduction velocity depend on?
fiber diameter (directly proportional), maximum upstroke of action potential and overshoot of action potential
Conduction velocity is inversely proportional to __________
RMP
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
________ is a decrease in conduction velocity when conduction spreads
decremental conduction
Current is passed between cells via cardiac ________
gap junctions
________ is the ability for cardiac cells to initiate action potentials in respond to inward, depolarizing current
excitability
__________ are changes in excitability throughout the course of the action potential
refractory periods
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.
Refractory periods depend on what four factors?
sodium conductance, membrane potential, recovery from inactivation and magnitude of outward K+ current during repoarlzation
What is excitability in non-pacemaker cells related to? In Pacemaker cells?
increase in Na+ conductance. In pacemaker, would be Ca++
What are the three classes of ion channels?
channels activated or suppressed by a ligand, voltage-dependent, or background/leak channels
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
How does vagal output slow down pacemaker activity? [in terms of pressure and slope]
Lowers mean diastolic pressure and decreases slope of phase 4
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
What are the effects of vagal response on the atria?
Reduction in action potential duration by Ach-mediated activation of K+ channels
What are the effects of vagal output on ventricles?
little effect, antagonizes the stimulator effects of beta-adrenergic stimulation DOE
What are the effects of vagal output on the AV node?
reduces excitability and thereby reduces transmission through ventricles –> ventricular escape in purkinje fibers
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
What are the effects of sympathetic stimulation on atria and ventricles?
increased contractibility
What are the effects of sympathetic stimulation on AV node?
increased excitability and transmission of impulse –> increased conduction velocity
True/False : Sympathetic stimulation lengthens action potential duration
FALSE
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
What happens to automaticity of SA nodal cells in hyperkalemia?
Decreases
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)
What happens to automacity of AV nodal cells in hypokalemia?
enhanced
Variation in PR interval is caused by what?
variation in conduction velocity through AV node (inversely proportional)
The negative Q wave represents initial depolarization of the _____ whereas the negative S deflection represents initial depolarization of the _____
septum, base
What does the QT interval represent?
Entire period of depolarization of the ventricles
What does the ST segment represent?
period when the ventricles are depolarized
What does the T wave represent?
ventricular repolarization
What does each thick line on the Y axis represent?
0.1 mV
The heart can be viewed as a _____ in terms of EKG and a given set of loads will detect the _______
dipole, vectorial sum
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)
Where are the positive and negative electrodes found in lead II? Degrees?
Positive is on left foot, negative is on right arm. 60 degrees.
Where are the positive and negative electrodes found in lead III? Degrees?
Positive on left foot, negative on left arm. 120 degrees.
What are the unipolar leads? The bipolar leads?
Unipolar are AVF, AVL, AVR. Bipolar are I, II, and III
Where is the positive electrode on AVF?
left foot, 90 degrees
Where is the positive electrode on AVL?
left arm, 330 degrees.
Where is the positive electrode on AVR?
right arm, 210 degrees
In ________ the voltage is measured relative to a common ground obtained by connecting the three electrodes together
V1-V6 precordial leads
What are two types of supraventricular arrythmia?
atrial flutter and atrial fibrillation
What are the 4 types of arrhythmias from junctional origin?
AV blocks, premature junctional contractions, junctional escape rhythm, junctional tachycardia
What are the four types of ventricular arrhythmias?
PVC’s, v tach, v fib, ventricular asystole
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)
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)
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
An _______ is any disorder of rate, rhythm, origin or conduction of impulses with the heart
arrhythmia
Why of the following does not commonly cause arrhythmias?
a) myocardial infarction
b) digitalis
c) running
d) anesthesia
c
_______ are abnormal sites of excitation
ectopic foci
What are the two general categories of arrhythmias?
abnormal impulse formation and disorders of impulse conduction
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
A ___________ is an abnormal Ca++ release event which includes transient membrane depolarization after final phase of repolarization
delayed after depolarization
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
What would cause a delayed after depolarization?
seen in conditions favoring Ca++ overload
A arrhythmia of impulse conduction without reentry would be classified as a ______
AV block
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
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
What are the three types of reentry arrhythmias?
reflection, circus movement, phase 2
What is an example of an anatomical block for circus movement arrhythmia?
inexcitable valve
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
What are the three types of non-anatomical block circus movement arrhythmias?
leading circle, figure of 8, spiral wave
The _________ is the temporal change in concentration of free intracellular Ca++ concentration during one cardiac beat
Ca++ transient
What does the amplitude of the Ca++ transient regulate?
contractile force
What plays a primary role in determining the size of the Ca++ transient?
action potential
When the plateau level of the action potential is elevated, what happens to the Ca++ transient?
it increases
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.
True/False: Most of Ca++ transient is from direct Ca++ entry through voltage and time dependent Ca++ channels
FALSE, only 10% at most
Where does the majority of Ca++ influx in the Ca++ transient come from?
Ca++ induced Ca++ release (CICR)
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.
What are the Ca++ channels found on t-tubules called
Ryanodine receptors (RyR)
Ca++ binding opens Ryr channels. What closes them?
decreased driving force for Ca++ and intrinsic inactivation
______ is the main Ca++ transporter involved in relaxing the Ca++ transient
Ca++ ATPase in the SR membrane
Describe the action of Ca++ ATPase in the SR membrane
it drives Ca++ back into the SR
______ is a Ca++ transporter found in the t-tubules and sarcolemma that does not require ATP
3Na+/Ca++ transporter, pumps Ca++ out
True/False: 3Na+/Ca++ transporter is the major mechanism for balancing Ca++ entry
TRUE
How does intracellular Ca++ stimulate contraction?
Free Ca++ binds to troponin C which initiates acto-myosin bridge cycling
Myocardial cells are packed with ________ which are regular arrays of filamentous proteins
myofibrils
What are myofibrils made up of?
actin, myosin, and structural proteins
Myofilaments are surrounded by the _______ which is an extensive intracellular membrane network
sarcoplasmic reticulum
_______ surround the myofibrils and make up ___ of muscle cell volume
mitochondria, 35%
The plasma surface of cardiac myocytes is called the _______
sarcolemma
At fixed intervals, the sarcolemma protrudes into the cell and forms the ________
transverse t-tubules [interior contigious with extracellular space]
True/False: Transverse t-tubules are much wider in skeletal muscle cells than cardiac cells
FALSE CARDIAC CELLS
The close juxtaposition of _____ with the ____ forms the dyad
portions of the SR and t-tubules
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
The ______ are the clear light areas composed of thin filaments, mostly actin
I
The _______ is the thin dark line in the middle of the I band
Z line
The space between two Z lines is called the _____
sarcomere
The _________ is an opaque, dark area consisting of ordered overlap between thick filaments (mainly myosin)
A band
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
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
How does NE/epi affect Ryr in the SR?
stimulates Ca++ influx to increase Ryr channel activity which improves Ca++ release
How does NE/epi affect phospholamban (PLB)?
represses activity of Ca++/ATPase pump and therefore inhibits relaxation of Ca++ transient
How does NE/epi affect troponin?
phosphorylation reduces affinity of troponin complex for Ca++ which facilitates relaxation
Which sympathetic stimulation mechanism is most important in increasing the size of the Ca++ transient and contraction?
Ca++ influx to increase Ryr channel activity
The basic unit structure responsible for contraction of striated muscle is the _________
sarcomere
Shortening of muscle results from interaction between ________ and ______ in the sarcomere
thin (actin) and thick (myosin)
True/False: Thick filaments are made of actin
FALSE - made of myosin
The __________ of myosin reacts with actin
globular region - made up of two heavy chains wound around each other
The globular regions of myosin exhibit ________
ATPase activity (cross bridge cycling?!)
Myosin filaments are arranged how?
globular regions oriented opposite of each other
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
Each actin chain made up of a monomer called ________
G-actin
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
Describe the function of tropomyosin
allow or prevent interaction of actin and myosin.
The ___________ is found tightly packed on thin filaments, evenly spaced
troponin complex
Describe the function of troponin C.
Troponin C binds to Ca++. Two globular regions.
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.
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)
What enhances the inhibitory activity of troponin I?
phosphorylation by PKA - accelerates relaxation - responsible for inhibiting acto-myosin bridge cycling during diastole
Describe the function of troponin T
Binds to TnI and Tropomyosin. Maintains structural integrity of complex.
