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HLSC-126 > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

1
Q

What is the name of the right AV valve?

A

Tricuspid valve

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2
Q

What is the name of the left AV valve?

A

Bicuspid or mitral valve

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3
Q

What helps anchor the AV valves?

A

Chordae Tendineae
• Tendon like cords that connect the atrioventricular valve to the papillary muscles
• Prevent extroversion

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4
Q

What is the fibrous skeleton of the heart and what is its function?

A

• 4 dense connective tissue rings that surround the valves of the heart
o Pulmonary fibrous ring
o Aortic fibrous ring
o Right atrioventricular fibrous ring
o Left atrioventricular fibrous ring
• Rings fuse one another and merge with the interventricular septum
• Functions
o Structural foundation for valves
o Prevents over stretching of valves
o Point of insertion for bundles of cardiac muscle fibers
o Act as an electrical insulator between the atria and ventricles

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5
Q

What are the 3 layers of the heart?

A

Endocardium - inner layer
Myocardium - middle muscular layer
Epicardium - outer layer

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6
Q

Describe the endocardium

A

• Innermost layer
• Made of 2 layers
o Thin layer of endothelium
 Continuous with endothelium of great vessels
o Thin layer of connective tissue
• Provides smooth lining for chambers of the heart which reduces friction of blood
• Covers valves of heart

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7
Q

Describe the myocardium

A
  • Responsible for pumping action of heart
  • Composed of cardiac muscle tissue
  • Muscle fibers arranged spirally around the heart
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8
Q

Describe the epicardium

A

• Outer most layer composed of 2 tissue layers

Visceral Pericardium
• Thin transparent outer layer composed of mesothelium

Deeper Layer
• Variable layer or delicate fibroelastic tissue and adipose tissue
• Adipose tissue thicker over ventricles where arteries are
• Amount of adipose tissue varies
o Corresponds with body fat of individual
o Increases with age
• Contains blood vessels, lymphatics, and nerves that supply the myocardium

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9
Q

Describe heart muscle tissue

A

• Striated involuntary muscle
• Troponin-tropomyosin complex like with skeletal muscle
• Display autorhythmicity
o Ability to repeatedly generate spontaneous action potentials
o Can cause alternating contraction and relaxation of the heart muscle fibers
• Branching gives a stair-step appearance

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10
Q

Describe intercalated discs

A

• Irregular transverse thickenings of sarcolemma
• Used to connect ends of cardiac muscle fibers to neighboring fibers
• Contains
o Desmosomes
 Hold fibers together
o Gap Junctions
 Allow action potentials to spread from one cell to another
 Both atria contract together as a singly functional syncytium
 Both ventricles contract together as a singly functional syncytium
 No gap junctions between the atria and ventricles

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11
Q

How is an action potential prevented from moving from the atria to ventricles?

A

No gap junctions

Nonconductive fibrous skeleton surrounding the valves

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12
Q

What is the pericardial sac?

A

• Membrane that surrounds and protects the heart
• Holds heart in position while allowing it to freedom to move to beat
Composed of fibrous layer and serous membranes

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13
Q

Describe the fibrous pericardium

A

• Composed of tough, inelastic, dense irregular connective tissue
• Top is fused to connective tissues of blood vessels
• Prevents overstretching
• Anchors heart in mediastinum
• Apex partially fused to central tendon of diaphragm
o Deep breathing facilitates movement of blood by heart
• Provides protection for heart

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14
Q

Describe the serous pericardium including the layers and fluid

A
  • Thinner, more delicate mesothelial membrane
  • Formed double layer around the heart
  • Folds over itself at the top where the major blood vessels are so the 2 layers are continuous

Visceral Layer
• Adheres tightly to surface of the heart

Parietal Layer
• Lines inside of fibrous pericardium

Pericardial Cavity
• Small space between the parietal and visceral layer
• Contains a few mL of pericardial fluid

Pericardial Fluid
• Thin film of lubricating fluid
• Released by pericardial cells
• Reduces friction between membranes as heart beats

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15
Q

What is pericarditis?

A

Inflammation of the pericardial sac that results in a painful friction rub between the two pericardial layers, occurs occasionally because of viral or bacterial infection

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16
Q

Name and discuss the functions of the 4 heart valves

A

AV valves let blood flow from the atria to ventricles during ventricular filling, but prevent backflow of blood from the ventricles into the atria during ventricular emptying

Semilunar valves let blood flow from ventricles into aorta and pulmonary arteries during ventricular emptying but prevent backflow of blood from these major arteries into the ventricles during ventricular filling

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17
Q

Describe the various pacemakers sites and their intrinsic rates

A

• Sinoatrial node 70-80 beats per minute

Latent Pacemakers
• Atrioventricular node 40-60 beats per minute
• Bundle of His 20-40 beats per minute
• Purkinje fibers 20-40 beats per minute

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18
Q

What is pacemaker potential

A
  • Display pacemaker activity
  • Membrane potential slowly depolarizes between action potentials until threshold is reached and another action potential generated
  • Result in cyclically initiated action potentials for rhythmic heartbeats
  • A few ion channels contribute to this potential
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19
Q

What is the initial ion channel that opens after hyperpolarization in the pacemaker cells?

What does this result in?

A

If
• Current activated upon hyperpolarization
• Allows slow influx of sodium and potassium
• Results in slow depolarization
o Rate is different in each pacemaker site resulting in different firing rates

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20
Q

What family are I(f) channels a part of and what does this allow for?

A

Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels (HCN Channels)
• Activity modulated by cyclic nucleotides, which function as second messengers in most cell types

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21
Q

Which channels open in cardiac cells to help bring the membrane to threshold level? What does this result in?

A

T-Type Ca2+ Channel (ICa, T)
• Transient calcium channel
• Open at lower membrane potentials than the voltage-gated calcium channels
• Open during slow depolarization prior to reaching threshold
• Results in further depolarization to bring membrane to threshold

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22
Q

Which channel opens when threshold potential in cardiac pacemaker cells is reached?

A

L-Type Ca2+ Channel (ICa, L)
• Longer lasting, voltage gated calcium channel
• Activated when threshold is reached
• Resulting influx of calcium results in depolarization
o Slower than depolarization with sodium

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23
Q

Which channels in cardiac pacemaker cells open after depolarization has occurred? What does this result in?

A 
Ik 
•	Voltage-gated potassium channels
•	Activation causes efflux of potassium 
•	Results in repolarization 
•	Slow closing results in hyperpolarization, in turn activated If channels
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24
Q

What is an abnormally excitable area in the heart that results in a prelature action potential?

A

Ectopic focus

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25
Q

How does ventricular filling occur?

A

Cardiac relaxation results in AV valves open and ventricles passively fill about 80%

During atrial excitation and contraction, the ventricles remain relaxed, and the last 20% is squeezed into the ventricles

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26
Q

During a normal heartbeat, how soon before a ventricular contraction does an atrial contraction occur?

A

160 msec

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27
Q

What is the random, uncoordinated excitation and contraction of cardiac cells called?

A

Fibrillation

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28
Q

What ensures that both atria contract simultaneously?

A

Interatrial pathway extends from SA node in the right atrium to the left atrium

Transmission of action potentials via gap junctions ensures that left and right atrium are excited at the same time

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29
Q

What is the only way an action potential in the atria can spread to the ventricles?

A

Passing through the AV node

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30
Q

What extends from the SA node to the AV node carrying the action potential down the heart?

A

Internodal pathway

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31
Q

How long does it take for the action potential to move from the SA node to the AV node?

A

30 msec

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32
Q

How long does it take for the action potential to spread through the entire Purkinje fiber system?

A

30 msec

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33
Q

Where do most Purkinje fibers terminate?

A

Ventricular muscle cells near the endocardial surface and spreads across the ventricular wall to the epicardial surface via gap junctions

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34
Q

What helps to ensure smooth, coordinated contraction of both ventricles?

A

Rapid conduction down the Bundle of His and swift, diffuse distribution down Purkinje fibers allows for almost simultaneous contraction of all ventricular cells

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35
Q

What is the resting membrane potential of cardiac contractile cells?

A

-80 mV

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36
Q

What is the membrane potential of cardiac contractile cells at the peak of depolarization?

A

Approaches +50mV

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37
Q

What are the ion channels that result in cardiac contractile cells depolarization and repolarization?

A

INa
• Sodium channels result in rapid influx
• Membrane potential peaks approaching +50mV

Ito
• Depolarization opens transient outward potassium channels (Ito)
• Rapid efflux of potassium

L-Type Ca2+ Channel (ICa, L)
• Longer lasting, voltage gated calcium channel
• Results slow influx of calcium
• Results in a plateau phase

Disruption of Plateau
• Time-dependent inactivation of both Ito and ICa, L channels
• Disrupts ionic flux balance of the plateau

Ik
• Referred to as a delayed rectifier
• Allows efflux of potassium resulting in repolarization

Inward Rectifier K+ Channel
• Unique channel that allows potassium to go in and out of the cell to keep membrane potential constant

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38
Q

Describe the ion channels that contribute to the pacemaker potential cycle of the autorhythmic cells

A

If
• Current activated upon hyperpolarization
• Allows slow influx of sodium and potassium
• Results in slow depolarization
o Rate is different in each pacemaker site resulting in different firing rates

Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels (HCN Channels)
• If channels are part of this family
• Activity modulated by cyclic nucleotides, which function as second messengers in most cell types

T-Type Ca2+ Channel (ICa, T)
• Transient calcium channel
• Open at lower membrane potentials than the voltage-gated calcium channels
• Open during slow depolarization prior to reaching threshold
• Results in further depolarization to bring membrane to threshold

L-Type Ca2+ Channel (ICa, L)
• Longer lasting, voltage gated calcium channel
• Activated when threshold is reached
• Resulting influx of calcium results in depolarization
o Slower than depolarization with sodium

Ik 
•	Voltage-gated potassium channels
•	Activation causes efflux of potassium 
•	Results in repolarization 
•	Slow closing results in hyperpolarization, in turn activated If channels
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38
Q

Describe the ion channels that contribute to the pacemaker potential cycle of the autorhythmic cells

A

If
• Current activated upon hyperpolarization
• Allows slow influx of sodium and potassium
• Results in slow depolarization
o Rate is different in each pacemaker site resulting in different firing rates

Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels (HCN Channels)
• If channels are part of this family
• Activity modulated by cyclic nucleotides, which function as second messengers in most cell types

T-Type Ca2+ Channel (ICa, T)
• Transient calcium channel
• Open at lower membrane potentials than the voltage-gated calcium channels
• Open during slow depolarization prior to reaching threshold
• Results in further depolarization to bring membrane to threshold

L-Type Ca2+ Channel (ICa, L)
• Longer lasting, voltage gated calcium channel
• Activated when threshold is reached
• Resulting influx of calcium results in depolarization
o Slower than depolarization with sodium

Ik 
•	Voltage-gated potassium channels
•	Activation causes efflux of potassium 
•	Results in repolarization 
•	Slow closing results in hyperpolarization, in turn activated If channels
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39
Q

Where are the L-Type Ca2+ Channel (ICa, L) located in the cardiac contractile cells?

A

Primarily in the T tubules

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40
Q

Describe how the calcium moves to the cytoplasm of cardiac contractile cells

A

Calcium Release
• L-Type Ca2+ Channel (ICa, L) lie primarily in T tubules
• Depolarization results in slow influx of calcium
• Calcium then directly interacts with contractile mechanisms

Calcium Induced Calcium Release
• Calcium brought from ECF activates ryanodine receptor of sarcoplasmic reticulum
• Results in SR releasing its own calcium stores
• Can be up to 90% depending on the species

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41
Q

Describe the contractile mechanism and how it relaxes in the contractile cells of the heart

A

Excitation-Contraction Coupling
• Calcium binds with troponin and troponin-tropomyosin complex is pulled away
• Extent of cross-bridge activity varies with amount of cytosolic calcium levels
• Energy-dependent mechanisms remove calcium from cytosol
o Located in both plasma membrane and SR
o Restores blocking action of troponin-tropomyosin complex

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42
Q

How does elevated ECF potassium affect the hearts contractile cells?

A
  • Normally much more potassium in the ICF than ECF
  • When ECF potassium elevated, less potassium leaves the cell
  • Results in reduction of resting potential
  • Consequences include ectopic foci and cardiac arrhythmias
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43
Q

How does alterations in ECF calcium levels affect the hearts contractile cells?

A

• ECF augments strength of contraction by altering amount of cross-bridge activity
• Elevated ECF calcium
o Increases cytosolic concentration of calcium
 Increases cardiac contractility
o Prolongs plateau phase
o Contractions then take longer, so less rest between contractions
• Decreased ECF calcium
o Reduces force of cardiac contraction

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44
Q

Describe the refractory period of the cardiac contractile cells

A

• Second action potential cannot be triggered
• Protective mechanism so that heart cannot experience summation or tetanus
• Refractory period lasts about 250 msec and contraction averages 300 msec
o So next contraction cannot happen until muscle is nearly entirely relaxed
• Results primarily due to sodium channels become inactivated after depolarization
• Factors underlying maintenance of plateau phase also critical as they directly affect time it takes for sodium channels to return to resting state

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45
Q

Is the ECG a direct recording of the actual electrical activity of the heart?

A

No, it is a recording of the part of the electrical activity induced in body fluids by the cardiac impulse that reaches the body surface

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46
Q

What occurs in the heart during the ST segment?

A

Ventricles have depolarized and cardiac contractile cells are undergoing plateau phase of their action potential before they repolarize, so ventricles are contracting and emptying

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47
Q

Why is the ST segment elevated during a heart attack?

A

Infarcted zone repolarizes slower than the rest of the ventricle, this causes the illusion of a delayed current moving away from the recording electrode, and this results in the elevated ST segment; it’s just an error of the ECG machine

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48
Q

What is a pulse defecit?

A

When the heart rate on the ECG exceeds the pulse taken; basically the heart has been stimulated but the ejection is low enough it is not palpable at the wrist

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49
Q

What is damage of the heart muscle called?

A

Cardiac myopathy

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50
Q

List the autorhythmic tissues of the heart, and indicate the normal rate of action potential discharge of each

A

SA node 70-80
AV node 40-60
Bundle of His and Purkinje fibers 20-40

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51
Q

Explain why no separate wave for atrial repolarization is visible on a normal ECG

A

The electrical activity associated with atrial repolarization occurs simultaneously with ventricular depolarization, and is masked by the QRS complex on a normal ECG

52
Q

What is the end-diastolic volume (EDV)? How much is this?

A

Volume of blood in the ventricle at the end of diastole

Averages 135 mL

53
Q

What is the isovolumetric ventricular contraction?

A

A period of time at the beginning of systole where the ventricle is a closed chamber (both AV and aortic valves are closed); the pressure quickly increases to become higher and this period ends when the aortic valve opens

Isovolumetric means constant volume and length; muscle fibers remain the same length like an isometric contraction in skeletal muscle

54
Q

What is stroke volume? How much is this?

A

Amount of blood pumped out with each contraction

70 mL

55
Q

What is the end systolic volume (ESV)? How much is this?

A

Amount of blood left in the ventricle at the end of systole

About 65 mL

56
Q

What is stroke volume? What is the average amount? How is it calculated?

A

Amount of blood pumped up during each ventricular contraction
About 70 mL
End diastolic volume (EDV) - End systolic volume (ESV) = stroke volume (SV)

57
Q

What is the notch that occurs on the aortic pressure curve when the aortic valve closes?

A

Dicrotic notch

58
Q

What is isovolumetric ventricular relaxation?

A

Ventricle is a closed chamber for a brief period as the aortic valve has closed but the ventricular pressure is still too high for the AV valve to open; this falls at the beginning of ventricular diastole

Muscle fiber length and chamber volume again remain constant

Ventricles will continue to relax and pressure continues to fall. This period ends when the pressure drops enough the AV valve opens

59
Q

How long is a complete cardiac cycle at rest? How much of this is devoted to ventricular systole and diastole?

A

800 msec
300 msec - V systole
500 msec - V diastole

60
Q

At about what heart rate is fast enough to impair adequate ventricular filling?

A

200 bpm

61
Q

When are the 2 highest peaks of the ventricles filling?

A

At the beginning when blood stored in the atrium rushes in

At the end with atrial systole

62
Q

Describe the heart sounds

A

First heart sound (lub) - closure of AV valves and signals onset of ventricular systole

Second heart sound (dup) - closure of semilunar valves and signals onset of ventricular diastole

Its not actually the sound of the valves closing but rather vibrations set up within the walls of the ventricles and major arteries during valve closure

63
Q

What are abnormal heart sounds?

A

Murmurs

64
Q

What are murmurs not involving heart pathology? Who is more likely to have them?

A

Functional murmur

Young people

65
Q

What causes the abnormal heart sounds?

A

Turbulent blood flow creating vibrations in the surrounding structures

66
Q

What is rheumatic fever, and how can it affect the heart?

A

• Autoimmune disease triggered by streptococcus bacterial infection
• Antibodies interact with bodies own tissues, resulting in damage
• Heart valves very susceptible to damage
• Large, hemorrhagic, fibrous lesions form along inflamed edges of an affective heart valve
o Results in thick, stiff, scarred valve
o Depending on extent of damage, may cause stenotic or leaky valves
 Most common cause of these issues

67
Q

What is a stenotic valve? What sounds does it make?

A
  • Stiff, narrowed valve that does not open completely
  • Blood flowing through the smaller passageway have to go through faster, resulting in turbulence
  • Sounds similar to a whistling
68
Q

What is an insufficient or incompetent valve? What does it sound like?

A

• Also called a leaky valve
• Valve cannot close completely
o Commonly caused by scarred edges that do not fit together properly
• Blood flows backwards through valve creating turbulence
o Called regurgitation
• Sounds like a swishing or gurgling

69
Q

What is a murmur called when it occurs between the first and second heart sounds?

A

Systolic murmur because it occurs after the onset of ventricular systole

70
Q

What is a murmur called when it occurs between the second heart sound and the first heart sound of the next beat?

A

A diastolic murmur as it occurs after ventricular diastole

71
Q

A patient has a whistling sound between the first and second heart sounds. What type of heart murmur is this likely to be?

A

Whistling = stenosis

Occurs between first and second sounds = systolic

Indicates stenosis is in a valve that should be open during systole.

This could be either the aortic or pulmonary semilunar valves

72
Q

What is the main concern with heart murmurs?

A

The circulatory results of the defect

73
Q

Define systole and diastole

A

Systole - Period of contraction and emptying

Diastole - Period of relaxation and filling during the cardiac cycle

74
Q

State the pressure relationships among the aortic, atrial, and ventricular pressures during each of these phases of the cardiac cycle

  1. Ventricular filling
  2. Isovolumetric ventricular contraction
  3. Ventricular ejection
  4. Isovolumetric ventricular relaxation
A
  1. aortic pressure > atrial pressure > ventricular pressure
  2. aortic pressure > ventricular pressure > atrial pressure
  3. ventricular pressure > aortic pressure > atrial pressure
  4. aortic pressure > ventricular pressure > atrial pressure
75
Q

How do heart sounds relate to the cardiac cycle?

A

First heart sound is associated with closure of AV valves, this occurs at the beginning of isovolumetric ventricular contraction

Second heart sound is the semilunar valves, this occurs at the beginning of isovolumetric ventricular relaxation

76
Q

What is cardiac output and what would the average cardiac output be for someone with a heart rate of 70 beats/min?

A 
Cardiac output (CO) is the volume of blood pumped by each ventricle per minutes (left and right are usually equal)
•	Cardiac Output = heart rate x stroke volume
o	CO = 70 beats/min x 70 mL/beat = 4900 mL/min or 4.9 L/min 
o	Often measured in mL/min or L/min
77
Q

What is cardiac reserve?

A

The difference between the cardiac output at rest and at maximum exercise

78
Q

What are the two types of controls influencing stroke volume?

A

Intrinsic control - extent of venous return

Extrinsic control - extent of sympathetic stimulation

79
Q

How does parasympathetic stimulation affect the heart? What is the action of it and how does it affect the various parts of the heart?

A
  • Results in slower heart rate and weaker atrial contraction
  • Supplied by vagus nerve
  • Primarily supplies atrium, especially SA and AV nodes
  • Supply to ventricles is sparse

Action
• Acetylcholine from vagus nerve binds to muscarinic receptor
• Coupled to an inhibitory G protein reducing activity of cAMP pathway

SA node influence
• Slows closure of potassium channels increases permeability causing
o More hyperpolarization so it takes longer to drift back to threshold
o Opposes If current responsible for initiating gradual depolarization to threshold

AV node influence
• Decreases node’s excitability resulting in longer AV nodal delay
• Due to increased potassium channel permeability resulting in increased hyperpolarization

Atrial contractile cell influence
• Plateau phase is shortened resulting in weaker contraction
• Due to shorter action potential which reduces the influx of calcium

Ventricular influence
• Very little effect

80
Q

What is the parasympathetic nerve that supplies the heart?

A

Vagus

81
Q

How does sympathetic stimulation affect the heart? What is the action of it and how does it affect the various parts of the heart?

A
  • Improves effectiveness of the heart and increases rate and force of contraction
  • Supply atrium, including SA and AV nodes
  • Rich supply to ventricles

Action
• Norepinephrine binds to β1 adrenergic receptor
• Coupled to a stimulatory G protein accelerating cAMP pathway in the target cells

SA node influence
• Enhanced pacemaker currents, reducing time to reach threshold
o Permits more frequent action potential

AV node influence
• Reduction in AV nodal delay
• Due to increased conduction velocity
o Presumably by enhancing influx of calcium

Atrial and Ventricular influence
•	Faster spread of action potential 
•	Increased contractile strength
o	Caused by increased calcium influx 
o	Intensifies excitation coupling
82
Q

How does the sympathetic nervous system stimulation affect the heart via the adrenal gland?

A

Adrenal Medulla
• Promotes secretion of epinephrine
o Augments the sympathetic nervous systems actions on the heart

83
Q

How does the sympathetic nervous system stimulation affect the heart via the veins?

A

• Increased venous return increases strength of cardiac contraction
o Frank-Starling mechanism

84
Q

Describe the Frank-Starling heart law? How does it work? What are the advantages of it?

A
  • The intrinsic relationship between end-diastolic volume and stroke volume
  • Resting cardiac length is less than optimal length
  • Increasing EDV increases the muscle fiber length, moving it closer to optimal length, which in turn increases contractile tension
  • The greater the diastolic filling, the greater the EDV, the greater the stretch of heart
  • The farther each muscle cell is stretched, the greater the force of the subsequent contraction

Mechanism of Action
• Based on the dependence of calcium sensitivity to fiber length
• Increased stretch reduces the space between the thick and thin filaments
• When calcium pulls away the troponin-tropomyosin, this closer relationship allows for more cross-bridge interactions

Advantages
• Equalizes output between right and left sides
• When larger CO is needed, venous return increases, resulting in an increased EDV, and therefore stroke volume increases

85
Q

Describe the effect of afterload on stroke volume

A

• Afterload
o Forces that the heart is contracting against
• Increased afterload caused by increased pressure in the aorta that the left ventricle has to overcome
• Intrinsic control will see an increase in EDV to compensate, if it doesn’t, extrinsic control will need to compensate

86
Q

Describe the effects of sympathetic stimulation in relation to stroke volume

A
  • Extrinsic control of stroke volume (SV)
  • Epinephrine enhances contractility
  • Causes greater ejection %
  • Greater calcium influx increases cross-bridge cycling resulting in more force being exerted

• Also increases venous return, which increases EDV, further increasing SV

87
Q

What are the most common causes of heart failure?

A

HTN and damage via AMI

88
Q

Describe the compensatory measures the body takes when experiencing heart failure

A

• Sympathetic stimulation increases heart contractility towards normal
o Only works for a limited time
o Heart becomes less responsive to norepinephrine
o Stores of norepinephrine in nerve terminals become depleted
• Kidneys retain extra salt and water to expand blood volume
o Increases EDV returning stroke volume to normal
o Working with greater cardiac muscle length

89
Q

Describe what happens when the heart begins to decompensate in heart failure. What is forward and backward failure?

A

• Heart unable to compensate and so stroke volume falls
• Heart operating in the descending limb of the length-tension curve
• Forward failure
o Heart fails to pump adequate amount of blood forward as stroke volume falls
• Backward failure
o Blood dams up in the venous system as a result of forward failure

90
Q

Describe left sided heart failure

A

• Backward failure leads to pulmonary edema
o Reduces gas exchange
• Forward failure
o Inadequate blood flow to kidneys
 Inhibits adequate kidney function
 Retention of additional salt and water to attempt to increase blood volume. This further exacerbates venous congestion

91
Q

Describe pulmonary heart disease

A

• Sometimes called cor pulmonale
• Caused by increased pulmonary resistance due to
o COPD
o Pulmonary HTN
• Heart develops hypertrophy on the right side to try to compensate
• Eventually right sided heart failure occurs

92
Q

Describe acute heart failure

A

• Caused by relatively sudden inability of heart to pump normally, such as
o AMI
o Pulmonary edema which will affect right ventricular function
• Develops over days to weeks
• Heart does not have time to compensate for increased demands

93
Q

Describe diastolic heart failure

A 
Diastolic Heart Failure
•	Abnormal ventricle filling
o	Heart muscle may not adequately relax 
o	Heart muscle stiffens and cannot expand normally 
•	Results in decreased stroke volume
94
Q

When does most coronary blood supply occur?

A

During diastole

95
Q

How does the heart increase oxygen availability when it has increased demands? How is this accomplished? Why doesn’t the heart cells just take more oxygen out of the blood flowing by it?

A

By vasodilating coronary blood flow.

Likely due to an increase in adenosine released during increased ATP use which acts as a paracrine inducing dilation

It already removes 65% of oxygen at rest so there is not much oxygen reserve for the coronary arteries

96
Q

How is does cardiac vascular spasm occur?

A

Too little oxygen available so endothelium (blood vessel lining) releases platelet-activating factor (PAF), whch diffuses to the underlying vascular smooth muscle causing contraction

97
Q

Describe the steps of development of an atherosclerotic plaque?

A

Inflammatory Response
• Injury occurs to the vessel wall
• Low-grade inflammation over decades can lead to plaque formation
• Artery-abusing agents may set off this inflammation, the most common is cholesterol

LDL Accumulation
• Low-density lipoprotein (LDL, bad cholesterol) accumulates below the endothelium
• Cholesterol oxidizes by free radicles
• Antioxidant vitamins have been shown to slow plaque deposition

Monocyte Activation
• Oxidized LDL causes endothelial cells to produce chemicals that attract monocytes
• Monocytes trigger local inflammatory response

Macrophage Activity
• Monocytes enter the blood vessel wall and become macrophages
• Phagocytose the oxidized LDL now called foam cells due to their fatty appearance under a microscope
• Foam cells accumulate beneath the vessel lining forming a fatty streak
• Earliest form of plaque

Mature Plaque Develops
• Chemicals released at inflammatory site cause smooth muscle cells in the vessel wall to migrate on top of the lipid accumulation
• Atheroma’s develop
o Benign tumors of smooth muscle cells within the vessel walls
o Build by continuous mitosis and enlargement of smooth muscle cells

Blood Vessel Narrowing
• Protruding plaque progressively bulges into the lumen narrowing it
• Oxidized LDL inhibits nitric oxide which works locally to allow vasodilation

Sclerosis Develops
• Thickening plaque interferes with nutrient exchange for the vessel wall
• Area becomes invaded by fibroblasts forming the connective tissue cap over the plaque

Calcification
• Calcium precipitates in the plaque, making artery hard and unable to distend easily

98
Q

Which one of the following is the correct flow of blood throughout the body when starting from the right ventricle?

a) systemic arteries - systemic veins - pulmonary arteries - pulmonary veins
b) pulmonary arteries - pulmonary veins - systemic arteries - systemic veins
c) systemic arteries - systemic veins - pulmonary veins - pulmonary arteries
d) pulmonary arteries - pulmonary veins - systemic veins - systemic arteries

A

B

99
Q

Which one of the following is the primary pacemaker of the heart?

a) sinoatrial node
b) atrioventricular node
c) bundle of His
d) Purkinje fiber

A

A

100
Q

Typically, stroke volume is approximately

a) 30 mL
b) 50 mL
c) 70 mL
d) 90 mL

A

C

101
Q

A cardiac muscle fiber’s length normally is

a) below optimal length
b) at optimal length
c) above optimal length

A

A

102
Q

What percentage of ventricular filling is normally accomplished before atrial contraction occurs?

a) 20%
b) 50%
c) 80%
d) 100%

A

C

103
Q

State the 3 basic components of the circulatory system

A

Heart, blood vessels, blood

104
Q

Describe where the atrioventricular valves are located and how they function

A

AV valves are located between each atria and ventricle
Bicuspid (Mitral) valve is on the left side of the heart
Tricuspid valve is on the right side of the heart

They open together at the beginning of ventricular filling during diastole and close together at the beginning of systole

105
Q

List the 3 layers of the heart wall

A

Endocardium - inner
Myocardium - middle muscle layer
Epicardium - outer

106
Q

Define the following:

  • end diastolic volume
  • end systolic volume
  • stroke volume
  • heart rate
  • cardiac output
A

EDV - amount of blood in each ventricle at the end of diastole (average is 135 mL)
ESV - amount of blood in each ventricle at the end of systole (averages 65 mL)
SV - amount of blood ejected from the heart during one contraction (average is 70 mL)
HR - number of heart beats per minute (averages 70 bpm)
CO - amount of blood ejected from the heart per minute (SV x HR = 70 x 70 = 4.9L/min)

107
Q

When compared to skeletal muscle, which one of the following properties is unique to cardiac muscle?

a) the muscle fibers run the length of the heart
b) contraction requires an electrical stimulus
c) single muscle cells are connected end-to-end
d) contraction requires calcium

A

C

108
Q

Using your knowledge of cardiac action potentials, which of the following ion channels dominates during the upstroke?

a) L-type Ca2+ channels
b) Na+ channels
c) If channels
d) Ik channels

A

B

109
Q

Interpreting an ECG, atrial repolarization is hidden by the

a) P wave
b) QRS complex
c) QT interval
d) R-R interval

A

B

110
Q

Contrasting isovolumetric ventricular contraction to isovolumetric ventricular relaxation, which of the following parameters is significantly decreased during isovolumetric relaxation?

a) aortic pressure
b) left ventricular pressure
c) left atrial pressure
d) left ventricular volume

A

D

111
Q

Implementing your knowledge of the Frank-Starling Law of the heart, state what happens when end diastolic volume decreases?

a) stroke volume decreases
b) stroke volume increases
c) heart rate decreases
d) heart rate increases

A

A

112
Q

Compare and contrast how the sympathetic and parasympathetic nervous system innervate the SA node to alter its function

A

Both sympathetic and parasympathetic systems innervate the SA node where sympathetic signals will increase its pacing rate, while parasympathetic signals will decrease its pacing rate

113
Q

Applying your knowledge of both skeletal and cardiac muscle, distinguish why cardiac muscle is resistant to tetanus

A

Due to the long plateau phase of cardiac action potentials, sodium channels remain inactivated, resulting in a refractory period that lasts almost as long as the contraction. This restricts twitch summation and tetanus

114
Q

Describe the normal spread of cardiac excitation and interpret the significance of the AV nodal delay

A

SA node depolarizes and sends wave of excitation throughout both atria (interatrial pathway) and to the AV node (intermodal pathway). After a short delay, the AV node sends the signal down the left and right bundle of His to the Purkinje fibers that directly excite the cardiac muscle.

The AV node delay allows the atrium to contract and complete ventricular filling before ventricular contraction

115
Q

During heavy exercise, the cardiac output of a trained athlete may increase to 40 L/min. If stroke volume remained constant at 70 mL, what heart rate would be necessary to achieve this cardiac output? Is this heart rate physiologically possible?

A

CO = SV x HR
40 000 mL/min = 70 mL x HR
HR = 571
Definitely not

116
Q

Differentiate between the two heart sounds and their underlying causes

A

First heart sound occurs when AV valves close
Second sound occurs when semilunar valves close
Sounds cause by vibrations in the ventricles and turbulent blood flow in the arteries

117
Q

With increased parasympathetic nervous system stimulation, which of the following effects on the heart would you NOT expect to observe?

a) decreased heart rate
b) decreased atrial contractility
c) decreased ventricular contractility
d) increased AV node delay

A

C

118
Q

Increasing afterload will have what effect?

a) decreased heart rate
b) shorten the time between initiation of contraction and ventricular emptying
c) decrease end diastolic volume
d) decrease stroke volume

A

D

119
Q

When isovolumetric ventricular relaxation time is decreased, which one of the following is correct?

a) atrial volume is decreasing
b) atrial volume is increasing
c) left ventricular volume is decreasing
d) left ventricular volume is increasing

A

B

120
Q

Select the most appropriate condition in which coronary blood flow is reduced the most

a) faster heart rates
b) slower heart rates
c) stronger ventricular contractions
d) weaker ventricular contractions

A

A

121
Q

Using your knowledge of heart sounds, appraise what kind of valve disorder is likely caused by a whistling diastolic murmur

a) stenotic semilunar valve
b) insufficient semilunar valve
c) stenotic AV valve
d) insufficient AV valve

A

C

122
Q

If there were no calcium ions in the ECF predict how this would affect cardiac contractility

A

Since cardiac muscle requires external calcium to enter and trigger further release of calcium from the SR, the absence of calcium in the ECF would mean the heart would stop contracting

123
Q

If right ventricular stroke volume was 70 mL, and left ventricular stroke volume was 69 mL, describe the consequences over 1 minute. Over 1 hour.

A

Over one minute, 60 mL of extra blood would be pooled in the pulmonary circulation. In an hour, 3.6 L of extra blood would be pooled in the pulmonary circulation, which is not sustainable for life

124
Q

How is stroke volume affected by decreasing the duration of ventricular diastole?

A

If the duration of left ventricular diastole was suddenly decreased, this would lead to a decrease in EDV and thus stroke volume

125
Q

Argue which is more of a problem, diastolic heart failure or systolic heart failure

A

One may argue that diastolic heart failure, characterized by decreased ventricular filling, is worse over the long term.

Systolic failure is characterized by a decrease in cardiac contractility.

Currently, there are no drugs in effect for diastolic heart failure, whereas there are drugs that can increase cardiac contractility.

126
Q

Defend the concept that LDL is worse than HDL

A

HDL has the most protein and least cholesterol
LDL has less protein and more cholesterol

LDL is worse because it transports cholesterol to the cells. When delivered to a vessel, oxidized LDL can act as a trigger for atherosclerosis.

HDL actually carries cholesterol away from cells to the liver for partial elimination

127
Q

In a physical exam, Rachel’s heart rate was rapid and very irregular. Furthermore, her heart rate, determined directly by listening to her heart with a stethoscope, exceeded the pulse rate taken concurrently at her wrist. No definite P waves could be detected on Rachel’s ECG. The QRS complexes were normal in shape but occurred sporadically.

Given these findings, what is the most likely diagnosis of Rachel’s condition?

Explain why the condition is characterized by a rapid, irregular heart beat.

Would cardiac output be seriously impaired by this condition? Why or why note?

What accounts for the pulse deficit?

A

A fib with rapid conduction

Only some of the impulses are being let through the AV node so the heart rate becomes erratic

CO is usually not seriously impaired. Most ventricular filling occurs at the beginning of diastole, so even with varying times, it should still have enough time to fill adequately leading to only a slight decrease in SV which is offset by the rapid heart rate.

Only when ventricular filling time is significantly reduced will there be an issue, as the contraction, due to the Frank-Starling Law, will be weakened. This may only eject a small volume or no stroke volume, resulting in a non-perfusing beat

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