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BIOL*235 Midterm 2 > Chapter 20: Cardiovascular System and Heart > Flashcards

Chapter 20: Cardiovascular System and Heart Flashcards

1
Q

The anterior surface of the heart is:

A

Deep to the sternum and ribs.

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2
Q

The inferior surface of the heart is:

A

Between the apex and right surface, and rests mostly on the diaphragm.

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3
Q

The valves of the heart are composed of:

A

Dense connective tissue covered by endocardium.

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4
Q

Pericardium.

A

Membrane that surrounds and protects the heart. Confines the heart to its position in the mediastinum while allowing sufficient freedom of movement for vigorous and rapid contraction.

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5
Q

Fibrous pericardium.

A

Superficial. Tough inelastic dense irregular connective tissue. Resembles a bag that rests on and attaches to the diaphragm. Open end is fused to connective tissue of the blood vessels entering and leaving the heart. Prevents overstitching of the heart. Provides protection. Anchors heart to mediastinum. Movement of diaphragm during deep breathing facilitates movement of blood by the heart.

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6
Q

Serous pericardium.

A

Deep. Thin delicate membrane. Forms a double layer around the heart. Between the parietal and visceral serous layers is a thin film of lubricating serous fluid called pericardial fluid that reduces friction between layers as the heart moves. The space that contains this pericardial fluid is the pericardial cavity.

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7
Q

Outer layer of serous pericardium.

A

Parietal. Fused to fibrous pericardium.

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8
Q

Inner layer of serous pericardium.

A

Visceral. Epicardium. One of the layers of the heart wall. Adheres tightly to heart surface.

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9
Q

Epicardium.

A

Outer layer of heart wall. Composed of two tissue layers. Creates a smooth slippery texture to the outermost surface of the heart. Contains blood vessels, lymphatics, and vessels that supply the myocardium.

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10
Q

Describe the two tissue layers of the epicardium.

A

Visceral layer: outer, thin, transparent, composed of mesothelium. Beneath the mesothelium is a variable layer of delicate fibroelastic tissue and adipose tissue. This adipose tissue becomes thickest over the ventricular surfaces where it houses the major coronary and cardiac vessels.

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11
Q

Myocardium.

A

Middle layer of heart wall. Responsible for the pumping action of the heart. Composed of cardiac muscle tissue. Makes up 95% of heart wall. Muscle fibres are wrapped and bundled with connective tissue sheaths composed of endomysium and perimysium. Striated muscle fibres are organized in bundles that swirl diagonally around the heart and generate pumping actions.

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12
Q

Endocardium.

A

Inner layer of heart wall. Thin layer of endothelium overlying a thin layer of connective tissue. Provides a smooth lining for the chambers of the heart, and covers the valves of the heart. Minimizes surface friction as blood passes through the heart. Continuous with endothelial lining of large blood vessels.

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13
Q

Atria.

A

Two superior chambers that receive blood from veins.

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14
Q

Ventricles.

A

Two inferior chambers that eject blood into arteries.

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15
Q

Auricle.

A

On the anterior surface of each atrium. Wrinkled pouch that increases the capacity of the atrium.

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16
Q

Sulci.

A

Contain coronary blood vessels and fat on the surface of the heart. Each sulcus marks the external boundary between two chambers of the heart.

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17
Q

Coronary sulcus.

A

Deep groove that encircles most of the heart. Marks the external boundary between atria and ventricles.

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18
Q

Anterior interventricular sulcus.

A

Shallow groove on anterior surface of heart. Marks external boundary between right and left ventricles on anterior aspect of heart.

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19
Q

Posterior interventricular sulcus.

A

Anterior interventricular sulcus continues around to the posterior side. Marks the external boundary between right and left ventricles on posterior aspect of heart.

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20
Q

Right atrium.

A

Forms right surface of heart. Receives blood from superior vena cava, inferior vena cava and coronary sinus. The inside of the posterior wall is smooth. The inside of the anterior wall is rough due to pectinate muscles.

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21
Q

Interatrial septum.

A

Thin partition between right and left atrium.

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22
Q

Fossa ovalis.

A

Oval depression. Opening in interatrial septum of the fetal heart that usually closes after birth.

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23
Q

Tricuspid valve.

A

Right atrioventricular valve. Blood passes from right atrium to right ventricle through this valve.

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24
Q

Right ventricle.

A

Forms most of the anterior surface of the heart. The inside contains a series of ridges formed by trabeculae carneae, which convey part of the conduction system of the heart. The cusps of the tricuspid valve are connected to chordae tendineae which are connected to cone-shaped trabeculae carneae called papillary muscles.

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25
Q

Interventricular septum.

A

Between right and left ventricles.

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26
Q

Pulmonary valve.

A

Semilunar valve. Blood passes from the right ventricle into the pulmonary trunk through this valve. This divides into right and left pulmonary arteries, and carries blood to lungs.

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27
Q

Left atrium.

A

Forms most of base of heart. Receives blood from the lungs through 4 pulmonary veins. The inside has a smooth posterior wall and anterior wall.

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28
Q

Bicuspid valve.

A

Left atrioventricular valve. Blood passes from left atrium to left ventricle through this valve.

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29
Q

Left ventricle.

A

Thickest chamber. Forms the apex of the heart. Contains trabeculae carneae. Has chordae tendineae that anchor the cusps of the bicuspid valve to papillary muscles.

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30
Q

Aortic valve.

A

Semilunar valve. Blood passes from left ventricle into ascending aorta through this valve. Some of the blood in the aorta flows to coronary arteries which branch from ascending aorta to carry blood to heart wall. The remainder of the blood in the aorta passes into the arch and descending aorta to carry blood throughout the body.

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31
Q

Ductus arteriosus.

A

A temporary blood vessel present in fetal life. Shunts blood from pulmonary trunk into aorta so only a small amount of blood enters their non-functioning fetal lungs. The vessel normally closes after birth, leaving the ligamentum arteriosum, which connects the arch of the aorta and pulmonary trunk.

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32
Q

The thickness of the myocardium of the chambers varies accordingly to:

A

The chamber function. The thin-walled atria deliver blood under less pressure. The thick-walled ventricles pump blood under high pressure and over greater distances.

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33
Q

Fibrous skeleton of heart.

A

Consists of 4 dense connective tissue rings that surround the valves of the heart, fuse with one another, and merge with the interventricular septum. Prevents overstitching of the valves. Serves as a point of insertion for bundles of cardiac muscle fibres. Act as an electrical insulator between atria and ventricles.

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34
Q

Atrioventricular valves (AV).

A

Tricuspid and bicuspid. When an AV valve is open, the rounded ends of the cusps project into the ventricle. When the ventricles are relaxed, the papillary muscles are relaxed, the chordae tendineae are slack, and blood moves from a higher pressure in the atria to a lower pressure in the ventricles through open AV valves. When the ventricles contract, the pressure of the blood drives the cusps upward until their edges meet and close. Papillary muscles also contract, tightening the chordae tendineae to prevent the cusps from everting (opening into atria).

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35
Q

Semilunar valves (SL).

A

Aortic and pulmonary. Made of 3 crescent moon-shaped cusps, where each cusp attaches to the arterial wall. Allows ejection of blood from heart into arteries and prevents backflow of blood into ventricles. The free borders of the cusps project into the lumen of the artery. When the ventricles contract, pressure builds up within the chambers –> SL valves open when pressure in ventricles exceeds pressure in arteries –> permitting ejection of blood from ventricles into pulmonary trunk and aorta. As the ventricles relax, blood flows back toward the heart –> this back flowing blood fills the valve cusps which causes the free edges of the SL valves to contact each other tightly and close the opening between the ventricle and artery.

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36
Q

Where are there no valves?

A

Guarding the junctions between the venae cavea and right atrium, or pulmonary veins and left atrium. As the atrium contract, a small amount of blood flows backward from atria into these vessels. Backflow is minimized by a different mechanism: as atrial muscle contracts, it compresses and nearly collapses the weak walls of the venous entry points.

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37
Q

Systemic circulation.

A

Left side of heart receives bright red oxygenated blood from lungs –> LV ejects blood into aorta –> divides into separate streams entering progressively smaller systemic arteries –> carry blood throughout the body –> exchange of nutrients and gases through capillary walls –> unloads O2 and picks up CO2 –> blood flows back to right atrium through systemic veins.

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38
Q

Pulmonary circulation.

A

Right side of heart receives dark red deoxygenated blood returning from systemic circulation –> RV ejects blood into pulmonary trunk –> branches into pulmonary arteries –> lungs –> blood unloads CO2 for exhalation and picks up O2 from inhalation –> pulmonary veins –> flows back to left atrium.

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39
Q

Coronary circulation.

A

The network of blood vessels that supplies the myocardium. Coronary arteries branch from ascending aorta and encircle the heart. When heart contracts, little blood flows in the coronary arteries because they are squeezed shut. When heart relaxes, the high pressure of blood in the aorta propels blood through coronary arteries –> capillaries –> coronary veins.

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40
Q

Left and right coronary arteries branch from:

A

Ascending aorta, and supply oxygenated blood to myocardium.

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41
Q

Left coronary artery.

A

Passes inferior to the left auricle and divides into anterior interventricular and circumflex branches. Anterior interventricular branch (left anterior descending artery) is in the anterior interventricular sulcus, and supplies oxygenated blood to walls of ventricles. Circumflex branch is in coronary sulcus, and supplies oxygenated blood to walls of left ventricle and left atrium.

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42
Q

Right coronary artery.

A

Passes inferior to right auricle and divides into posterior interventricular and marginal branches. Posterior interventricular branch follows posterior interventricular sulcus, and supplies oxygenated blood to walls of ventricles. Marginal branch follows the right margin of the heart, and supplies oxygenated blood to the wall of the right ventricle. Also supplies small branches to right atrium.

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43
Q

The heart muscle may receive sufficient oxygen even if one of its coronary arteries is partially blocked.

A

True.

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44
Q

Most deoxygenated blood from the myocardium drains into:

A

Coronary sinus. In coronary sulcus on posterior surface of heart. Empties into right atrium.

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45
Q

Cardiac muscle fibres.

A

Short, less circular, one centrally located nucleus, many large mitochondria, wider transverse tubules. The ends of cardiac muscle fibres connect to neighbouring fibres by intercalated discs, which contain desmosomes and gap junctions.

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46
Q

Desmosomes.

A

Hold fibres together.

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47
Q

Gap junctions.

A

Allow muscle APs to conduct from one muscle fibre to its neighbours. Allow the entire myocardium of the atria and ventricles to contract as a single coordinated unit.

48
Q

Why does cardiac muscle have a smaller intracellular reserve of calcium?

A

Smaller SR.

49
Q

Autorhythmic fibres.

A

Conduction system. Source of electrical activity of heart. Self-excitable. Repeatedly generate APs that trigger contractions. Continue to stimulate a heartbeat even after the heart is removed from the body. Problems with these fibres can result in arrhythmias.

50
Q

Autorhythmic fibre functions.

A

Act as pacemaker to set the rhythm of electrical excitation that causes heart contraction. Also forms the cardiac conduction system, which is a network of specialized cardiac muscle fibres that provide a path for each cycle of cardiac excitation to progress through the heart.

51
Q

Describe the process of contraction by autorhythmic fibres.

A

Cardiac excitation begins in SA node –> pacemaker potential reaches threshold –> AP is triggered –> propagates throughout both atria via gap junctions in intercalated discs of atrial muscle fibres –> atria contract at same time –> AP reaches AV node –> AP slows due to differences in cell structure at AV node –> provides time for atria to empty into ventricles –> AP enters AV bundle –> AP enters right and left bundle branches which extend through interventricular septum toward apex –> large diameter Purkinje fibres rapidly conduct AP beginning at apex upward to remainder of ventricular myocardium –> ventricles contract to push blood upward toward semilunar valves.

52
Q

Sinoatrial node.

A

Located in right atrial wall inferior and lateral to superior vena cava opening. Set the rhythm for contraction. Natural pacemaker. SA node cells do not have a stable resting potential; they repeatedly depolarizes to threshold spontaneously. The spontaneous depolarization is a pacemaker potential.

53
Q

Atrioventricular node.

A

Located in interatrial septum anterior to opening of coronary sinus.

54
Q

Atrioventricular bundle.

A

Bundle of His. Only site where APs can conduct from the atria to the ventricles.

55
Q

On their own, autrorhythmic fibres in SA node would initiate an AP every:

A

0.6 seconds or 100 times a minute.

56
Q

How does the SA node act as the natural pacemaker?

A

APs from SA node spread through the conduction system and stimulate other areas before they are able to generate APs at their own slower rate.

57
Q

Depolarization.

A

Contractile fibres have a stable resting membrane potential that is around -90mV. When a contractile fibre is brought to threshold by an AP from neighbouring fibres, its voltage gated fast Na2+ channels open to allow Na2+ inflow. This produces a rapid depolarization. The fast Na2+ channels automatically inactivate and Na2+ inflow decreases.

58
Q

Plateau.

A

A period of maintained depolarization due to opening of voltage gated slow Ca2+ channels in sarcolemma. Ca2+ moves from interstitial fluid to cytosol, which causes even more Ca2+ to leave the SR and into the cytosol. This triggers contraction. Plateau lasts 0.2 seconds, and the membrane potential is 0mV.

59
Q

Repolarization.

A

Recovery of the resting membrane potential. After a delay, additional voltage gated K+ channels open to allow the outflow of K+, and restore the resting membrane potential of -90mV. Ca2+ channels in sarcolemma and SR close.

60
Q

As calcium concentration rises inside the contractile fibre:

A

Calcium binds to troponin –> actin and myosin filaments slide past one another –> tension develops.

61
Q

Refractory period in muscle.

A

Interval during which a second contraction cannot be triggered.

62
Q

Refractory period in cardiac muscle fibre.

A

Lasts longer than the contraction itself. Another contraction cannot begin until relaxation. Tetanus (maintained contraction) cannot occur in cardiac muscle since this would result in blood flow ceasing.

63
Q

ATP production.

A

Cardiac muscle produces little of the ATP it needs by anaerobic cellular respiration. It relies mostly on aerobic cellular respiration in its mitochondria.

64
Q

At rest, the heart’s ATP comes mainly from:

A

Oxidation of FAs (60%) and glucose (35%), with smaller contributions from lactic acid, creatine phosphate, amino acids, and ketone bodies. During exercise, the heart’s use of lactic acid increases.

65
Q

A sign that a myocardial infarction has occurred is the presence of:

A

Creatine kinase in blood. This enzyme catalyzes CP –> ADP –> ATP. Injured or dying cardiac or skeletal muscle fibres release CK into bloodstream.

66
Q

Electrocardiogram.

A

Record of APs produced by all of the heart muscle fibres during each heartbeat. Amplifies the heart’s electrical signals and produces 12 different tracings from different combinations of limb and chest electrodes. Can determine if the conducting pathways is abnormal, if heart is enlarged, if certain regions of the heart are damaged, and the cause of chest pain.

67
Q

P-wave.

A

First wave. Small upward deflection. Represents atrial depolarization which spreads from SA node through contractile fibres in both atria.

68
Q

Large P-wave may indicate:

A

Enlarged atria.

69
Q

QRS complex.

A

Second wave. Begins as downward deflection and continues as a large upright triangular wave, and ends as a downward wave. Represents rapid ventricular depolarization as the AP spreads through ventricular contractile fibres.

70
Q

Large Q-wave may indicate:

A

Myocardial infarction.

71
Q

Large R-wave may indicate:

A

Enlarged ventricles.

72
Q

T-wave.

A

Third wave. Dome-shaped upward deflection. Represents ventricular depolarization. Occurs just as the ventricles start to relax. Smaller and wider than QRS.

73
Q

Flat T-wave may indicate:

A

Heart muscle is receiving insufficient oxygen. CAD.

74
Q

Large T-wave may indicate:

A

Hyperkalemia. High blood K+.

75
Q

ECG is flat during which phase?

A

Plateau.

76
Q

P-Q interval.

A

Time from beginning of P-wave to beginning of QRS complex. Represents the conduction time from the beginning of atrial excitation to the beginning of ventricular excitation. The time required for the AP to travel through the atria –> AV node –> remaining fibres of conduction system.

77
Q

P-Q interval lengthens if:

A

AP is forced to detour around scar tissue.

78
Q

S-T interval.

A

Begins at end of S-wave and ends at beginning of T-wave. Represents time when ventricular contractile fibres are depolarized during plateau phase.

79
Q

S-T interval is elevated in:

A

Acute myocardial infarction.

80
Q

S-T interval is depressed when:

A

Heart muscle receives insufficient oxygen.

81
Q

Q-T interval.

A

Time from start of QRS complex to end of T-wave. Represents time from beginning of ventricular depolarization to end of ventricular repolarization.

82
Q

Q-T interval is elevated in:

A

Myocardial damage, myocardial ischemia, and conduction abnormalities.

83
Q

Systole.

A

Phase of contraction.

84
Q

Diastole.

A

Phase of relaxation.

85
Q

Describe the process of atrial and ventricular systole and diastole.

A

Cardiac AP arises in SA node –> propagates through atrial muscle and down to AV node in 0.03 sec –> atrial contractile fibres depolarize and P-wave appears –> atria contract –> conduction of AP slows at AV node –> 0.1 sec delay –> AP propagates rapidly again after entering AV bundle –> 0.2 sec after P-wave onset, it has propagated through the bundle branches, Purkinje fibres, and entire ventricular myocardium –> depolarization progresses down septum, upward from apex, and outward from endocardial surface to produce QRS complex –> atrial repolarization occurs at same time –> contraction of ventricular contractile fibres begins after QRS complex appears and continues during S-T interval –> blood flows toward semilunar valves –> repolarization of ventricular contractile fibres begins at apex and spreads throughout ventricular myocardium –> produces T-wave 0.4 sec after P-wave onset –> ventricles relax –> ventricular repolarization is complete and ventricular contractile fibres are relaxed by 0.6 sec –> during the next 0.2 sec, contractile fibres in atria and ventricles are relaxed –> at 0.8 sec, P-wave appears again, atria contract and cycle repeats.

86
Q

Atrial systole.

A

0.1 sec. Contraction of atria. Relaxation of ventricles.

87
Q

Ventricular systole.

A

0.3 sec. Contraction of ventricles. Relaxation of atria.

88
Q

Relaxation period.

A

0.4 sec. Relaxation of atria and ventricles. As the heart beats faster, the relaxation period becomes shorter.

89
Q

Isovolumetric contraction.

A

0.05 sec when SL and AV valves are all closed. Cardiac muscle fibres are contracting and exerting force, but are not yet shortening.

90
Q

Isovolumetric relaxation.

A

When SL and AV valves are all closed after ventricular repolarization.

91
Q

Auscultation.

A

The act of listening to sounds within the body with a stethoscope.

92
Q

The sounds of the heartbeat come from:

A

Blood turbulence caused by closing of heart valves.

93
Q

Which two sounds are loud enough to be heard through a stethoscope in a normal heart?

A

S1 and S2.

94
Q

S1.

A

LUBB. Loud. Longer than S2. Caused by blood turbulence associated with closure of AV valves soon after ventricular systole begins.

95
Q

S2.

A

DUPP. Caused by blood turbulence associated with closure of SL valves at beginning of ventricular diastole.

96
Q

S3.

A

Caused by blood turbulence during rapid ventricular filling. Not loud enough to be heard in a normal heart.

97
Q

S4.

A

Caused by blood turbulence during atrial systole. Not loud enough to be heard in a normal heart.

98
Q

Cardiac output.

A

Volume of blood ejected from LV into aorta each minute, or from RV into pulmonary trunk each minute.

99
Q

Cardiac reserve.

A

Difference between a person’s maximum CO and resting CO. The average person has a CR of 4-5x the resting value. Athletes have a CR of 7-8x the resting value. People with severe heart disease usually have a CR of 0x the resting value.

100
Q

At rest, the stroke volume is 50-60% of the end-diastolic-volume because:

A

40-50% of the blood remains in the ventricles after each contraction.

101
Q

Preload.

A

The degree of stretch on the heart before it contracts. A greater preload on cardiac muscle fibres prior to contraction increases their force of contraction. Preload is proportional to EDV.

102
Q

Frank-Starling Law of the Heart.

A

The more the heart fills with blood during diastole, the greater the force of contraction during systole. Equalizes the output of the right and left ventricles. Keeps the same volume of blood flowing to both the systemic and pulmonary circulations.

103
Q

What can determine EDV?

A

The duration of ventricular diastole, and venous return.

104
Q

Stroke volume declines due to short filling time at which heart rate?

A

160 bpm. Low EDV and low preload.

105
Q

Contractility.

A

The forcefulness of contraction of individual ventricular muscle fibres. The strength of contraction at any given preload.

106
Q

What increases contractility?

A

Positive inotropic agents. They promote calcium inflow during cardiac APs which strengthens the force of contraction. Example: stimulation of sympathetic division of ANS, EP, NE, increased calcium in interstitial fluid, digitalis drug.

107
Q

What decreases contractility?

A

Negative inotropic events. They reduce calcium inflow to decrease the strength of the heartbeat. Examples: inhibition of sympathetic division of ANS, anoxia, acidosis, anesthetics, increased K+ in interstitial fluid.

108
Q

Afterload.

A

The pressure that must be exceeded before ejection of blood from ventricles can occur. The pressure that must be overcome before a SL valve can open. Ejection of blood from the heart begins when pressure in the RV exceeds the pressure in the pulmonary trunk, and when the pressure in the LV exceeds the pressure in the aorta.

109
Q

What increases afterload?

A

Hypertension and narrowing of arteries by atherosclerosis.

110
Q

An increase in afterload causes the strove volume to:

A

Decrease so that more blood remains in ventricles at the end of systole.

111
Q

Homeostatic mechanisms maintain adequate cardiac output by increasing:

A

HR and contractility.

112
Q

Autonomic regulation of HR.

A

Originates in the cardiovascular centre in the medulla oblongata, which directs appropriate output by increasing/decreasing the frequency of nerve impulses in sympathetic and parasympathetic branches of ANS. Before physical activity begins, HR may climb because the limbic system sends nerve impulses to cardiovascular centre. As physical activity begins, proprioceptors send nerve impulses at an increased frequency to the cardiovascular centre. Other sensory receptors are chemoreceptors and baroreceptors.

113
Q

Sympathetic regulation of HR.

A

Sympathetic neurons extend from medulla –> thoracic spinal cord –> sympathetic cardiac accelerator nerves –> SA node –> AV node –> myocardium. Release NE, which speeds the rate of spontaneous depolarization, and enhances calcium entry through channels to increase contractility.

114
Q

With maximal sympathetic stimulation, HR can reach:

A

200 bpm in a 20-year-old.

115
Q

Parasympathetic regulation of HR.

A

Parasympathetic nerve impulses reach the heart via the right and left vagus nerves. Vagal axons terminate in SA node, AV node and atrial myocardium. They release ACh, which decreases HR by slowing rate of spontaneous depolarization in autorhythmic fibres. As only a few vagal fibres innervate ventricular muscle, changes in parasympathetic activity have little effect on contractility of ventricles.

116
Q

With maximal parasympathetic stimulation, HR can reach:

A

20-30 bpm, or even stop momentarily.

117
Q

Chemical regulation of HR.

A

Hormones and cations. EP and NE enhance pumping effectiveness, and increase HR and contractility. Thyroid hormones increase contractility and HR. Elevated K+ or Na+ decrease HR and contractility. Elevated interstitial Ca2+ increases HR and strengthens heartbeat.

BIOL*235 Midterm 2 (10 decks)

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