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Cardiac Flashcards

0
Q

What is the Space Constant?

A

The distance over which a subthreshold depolarizaion will spread and influence the next segment of membrane.

Longer space/length constant = faster conduction.

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1
Q

Skeletal muscle, motor neuron, cardiomyocyte.

What has the fastest action potential?
The slowest?

A

Motor neuron > skeletal muscle&raquo_space; cardiac muscle

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2
Q

What effect does axon diameter have on conduction velocity?

A

Larger diameter –> lower internal (axial) resistance –> faster conduction.

Membrane resistance is higher with larger diameter but the change in internal resistance more than compensates.

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3
Q

What does negative resting membrane potential mean with regard to charges inside vs. outside the cell?

A

The inside of the cell is more negative than the outside.

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4
Q

In nerves, what ion channel is responsible for depolarization?
Repolarization?

A

Depolarization = increase in Na+ conductance

Repolarization = increase in K+ channel conductance

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5
Q

What will the spike of an action potential always be within?

A

It will be contained within the Na+ and K+ membrane potentials.

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6
Q

Define the possible states of a Na+ Channel.

A

Resting = m activation gate closed, h inactivation gate open

Activated = both gates open –> Na+ influx

Inactivated = m gate open, h gate closed

Recovery (inactivated –> resting) is dependent on time and voltage.

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7
Q

What is Regenerative Depolarization?

A

As a membrane depolarizes, more Na+ channels open, causing further depolarization. This is a positive feedback loop.

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8
Q

What is the refractory period of a Na+ channel caused by?

A

It is voltage and time dependent. More negative membrane potentials are needed for transition from inactivation –> resting.

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9
Q

What is the difference between inactivation of Na+ and K+ channels?

A

Na+ are time dependent with inactivation. K+ are only voltage dependent and will thus stay open if depolarization is maintained.

K+ have no inactivation gates. They just deactivate once repolarization is achieved.

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10
Q

What can influence the overall length of a refractory period in nerve or heart cells?

A

The initial resting membrane potential can. At less negative potentials, Na+ channels are more likely to be inactivated. Thus, it takes a stronger stimulus to elicit an AP.

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11
Q

What is the difference between absolute and relative refractory periods?

A

Absolute –> the TIME during which a regenerative response (AP) cannot be elicited.

Relative –> the TIME during which a stimulus can elicit an abnormal regenerative response.

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12
Q

What resting membrane potential corresponds to 50% of Na+ channels being available?

A

-60

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13
Q

What is the effect of Hypercalcemia on membrane excitability?
Hypocalcemia?

A

Hypercalcemia raises threshold.

Hypocalcemia lowers threshold.

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14
Q

How does ventilation affect free plasma Ca2+?

A

Hyperventilation –> blow off CO2 –> Resp. Alkalosis –> decreased free Ca2+.

H+ and Ca2+ compete for same binding sites in solution.

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15
Q

What effect does hyperkalemia have on resting membrane potential?
Excitability?

A

It raises RMP –> less Na+ channels available –> current decreases & conduction slows.

It makes nerves/muscles less excitable.

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16
Q

What parameter of a cell does myelination affect?

A

It increases membrane resistance. This increases the length constant of the axon & conduction velocity.

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17
Q

What do transverse tubules do?

A

They propagate an action potential transversely into the interior of a muscle fiber.

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18
Q

What neurotransmitter is released onto muscle cells?

A

Acetylcholine

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19
Q

What receptors are found at a triad within muscle?

A

DHPR is found in the plasma membrane.

RYR is found on the sarcoplasmic reticulum.

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20
Q

What is the difference between skeletal and cardiac excitation-contraction coupling?

A

DHPR on skeletal muscle physically open RYR on the SR, allowing Ca2+ efflux into cytosol. Extracellular Ca2+ is not required and does not flow through the DHPR.

In cardiac muscle, DHPR open to allow Ca2+ influx, which then activates RYR to open and release SR calcium stores.

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21
Q

What are the two methods of Ca2+ release in skeletal vs. cardiac muscle?

A

Skeletal = voltage-dependent Ca2+ release

Cardiac = Ca2+ induced Ca2+ release

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22
Q

What effect do calcium levels have on cardiac contractility?

A

More extracellular Ca2+ –> more influx into myocyte –> more release from SR –> greater force

In skeletal muscle, SR release of Ca2+ yields almost fully active myofilaments every time.

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23
Q

What enzyme pumps Ca2+ back into the sarcoplasmic reticulum?

A

SERCA

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24
Q

What is the optimal sarcomere length?

Why?

A

2-2.2 um

This offers the best overlap of thick & thin filaments (maximum # of available crossbridges)

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25
Q

How many motor units per muscle fiber?

A

Each fiber only responds to one nerve, however a motor unit can be composed of many muscle fibers responding to the same nerve.

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26
Q

How is force regulated with skeletal muscles as a whole?

A

The necessary amount of motor units are recruited.

Each twitch is ~equal in duration & force, so # of muscle cells recruited is how force is varied.

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27
Q

Why is summation/tetanus possible?

A

The twitch is much longer than the AP, so another AP can arrive before a twitch is completed.

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28
Q

What is isotonic contraction?

Isometric contraction?

A

Isotonic = force stays the same, muscle length changes

Isometric = force changes, muscle length stays the same

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29
Q

How are thick filaments regulated in smooth muscle?

A

Via Myosin Light Chain Kinase (MLCK)

MLCK is activated by Calmodulin (activated by Ca2+)

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30
Q

What signals the formation of Latch Bridges in smooth muscle?
Why is this important?

A

Dephosphorylated myosin (via MLCP) can form latch bridges.

This allows smooth muscle to maintain a tonic level of tension without expending much ATP.

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31
Q

What are the 3 methods of activating smooth muscle?

A

Hormone/NT –> IP3 –> Ca2+ release from SR

Voltage gates Ca2+ channel opens –> influx of Ca2+ across PM

Hormone or NT –> ligand coupled Ca2+ channel –> influx of Ca2+ across PM

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32
Q

What can inhibit the Na+/K+ ATPase?

A

Digitalis

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33
Q

What is inward rectification?

A

Anomalous (inward) rectification is a decrease in K+ permeability seen when the driving force on K is strengthened (i.e. hypokalemia, depolarization).

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34
Q

How do inward rectifying channels respond to voltage?

What does this type of channel allow for in the action potential?

A

Lower voltage = more inward K+ flux permeability

Higher voltage = less inward K+ flux permeability

This channel allows for an action potential plateau (delayed repolarization) in cardiomyocytes.

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35
Q

Is the K+ gradient across the PM in cardiomyocytes greater in hyperkalemia or hypokalemia?
What is the effect on RMP?

A

The gradient is greater in hypokalemia due to a decrease in permeability due to “inward rectifying” K+ channels.

Thus, hyperkalemia –> RMP more positive
Hypokalemia –> RMP changes very little

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36
Q

What is occurring ionically during the plateau phase of a cardiomyocyte AP?

A

Calcium is flowing in and K+ is flowing out.

Once Ik channels open –> repolarization begins –> Ik1 (inward rect.) channels can open –> full repolarization.

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37
Q

What causes the small repolarization seen at the peak of a cardiomyocyte AP?

A

Ito channels (transient outward K+)

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38
Q

What does Tetrodotoxin (TTX) do?

What is the effect on cardiac AP’s?

A

It selectively blocks Na+ channels.

This can turn a fast response AP into a slow response AP (reliant on Ca2+ for upstroke).

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39
Q

What causes the slow conduction seen through infarcted portions of the heart?

A

Intracellular K+ leaks out of damaged cells –> local hyperkalemia –> more positive RMP –> Less Na+ channels available –> slower upsteoke –> conduction slowed.

This can cause reentry

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40
Q

What parts of the heart exhibit slow responses?

Fast responses?

A

Slow: SA node, AV node

Fast: Atria, His-Purkinje, Ventricle

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41
Q

Compare slow vs. fast cardiac AP’s:
RMP
Threshold
Duration

A

RMP: Slow = -60, fast = -80
Threshold: Fast have higher threshold
Duration: Fast have longer duration

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42
Q

What are the 3 mechanisms of cardiac arrhythmias?

A
  1. Altered automaticity
  2. Re-entry of excitation
  3. Triggered activity
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43
Q

What is healing over?

How is this tissue recognized?

A

The heart electrically isolates damaged tissue by decreasing the number of gap junctions with it.

Tissue reduces its number of gap junctions in response to high Ca2+ or H+ (low pH).

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44
Q

What is the space constant proportional to?

A

membrane resistance/internal resistance

The fastest cell:
Low K+ permeability
Many gap junctions
Large diameter

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45
Q

At what RMP are all Na+ channels available?

How about almost no channels?

A

100% available: -80 to -90 mV

0% available: -50 mV

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46
Q

What does the P-R interval correspond to?

A

AV nodal conduction time

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47
Q

How does conduction occur in the ventricles?

A

Endo –> epi

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48
Q

What does the QRS complex represent?

How long should it be?

A

Intraventricular conduction time.

It should be < 100 msec

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49
Q

What does a notched QRS indicate?

A

Asynchronous activation of L & R ventricle.

This can be due to a bundle branch block.

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50
Q

Is ventricular wall motion normal in SVT?

VT?

A

Supraventricular tachycardia = normal conduction & normal all motion –> stroke volume not compromised

Ventricular tachycardia = impulse originates in ventricles –> conduction not normal –> abnormal wall motion –> stroke volume compromised.

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51
Q

What does Ach (parasymp.) affect in the heart?

NE?

A

Ach does not affect the ventricles.

NE affects all areas of the heart.

Most importantly, these modulate the slow-inward Ca2+ current. Ach inhibits cAMP & NE increases cAMP to do so.

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52
Q

What is an R on T?

A

A premature ventricular beat that occurs during the relative refractory period. This can often lead to non-sustained ventricular tachycardia (repeated PVC’s).

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53
Q

What does post-repolarization refractoriness refer to?

What causes it?

A

This is seen in slow responses (nodes).

The refractory period is much longer than the action potential duration. This is because slow-Ca2+ channel recovery is more dependent on time than on voltage.

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54
Q

What shortens the most on an EKG as heart rate is increased?

A

The Q-T interval does. This is equivalent to the duration of the action potential.

Systole shortens to protect diastolic filling time.

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55
Q

What could cause prolonged Q-T syndrome?

A

Acquired: bradycardia, hypokalemia, drugs

Congenital: genetic lesions in Na+ or K+ channels

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56
Q

What is the fastest pacemaker in your heart?

How is anatomical organization important?

A

The fastest pacemaker is the SA node.

SA node > latent atrial pacemakers > AV nodal/His bundle > bundle branches > Purkinje fibers

These are anatomically arranged from fastest to slowest.

57
Q

What is the mechanism of delayed afterdepolizations?

A

Usually occur with fast heart rates.

SR overloaded with Ca2+ –> Ca2+ release AFTER AP has ended –> Na+/Ca2+ exchanger allows Na+ into the cell –> depolarization

58
Q

What aspect of an action potential puts it at risk of an early afterdepolarization?

A

Long action potential duration is associated with EAD’s.

The mechanism is not well understood.

59
Q

How long should a P-R interval be?

A

120-200 msec

60
Q

How long is a normal Q-T interval?

A

250-430 msec

61
Q

What is the most important factor that affects the rate of automaticity in a pacemaker cell?

A

The slope of diastolic depolarization.

62
Q

What is Overdrive Suppression?

A

The pacemaker that is driven at the highest frequency will suppress all pacemaker activity.

63
Q

What causes sinus arrhythmia?

A

Inspiration –> inhibition of parasymp. –> ^ HR

Expiration –> stimulation of parasymp. –> decreased HR

64
Q

What are the three requirements for re-entry of excitation?

A
  1. Geometry for a conduction loop
  2. Slow or delayed conduction
  3. Unidirectional conduction block
65
Q

What is the purpose of the Na+/Ca2+ exchanger?

What is its stoichiometry?

A

To aid in clearing Ca2+ out of myocytes.

3Na+ influx for every Ca2+ extruded

66
Q

How can you estimate heart rate on an EKG?

A

300/# of large boxes between Q waves

67
Q

What does ventricular ischemia show up as on an EKG?

A

ST segment depression

68
Q

What effect will an inferior heart wall infarct have on the CNS?

A

Induces a vagal response.

69
Q

What are the 3 methods of removing calcium from the cardiomyocyte cytosol?

A

SERCA (80%)
Na+/Ca2+ exchange (18%)
Ca2+ pump in sarcolemma (2%)

70
Q

How do catecholamines influence cardiac contractility?

A

Beta adrenergic receptor –> ^ cAMP –> PKA phosphorylates:

Ca2+ channels (increased Ca2+ influx)
Phospholamban (increased SERCA uptake –> relaxation)

71
Q

What is the mechanism of cardiac glycosides?

A

Digitalis = glycoside

Inhibits Na+/K+ pump –> Na+ gradient dissipated –> decreases Ca2+ extrusion by Na+/Ca2+ exchanger –> more Ca2+ stored in SR –> more Ca2+ release

Inotropic agent = strengthens contraction

72
Q

What are Ca2+ channel blockers used for?

A

Vasodilators & anti-arrhythmic agents.

Less Ca2+ present in vascular smooth muscle –> vasodilation

Inhibit slow Ca2+ current –> inhibits AV conduction (blocks SVT)

73
Q

What is seen in the force-frequency relationship?

A

Faster HR –> stronger contraction

Due to less time for Ca2+ efflux –> more Ca2+ stored in SR

74
Q

Is a premature beat stronger or weaker?

How about the next beat?

A

Premature beat = weaker due to less time for Ca2+ handling

Post-extrasystolic Potentiation = Beat following a premature beat is stronger (more time for Ca2+ handling). Often felt as a thump in the chest.

75
Q

What does an upward deviation on an EKG mean?

A

A wavefront of depolarization moving in the same direction of the lead.

76
Q

What direction does the heart repolarize?

A

Epi –> endo

Epi myocytes are different from endo ones, they repolarize faster (transient outward current is stronger).

77
Q

What tissues can an EKG record from?

A

Only atrial and ventricular myocytes. The conduction system does not generate large enough impulses.

78
Q

What has the longest refractory period in the heart?

A

Purkinje fibers

79
Q

On an EKG, when is AV nodal conduction initiated?

A

The peak of the P wave

80
Q

On an EKG, what would a first degree heart block appear as?

A

> 200 msec between P & Q waves (>1 box)

81
Q

How long should a QRS complex be?

A

70-100 msec

82
Q

Which way do all of the EKG leads point?

A

Bipolar:
I = horizontal to left arm
II = down & left
III = down & right

Unipolar:
vR = up & right
vL = up & left
vF = straight down

Precordial:
v1 = forward and to the right
v6 = straight left

83
Q

Why do PVC’s often fail to open the aortic valve?

A

Ca2+ cycling has not occurred –> less forceful contraction

Preload is not very high –> less forceful contraction

Afterload is still high –> more resistance

84
Q

What is considered a normal cardiac mean plane vector?

A

-30 to 105 degrees

85
Q

How can one calculate mean plane vector?

A

Count the net boxes deviated (upward minus downward) for two leads and plot the point of intersection on Einthoven’s triangle.

86
Q

What 4 factors influence cardiac output?

A

Heart rate
Contractility
Preload
Afterload

87
Q 
What determines the slope of the resting (diastolic) tension curve?
The active (systolic) tension curve?
A

Diastolic tension curve = muscle compliance

Systolic tension curve = contractility

88
Q

What factor determines cardiac contractility?

How does a positive inotropic agent shift the slope of the systolic tension curve?

A

Intracellular Ca2+ release primarily determines contractility.

Up and to the left. This allows the muscle to reach a shorter length at a given afterload.

89
Q

How does preload affect cardiac muscle shortening?

Afterload?

A

Increased preload –> increased shortening

Increased afterload –> decreased shortening

90
Q

How is cardiac ejection fraction calculated?

What is a normal ejection fraction?

A

EF = (EDV-ESV)/EDV * 100

Normal EF = 60%

91
Q

Does preload change the maximum tension developed?

Does contractility?

A

Preload does not change maximum tension, but contractility does.

92
Q

What factors affect stroke volume?

A

EDP (Preload), MAP (afterload), and contractility.

93
Q

Why is the top of a cardiac pressure-volume loop bowed?

A

The afterload is constantly changing during systole.

94
Q

What effect does an increased afterload have on tension developed & total shortening?

A

Increased afterload –> more tension developed, less total shortening.

95
Q

What are the two types of heart failure caused by?

A

Systolic HF = decreased ventricular contractility

Diastolic HF = decreased ventricular compliance

96
Q

What causes the dicrotic notch seen in arterial pressure tracing?

A

The elasticity of the aorta causes the dicrotic notch.

The aorta works as a secondary pump and distributes some of the pressure of systole over diastolic times. A loss in aortic elasticity leads to increased pulse pressure.

97
Q

Venous pulse:
What is the a wave?
c wave?
v wave?

A

a wave = contraction of R. atrium

c wave = tricuspid valve bulging due to R. ventricular contraction

v wave = filling of atria

98
Q

What is physiological splitting?

How does respiration affect it?

A

Inspiration –> reduced intrathoracic pressure –> increased EDV of R. ventricle –> delayed closure of pulmonic valve

Inspiration exacerbates it

99
Q

What is paradoxical splitting?

How does respiration affect it?

A

Aortic valve closes after pulmonic valve.

This is due to a L. bundle branch block.

It is attenuated upon inspiration?

100
Q

What can cause a systolic murmur?

Diastolic murmur?

A

Systolic = semilunar stenosis or AV insufficiency (regurgitation)

Diastolic = Semilunar insufficiency or AV stenosis

101
Q

What is a normal pulmonary blood pressure?

A

25/10

102
Q

What is pulmonary wedge pressure used to measure?

What is the average wedge pressure?

A

L. atrial pressure.

The wedge is placed in the pulmonary artery and pressure is measured downstream after lungs equilibrate with L. atrium.

Average wedge pressure = 6 mmHg

103
Q

What is the mean brachial artery pressure?

A

95 mmHg

104
Q

Where does systole take place on an EKG?

A

Just after the peak of the R wave, to the end of the T wave.

105
Q

What is a normal duration of atrial depolarization (p wave)?

A

80-100 msec

106
Q

How is the PR interval measured on an EKG?
What is a typical duration?
What is the interval indicative of?

A

Beginning of P wave to beginning of Q wave.

120-200 msec is normal

Important in identification of AV conduction defects (heart block)

107
Q

What causes S3?

S4?

A

S3 = rapid inflow of blood into the ventricles

S4 = atrial kick

108
Q

How would an increase in central venous pressure affect the cardiac output/venous return curve?

A

^ CVP –> ^ CO –> reduced CVP due to suction –> equilibrium is achieved.

109
Q

What is the mean systemic circulatory pressure?

What is its value?

A

The pressure found if cardiac output were reduced to zero & the body was allowed to equilibriate.

Its value is typically 7 mmHg

110
Q

What factors influence the cardiac function curve?

A

Sympathetic stimulation
Inotropic drugs
Heart failure

111
Q

What occurs in uncompensated heart failure?

Compensated heart failure?

A

Uncompensated: CO is decreased, and CVP is increased

Compensated: When blood volume increases to compensate, CO is increased, but CVP rises even higher.

Moderate CHF can be compensated for, with CO going back to normal. Severe CHF cannot bring CO back to normal.

112
Q

What compensatory mechanisms occur in response to hemorrhage?

A

A sympathetic increase in venous tone and increased cardiac function.

113
Q

How does in increase in afterload affect velocity of shortening?
Amount of total shortening?

A

Increased afterload –> decreased velocity and total amount of shortening

114
Q

What does thrombin do?

Plasmin?

A

Thrombin converts Fibrinogen –> Fibrin

Plasmin converts Fibrin –> Split Products

115
Q

What are the enzymes involved in extrinsic & intrinsic blood clotting?

When is each pathway typically seen?

A

Intrinsic: 12, 11, 9, 8
Extrinsic: 7, Tissue Factor

Intrinsic: Endogenous activation of coagulation. Seen in bedridden patients.

Extrinsic: Trauma (surgery, car accident)

116
Q

What do serine protease inhibitors do?

A

They inhibit coagulation proteases involved in the coagulation cascade.

117
Q

How does radius of a vessel affect blood flow?

A

Increased radius –> increased blood flow.

The relationship is to the 4th power.

118
Q

What is a non-Newtonian fluid?

A

A fluid whose viscosity changes over a range of shear rates and shear stress.

119
Q

What effect does vessel diameter have on hematocrit?

A

Smaller vessels have a relatively lower hematocrit. This is due to axial streaming and plasma skimming.

120
Q

What factors influence Reynold’s number?

What does Reynold’s number indicate?

A

Density, diameter, and velocity all increase Reynold’s number.
Viscosity decreases Reynold’s number.

A high Reynold’s number indicates a high chance for turbulent flow.

121
Q

What happens to transmural pressure at a stenotic site?

A

Transmural pressure decreases as potential energy is converted into kinetic energy (velocity).

122
Q

What is the equation for wall tension?

What does this mean for aneurysms?

A

Wall Tension = Pressure * Radius/Wall thickness

This means that aneurysms get wider radii and thinner walls –> worse and worse –> rupture.

123
Q

What is total resistance like for resistors in series?

In parallel?

A

In series, resistances are additive.

In parallel, the total resistance is less than any individual resistance.

124
Q

What has the highest resistance in the cardiovascular system?
The lowest resistance?

A 
Arterioles = highest R
Capillaries = lowest R.

This is because there are so many capillaries, that together they have a low resistance. They have the highest combined cross-sectional area in the CV system.

125
Q

What is the equation for mean arterial pressure?

A

Diastolic + 1/3 Pulle Pressure

126
Q

What effect does exercise have on systolic pressure?

Diastolic?

A

It increases systolic.

Diastolic can remain the same or decrease.

127
Q

What cardiovascular effects take place in response to exercise?

A

Pulse pressure widens
Metabolic vasodilation of active muscle & heart
Enhanced O2 extraction –> increased AV O2 difference
Increased venous return (venoconstriction, muscle pump, respiratory pump)

128
Q

What causes filtration in capillary beds?

Absorption?

A

Capillary hydrostatic pressure –> filtration

Plasma oncotic pressure –> absorption

129
Q

Does arterial or venous pressure exert a stronger influence on capillary hydrostatic pressure?

A

Venous pressure does. This is because significant pre-capillary resistance prevents arterial pressure from affecting it greatly.

130
Q

What is the primary determinant of capillary hydrostatic pressure?

A

pre/post capillary resistance ratio

131
Q

What occurs to baroreceptors in chronic hypertension?

A

They become less sensitive.

132
Q

What occurs physiologically upon stimulation of the aortic/carotid bodies?

A

Low pO2/high pCO2/low pH –> increased ventilation

Also, stimulates vasoconstriction & bradycardia but bradycardia is blocked in real life due to stretch receptors in lungs.

133
Q

What organs have strong autoregulation of blood flow?

Little autoregulation?

A

Strong: heart, brain, kidney, skeletal muscle
Little: skin, lungs

134
Q

When is the left ventricle perfused with blood?

A

Mostly during diastole

135
Q

What is coronary steal?

A

If an area is partially occluded (and thus fully vasodilated), vasodilation of another area can steal the blood from the occluded area, causing further ischemia.

136
Q

What is claudication?

A

Peripheral Arterial Disease (PAD) in which walking causes a pain int he thigh that ceases upon rest.

This is an example of the “steal” phenomenon.

137
Q

How is brain blood flow related to pH?

A

Inversely. Lower pH due to carbonic acid buildup –> increased blood flow.

This only applies to respiratory acidosis/alkalosis, and can be used clinically to modulate blood flow to the brain.

138
Q

What is the Cushing response?

A

Bradicardia and high systemic blood pressure seen with elevated intracranial pressure.

139
Q

What is the effect of 2,3, DPG?

A

It shifts the O2 binding curve of Hb to the right, leading to less affinity for O2.

DPG cannot affect HbF!

140
Q

Where does fetal hematopoiesis occur?

A

In the liver and spleen up to 30 weeks of gestation. Then it occurs in the bone marrow.

FHB (8 decks)

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