Cardiovascular Flashcards

1
Q

What are the two key parts of the cardiovascular system and what is the roleof each?

A

The heart- pumps bloodThe blood vessels- carry blood to the body and return it back to theheart again

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2
Q

What is the function of the serous pericardium?

A

It is a sac of fluid that the heart sits inside of that has two layers, thevisceral and parietal layer, inside this fluid-filled sac, the heart canmove with each heartbeat with less friction

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3
Q

What are the two layers of the serous pericardium? Which is the inside layerand which is the outside layer?

A

Parietal layer (outside layer) and visceral layer (inside layer)

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4
Q

The epicardium is the outside layer of the heart, what is the middle layer ofthe heart and what is its function?

A

The myocardium is the muscular middle layer of the heart with cardiacmuscle cells that contract and pump blood.

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5
Q

What structures supply the myocardium with blood? Where are they located?

A

The coronary vessels supply the myocardium with blood, they arelocated on the outside of the heart

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6
Q

What is the inside layer of the heart called, what type of tissue is itcomprised of, and what does it do?

A

The endocardium, it is made of a relatively thin layer of endothelium,it lines the heart chambers and heart valves.

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7
Q

What two vessels bring deoxygenated blood from the body to the heart?

A

Superior vena cava and inferior vena cava

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8
Q

Where does deoxygenated blood enter the heart?

A

The right atrium

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9
Q

Where is the coronary sinus located and what is its function?

A

It is in the right atrium; it collects blood from coronary vessels returning from the myocardium and empties into the right atrium

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10
Q

What are AV valves and what is their function?

A

Atrioventricular valves, they separate the atria from the ventricles and when open they allow blood to flow from the atria to the ventricles.

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11
Q

What are the names and locations of the AV valves?

A

The tricuspid valve is between the right atrium and right ventricle

The mitral valve is between the left atrium and left ventricle

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12
Q

What is the function of chordae tendineae?

A

They tether the tricuspid valve to the papillary muscle in the right ventricle and the mitral valve to the papillary muscle in the left ventricle and become taut with heart contraction to help prevent regurgitation of blood back into the atrium from the ventricle.

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13
Q

Which valve separates the right atrium and the right ventricle? What is its function?

A

The tricuspid valve, it allows blood to flow one way from the right atrium to the right ventricle and prevents regurgitation of blood back into the right atrium

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14
Q

What valve separates the right ventricle from the pulmonary arteries? Does it have chordea tendineae?

A

The pulmonary valve, it does not have chordae tendineae

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15
Q

Is the blood in the pulmonary arteries oxygenated or deoxygenated?

A

Deoxygenated, it comes from the right ventricle, the pulmonary arteries carry blood away from the heart. Arteries carry blood Away from the heart

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16
Q

What is the path of deoxygenated blood through the blood vessels from the pulmonary artery to the vessels that line up with the alveoli of the lungs?

A

Pulmonary artery > pulmonary arteriole > capillary

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17
Q

What exchange occurs between the capillaries and alveoli in the lungs?

A

Carbon dioxide moves from the capillary to the alveolus and oxygen moves from the alveolus to the capillary

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18
Q

Approximately how many hemoglobin proteins are in each red blood cell?

A

Millions

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19
Q

How many oxygen molecules can bind to each hemoglobin protein?

A

4

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20
Q

Approximately how many oxygen molecules can be carried by each red blood cell when fully loaded?

A

Millions

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21
Q

What is the path of oxygenated blood through the blood vessels from the siteof oxygenation at the alveoli back to the heart?

A

Venule > pulmonary vein > left atrium

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22
Q

What is pulmonary circulation?

A

The path from the right ventricle of the heart through the pulmonary artery to the lungs and back to the left atrium of the heart.

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23
Q

What happens to the blood in the heart after it enters the left atrium?

A

It goes through the mitral valve into the left ventricle.

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24
Q

How many leaflets (cusps) are in each of the AV valves?

A

Tricuspid has 3, mitral has 2

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25
Q

What happens to the blood in the heart after it enters the left ventricle?

A

It gets pumped out through the aortic valve, to the aorta

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26
Q

Which is the largest artery in the body?

A

The aorta

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27
Q

What is the path of oxygenated blood through the blood vessels from the aorta to the target organs and tissues?

A

Aorta > arterioles > capillaries

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28
Q

What exchange occurs between the capillaries and tissues in the body?

A

The red blood cells line up alongside tissue cells and drop off oxygen and pick up carbon dioxide, the reverse of what happened with the alveolus in the lung.

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29
Q

What is the path of deoxygenated blood through the blood vessels from the organs and tissues to the heart?

A

Venules > veins > inferior or superior vena cava > right atrium

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30
Q

Which large blood vessel receives deoxygenated blood from veins of the lower half of the body?

A

Inferior Vena Cava

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31
Q

Which large blood vessel receives deoxygenated blood from veins of the upper half of the body?

A

Superior vena cava

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32
Q

What is systemic circulation?

A

The path from the left ventricle of the heart to the body and back to the right atrium of the heart.

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33
Q

Which has more blood vessels, the pulmonary circulation or the systemic circulation?

A

The systemic circulation

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34
Q

Which has greater resistance to blood flow (harder to pump blood) the pulmonary circulation or the systemic circulation

A

The systemic circulation because it has a lot more blood vessels there is about a 5 times greater resistance to blood flow even though it’s the same amount of blood being pumped as in the pulmonary circulation

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35
Q

Which ventricle’s myocardium is thicker, right or left? Why?

A

The left ventricle’s myocardium - is three times thicker than the right ventricle’s myocardium. The left ventricle needs to be stronger to pump blood through increased resistance of the systemic circulation compared with the pulmonary circulation, so its muscular layer is thicker.

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36
Q

What are the two heart sounds and what causes these sounds?

A

Lub- S1 from the tricuspid and mitral valves closing with ventricular contraction

Dub- S2 from the aortic and pulmonic valves closing

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37
Q

What happens after the S1 sound? What is this time called?

A

The aortic and pulmonic valves open and blood is pushed out, this time is systole

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38
Q

What starts and ends systole?

A

Opening of the aortic and pulmonic valves then closing of the aortic and pulmonic valves

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39
Q

What happens after the S2 sound? What is this time called?

A

The tricuspid and mitral valves open back up, allowing blood to fill up the ventricles again, this is diastole

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40
Q

What are the two phases of the cardiac cycle? What do each represent?

A

Systole – ventricular contraction and blood pumping

Diastole- ventricular relaxation and blood filling

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41
Q

What does the systolic blood pressure represent? Is this higher or lower than diastolic blood pressure?

A

The pressure in the arteries when the ventricles are squeezing outblood, it is higher pressure than diastolic blood pressure.

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42
Q

What does the diastolic blood pressure represent? Is this higher or lower than systolic blood pressure?

A

The pressure in the arteries when the ventricles are filling up with more blood, lower pressure

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43
Q

Very simply, what is cardiac output?

A

The amount of blood that is pumped out by the heart in one minute

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44
Q

Very simply, what is venous return?

A

The rate at which the veins return blood back to the atria

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45
Q

What is the relationship between cardiac output and venous return?

A

They are equal since the circulatory system is a closed-loop

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46
Q

How much blood is in the average adult?

A

5L

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47
Q

Is there more blood in the systemic or pulmonary circulation at any given time?

A

Systemic

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48
Q

Is there more blood in the systemic veins or arteries at any given time? Which is under higher pressure?

A

More blood in the systemic veins, veins are high-volume, low-pressure vessels and arteries are low-volume, high-pressure vessels

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49
Q

Do both veins and arteries have valves?

A

No, only veins have valves to help fight gravity and keep blood flowingin one direction. Arteries don’t need valves because they’re under higher pressure

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50
Q

What characteristic of the large arteries close to the heart, the aorta, its main branches, and the pulmonary arteries allow the arteries to keep their shape and absorb pressure?

A

Elasticity, they are sometimes referred to as the elastic arteries.

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51
Q

What is vasoconstriction?

A

Narrowing of the arterial blood vessels to decrease blood flow to a capillary bed for an organ or tissue

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52
Q

What is vasodilation?

A

Increasing the diameter of the arterial blood vessels to increase blood flow to a capillary bed for an organ or tissue.

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53
Q

What connects the arteriole and venule at the capillary bed?

A

Metarteriole

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54
Q

What type of exchanges occur at the capillaries?

A

Lipid-soluble molecules like oxygen and carbon dioxide can dissolve and then diffuse across the endothelial cell membranes

Nutrients like glucose can be delivered.

Fluid can move out of the blood vessel and into the interstitial space.

Water-soluble substances, like ions, cross the capillary wall either through water-filled spaces, called clefts, between the endothelial cells, or through large pores in the walls of fenestrated capillaries

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55
Q

What are the three types of muscle tissues?

A

cardiac, skeletal, and smooth muscle

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56
Q

How are cardiac and skeletal muscle cells different related to branching and nuclei?

A

Cardiac muscles are branched cells and have 1-2 centrally located nuclei

Skeletal muscles are not branched and have multiple nuclei located on the periphery of the cell

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57
Q

What are intercalated discs? What type of muscle tissue are they found in?

A

Specialized junctions between neighboring cardiac cells that allow the cells to have synchronized contractions and pump blood out of the heart efficiently.

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58
Q

What is a cardiac cycle?

A

The sequence of mechanical and electrical events that occurs withevery heartbeat

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59
Q

What are the two phases of each heartbeat and what do they represent?

A

Systole- when the heart contracts and pumps blood out of the ventricles

Diastole- when the heart relaxes, and ventricles fill with blood

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60
Q

Which phases of the cardiac cycle occur during ventricular systole?

A

Isovolumetric ventricular contraction, rapid ventricular ejection, and reduced ventricular ejection

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61
Q

Which phases of the cardiac cycle occur during ventricular diastole?

A

Isovolumetric ventricular relaxation, rapid ventricular filling, and reduced ventricular filling (AKA diastasis)

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62
Q

What starts the first phase of the cardiac cycle, atrial contraction?

A

The firing of the sinoatrial, or SA node, which sends an electrical signal that propagates outward through the walls of the heart and depolarizes the atria.

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63
Q

On the ECG, what does atrial depolarization correspond to?

A

The P wave

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64
Q

What happens after atrial depolarization?

A

Contraction of the right and left atrium and increased pressure in the atria

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65
Q

What happens to ventricular volume after atrial contraction?

A

Ventricular volume increases as the atria pump blood into the ventricle with a slight increase in ventricular pressure

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66
Q

On the ECG, what signals the isovolumetric contraction phase of the cardiac cycle?

A

The appearance of the QRS complex

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67
Q

On the ECG, what does the QRS complex represent?

A

Ventricular depolarization

68
Q

What pressure changes cause the AV valves to close and the production of the first heart sound, S1?

A

Prior to ventricular contraction, when the pressure within the ventricle exceeds the atrial pressure, the atrioventricular valves close

69
Q

What happens during the isovolumetric contraction phase of the cardiac cycle?

A

Ventricular depolarization causes ventricular contraction to occur,ventricular pressure to rise, but no blood emptying occurs yet so the blood volume within the ventricles remains the same

70
Q

What signals the end of isovolumetric contraction?

A

The pressure within the ventricles becomes higher than the pressure within the aorta and pulmonary arteries, so the aortic and pulmonary valves open.

71
Q

What phase of the cardiac cycle follows isovolumetric contraction? What occurs during this phase?

A

Rapid ventricular ejection- a sudden ejection of a large amount of blood from the ventricles

72
Q

When does the ventricular and aortic pressure reach its maximum?

A

As the left ventricle ejects the blood in rapid ventricular ejection

73
Q

On the ECG, what does the ST segment represent?

A

The flat section of the ECG between the end of QRS complex and the beginning of the T wave, which represents the period between ventricular depolarization and ventricular repolarization

74
Q

What phase of the cardiac cycle follows rapid ventricular ejection? What occurs during this phase?

A

Reduced ventricular ejection- during this phase, the blood outflow isn’t caused by ventricular contraction; instead, it occurs due to inertial energy of the blood. Ventricular pressure starts to decrease, and volume continues to decrease. Aortic pressure also decreases while atrial pressure increases with increased atrial filling.

75
Q

On the ECG, what does the T wave represent?

A

Ventricular repolarization

76
Q

What phase of the cardiac cycle follows reduced ventricular ejection? What occurs during this phase?

A

Isovolumetric ventricular relaxation: the AV, aortic, and pulmonary valves are all closed, no blood enters or leaves so ventricular volume stays the same and the ventricles are relaxed.

77
Q

What phase of the cardiac cycle follows isovolumetric ventricular relaxation? What occurs during this phase?

A

Rapid ventricular filling, when the atrial pressure exceeds the ventricular pressure, the two atrio ventricular valves open, and the two ventricles start to fill rapidly with blood from the atria.

78
Q

What phase of the cardiac cycle follows rapid ventricular filling? What occurs during this phase?

A

Reduced ventricular filling (aka diastasis), the ventricles continue to fill with blood, leading to 90% of ventricular filling occurring in rapid and reduced ventricular filling phases

79
Q

Which cardiac phase is the longest?

A

Reduced ventricular filling (aka diastasis)

80
Q

What do pacemaker cells do in the heart?

A

Generate action potentials to set the rhythm and pace of the heartbeat

81
Q

What percentage of heart cells are pacemaker cells?

A

About 1%

82
Q

What happens in Phase 0 of the cardiac muscle action potential?

A

Sodium channels open and there’s an influx of sodium ions that makes the myocyte depolarize

83
Q

What happens in Phase 1 of the cardiac muscle action potential?

A

The potassium channels open and there’s an outflux of potassium ions that brings down the charge a little bit.

84
Q

What happens in Phase 2 of the cardiac muscle action potential?

A

The calcium channels open and there’s an influx of calcium ions and that counterbalances the potassium ion outflux - so it’s called the plateau phase.

85
Q

What happens in Phase 3 of the cardiac muscle action potential?

A

The calcium channels close but the potassium channels remain open,so there’s an overall outflux of potassium ions that brings down the charge that repolarizes the myocyte and it enters the resting state again

86
Q

What happens in Phase 4 of the cardiac muscle action potential?

A

The myocyte is at rest and at its resting membrane potential.

87
Q

How do pacemaker cells set the heart rhythm and pace?

A

By automatically initiating action potentials for myocyte contraction or spreading action potentials from neighboring pacemaker cells

88
Q

Where are the pacemaker cells of the heart?

A

Sinoatrial node (SA node), internodal tracts between nodes, atrioventricular node (AV node), Bundle of His, Purkinje fibers

89
Q

What does the term functional syncytium mean in relation to heart function?

A

The mechanical, chemical, and electrical connections between myocytes allow them to act as one unit because of pacemaker cell activity

90
Q

Each depolarization wave causes heart muscle contraction so the rate of the depolarization waves through the heart does what?

A

Sets the heart rate, if depolarization waves are going through about once per second, that means that your heart beats once per second, or sixty times in a minute

91
Q

What is cardiac contractility?

A

It is is a measure of the strength of cardiomyocytes to contract.

92
Q

Where does the depolarization wave typically start in the heart?

A

The sinoatrial node (SA node)

93
Q

What structures in cardiac tissue allow ions like calcium (and therefore depolarization) to spread from one cardiomyocyte to the next?

A

Gap junctions in the intercalated discs that hold the myocytes together

94
Q

What organelle in the myocyte stores intracellular calcium?

A

The sarcoplasmic reticulum

95
Q

What is the function of the T-tubules in the heart?

A

They bring calcium deep into the myocyte to bind to receptors on the sarcoplasmic reticulum to release even more calcium into the cell to activate actin and myosin for myocyte contraction

96
Q

What energy is needed for myocyte contraction?

A

Adenosine-triphosphate (ATP)

97
Q

What is cardiomyocyte contractility directly related to?

A

The concentration of calcium within the cardiomyocyte

98
Q

What factors affect cardiomyocyte calcium concentration?

A

How much calcium there is intracellularly and how much calcium is stored within the sarcoplasmic reticulum available to be released

99
Q

How does the autonomic nervous system affect cardiac contractility?

A

By changing intracellular calcium through parasympathetic and sympathetic stimulation

100
Q

What is the effect of the sympathetic nervous system on intracellular calcium and cardiac contractility?

A

A positive ionotropic effect, sympathetic stimulation increases cardiac contractility by releasing catecholamines like norepinephrine.

101
Q

What type of receptors does norepinephrine bind to in cardiomyocytes due to sympathetic nervous system activity? What effect does it have?

A

Beta 1 receptors , which bind to beta 1 receptors on cardiomyocytes increasing the sarcoplasmic reticulum’s ability to release calcium leading to increased contractility.

102
Q

What is the effect of the parasympathetic nervous system on intracellular calcium and cardiac contractility?

A

A negative ionotropic effect, decreases contractility, mainly due to the release of acetylcholine.
Parasympathetic stimulation also acts on the sinoatrial node decreasing heart rate.

103
Q

What type of receptors does acetylcholine bind to in cardiomyocytes due to parasympathetic nervous system activity?

A

Muscarinic M2 receptors, this leads to the inhibition of calcium channels. Less calcium moving into the cell and less calcium released from the sarcoplasmic reticulum leads to decreased contractility.

104
Q

How can heart rate itself can also independently change cardiac contractility?

A

A higher heart rate results in more action potentials per unit of time, each action potential’s inward calcium influx increases the total calcium that enters the cell. With greater amounts of calcium entering the cell, the sarcoplasmic reticulum accumulates more calcium for subsequent action potentials.

105
Q

What does blood pressure measure?

A

The force that the blood exerts on the surface area of the walls of the blood vessels

106
Q

Are arteries higher or lower pressure vessels than veins?

A

Higher, arteries are high-pressure blood vessels and veins are low-pressure vessels

107
Q

What does the term blood flow mean?

A

The volume of blood that flows through a vessel or an organ over time

108
Q

What factors affect the amount of blood flow?

A

Blood pressure and resistance from the blood and blood vessels

109
Q

What is vasoconstriction, and what is its effect on blood flow?

A

Narrowing of the walls of the blood vessels, this decreases blood flow

110
Q

What is vasodilation, and what is its effect on blood flow?

A

Expanding of the walls of the blood vessels, this increases blood flow

111
Q

What is blood velocity?

A

The distance blood flows over time

112
Q

Are blood flow and blood velocity the same thing?

A

No, they are related but different, blood flow is volume/time while blood velocity is distance/time

113
Q

What is the flow rate?

A

The cross-sectional area of the blood vessel times the blood velocity

Flow= Area x Velocity

114
Q

What is the average cardiac output for an adult?

A

5 L/min

115
Q

Is blood pressure higher in large arteries or smaller arterioles and capillaries?

A

Large arteries

116
Q

What does the top number in blood pressure represent?

A

The systolic pressure or the force that the blood exerts on the walls of the arteries during systole, when the heart contracts to pump blood to the body

117
Q

What does the bottom number in blood pressure represent?

A

The diastolic pressure or the force on the walls of the arteries during diastole, when the heart relaxes and refills with blood between heartbeats

118
Q

What is normal blood pressure in an average adult?

A

120/80 mmHg

119
Q

What is the Mean Arterial Pressure (MAP)?

A

The average pressure on the arteries during a complete cardiac cycle, including the systolic and diastolic pressures

MAP=1/3 (SBP) + 2/3 (DBP)

120
Q

What happens to blood pressure when the vessels vasoconstrict? What equation represents this relationship?

A

Blood pressure increases with increased resistance from vasoconstriction, represented in the equation:

Mean Arterial Pressure = Cardiac Output x Systemic Vascular Resistance

MAP = Q x R

121
Q

What three factors contribute to vascular resistance and how?

A

Blood viscosity (increased viscosity increases resistance)

Total blood vessel length (increased length increases resistance)

Blood vessel radius (increased radius decreased resistance)

122
Q

Which of the three factors that contribute to vascular resistance can change most quickly and how?

A

Blood vessel radius, it is inversely proportional to the fourth power, so as the blood vessel radius decreases from vasoconstriction the resistance increases dramatically or the radius increases from vasodilation the resistance decreases dramatically.

123
Q

What impact does increased vascular resistance from a blockage have onblood flow?

A

Increased vascular resistance would decrease blood flow

124
Q

What impact does increased vascular resistance have on blood pressure?

A

Increased vascular resistance would increase blood pressure

125
Q

Is the resistance in the systemic circulation higher or lower than that of the pulmonary circulation?

A

Higher

126
Q

What is the end-diastolic point and end-diastolic volume?

A

The end-diastolic point is when the left ventricle is fully relaxed, at the end of filling or diastole. The end-diastolic volume is the volume of blood within the left ventricle at the end-diastolic point.

127
Q

What is the end-systolic point and end-systolic volume?

A

The end-systolic point is after the left ventricle contracts, forcing blood through the aorta and into the whole arterial system and the left ventricle is fully contracted at the end of contraction or systole. The end-systolic volume is the volume of blood within the left ventricle at the end-systolic point

128
Q

What is stroke volume? How is it calculated?

A

The volume of blood that the left ventricle ejects with every heartbeat.End-diastolic volume minus end-systolic volume equals stroke volume

EDV-ESV=SV

129
Q

Does stroke volume vary with a person’s size or do all humans have approximately the same stroke volume?

A

Stroke volume varies with size a larger person will typically have a higher stroke volume

130
Q

What is the ejection fraction? How is it calculated?

A

The percentage of a person’s blood volume pumped out of the left ventricle during each heartbeat

Ejection fraction = Stroke Volume / End- Diastolic Volume

131
Q

What is a normal ejection fraction range?

A

50 and 65%

132
Q

What result would low cardiac contractility have on a person’s ejection fraction?

A

Low cardiac contractility can lead to a lower ejection fraction than normal

133
Q

What is cardiac output? How is it calculated?

A

The total volume of blood the left ventricle ejects in one minute.

stroke volume x heart rate = cardiac output

134
Q

How much blood is normally contained in the body?

A

5L

135
Q

What is a normal cardiac output?

A

4.9 L/min

136
Q

How is blood flow to organs and tissues distributed?

A

Blood flow to organs and tissues is distributed according to the organ and tissue needs

137
Q

What is tissue perfusion?

A

The total amount of blood volume going to a gram of tissue over time

138
Q

What is Stroke Volume

A

The volume of blood pumped by the left ventricle in a single heartbeat

139
Q

What is Ejection fraction

A

The % of blood that is pumped out of the left ventricle with each heartbeat

140
Q

What is Cardiac output

A

The volume of blood pumped in one minute

141
Q

What is the Frank-Starling Relationship (Law)?

A

As the heart gets filled up with more blood during diastole, it contracts harder and pumps out more blood during systole

142
Q

The force of muscle contraction during systole depends on what factors?

A

The number of myosin heads that bind to actin, which depends on the overall length of the sarcomere. The length of the sarcomere depends on how much blood fills the ventricle during diastole - because that affects how stretched out the overall muscle wall and each sarcomere within it

143
Q

Based on the Frank-Starling Relationship, what happens to the stroke volume with a greater than normal end-diastolic volume?

A

Stroke volume starts to decrease as the myosin and actin get too far apart, the number of myosin and actin binding decreases, resulting in a weaker contraction

144
Q

Does the Frank-Starling Relationship inform us on intrinsic or extrinsic mechanisms to vary the strength of cardiac contraction?

A

Intrinsic, based on the ventricular end-diastolic volume

145
Q

What are some general extrinsic mechanisms to vary the strength of cardiac contraction?

A

Nerve or hormonal stimuli and medications that can increase or decrease the contractility of the heart

146
Q

Based on the Frank-Starling Relationship, when end-diastolic volume increases

A

A stronger cardiac contraction is achieved and Stroke Volume increases

147
Q

What is cardiac preload? Why is it important?

A

Ventricular wall stress at the end of diastole, it can also be defined by the length of cardiac muscle fibers (sarcomeres) at the end of diastole.

Cardiac preload is one of the main factors that influence how much blood the heart pumps out with each heartbeat

148
Q

Is cardiac preload the same as end-diastolic volume?

A

No, it is not the same as end-diastolic volume, but it is closely related so often measured that way using echocardiogram

149
Q

What are the five factors that affect end-diastolic volume and cardiac preload?

A

Venous pressure and rate of venous return, atrial contraction,resistance from valves, ventricular compliance, and heart rate.

150
Q

How does venous pressure and the rate of venous return affect end-diastolic volume and cardiac preload?

A

Decreased venous pressure, return of venous blood, and decreased blood volume leads to decreased left ventricular pressure and decreased end-diastolic volume and therefore decreased cardiac preload.

Increased venous pressure, return of venous blood, and increased blood volume leads to increased left ventricular pressure and increased end-diastolic volume and therefore increased cardiac preload.

151
Q

How does atrial contraction affect end-diastolic volume and cardiac preload?

A

Increased force of atrial contraction increases the volume of blood that enters the ventricle, causing an increase in end-diastolic volume and preload

Decreased force of atrial contraction decreases the volume of blood that enters the ventricle, causing a decrease in end-diastolic volume and preload

152
Q

How does valve resistance affect end-diastolic volume and cardiac preload?

A

Inflow resistance is created by the narrowing of atrioventricular valve openings, this results in decreased filling of the ventricles and decreased preload

Outflow resistance is created by the narrowing of aortic and pulmonic valves, this results in decreased emptying of the ventricles and increased preload

153
Q

How does ventricular compliance affect end-diastolic volume and cardiac preload?

A

Compliant, stretchy ventricles increase preload; while noncompliant,stiff ventricles, such as seen in ventricular hypertrophy,decrease preload

154
Q

How does heart rate affect end-diastolic volume and cardiac preload?

A

Normal heart rate, 60-100 beats per minute, allows adequate time for ventricles to fill, while abnormal heart rate, such as fast heart rhythm, or tachycardia, reduce the filling time, eventually decreasing preload

155
Q

What is cardiac afterload? Why is it important?

A

Cardiac afterload can be defined as the ventricular wall stress during systole or ejection

It can also be defined as the amount of resistance that the ventricles must overcome during systole

It is one of the main factors that influence how much blood the heart pumps out with each heartbeat, or stroke.

156
Q

What are factors that affect afterload?

A

Systemic vascular resistance, aortic pressure, and valve diseases

157
Q

How does systemic vascular resistance affect afterload?

A

Vasodilation causes decreased systemic resistance and decreased afterload, vasoconstriction causes increased systemic resistance and increased afterload

158
Q

How does aortic pressure affect afterload?

A

Increased aortic pressure means that the heart must contract harder and generate more pressure within the left ventricle to overcome aortic pressure and open the aortic valve.

Therefore, increased aortic pressure increases afterload, while decreased aortic pressure reduces afterload

159
Q

How many ATP per glucose molecule does anaerobic metabolism yield?

A

2

160
Q

During anaerobic metabolism, what is pyruvate converted to?

A

Lactic acid

161
Q

Release of which hormone causes increased heart rate and contractility, systemic vasoconstriction to visceral blood vessels, and vasodilation of skeletal muscle blood vessels?

A

Epinephrine

162
Q

What is functional hyperemia?

A

Increased blood flow as a result of increased activity in a specific organ (i.e. muscles during exercise)

163
Q

What is an example of a long-term body system adaptation from regular physical exercise?

A

Specific changes to help increase the efficiency and capacity during exercises, for example, the heart muscle hypertrophies, or enlarges, while the heart rate decreases. This allows for the same amount of blood per minute to be pumped even at rest, but the heart muscle uses less energy.

164
Q

During aerobic metabolism, what is pyruvate converted to?

A

Pyruvate molecules enter the mitochondria and they’re converted to acetyl CoA, which can enter the Krebs cycle and goes through oxidative phosphorylation for ATP regeneration

165
Q

What is beta oxidation?

A

Free fatty acids get released into blood circulation, and then transported to the working muscle cells, where they undergo beta-oxidation, which converts free fatty acids to acetyl CoA in the mitochondria which enters the Krebs cycle and goes through oxidative phosphorylation for ATP regeneration.

166
Q

With increased exercise which system is acting on the heart, the sympathetic or parasympathetic nervous system? How and what is the response?

A

Sympathetic stimulation causes the kidneys to release epinephrine, and when epinephrine gets to the heart, it binds to the adrenergic receptors of the heart muscle, making heart rate and contractility increase. The heart contracts faster and stronger and the cardiac output increases. Epinephrine also causes systemic vasoconstriction so there’s reduced blood flow to the kidneys, liver and the gastrointestinal system

167
Q

What are some general cardiac adaptations with regular physical exercise?

A

Hypertrophy of cardiac muscle tissue, decreased heart rate without changes in cardiac output